Todo Acido Peracetico

Peracetic Acid (CAS No.
79-21-0) and
its Equilibrium Solutions
JACC No. 40
ISSN -0733-6339-40
Brussels, January 2001
Peracetic Acid (CAS No. 79-21-0) and its Equilibrium Solutions
ECETOC JACC No. 40
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ECETOC JACC No.40

Peracetic Acid (CAS No. 79-21-0)
and its Equilibrium Solutions
CONTENTS
EXECUTIVE SUMMARY 1
THE ECETOC SCHEME FOR THE JOINT ASSESSMENT OF COMMODITY CHEMICALS 2
1. SUMMARY AND CONCLUSIONS 3
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS 7

2.1 Identity 7
2.2 Conversion Factors 8
2.3 EU Classification and Labelling 8
2.4 Commercial Formulations 9
2.4.1 Equilibrium PAA solutions 10
2.4.2 Distilled PAA solutions 10
2.5 Physical and Chemical Properties 10
2.5.1 Equilibrium PAA grades 11
2.5.2 Distilled aqueous PAA grades 14
2.5.3 Flashpoint and autoignition temperature 14
2.6 Stability 15
2.6.1 Stabilisers and impurities 15
2.6.2 Decomposition of PAA in air 15
2.6.3 Decomposition of PAA in aqueous solutions 15
2.7 Chemical Reactivity 16
2.7.1 Compatibility 16
2.7.2 Chemical characteristics 16
2.8 Analytical Methods 16
2.8.1 In aqueous solutions 17
2.8.2 In air 18
3. PRODUCTION, STORAGE, TRANSPORT AND USE 20
3.1 Production 20
3.1.1 Industrial production 20
3.1.2 Generation in situ 20
3.1.3 Quantities used 20
3.2 Compatibility 21
3.2.1 Storage and transportation containers 21
3.2.2 Non-compatible materials 21
3.3 Storage 21
3.4 Transportation 22
3.5 Use 23
4. ENVIRONMENTAL DISTRIBUTION AND TRANSFORMATION 26
4.1 Emissions 26
4.1.1 Natural sources 26
4.1.2 Emissions during production and use 26
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4.2 Environmental Fate and Biotransformation 27

4.2.1 Distribution 27
4.2.2 Atmospheric fate 27
4.2.3 Aquatic fate 27
4.2.4 Terrestrial fate 30
4.2.5 Biodegradation 31
4.2.6 Bioaccumulation 31
4.2.7 Evaluation 32
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE 33
5.1 Environmental Levels 33
5.1.1 Air 33
5.1.2 Water, soil and biota 33
5.2 Human Exposure Levels and Hygiene Standards 33
5.2.1 Non-occupational exposure 33
5.2.2 Simulated occupational exposure studies 34
5.2.3 Occupational exposure 35
5.2.4 Hygiene standards 36
6. EFFECTS ON ORGANISMS IN THE ENVIRONMENT 37
6.1 Micro-Organisms 37
6.2 Aquatic Organisms 37
6.2.1 Algae 40
6.2.2 Invertebrates 41
6.2.3 Fish 43
6.2.4 Birds 44
6.3 Summary and Evaluation 44
7. KINETICS AND METABOLISM 46
7.1 Absorption and Distribution 46
7.2 Evaluation 49
7.3 Metabolism 50
7.3.1 Enzymatic reactions in vitro 50
7.3.2 Non-enzymatic degradation 53
7.4 Elimination 53
7.5 Summary and Conclusions 54
8. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO TEST SYSTEMS 55
8.1 Acute Toxicity 55
8.1.1 Oral 55
8.1.2 Dermal 60
8.1.3 Inhalation 63
8.1.4 Intravenous 67
8.1.5 Summary and evaluation 68
8.2 Skin, Respiratory Tract and Eye Irritation, Sensitisation 68
8.2.1 Skin irritation 68
8.2.2 Eye irritation 71
8.2.3 Respiratory tract irritation 72
8.2.4 Skin sensitisation 73
8.3 Repeated Dose Toxicity 74
8.3.1 Oral 74
8.3.2 Dermal 78
8.3.3 Inhalation 81
8.3.4 Other studies 86
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8.4 Genetic Toxicity 87

8.4.1 Gene mutation in vitro 87
8.4.2 Gene mutation in vivo 91
8.5 Chronic Toxicity and Carcinogenicity 94
8.5.1 Chronic toxicity 94
8.5.2 Carcinogenicity 94
8.5.3 Tumour initiation-promotion 94
8.6 Reproductive Toxicity and Teratogenicity 96
8.6.1 Fertility 96
8.6.2 Developmental toxicity 98
8.6.3 Evaluation 98
8.7 Other Studies 98
8.7.1 Neurotoxicity 99
9. EFFECTS ON HUMANS 101
9.1 Acute and Subchronic Toxicity 101
9.2 Irritation 101
9.2.1 Skin irritation 101
9.2.2 Eye irritation 102
9.2.3 Respiratory irritation 103
9.3 Sensitisation 104
9.4 Evaluation 104
10. FIRST AID AND SAFE HANDLING ADVICE 106
10.1 First Aid 106
10.1.1 Skin and eye injuries 106
10.1.2 Inhalation 106
10.1.3 Ingestion 106
10.2 Safe Handling 106
10.2.1 Handling and safety at work 106
10.2.2 Storage 107
10.3 Management of Spillage and Waste 107
10.3.1 Spills and waste 107
10.3.2 Fire-fighting measures 108
11. BIBLIOGRAPHY 109
11.1 Databases Consulted 109
11.2 References Quoted 109
11.3 References Not Quoted 134
APPENDIX A. SPECIAL ABBREVIATIONS 139
APPENDIX B. CRITERIA FOR RELIABILITY CATEGORIES 140
MEMBERS OF THE TASK FORCE 141
MEMBERS OF THE SCIENTIFIC COMMITTEE 142
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EXECUTIVE SUMMARY
This report has been produced as part of the Joint Assessment of Commodity Chemicals
(JACC) programme. It presents a critical evaluation of the physicochemical, ecotoxicity
and toxicity data of peracetic acid (PAA) solutions. At present no other comprehensive
review is available. A risk assessment, inter alia, will be required under the EU Biocidal
Products Directivea.
Most studies have been performed with different grades of equilibrium PAA solutions,
i.e. formulations containing PAA, acetic acid and hydrogen peroxide dissolved in water
in different concentration ratios. PAA solutions are clear, colourless and acidic liquids
with a pungent vinegar-like odour. Upon dilution with water, their components tend
to re-equilibrate slowly within several days. Solutions with a high (> 15%) PAA content
can produce flammable vapours and exothermic decomposition can occur, liberating
large volumes of oxygen gas. To guard against this, commercial PAA formulations are
stabilised.
If released into the environment PAA will be distributed almost entirely to the aquatic
compartment, where it is degraded by hydrolysis or decomposition. Hydrolysis is faster
at high pH, such as in seawater. Biodegradation is rapid, although limited by the biocidal
effect of PAA at higher concentrations. Bioaccumulation is not expected to occur.
PAA solutions are acutely toxic to aquatic organisms. The toxicity is related to the
PAA content, except for solutions with a relatively high ratio of hydrogen peroxide. In
those cases, the toxicity is attributable to the hydrogen peroxide.
The studies of acute mammalian toxicity do not reveal a clear dose-response that could
be related to the PAA content or concentration alone. A particular problem with the
inhalation studies is the instability of the vapour/aerosol phase. The available repeated-
dose toxicity studies suffer from deficiencies in reporting, inadequate histopathological
examination and limited number of dose levels tested. The presence of infectious disease
in a number of the animal studies obscured and confounded the test findings. It was
thus not possible to derive clear, no-adverse effect levels from the existing studies.
In spite of these limitations, it can be concluded that the main effect of PAA seen in
experimental animals is severe irritation and corrosion of skin, eyes and mucous
membranes. This is consistent with information on human exposure. However, the
limited data available suggest that a systemic effect after repeated exposure to PAA
cannot be completely excluded. The skin sensitisation potential of PAA appears to be
low. The data do not raise immediate concern for mutagenicity, carcinogenicity or toxicity
to reproduction.
a European Parliament and Council Directive 98/8/EC concerning the placing of biocidal products
on the market (EU, 1998)
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THE ECETOC SCHEME FOR THE JOINT ASSESSMENT OF COMMODITY

CHEMICALS
This report has been produced by an ECETOC Task Force as part of the Joint Assessment
of Commodity Chemicals (JACC) programme for preparing critical reviews of the
toxicology and ecotoxicology of selected existing industrial chemicals. In the programme,
commodity chemicals (i.e. those produced in large tonnage by several companies and
having widespread and multiple uses) are jointly reviewed by experts from a number
of companies with knowledge of the chemical. It should be noted that in a JACC review
only the chemical itself is considered; products in which it appears as an impurity are
not normally taken into account.
This report presents a critical evaluation of the ecotoxicology, toxicology and

physicochemical properties of peracetic acid (PAA, CAS No. 79-21-0) and its equilibrium
solutions. Commercial grades (formulations) of equilibrium PAA contain the main
components PAA, hydrogen peroxide (H2O2) and acetic acid (HOAc) dissolved in water
at a number of different concentration ratios. A distilled (non-equilibrium) solution
containing PAA and water is also marketed. These PAA solutions are reviewed here
together because they contain PAA and have similar physicochemical properties,
environmental and (eco)toxicity profiles and use patterns.
In this report, for each study, the composition of the solution (formulated product) tested
has been specified as far as possible in terms of its content of PAA, H2O2 and HOAc.
In addition, for each of the toxicological and ecotoxicological studies the actual dose
or concentration of the main component PAA is given.
Where relevant, the Task Force has assigned a Code of Reliability (CoR) a to
(eco)toxicological studies to reflect the degree of confidence that can be placed on the
reported results. The criteria used to assess and categorise reliability are included in
Appendix B.
a A list of special abbreviations used throughout this report is at Appendix A
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1. SUMMARY AND CONCLUSIONS
This report reviews the available physicochemical, ecotoxicity and toxicity data on
different peracetic acid (PAA) solutions. PAA is completely soluble in water and solutions
are clear and colourless with a pungent vinegar-like odour. PAA solutions are acidic
(pH < 1).
PAA is produced commercially as a solution in which PAA is in equilibrium with

hydrogen peroxide (H2O2), acetic acid (HOAc) and water, or as a distilled (non-
equilibrium) solution containing primarily PAA and water. Equilibrium solutions are
generally prepared by reacting glacial HOAc with H2O2 in the presence of a catalyst
such as mineral acid. Specific grades are formulated by controlling the concentration
and amount of H2O2 and HOAc used during the manufacturing process. Commercial
PAA grades (formulations) are available in PAA concentrations ranging from about 0.3%
to 40% by weight.
The production of non-equilibrium solutions involves the vacuum distillation of PAA

from a mixture containing HOAc, H2O2, a catalyst (e.g. mineral acid) and de-ionised
water. Final formulations contain only minor amounts of HOAc and H2O2. Distilled
PAA solutions are produced on site or shipped, normally in concentrations ranging from
25 to 40%. These grades are usually shipped cooled (< 0°C) to slow down the hydrolysis
reaction.
Major uses of PAA are in chemical synthesis, disinfection and bleaching. PAA is also
generated in situ from laundry detergents containing sodium perborate or sodium
percarbonate and tetra-acetyl ethylenediamine (TAED).
Emissions of PAA to the environment through production and use are considered
negligible due to the processes applied. However, the current emission situation is
not well described.
Possible routes of human exposure to PAA are by inhalation of vapours or aerosols

during production and use as well as dermal contact, mostly to diluted solutions. The
available data on workplace exposure are limited. This may be due partly to difficulties
in the analytical determination of PAA in air samples and to the instability of PAA in
air.
The decomposition of PAA is strongly exothermic, liberating large volumes of oxygen

gas. Decomposition can be initiated by high temperatures, high pH, and contamination
with metal catalysts such as copper, iron, chromium, and incompatible organic materials.
To prevent decomposition, commercially available equilibrium and distilled formulations
contain low concentrations of proprietary stabilisers, which protect against decomposition
induced by metal ions and minor contamination.
Most of the equilibrium grades containing less than 15% PAA exhibit closed-cup flash
points, but no open-cup flash point. Thus, these grades are not flammable where the
liquid is open to the atmosphere. Grades containing greater than 15% PAA exhibit both
open and closed-cup flash points and the vapours can be flammable.
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Volatilisation from aqueous solutions is relatively low, but dependent on the partial
vapour pressure. When PAA formulations are diluted with water, the solution slowly
begins to re-equilibrate in a temperature dependent reaction until a final equilibrium is
attained. At ambient temperature re-equilibration usually takes several days.
Mackay level 1 calculations suggest that, once released into the environment, PAA is
expected to partition mainly ( > 99%) to the aquatic compartment, while a minor part
(< 1%) will be distributed into the atmosphere. No partitioning of PAA into soil,
suspended matter or biota is expected. Based on its chemical reactivity and short half-
life, PAA is not expected to persist in the atmosphere. Airborne PAA vapours have a low
stability, with a half-life of about 20 minutes at ambient temperature. When entering the
aquatic environment, PAA is subject to a concentration-, pH- and temperature-dependent
hydrolysis or decomposition; the half-life is lower as pH increases. At acidic pH, the
half-life of PAA will be around 7 to 12 days, while at neutral or alkaline pH, half-lives
may be 1 day or less. In seawater degradation is expected to be rapid (half-life < 1 h). In
soil a diluted PAA solution will be rapidly degraded by hydrolysis and decomposition
evoked by transition metals. At low PAA concentrations, biodegradation could contribute
to degradation in soil and surface waters. In sewage treatment plants with adapted
activated sludge PAA is rapidly biodegraded. The low octanol-water partition coefficient
of PAA (log Pow = -0.52) suggests that PAA has no potential to bioaccumulate.
Several studies on acute toxicity to aquatic species are available for all trophic levels.
PAA formulations were toxic to algae. The lowest 120-h no-observed-effect concentration
(NOEC) of 0.13 mg PAA/l was found for Selenastrum capricornutum, with an EC50 (median
concentration expected to have an effect in 50% of the test organisms) value of 0.18 mg/l
for growth inhibition. PAA was also toxic to Daphnia magna with 48-h EC50 values of 0.5
to 1.0 mg PAA/l. Toxicity to fish was lower and 96-h LC50 (median concentration expected
to cause the death of 50% of the test organisms) values ranged from 0.9 to 3.3 mg PAA/l
in most freshwater species. In general, the aquatic toxicity tests were reproducible if
concentrations were expressed as PAA irrespective of the concentrations of H2O2 and
HOAc. Thus, the PAA concentration alone may explain the toxicity of PAA formulations.
However, when PAA concentrations are low compared to H2O2 concentrations, H2O2
apparently contributes to the toxic effects, in particular for algae and daphnids. In these
cases, the effect concentrations of PAA formulations are close to those of H2O2 alone.
For fish there was not always evidence of an additional toxic effect of H2O2. The results
of the aquatic toxicity studies also suggest a relationship between the size of the organisms
and their sensitivity. Small test organisms were more sensitive than larger organisms,
probably because of their high body surface-weight ratio, which enables a relatively
high uptake of the test substance (per gram body weight). This phenomenon can be
related to the relatively non-specific mode of action of the compound, i.e. its oxidising
properties, which is relevant to all organisms.
Only few data on the toxicokinetic properties of PAA in mammals are available. Due to
the high water solubility and low octanol-water partition coefficients, absorption into
the circulation would be expected to be limited. However, PAA seems to be rapidly
absorbed through damaged skin when the skin barriers are destroyed due to the
corrosivity of PAA solutions.
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Distribution is only likely in body fluids and limited by the degradation of PAA. PAA
may be degraded in the organism either non-enzymatically, by hydrolysis, dismutation
or reaction with reducing agents such as cysteine and glutathione (GSH), or enzymatically
by catalases or peroxidases. The catalase reaction with PAA is independent of the PAA
concentration and may therefore be saturated. H2O2 is also degraded by peroxidases,
catalases and a number of antioxidants and thus the equilibrium between PAA, H2O2
and HOAc will also be influenced by the continuous elimination of H 2O2 from the
equilibrium under physiological conditions.
PAA possesses a moderate acute toxicity via the oral route. The acute oral toxicity of
PAA solutions is dependent on the composition (i.e. the relative content of PAA, H2O2
and HOAc) and concentration of the applied (diluted) test solution. Usually PAA solutions
containing less than 10% of PAA are of low oral toxicity. The acute dermal toxicity of
PAA solutions in rabbits is relatively low and depends upon the applied concentration
and presence of local irritations. The available acute inhalation toxicity studies in rats
and mice with aerosols and vapours derived from different PAA solutions suffer from
difficulties in achieving and measuring constant PAA concentrations due to the instability
of the substance itself and the aerosol droplets. Consequently, the LC50 values show a
relatively wide variation, the main effect being local irritation of the respiratory tract.
The predominant effect in all acute toxicity studies is local irritation at the site of contact,
which strongly depends on the applied concentration.
PAA solutions containing > 10% PAA were severely corrosive to rabbit skin already
3 minutes after application. Formulations containing between 3.4 and 5% PAA were
corrosive to rabbit skin after occluded exposure for 4 or 24 hours. Dilutions containing
0.034 to 0.35% PAA were reported to be not irritant or slightly irritant. PAA solutions
are corrosive or severely irritant to the rabbit eye at concentrations of 0.2% and higher.
A study of sensory irritation in rats revealed an RD50 (concentration inducing a 50%
reduction of respiratory rate) value of 21.5 to 24.1 mg PAA/m3.
No evidence for skin sensitisation was observed in two Bühler tests in guinea pigs with
different solutions of PAA. In one guinea pig maximisation test a positive result was
claimed, but the report does not allow a critical evaluation of the results. Despite the
use of PAA in hand and surface disinfection no cases of skin sensitisation have been
reported in humans. Taken together, there seems to be no indication for a skin sensitisation
potential of PAA solutions in humans.
The available repeated dose toxicity studies in experimental animals suffer from
deficiencies in reporting, including uncertainties about the composition, concentration
and stability of the test substance, inadequate histopathological examination and limited
number of dose levels tested. In a number of studies the test animals suffered from
infectious diseases and it remains unclear to what extent the reported effects are the
result of administration of PAA. It is not possible to derive clear, no-adverse effect levels
from the existing studies. In spite of these limitations, the following conclusions may
be drawn.
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The predominant effects after repeated oral, dermal or inhalation exposure of

experimental animals to PAA appear to be related to local irritation at the site of contact.
The toxicokinetic data suggest that PAA might become available systemically when the
detoxifying enzyme systems are saturated. The detoxification reaction could then be
slower than the speed of distribution to organs, such as liver and kidney.
Limited information is available on the effects of PAA on deoxyribonucleic acid (DNA)

and its potential to induce gene and chromosome mutations in vitro or in vivo. Bacterial
tests showed predominately negative results. These tests are of limited value because
PAA is a biocide and will exert cytotoxicity at low doses. In most cases, cytotoxicity
could be diminished by the addition of an exogenous metabolic system. Two DNA repair
tests in human foetal lung cells did not indicate a genotoxic potential of PAA. In the in
vitro chromosome aberration test, positive findings were obtained only at cytotoxic
concentrations. Under in vivo conditions, PAA did not produce micronuclei in two mouse
micronucleus tests after oral administration. In one study, the authors claimed to have
observed positive effects in a series of chromosomal aberration tests with single
intraperitoneal and dermal administration. The validity of this test is however highly
questionable due to serious deficiencies in the experimental procedure and reporting.
In an in vivo / ex vivo assay of unscheduled DNA synthesis (UDS) in rats after oral
administration, PAA did not show a genotoxic potential. Overall these data do not raise
immediate concern with regard to the mutagenic potential of PAA.
No specific data are available on the carcinogenicity or chronic toxicity of PAA. A limited
initiation-promotion study on mouse skin indicates that PAA might have a tumour-
promoting potential, which is not unusual for a corrosive substance.
Limited data are available on reproductive toxicity of PAA in experimental animals.

Summary publications on multiple-generation studies indicate no effect on reproduction
and development, offering some reassurance for this endpoint.
Human experience with PAA is limited to reported effects seen after acute inhalation
and dermal exposure. Vapour concentrations below 0.5 mg PAA/m3 (0.16 ppm) seem
to be well tolerated. Concentrations up to 1.2 mg/m3 (0.38 ppm) were not immediately
irritant but unpleasant after exposure for an extended time period. Human eye irritation
seems to be the most pronounced effect after exposure to PAA vapours or aerosols.
Washing hands with a 0.2% PAA solution was without effect; higher concentrations of
0.5% PAA caused skin irritation when used as a wash solution.
In conclusion, the main effect of PAA reported in mammalian toxicology studies was
severe irritation and corrosion of skin, eyes and mucous membranes. This is consistent
with reports of effects of human exposure. The skin sensitisation potential of PAA appears
to be low. The limited data available from the experimental studies suggest that a systemic
effect following repeated exposure to PAA cannot be completely excluded. The available
data do not indicate an immediate concern for mutagenicity, carcinogenicity or toxicity
to reproduction.
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2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL

METHODS
2.1 Identity
Name: Peracetic acid
IUPAC Name: Peroxyethanoic acid
Synonyms: Acetyl hydroperoxide

Ethaneperoxoic acid
Peroxyacetic acid
Danish: Pereddigesyre
Dutch: Perazijnzuur
Finnish: Peretikkahappo
French: Acide peracétique
German: Peressigsäure
Greek: Υπεροξικó οξú
Italian: Acido peracetico

Acetil-idroperossido
Norwegian: Perettikusyre
Portuguese Acido peracetico
Spanish: Acido peracético
Swedish: Perättiksyra
CAS Name: Ethaneperoxoic acid
CAS Registry No. 79-21-0
Formula: C2H4O3
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Structural formula:
Molecular Weight: 76.05
2.2 Conversion Factors

Conversion factors for concentrations of PAA in air at standard conditions (20°C and
1,013 hPa) are:
• 1 ppm = 3.162 mg/m3

• 1 mg/m3 = 0.316 ppm
In this report, converted values are given in parentheses.
2.3 EU Classification and Labelling

The following EU classification and labelling applies to pure PAA according to Directive
98/98/EEC, effective from 1 July 2000 (EC, 1998).
EC (EINECS) No. 201-186-8
Index No. 607-094-00-8
EEC classification: R 10, flammable
O, oxidising; R 7, may cause fire

Xn, harmful; R 20/21/22, harmful by inhalation /
in contact with skin / if swallowed
C, corrosive; R 35, causes severe burns
N, dangerous to the environment; R 50, very toxic
to aquatic organisms
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EEC labelling: Symbols: O, Oxidising

C, Corrosive
N, Dangerous to the environment
R-phrases: R 10, flammable

R 7, may cause fire
R 20/21/22, harmful by inhalation / in contact
with skin / if swallowed
R 35, causes severe burns
R 50, very toxic to aquatic organisms
S-phrases: S 1/2, keep locked up / keep out of the reach of

children
S 3/7, keep in a cool place / keep container tightly closed
S 14, keep away from ... (incompatible materials to be
specified by the manufacturer)
S 36/37/39, wear suitable protective clothing, gloves and
eye/face protection
S 45, In case of accident or if you feel unwell, seek medical
advice immediately (show the label where possible)
S 61, Avoid release to the environment. Refer to special
instructions/Safety data sheets
Preparations must be classified in accordance with Directive 1999/45/EC (EU, 1999).

Specific concentration limits for health hazards of PAA in preparations are specified
in Directive 98/98/EEC above.
Concentration ≥ 10% C, corrosive; R20/21/22, harmful by inhalation / in

contact with skin / if swallowed; R35, causes severe burns
5 ≤ Concentration < 10% C, corrosive; R34, causes burns
1 ≤ Concentration < 5% Xi, irritant; R 36/37/38, irritant to eyes / respiratory

system / skin
For the classification of equilibrium PAA solutions, the concentrations of hydrogen

peroxide (H2O2) and acetic acid (HOAc) have to be considered as well following the
same rules of the preparations Directive 1999/45/EEC.
2.4 Commercial Formulations

Peracetic acid (PAA) is produced commercially either as an equilibrium solution in
which PAA is in equilibrium with H2O2, HOAc and water (Swern, 1970) or as a distilled
product containing primarily PAA and water (Dalin, 1996; Jäkärä et al, 1998).
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2.4.1 Equilibrium PAA solutions
Equilibrium PAA solutions are generally prepared by reacting glacial HOAc with H2O2
in the presence of a catalyst such as a mineral acid. The equilibrium reaction is shown
in the following equation:
Specific grades are obtained by controlling the concentration and amount of H2O2
and HOAc used during the manufacturing process. Adding an acid such as sulphuric
acid or increasing the temperature during the manufacturing process can accelerate the
establishment of the final equilibrium concentration (grade). The final solution contains
PAA in equilibrium with H2O2, HOAc and water. Commercial PAA grades are available
in PAA concentrations ranging from about 0.3% to 40% by weight. For a given PAA
formulation, the equilibrium concentration is temperature dependent, so that a decrease
of temperature will increase the PAA content. The equilibrium aspects are further
discussed in Section 2.5.
2.4.2 Distilled PAA solutions
The production of distilled solutions involves vacuum distillation of PAA from a mixture
containing HOAc, H2O2, a catalyst (e.g., mineral acid) and de-ionised water. Final
formulations contain only minor amounts of HOAc and H2O2. Distilled solutions of
PAA in water are produced on site or shipped in concentrations normally ranging from
25 to 40%. These grades are usually shipped cooled (< 0°C) to slow down the hydrolysis
reaction, which in effect slows down the formation of HOAc and H2O2.
2.5 Physical and Chemical Poperties

All PAA solutions are clear, colourless liquids with a pungent vinegar-like odour and
are soluble in polar solvents, aromatics and acetates (Swern, 1970). Physical and chemical
properties characteristic of the component PAA are shown in Table 1.
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Table 1: Physical and Chemical Properties of PAA
Property Value, unit Reference

pH <1 Safety data sheetsa
Solubility in water at 20°C 1,000 g/kgb Swern, 1970; Safety data sheetsa
pKa at 20°C 8.2 Swern, 1970
Partition coefficient, log Kow - 0.52c Byers, 1998
(octanol/water) at 25°C - 1.25d Thus, 1994
Odour threshold 50 ppb Ancker and Zetterberg, 1997
Henry's law constant at 25°C 0.22 Pa·m3/mole Lind and Kok, 1986
a Ausimont, 1997a,b; Bactria, 1995, 1997; Bioxal, 2000a,b; Chemoxal, 1997; Degussa, 1996a,b, 1997;
FMC, 1998a,b,c; Henkel, 1995, 1997a,b; Solvay, 1997a,b,c,d
b Reported as 100%
c Measured, reported as Kow = 0.30
d Calculated
e Measured, reported as 467.6 mol/l·atm
Other physical and chemical properties are specific to the concentration ratio of the
individual components in the formulation.
2.5.1 Equilibrium PAA grades
Equilibrium grades of PAA are produced in various concentrations ranging from about
0.3% to 40%. Many of the chemical and physical properties are specific to the
concentrations (ratios) of each component, i.e. PAA, H2O2, HOAc and water, in the
different grades. Generally, most commercial 5% to 35% equilibrium grades from different
producers have similar compositions and physico-chemical properties. Table 2 shows
chemical and physical properties specific for equilibrium grades of 5%, 15% and 35%
PAA. Producers' material safety data sheets should be consulted for data pertaining
to their commercial grades.
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Table 2: Physical and Chemical Properties of Three Equilibrium Grades of PAA
Property Value, unit Reference

5% 15% 35%
Ratio components PAA: H2O2:HOAc:H2O 5 : 22 : 10 : 63%a 15 : 20 : 15 : 50%a 35 : 7 : 40 : 18%a Safety data sheetsb, c, d
Melting point -26 to -30°Ce -30 to -50°Ce -44°Ce Safety data sheetsb, c, d
Boiling point 99 to 105°C > 100°C > 105°C Safety data sheetsb, c, d
Relative density D420 at 20°C (density of 1,120 kg/m3 1,150 kg/m3 1,130 kg/m3 Safety data sheetsb, c, d
water at 4°C is 1,000 kg/m3)
Vapour Pressure at 20°C 21 to 27 hPa 25 hPa 17 hPa Safety data sheetsb, c, d
Partial pressure at 20°C PAA 0.3 hPa (4%) 1.1 hPa (14%) 2.7 hPa (32%) Caropreso, 2000
(vapour phase concentrations) H2O2 0.4 hPa (2%) 0.5 hPa (3%) 0.2 hPa (1%)
HOAc 0.8 hPa (9%) 1.6 hPa (16%) 4.1 hPa (38%)
H2O 25.0 hPa (85%) 21.8 hPa (67%) 10.1 hPa (28%)
Flash point, open cup No data > 100°C No data Safety data sheetsb, c, d
closed cup 74 to 83°C 68 to 81°C 46 to 62°C
Auto ignition temperature 270 to 430°C ≈ 265°C ≈ 218°C Safety data sheetsb, c, d
SADTf (55 US gallonsg drum) > 55 to > 65°C > 50°C > 55°C Safety data sheetsb, c, d
Sustained flammability No No Yes, flammable FMC, 1998a, b, c
a Each producer will have specified concentrations

b 5% PAA grade: Bactria, 1995; Henkel, 1995; Ausimont, 1997a; Degussa, 1997; Solvay, 1997a,b ; FMC, 1998a; Bioxal, 2000a
c 15% PAA grade: Henkel, 1995; Degussa, 1996a; Ausimont, 1997b; Bactria, 1997; Chemoxal, 1997, 1999; Solvay, 1997c,d; FMC, 1998b; Bioxal, 2000b
d 35% PAA grade: Degussa, 1996b; Henkel, 1997b; Akzo Nobel, 1998; FMC, 1998c.
e Decomposes
f Self-accelerating decomposition temperature
g One US gallon = 3.758 l
However, there are formulations on the market which have the same PAA concentration
but different concentrations of HOAc and H2O2, so that the physico-chemical properties
may be completely different. The equilibrium equation (Eq. 1, Section 2.4) shows that
by changing the concentration of one component in a PAA formulation, the concentration
of the other components will also change to re-establish the equilibrium (Section 2.4.1).
Examples of formulations with the same PAA concentrations but with different
concentrations of the other components are given in Tables 3 and 4.
Table 3: Composition of Two Commercial PAA 10% Formulations (Steiner, 2000)
PAA (%) H2O2 (%) HOAc (%) H2O (%)

Formulation 1 10 1 78 11
According to the UN classification system for transport of dangerous goods (UN, 1995),
formulation 2 in Table 3 is an organic peroxide type F, while formulation 1 is an organic
peroxide type D that is also flammable because of the high HOAc content. The UN
system is explained in Section 3.4.
Table 4: Composition of Two Commercial PAA 15% Formulations (Block, 1991)
PAA (%) H2O2 (%) HOAc (%) H2O (%)

Although the composition of these two 15% PAA grades is different, the formulations
exhibit similar physical properties and both are classified as organic peroxide type F.
As soon as water is added, the solution slowly begins to re-equilibrate until a new final
equilibrium composition is attained. Usually, re-equilibration takes several days. If
the diluted solution is not going to be used within a few days, the amount of water
needed to halve the concentration of PAA will be different from that calculated by simple
material balance. Cooling to about 20°C can decrease the rate at which equilibrium is
established. Conversely, increasing the temperature can increase the rate. As can be seen
in Table 5, the PAA concentration of a 1:1 dilution mixture of a commercial 15% PAA
acid formulation with water dropped from 7.3% to 2.8% after 12 days storage at 20°C.
The active oxygen concentration remained constant, i.e. no decomposition occurred.
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Table 5: Re-equilibrium of PAA 15%a after Dilution with Deionised Water at 20°C
(Reinold, 2000)
Dilution: 1:1 1:2 1:3

Time after dilution PAA concentration (%)
1 min 7.3 4.9 3.7
12 d 2.8 1.2 0.8
a Measured composition of test solution: 14.7% PAA and 21.9% H2O2
2.5.2 Distilled aqueous PAA grades
Table 6 shows chemical and physical properties for a 38% distilled aqueous grade of
PAA. Producers' material safety data sheets should be consulted for data specific to their
commercial grades.
Table 6: Physical and Chemical Properties of Distilled PAA (38%) (Akzo Nobel, 1998)
Property Value, unit

Ratio Components PAA: H2O2 :HOAc 38 : < 1 : < 3%
pH ≈2
Melting point ≈ -12°C
Boiling point 105 - 110°Ca
Relative density at 20°C 1,070 kg/m3
Vapour pressure at 20oC No data
Flash point open cup No data
closed cup ≈ 65 to 70°C
Auto ignition No data
SADT (55 gal drum) No data
Sustained flammability Not flammable
a Decomposes
2.5.3 Flashpoint and autoignition temperature
A comparison of producers’ safety data sheets shows considerable scatter in measured

flashpoints (Table 2). This scatter may be attributed to several factors e.g., PAA reacting
with the sample container used in the flash point determination, thermal instability of
the PAA solutions, loss of volatile material during analysis due to decomposition and
excessive gassing, releasing oxygen and water which tend to extinguish any flame. While
the reported flash point value may not be exact, it is an indication of the temperature at
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which vapours can ignite. Most of the PAA equilibrium grades ranging from 5% to 15%
exhibit closed-cup flash points but no measurable open-cup flash points. Thus, these
grades are not flammable under conditions where the liquid is open to the atmosphere.
However, a sustained flame is possible in a closed system. Decomposition of PAA
produces oxygen. A closed system prevents the release of the oxygen, which in the
presence of the organic (acetic acid) can sustain a flame. Thus, all the gases produced
remain in the system and they can burn. Equilibrium grades of concentrations ≥ 30%
PAA or higher exhibit both open and closed-cup flash points and are flammable.
Equilibrium PAA grades exhibit autoignition temperatures ranging from 218 to 430°C
(Table 2).
2.6 Stability
The decomposition of PAA is strongly exothermic, liberating large volumes of oxygen
gas. Decomposition can be initiated by high temperatures, high pH, and contamination
with metal catalysts such as copper, iron and chromium, and incompatible organic
materials.
2.6.1 Stabilisers and impurities
To prevent decomposition, commercially available equilibrium and aqueous formulations

contain low concentrations of proprietary stabilisers, which protect against decomposition
induced by metal ions and minor contamination. The concentration of impurities in
commercially available PAA solutions is generally low. Common stabilisers include
dipicolinic acid and phosphonates.
2.6.2 Decomposition of PAA in air
PAA vapour in air is found to have limited stability. For example, measurements taken
at ambient temperature showed a decrease in concentration from 1 ppm (3.16 mg/m3)
to 0.5 ppm (1.58 mg/m3) in 22 minutes (Ancker and Zetterberg, 1997).
2.6.3 Decomposition of PAA in aqueous solutions
Yuan et al (1977a,b) reported that decomposition of PAA solutions can involve three
competitive reactions:
Spontaneous 2 CH3C(O)OOH 2 CH3C(O)OH + O2 (Eq. 2)
Metal [M] catalysed 2CH3C(O)OOH + [M] 2CH3C(O)OH + O2 + [M] (Eq. 3)
Hydrolysis CH3C(O)OOH + H2O CH3C(O)OH + H2O2 (Eq. 4)
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Increasing temperature or pH will result in accelerated decomposition (Mücke, 1977;

Yuan et al, 1977a). For example, Mücke (1977) showed that in the absence of heavy metal
ions, dilute PAA solutions undergo hydrolytic decomposition (Eq. 4) in a manner that
is the reverse of the formation reaction, to form HOAc and H2O2. The rate of hydrolysis
increases with increasing temperature and pH.
Drimus and Matasa (1966) studied the thermal decomposition of PAA solutions. Analysis
of the gas evolved during decomposition suggested that the decomposition process
consisted of several distinct reactions, such as:
2 CH3C(O)OOH 2 CH3C(O)OH + O2 (Eq. 2)
CH3C(O)OOH CH3OH + CO2 (Eq. 5)
2.7 Chemical Reactivity
2.7.1 Compatibility
Good stability has been achieved in the presence of certain surfactants, mineral acids,
thickening agents and perfumes (James and Shehad, 1995). However, it is important
that all materials are tested for compatibility and stability in the presence of the specific
PAA solution before being added to the formulation. Incompatible materials could cause
the PAA solutions to decompose rapidly with the evolution of large quantities of oxygen
and other vapours.
2.7.2 Chemical characteristics
PAA is a strong oxidising agent. For that property, it is used commercially in a variety
of applications (Section 3.5).
2.8 Analytical Methods

An EU Project with the objective to develop methods for the quantitative determination
of PAA in air and aqueous solutions will be finalised by the end of year 2000 and public
reports will follow (Euperox, 1997). Several publications mentioned in this section
originate from this project. One of these (Effkemann et al, 1999b) includes useful
recommendations on choice of analytical methods for different purposes, as explained
below.
Concerning animal experiments and other studies in air or in water, one has to consider
that if the (diluted) PAA formulation used contains H2O2 it is necessary to record both
compounds using a method that fits from the viewpoint of sensitivity and accuracy.
Even when a H2O2-free PAA formulations is used, it might be necessary to record the
levels of both compounds since H2O2 may be formed as a hydrolysis product of PAA.
Due to the instability of PAA (and H2O2) in vapours and also in water, it is important
to record continuously or regularly the concentrations of the components.
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2.8.1 In aqueous solutions
Table 7 gives a summary of analytical methods for concentrated and diluted PAA
solutions.
Table 7: Analysis of PAA in Aqueous Solutions
Analytical technique Range Detection limit Reference

(mg PAA/l) (mg PAA/l)
Concentrated (and diluted) products
Titration with cerium sulphate 10 - 50,000 10 Greenspan and MacKellar, 1948
(for H2O2) followed by iodometric
titration (for PAA)
Titration at 0ºC with KMnO4 in 10 - 50,000 10 Senf, 1984
presence of NaF (for H2O2) followed by
iodometric titration (for PAA)
Dilute solutions
Colorimetric oxidation of DPDa 5 - 50 5 Merck, 1995, 1998
reagent (Merckoquant test strips)
Colorimetric oxidation of 1 - 100 1 Fischer et al, 1989;
tetra-methylbenzidine in buffered Merck, 1994
potassium iodide (RQflexb photometer
with Reflectoquant test strips)
Successive reaction of PAA with MTSc 0.1 - several 0.1 Pinkernell et al, 1994, 1997a
and of H2O2 with triphenylphosphine, 1,000
HPLCd analysis
Selective oxidation of enzyme substrate Not stated 0.1 Pinkernell et al, 1997b
ABTSe, HPLC analysis
Oxidation of ADSf. HPLC , 0.007 - 0.7 0.002 Effkemann and Karst, 1998
detection at 410 nm
HPLC with electrochemical detection 10 - 200 or 10 Pinkowski, 1995; Prominent, 1997
on line (Prominent Perox Controller) 100 - 2,000
HPLC with electrochemical detection Not stated 0.1 Kirk et al, 1992;
Qi and Baldwin, 1993
a N,N'-diethyl-p-phenylenediamine
b Reflectometer Quality flexible (strips)
c Methyl p-tolyl sulphide
d High performance liquid chromatography
e 2,2´-Azino-bis-(3-ethyl-benzo-thiazoline)-6-sulphonate
f 2-((-3(2-(4-Amino-2-(methylsulphanyl)phenyl)-1-diazenyl)phenyl)sulphonyl)-1-ethanol
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The generally accepted method, suitable for concentrated solutions (10 - 500,000 mg
PAA/l), starts with the determination of the concentration of H2O2 by cerium sulphate
titration. The PAA content is then measured by iodometric titration with sodium
thiosulphate. This procedure is carried out at low temperature (< 0°C) to prevent re-
equilibration (Greenspan and MacKellar, 1948). An alternative method is to determine
the H2O2 content by titration with potassium permanganate (KMnO4) at 0° C, and then
determine the PAA content with iodometric titration as described above (D'Ans, 1912
as quoted in Swern, 1970; Senf, 1984). The cerium-based method is regarded as more
accurate and less dependent on operator skill compared to the KMnO4/iodometric
method.
The method according to Pinkernell (1994, 1997a) is suitable for the analysis of PAA +
H2O2 in dilute solutions but too cumbersome for determination of PAA alone. The Merck
RQflex-Reflectoquant test is considered more selective than the DPD method, which
cannot be used in the presence of active chlorine compounds. The electrochemical method
of Prominent (1997) is easy to use (e.g. calibration) and useful, amongst others, for on-
line control of disinfectant solutions in the food industry.
2.8.2 In air
Table 8 summarises analytical methods for the determination of PAA in air. All of these
methods are selective for PAA, rather than determining total PAA + H2O2 concentrations.
An overview of nine existing gas monitoring methods for PAA has been made, including
applicability of the methods and costs (Solvay, 1999). Five of these are included in Table 8.
Table 8: Analytical Methods in Air
Analytical technique Detection limit Air sample Reference

(mg PAA/m3) volume (l)
Iodide catalysed oxidation of ABTSa in 0.35 3-5 Effkemann et al, 2000

coated test tubes or impingers
Oxidation of ADSb on coated test tubes 0.13 5 Effkemann et al, 1999a

or impingers. HPLCc, detection at 410 nm
Oxidation of MTSd, HPLC, UV detection 0.035e NS Thus et al, 1996
Impinger. Amine colour reaction 0.5 20 Fischer et al, 1989,

(Merck PAA test 15975) Solvay 1999
Direct measurement in vapour phase with 0.15 1,000g Ancker and Zetterberg, 1997
FTIRf and Michelson interferometer
Photo-acoustic FTIR 0.09h NS Solvay, 1999
NS Not Stated
a 2,2´-Azino-bis-(3-ethyl-benzo-thiazoline)-6-sulphonate
b 2-((-3(2-(4-Amino-2-(methylsulphanyl)phenyl)-1-diazenyl)phenyl)sulphonyl)-1-ethanol
c High performance liquid chromatography
d Methyl p-tolyl sulphide
e H2O2 0.16 mg/m3
f Fourier transform infrared (spectroscopy)
g Range 0.15 - 100 mg PAA/m3 or higher
h H2O2 0.1 mg/m3
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For ambient workplace air and personal measurements at the workplace, the method
by Thus et al (1996) provides high sensitivity for both PAA and H2O2 without interference
between PAA and H2O2. Another sensitive and portable technique is the photo-acoustic
Fourier transform infrared (FTIR) spectroscopy technique of Solvay (1999). Among
the two methods developed by Effkemann et al (1999a, 2000), the ABTS test tube method
is recommended for screening purposes. The ABTS impinger method and also the ADS
impinger or test tube methods are more selective and accurate. The direct FTIR
spectroscopic method according to Ancker and Zetterberg (1997) is suitable for personal
and area measurements at the workplace, indoors and outdoors.
There are few methods available which are sensitive enough for atmospheric PAA
measurements. An enzyme fluorometric method developed mainly for H2O2 (Lazrus
et al, 1986) might be further developed for such a purpose.
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3. PRODUCTION, STORAGE, TRANSPORT AND USE
3.1 Production
3.1.1 Industrial production
In general, peroxycarboxylic acids can be made by numerous methods generally involving

the reaction of H2O2 with the corresponding carboxylic acid or carboxylic acid derivatives
(Klenk et al, 1991; Swern, 1970).
Peroxyacetic acid (PAA) solutions are produced by three industrial methods. Equilibrium
mixtures of PAA are obtained by reacting HOAc, H2O2 in the presence of an acid catalyst,
normally sulphuric acid. Equilibrium PAA grades of this type are commercially available
with a PAA content of up to 40%.
Optionally, PAA can be distilled from equilibrium mixtures of HOAc and H2O2 to yield
an aqueous PAA solution with low residual H2O2 and HOAc. Commercially, distilled
PAA is available with a content of 25-40% PAA.
Alternatively, PAA is produced by the oxidation of acetaldehyde in the presence of a

solvent, e.g. ethylacetate, yielding a product with approximately 25% PAA content
(Swern, 1970).
Accurate data on the quantities of PAA produced in Europe or USA are not available.
CEFIC (2000a) estimated a figure of > 32,430 tonnes for western Europe.
3.1.2 Generation in situ
PAA acts as a low temperature bleaching agent and is generated in situ during the
washing process from sodium perborate / percarbonate and TAED (Jakobi and Löhr,
1991). In Europe, powder detergents with bleach typically contain 15-25% persalt and
up to 5% TAED corresponding to approximately 3.5% PAA equivalent (100%) (Jakobi
and Löhr, 1991).
Minor quantities of PAA precursors such as TAED, acetyl salicylic acid or HOAc
anhydride are used for generation in situ of PAA in the sterilisation of medical instruments
and in the textile industry (Wurster, 1992).
In 1999, approximately 48,500 tonnes of TAED (corresponding to 32,300 tonnes PAA

(100%) generated in situ) were employed in European detergents (Battelle, 1999). AISE
(2000) estimated that approximately 60,000 tonnes PAA is generated in this way
worldwide, excluding South America and Africa.
3.1.3 Quantities used
In Europe, the equilibrium PAA consumption (as such) is estimated at 25,000 t/y. This
is mainly used for disinfection and does not include use in chemical synthesis (CEFIC,
1998). In Scandinavia the consumption of distilled PAA in pulp bleaching is estimated
at 2,000-3,000 tonnes (100%) mainly driven by demand for total chlorine free (TCF) pulp
grades (Sandström et al, 1999).
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In the USA, the PAA consumption is estimated to be less than 10,000 t/y (as such) for
non-synthesis applications (CEFIC, 1998). Approximately 20,000 tonnes of PAA were
produced in the USA by autoxidation of acetaldehyde (Johnson, 1995).
Worldwide consumption in chemical synthesis including captive use and in situ

generation has been estimated at 45,000-50,000 tonnes (PAA 100%) in 1998 (CEFIC,
2000b). In 1999 the worldwide consumption of acetaldehyde for PAA production was
expected to be 41,000 tonnes corresponding to 72,500 tonnes PAA (100%) (Tecnon
Consulting, 1999). The Task Force was not aware of any production by this route in
Europe.
3.2 Compatibility
3.2.1 Storage and transportation containers
Generally, PAA is stable in containers made from glass, certain high density linear
polyethylene grades, polyvinylchloride, poly-tetra-fluoroethylene and properly passivated
stainless steel 304L and 316. However, it is important to check the compatibility and
stability with all containers before long-term use; PAA can degrade (embrittle) plastics
with extended contact time. Degradation rates are enhanced by elevated temperature.
The German authorities have restricted the maximum storage time for PAA > 17% in
standard polyethylene containers to 6 months from the day of filling. Extensions can be
obtained for containers that exhibit long-term storage stability with PAA by passing the
required tests (drop test) after contact with PAA for a defined time period (BAM, 1999).
PAA solutions are capable of leaching metal ions from stainless steel. This effect is
enhanced by some of the mineral acids (e.g. H2SO4) added as catalysts. Many of these
metal ions, e.g., iron, nickel, chromium, and molybdenum can cause product instability.
3.2.2 Non-compatible materials
Concentrated PAA is not compatible with aluminium, carbon steel, some cross-linked
polyethylene and metal alloys containing copper. It is important to determine
compatibility before using PAA with any material. PAA is rapidly decomposed upon
contact with metal salts, alkalis and activated carbon.
3.3 Storage
Equilibrium PAA is stabilised and stored at ambient conditions in certain polyethylene,
polyvinylidene fluoride containers, or passivated stainless steel tanks, with the
appropriate safety measures e.g. pressure relief. PAA should be kept away from metals,
metal salts, alkalis and reducing agents. PAA storage containers made of polyethylene
are protected from UV radiation. Storage temperature conditions are determined
individually for every formulation depending on the physical properties, in particular
flash point and self-accelerating decomposition temperature (SADT).
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Distilled PAA is typically stored and transported in cooled (< 0°C) stainless steel
containers, in order to prevent an equilibrium shift from PAA to H2O2 and HOAc.
For storage in stainless steel containers the addition of special corrosion inhibitors may
be required in order to prevent accelerated leaching of metals into the product causing
enhanced decomposition (see also Section 3.2).
Several national regulations apply for the storage and handling of PAA, e.g. in Germany
on precautions for the handling of organic peroxides (BG Chemie, 1993) and on explosive
substance regulations in other countries. In Germany, PAA is listed as water polluting
in “Wassergefährdungsklasse (WGK) 2” (Bundesminister, 1999; Umweltbundesamt,
2000).
3.4 Transportation
Mixtures of H2O2 and PAA ≤ 5% may be classified as Oxidiser in division 5.1 of UN
Recommendation 3149, provided they are thermally stable, do not detonate in the
cavitated state, do not deflagrate at all, nor show any effect when heated under
confinement nor any explosive power (UN, 1995; ECE, 1996). PAA solutions > 5% or not
meeting the above-mentioned provision are classified as organic peroxides in division
5.2 (type D = UN 3105, type E = UN 3107 or type F = UN 3109). The appropriate type
has to be determined by testing pursuant to the UN Recommendations on the Transport
of Dangerous Goods, Manual of Tests & Criteria, Part II (UN, 1995; ECE, 1996).
In the USA, a mixture of PAA 6% and H2O2 may be classified as Oxidiser in division 5.1
(UN 3149) pursuant to an approval of the national competent authority (US-DOT, 1995).
PAA solutions are subjected to temperature control during carriage if the SADT is
≤ 45°C for type E and F, or ≤ 50°C for type D showing a medium effect when heated
under confinement, or ≤ 45°C for type D showing a low or no effect when heated under
confinement.
Equilibrium PAA is permitted for transport by road, rail and sea in plastic drums made
of high-density polyethylene. Intermediate bulk containers (IBCs) made of stainless
steel or rigid plastic (high-density polyethylene) and portable tanks made of stainless
steel are permitted for type F for European and US American land transport with an
upper limit of 43 % PAA. Transport by portable tanks requires approval of the competent
authorities of the country of origin. For transport by sea, IBCs made of stainless steel or
rigid plastic (high-density polyethylene) and portable tanks made of stainless steel
are permitted for type F with an upper limit of 17% PAA only. Approval of the competent
authorities is required for both IBCs and portable tanks.
At present distilled PAA is permitted for transport by road and rail, pursuant to an
exemption of the competent authority of Finland, which submitted the content of the
approval as proposal document ST/SG/AC.10/C.3/2000/10 to the 18th session of
the UN Sub-Committee of Experts session held in Geneva on July 2000. Depending
on the concentration and the individual product properties cooling may be required.
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3.5 Use
Major uses of PAA are in chemical synthesis, disinfection and bleaching (Table 9).
Low concentrations (1-15%) are used as sanitisers, disinfectants and sterilants in the
food, beverage and medical industries. Concentrated (> 15%) solutions are used for the
oxidation of organic compounds.
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Table 9: Applications Ranked by Decreasing Quantity
Application Method of use Reference

Food Industry
Clean-in-place (breweries and dairies) In-line into closed vessels or pipework Lever Industrial,
Surface cleaning High or low pressure spray systems 1987; Lenahan,
Fish/meat/poultry processing In process water 1992
Vegetable processing In process water
Sugar beet processing In-line into process liquors Bowler et al, 1996
Starch processing In-line into process liquors Pehrsson et al,
Bottle cleaning Spray into bottles 1995
Agriculture / horticulture
Animal house and glasshouse surface High or low pressure spray and fogging
disinfection
Equipment disinfection Open bath
Animal waste / slurry In slurry or liquid waste
Irrigation water Loosely covered tanks and pipelines
Harvested fruit and vegetables Open bath or spray
Pulp and paper
Chemical pulp bleaching In-line into pulp Kramer, 1997;
White water In-line into white water LaZonby, 1997
Pulp de-inking In-line into pulp
Health
Renal dialysis machines and cartridges Open baths or soak treatment or in line Fischbach, 1985;
in pipework Crow, 1992
Endoscopes Open baths or automated washing systems
Dental instruments Open baths
Consumer
Household cleaners Open operations
Chemical Industry
Oxidiser during synthesis of chemicals Closed reaction vessels
Miscellaneous
Effluent treatment In-line in open pipes or lagoons Baldry et al, 1990,
Sludge debulking In-line in pipework, sump or lagoon 1991, 1995;
Algal control Low pressure spray onto water or solid Rudd, 1989
surface
Industrial laundries Into closed washing machines
PAA is employed as a sanitiser in the food processing and beverage industry. This
includes meat and poultry processing plants, canneries, dairies, animal houses, green
houses breweries, wineries and soft drink plants where it is used in clean-in-place (CIP)
systems at concentrations of 50 to 200 ppm PAA (158 - 632 mg/m3) (Jäger and Püspok,
1980; Schröder, 1982; Lever Industrial, 1987; Baldry and Fraser, 1988; Dychdala, 1988;
Cords and Dychdala, 1993; Cords, 1994; Mrazek, 1996). At lower temperatures (up to
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40°C), PAA (0.04-0.1%) is an alternative for H2O2 in aseptic packaging (Mrazek, 1996;
Blakistone et al, 1999).
Another major use of PAA is as a bleaching and disinfecting agent in industrial and
hospital laundries (Potokar et al, 1996).
PAA has been found useful in the disinfection of vegetables, fruits, starch products and
plant growing media such as coir (strong fibre of coconut husk) (Chalkley, 1992). PAA
is permitted in the US as a secondary and indirect food additive (US-FDA, 1996a,b) at
concentrations up to 100 mg/l. PAA is also used as a disinfectant in sugar beet extraction
(Bowler et al, 1996).
Because PAA has agricultural applications, residues potentially could be found in animals.
Council Regulation 2377/90 of 26 June 1990 established a Community procedure for
maximum residue limits of veterinary medicinal products in foodstuffs of animal origin
(EEC, 1990). According to Commission Regulation 1433/96 of 23 July 1996, PAA is not
subject to these limits (EC, 1996).
PAA has found applications in sewage sludge oxidation (Fraser, 1986) and municipal
wastewater treatment (Baldry et al, 1991). Treatment of municipal wastewater with 10
mg PAA/l for 30 minutes proved sufficient to meet WHO faecal coliforms guideline
values and for the water to be reused in agricultural irrigation (Liberti et al, 1998, 1999).
PAA has also been evaluated for the disinfection of drinking water (Profaizer et al, 1997).
In process water of paper mills PAA is employed as a slimicide in order to avoid corrosion
and odour problems (Klahre, 1996a,b). PAA is also effective in removal and growth
inhibition of biofilms and algae in cooling systems (Kramer, 1997).
PAA based systems are used for the sterilisation of medical equipment (Block, 1991;
Malchesky, 1993). Pyrogens were significantly reduced at a concentration of 0.1% PAA
for 30 minutes (Werner, 1988).
PAA is also applied for disinfection of stables and for drinking water conservation in
animal farming (Krüger et al, 1977; Kurzweg et al, 1988). It has been employed for
farm effluent disinfection where concentrations of up to 0.4% (PAA 100%) are applied
for 15 minutes (Meyer, 1976). In greenhouses, PAA is used as a cleaner and disinfectant
in water circuits.
Distilled PAA has found application as a bleaching agent mainly in TCF cellulose pulp
production processes replacing chlorine dioxide (Basta et al, 1995; Thomasfolk et al, 1996;
Ruohoniemi et al, 1998; Sandström et al, 1999). Small quantities of PAA are used in the
bleaching of recycled fibres, de-inking and in textile finishing (Steiner, 1995).
High-strength equilibrium (> 15%) and distilled PAA products are in general employed
as oxidising agents in the manufacture of organic chemicals and pharmaceuticals.
Examples of oxidation reactions include the epoxidation of olefins and the production
of sulphoxides and sulphones, such as in the synthesis of cephalosporins. Other examples
are ε-caprolactone, epoxidised soybean oil (Swern, 1970), modified starch products and
penicillin (V) sulphoxide, a key intermediate in the synthesis of cephalosporin antibiotics
(Feigenbaum, 1997).
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4. ENVIRONMENTAL DISTRIBUTION AND TRANSFORMATION
4.1 Emissions
4.1.1 Natural sources
Organic hydroperoxides such as PAA are thought to be formed in air by the reaction
of peroxyl and hydroxyl radicals as follows (Gunz and Hoffmann, 1990).
R - C = OO. + HO.2 R - C = OOH + O.2 (Eq. 6)
The origin of these atmospheric radicals in polluted and unpolluted air has been reviewed
(Wayne, 1991; Thompson, 1994).
The formation of PAA and other hydroperoxides has been demonstrated in smog chamber
studies using chlorine atoms as initiator (e.g. Hanst and Gay, 1983).
Traces of PAA were found in mountain air, but have not been demonstrated in ambient
air or atmospheric deposition samples (Section 5.1.1).
4.1.2 Emissions during production and use
Emissions to the atmosphere during production are normally avoided by scrubbing the
exhaust using an alkaline scrubber. For the manufacture of equilibrium PAA an effluent-
free process is applied. Thus no emissions to the aquatic environment are expected under
normal operating conditions.
In the manufacture of distilled PAA, a minor liquid effluent flow essentially free of PAA
is produced.
Water emissions during bleaching of pulp with distilled PAA are expected to be negligible
due to the low stability of PAA in the bleaching liquids.
In the USA, the Toxic Release Inventory lists the reported releases (annual quantities
emitted) from industrial facilities having 10 or more full-time employees and
manufacturing or processing ≥ 25,000 lbs (11,364 kg)a or otherwise using ≥ 10,000 lbs
(4,545 kg). The latest available figures indicate a total quantity release on- and off-site
of 7,345 lbs (3,330 kg) PAA in 1997 (US-EPA, 1999a). These release figures represent a
worst-case estimate, because they are based on conservative assumptions and do not
take into consideration any breakdown on-site by biological or physical means such
as waste-water treatment, incineration and flaring (US-EPA, 1999b).
1 lb = 1 pound = 0.4535924 kg
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4.2 Envionmental Fate and Biotransformation
4.2.1 Distribution
The theoretical distribution of PAA has been estimated using the fugacity model of
Mackay, Level 1 (Mackay et al, 1992). The calculations were conducted for the equilibrium
grades of PAA in Table 10, using the partial vapour pressure of PAA in those solutions.
According to the model, the majority of PAA (99.3 to 99.9%) released into the environment
enters the water phase, while the remainder is found in air. No partitioning into soil,
suspended matter or biota is expected (Table 10).
Table 10: Distribution of PAA, for Different Grades of PAA, between Environmental
Compartments at 25°C (Jacobi, 1997)
Grade (%): 5 15 35
Compartment / Distribution: (%) (%) (%)
Air 0.08 0.29 0.70
Water 99.92 99.71 99.29
Soil 0.00 0.00 0.00
Sediment 0.00 0.00 0.00
Suspended matter (aquatic) 0.00 0.00 0.00
Biota 0.00 0.00 0.00
4.2.2 Atmospheric fate
Henry's Law constant of PAA, measured in the concentration range of 1 x 10-6 1 x 10-4
mol/l at 25°C, is 0.22 Pa·m3/mol (Lind and Kok, 1986) (Table 1). This value is 2-3 orders
of magnitude lower than the value determined for H2O2 (Gunz and Hoffmann, 1990).
So PAA may be washed out by rain but less easily than H2O2.
As stated in Section 2.6.2, PAA is quickly decomposed by 50% in the vapour phase within
22 minutes (Ancker and Zetterberg, 1997). This value may be taken as the atmospheric
half-life, assuming first-order kinetics. Based on its chemical reactivity and short half-
life, PAA is not expected to persist in the atmosphere.
4.2.3 Aquatic fate
The Henry's Law constant for PAA is measured as 0.22 Pa·m3/mol at 25°C (Table 1).
This value indicates that PAA will volatilise slowly from water surfaces.
Table 10 above shows that PAA will not partition into sediment, suspended matter or
biota and for this reason the aquatic fate of PAA is mainly determined by degradation
in the water phase. Degradation could be due to abiotic decomposition, hydrolysis,
biodegradation or reaction with organic compounds, following the general reaction:
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Decomposition can be spontaneous or initiated by metal catalysts such as copper, iron

and chromium. Enzyme-calalysed degradation by catalase and peroxidase is also possible
(Kirk et al, 1994) (Section 7.2.1). Decomposition results in a decrease of the active oxygen
content of the solution.
Hydrolysis
Hydrolysis of PAA is based on the following reaction:
CH3C(O)OOH + H2O CH3C(O)OH + H2O2 (Eq. 4)
When hydrolysis takes place the active oxygen content of the solution remains the same,
which is in contrast to decomposition.
Yuan et al (1977a,b) calculated theoretical half-lives of PAA in water using a kinetic

equation. The results revealed extensive half-lives which are not supported by
experimental data. Both Yuan et al (1977a,b) and Mücke (1977) reported that the rate
of hydrolysis is accelerated by increasing temperature, and more so by increasing pH.
Mücke (1977) suggests that hydrolysis occurs almost exclusively by hydrolytic cleavage.
He showed hydrolysis half-lives at 20°C, for a 2% PAA solution, of about 1 week at
pH 4.4 and less than 1 day at pH 7.
Bioxal (1999) showed that the loss of PAA by hydrolysis of a 5% commercial grade of
equilibrium PAA diluted to 1,000 mg PAA/l and 100 mg/l at 15°C, pH 3.4, was about
34% to 36% in 8 days.
Dychdala (1988) showed a 50% loss of PAA from a solution containing 170 mg PAA/l,
at 21°C, pH 3.4, within 12 days (half-life). Teral and Gouges (1997) determined the
rate of hydrolysis for a 19.7% distilled (non-equilibrium) PAA solution at various
temperatures. Results at 20°C showed the half-life to be about 12 days. The pH was not
stated, but a low pH may be assumed.
These data suggest that at acidic pH, the half-life of PAA will be around 7 to 12 days,
while at neutral or alkaline pH, the rates will be more rapid, with half-lives of 1 day
or less.
Degradation Studies
Abiotic degradation tests with diluted PAA solutions studies were performed according
to EEC method C7 of Directive 92/69/EEC. Buffered solutions were prepared according
to document L 383A (appendix to Directive 92/69 EEC). High PAA concentrations were
measured by cerimetric titration, low concentrations by Merckoquant or Reflectoquant
colorimetry (Table 7). Both decomposition and hydrolysis were expected to occur in
these PAA degradation tests. The results (Table 11) show that the degradation was more
rapid at a high temperature and increased with increasing pH. Decomposition half-lives
seemed to be shorter when diluted solutions were used.
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Table 11: Abiotic degradation of equilibrium PAA at different temperatures, pH and

concentrations in buffered solution
Concentration Temperature pH Half-life Reference

(mg/l) (°C) (h)
20 25 4 31a Chemoxal, 1995a,b
20 50 4 3.3
10 50 4 3.1
20 50 7 1.6
20 50 9 < 0.25
20 60 4 1.7
20 70 4 0.7
748 25 4 62 Pierre et al, 2000

748 25 7 63
748 25 9 < 64b
95 25 4 48
95 25 7 48
95 25 9 < 3.6c
a Obtained by calculation
b Based on the results the half-life was 64 hours. However, the pH at the end of the test was 5.3
and therefore the half-life is reported as < 64 hours
c Based on the results the half-life was 3.6 hours. However, the pH at the end of the test was not
measured and it could have decreased. Therefore the half-life is reported as < 3.6 hours
In another test, Pierre et al (2000) studied the abiotic degradation of PAA in distilled
water (pH 2) at 25°C and at concentrations of 95 and 748 mg/l. In this case the half-
life was 18 and 19 days, respectively.
Solutions containing approximately 100 mg PAA/l in fresh water from a pond or a

stream were found to degrade for 66% in 96 hours and completely (99%) in 3 weeks.
The same solution in demineralised water was found to degrade for 80% within 3 weeks.
H2O2 decomposition in the same period was comparatively small with a maximum loss
of 8% in 96 hours. The overall breakdown of a 0.2% PAA solution (2,000 mg/l) was 45%
in 120 hours. In drinking water and pond water, PAA degraded more rapidly than in
demineralised water or lake or stream water. The tests were conducted under laboratory
conditions (Chalkley, 1991a,b).
Half-lives of diluted PAA solutions (prepared from equilibrium PAA 40%, 14% H2O2
and 27% HOAc dissolved in drinking water) containing up to 200 mg PAA/l were
less than 24 hours (Krüger et al, 1977). PAA concentrations measured in drinking-water
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bottles of rats were found to decrease rapidly within 1 day. Concentrations between 3.1
and 200 mg/l decreased up to one third and one half of the original concentration,
respectively. After 4 days the concentration decreased slowly to one fourth of the original
concentration (Juhr et al, 1978).
PAA concentrations have also been measured during ecotoxicity studies with PAA in
fish and water fleas (Section 6.2). During a semi-static test with the fish Brachydanio rerio,
the mean loss of a 1 mg/l PAA solution was 7.5% in 4 hours. The loss of a 10 mg/l
PAA solution was 5.1% in 4 hours (Bazzon et al, 1997). During the test with water fleas
(Daphnia magna) the loss at 0.1 mg/l was 21% in 4 hours (Lamy et al, 1997).
The degradation of PAA in demineralised water, drinking water and seawater has been
compared (Table 12). The data show 97% and 96% degradation in seawater after 1 day
when the initial nominal concentration was 20 and 10 mg PAA/l, respectively.
Table 12: Degradation of PAA in Water at 20°C (Teral and Hamon, 1995)
Type of water Nominal Measured concentration (mg/l)

concentration
pH (mg/l) Day 0 Day 1 Day 2 Day 4
Demineralised water 5 20 19.1 16.7 16 13.7
Drinking water 6 20 18.8 1 0 NS
Seawater 7 20 18.5 0.5 0 NS
Demineralised water 5 10 12 8.3 7.9 6.4

Drinking water 6 10 10.3 0.5 0 NS
Seawater 7 10 12.1 0.5 0 NS
NS Not Stated
The degradation of PAA in synthetic seawater was studied using a 15% PAA solution.
With an initial concentration of 52.5 mg PAA/l, the half-life was 2 minutes at 3.3%
and 2% salinity. When the concentration was doubled to 105 mg PAA/l, the respective
half-lives at 3.3% and 2% salinity were 7 and 20 minutes. Thus, increased salinity enhanced
the degradation rate (Kuhn, 2000).
The degradation of PAA is seawater seems to be faster than the degradation in fresh
water, which could be related to the high pH and salinity (ionic strength).
4.2.4 Terrestrial fate
Degradation of a 1.1% PAA solution (11,190 mg PAA/l) was tested on a sample of dried
soil (not specified). Following extraction with demineralised water, 99.2% of the
compound appeared to have been destroyed in about 20 minutes (Chalkley, 1991c).
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The penetration of PAA into soil (John Innes compost) columns was investigated with
a solution containing approximately 2,000 mg PAA/l, prepared from equilibrium
PAA 5% (20% H2O2 and 27% HOAc). One ml of the test solution was added to the top
of each soil column. After 5 minutes, each column was washed with 100 ml of
demineralised water (sufficient to remove all PAA) and the eluate content determined.
Of the PAA, 21.5% was recovered at a soil depth of 25 mm, while 42% H2O2 was found
at the same depth. PAA recovery decreased to 3.2% at 50 mm, 0.3% at 100 mm and
< 0.2% at 150 mm, where 10% of the H2O2 was still present. Similarly after 10 minutes
only 8.7% PAA was recovered at 25 mm depth (Chalkley, 1991a).
4.2.5 Biodegradation
The biodegradability of PAA was evaluated in various experimental test systems.
PAA appeared to be not readily biodegradable in the OECD Closed Bottle Test. However,
when inoculum of adapted bacteria derived from a Zahn-Wellens Test with the same
compound was added, PAA (initial concentration of 2 - 5 mg/l) proved to be highly
(> 79%) degradable (Gerike and Gode, 1990).
In a Coupled Units Test with PAA, where the organic carbon is measured to estimate
ultimate biodegradability, 56% carbon removal was found. In another test using detection
of recalcitrant metabolites 98% carbon removal was measured (Gerike and Jasiak, 1983;
Gerike and Gode, 1990).
Inhibition of the microbial degradation by PAA was measured with an oxygen

consumption inhibition test. PAA was shown to have inhibitory activity at 90 mg/l
(Gerike and Gode, 1990).
In a Modified OECD Screening Test (OECD 301 E) which determines ultimate

biodegradation by measurement of removal of dissolved organic carbon (DOC), PAA
was added once at a concentration of 5 mg DOC/l. A bactericidal effect was found
and a biodegradable reference substance was not degraded. Therefore, the test procedure
was modified and PAA doses were increased stepwise over 2 weeks until the nominal
concentration of 5 mg DOC/l was reached. Thus, a very high DOC removal of 98% was
achieved within the 28-day test period (Richterich and Gode, 1986), supporting the view
of the ready biodegradability of the compound. Based on a simple distribution (PAA
is very soluble in water and the volume of bacterial cells is very low compared to the
volume of the medium), no significant uptake of PAA is expected to have taken place.
Active uptake is very unlikely.
The hydrolysis products HOAc and H2O2 are both readily biodegradable (Verschueren,
1983; Groeneveld and De Groot, 1999).
4.2.6 Bioaccumulation
The octanol-water partition coefficient was measured for PAA and H2O2 using the US
Environmental Protection Agency (EPA) shake flask method (Byers, 1998). The values
were 0.30 ± 0.13 and 0.40 ± 0.07 for PAA and H2O2, respectively. Compounds with such
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a low octanol-water partition coefficient are not considered to be bioaccumulable.
4.2.7 Evaluation
PAA released in the environment will partition almost exclusively (> 99%) to the water
compartment. Only a minor part (< 1%) will remain in the atmosphere, where it is
expected to undergo rapid decomposition with a half-life of 22 minutes. The fate of PAA
in the environment is mainly determined by its degradation.
The fate of PAA in water will be influenced by abiotic degradation, which yields HOAc
and oxygen and hydrolysis which forms HOAc and H2O2, both of which are easily
(bio)degradable compounds. The abiotic degradation increases with temperature and
pH. At acidic pH, the half-life of PAA will be around 7 to 12 days, while at neutral or
alkaline pH, half-lives may be 1 day or less. In seawater degradation is expected to be
rapid (half-life < 1 h). Most abiotic degradation studies of PAA in water were done at
concentrations that resulted in acute effects on aquatic organisms. In these situations,
abiotic degradation is the single degradation pathway of PAA. However, these
concentrations are not realistic environmental concentrations during normal use of PAA
products. At low PAA levels (< 1 mg/l), the biotic degradation by algae, and micro-
organisms could significantly increase the degradation in aquatic ecosystems.
In the soil, a diluted PAA solution is rapidly and easily degraded by hydrolysis and
transition metal decomposition, which is an instantaneous reaction. At low concentrations
biodegradation could contribute to the degradation in soils.
Biodegradation studies with PAA show a rapid degradation of PAA if the biocidal effect
is not too strong. Sewage treatment plants with adapted activated sludge, would easily
degrade PAA. The biodegradation is also enhanced when the biomass is high (as in the
case of sewage treatment plant).
Based on the low octanol-water partition coefficient and the rapid degradation in the
environment, PAA is not bioaccumulable.
In conclusion PAA should be easily degraded in air, water and soil and does not persist
or accumulate in the environment.
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5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1 Environmental Levels
5.1.1 Air
No specific measurement data are available.
Based on atmospheric model calculations, trace levels (4 ppbva) of PAA were predicted
by Calvert et al (1985) and Gaffney et al (1987).
Hellpointer and Gäb (1989) could not demonstrate PAA (detection limit 0.07 µmol/l) in
32 rainwater samples collected at Freising near Munich in Germany (April and May
1988).
Junkermann et al (1993), using the sensitive (detection limit 0.06 ppb) enzyme fluorometric
method developed by Lazrus et al (1986) (Section 2.8), found PAA to be present among
other hydroperoxides and H2O2 in mountain air at two different altitudes at sites in
Germany (Schafberg 1,175 m and Wank summit 1,780 m). A pronounced seasonal and
daily variation in the total concentration and composition of the hydroperoxides was
seen (Junkermann et al, 1993).
Heikes et al (1991) measured soluble organic peroxides, including PAA, in remote marine
air over the South Pacific ocean (Australia and Fiji). The total concentration was 0.4 ppbv
near the sea surface (< 91.4 m) and 0.6 ppbv between the marine layer and the free
troposphere (914.4 m to 3,352 m). At high altitude (5,638 m), the level was 0.2 ppbv.
No specific concentrations for PAA were given.
Tanner and Schorran (1995) reported total gaseous peroxide levels near the Grand Canyon
(USA) in the range of 1.0 - 5 ppbv. The results varied, depending on the daylight and
the season.
Peroxide measurements of cloud and rainwater collected (48 samples) in the eastern
USA indicated the presence of organic hydroperoxides in only some of samples (Kelly
et al, 1985).
5.1.2 Water, soil and biota
No data are available on concentrations of PAA in water, soil and biota.
5.2 Human Exposure Levels and Hygiene Standards
5.2.1 Non-occupational exposure
No data are available.
a Parts per billion by volume
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5.2.2 Simulated occupational exposure studies
A number of measurements of atmospheric concentrations were performed in an

experimental setting to obtain an indication of possible occupational exposures levels
during certain operations (Table 13).
Table 13: Simulated Occupational Exposure Studies
Description Results Reference

(mg PAA/m3)
Fogging of 0.2% PAA in closed shed, measured at different distances 0.7 - 7 H2O2a Fraser and
Fogging of 0.2% PAA in closed shed, measured 5 - 60 minutes ND - 3 H2O2 b Thorbinson, 1986
Pulp mill A, refrigeration room, doors closed 1.8 Cerne et al, 1999
Pulp mill A, refrigeration room, doors open 0.45
Pulp mill B, refrigeration room, doors closed 0.45
Pulp mill B, refrigeration room, doors open < 0.15 (ND)
Distillation, spill of 20 litres cold PAA (intentional), doors closed 1.5 Ancker and
Container filling above manhole outdoors 0.5 Zetterberg,1997
Laboratory, beakers w/o lid 0.15 - 0.5
Laboratory, beakers w/o lid in vented hood 0.3-3
Bath with 0.35% PAA, measured at 0.4 meter above bath 0.8 - 1.0c Simms, 1995
Bath with 0.35% PAA, measured at 0.1 meter above bath 3.3d
Bath with 0.35% PAA, measured at 2.7 meter from bath < 0.3e
Ten litre 0.35% PAA in water bath (50 x 29 x 19 cm) at 28°C in < 0.7 Harvey, 1992
room without ventilation or air changes
Filling of 1,000 kg IBCf with 15% PAA, measured at 0.6 m from 0.3 - 0.5g Rowbottom, 1996a
top of container
Filling of 1,000 kg IBC with 5% PAA, measured at 0.6 m from < 0.5h
top of container
Distillation house A of PAA, near ground floor, small leak in pump 0.9 - 1.2i McDonagh, 1997;
Distillation house A and B of PAA, first floor 0.4 - 0.5ij Rowbottom, 1996b
Ten litre 0.35% PAA in water bath, ambient temperature, < 0.02 Harvey, 1993
closed room
Ten litre 0.35% PAA in water bath, temperature of 32°C, < 0.02
sealed room
a Reported as 0.5 - 5 ppm H2O2 f Intermediate bulk container

b Reported as < 0.5 - 2.0 ppm H2O2 g Reported as 0.1 - 0.15 ppm PAA
c Reported as 0.35 - 0.46 mg/m3 H2O2 h Reported as < 0.15 ppm PAA
d Reported as 1.46 mg/m3 H2O2 i Reported as 0.3 - 0.4 ppm PAA
e Reported as < 0.15 mg/m3 H2O2 j Reported as 0.13 - 0.17 ppm PAA
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During the studies of Fraser and Thorbinson (1986), Harvey (1992 and 1993), Simms
(1995), Rowbottom (1996a,b) and McDonagh (1997), the air samples were drawn through
an alkaline solution of phenolphthalein. Peracids and H2O2 produced a pink colour
by the formation of phenolphthalein, which was detected spectrophotometrically,
and the results were reported as total peroxygen concentrations.
Fraser and Thorbinson (1986) fogged a solution containing 0.2% PAA into a hen house,
which means that an aerosol was present. The product which was used (4% equilibrium
PAA) contained presumably also a relatively high content of H2O2 which meant that
a significant quantity of the measured atmospheric peroxygen might have been H2O2
(assuming a constant composition). Therefore, the results of this experiment are expressed
in Table 13 as H2O2 concentrations.
Also Harvey (1992, 1993), Simms (1995), Rowbottom (1996a,b) and McDonagh (1997)
measured the total peroxygen concentrations but in this case a vapour was present.
Because PAA has a higher vapour pressure than H2O2 (Section 2.5), the measured
peroxygen was probably mainly PAA. The results of these studies are presented in Table
13 as PAA concentrations.
The analytical measurements reported by Ancker and Zetterberg (1997) and Cerne et al
(1999) were based on FTIR spectroscopy (Table 8) . In this case the PAA concentration
was measured directly.
5.2.3 Occupational exposure
Given the applications of PAA there is a possibility for occupational exposure to aerosols
or vapours or dermal exposure to the liquid. Hygiene procedures are designed to
minimise skin, eye and inhalation exposure by appropriate technical and personal
protective equipment depending on the situation at the particular workplace.
Recommended safe handling procedures are provided (Section 10.2).
Workplace (area) measurements at Akzo Nobel, Eka Chemicals were reported in 1997
using direct FTIR spectroscopy (Table 8). PAA could only be measured near the distillation
reactor where short-term concentrations ranged from 0.15 mg PAA/m3 (detection limit)
to 0.30 mg PAA/m3 (original data given in ppm). No PAA was detected near the storage
tank or outside a laboratory hood (Ancker and Zetterberg, 1997). Using the same method,
no PAA was detectable at the dosage area of two pulp mills in 1998 (Cerne et al, 1999).
No further information is available.
Measurements carried out at Ausimont during 1999 indicate short-term workplace

concentrations of PAA ranging from < 0.1 to 0.9 mg PAA/m3 in different areas of the
production plant, in particular the filling area. Sampling was performed 3 x 2 h and
14 x 1 h. The analytical method was not stated (Ausimont, 1999, 2000).
Degussa (1990a) reported levels of < 0.1 to 0.5 mg PAA/m3 (20 - 30 min/area) during
bottle disinfection at a pharmaceutical company in 1990. The analytical method was not
detailed. PAA was calculated from the amount of active oxygen taking into account the
measured H2O2 levels.
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PAA exposure was determined in a university hospital where employees (150 workers)
used 0.12 to 2% aqueous disinfection and sterilisation solutions prepared from an
equilibrium PAA 40% (3.5% H2O2, 46% HOAc). There were 121 samples taken at 45
different areas (2 - 6 measurements at each workplace). PAA was determined by means
of a spectrophotometric technique (oxidative formation of iodine from a potassium
iodine solution) with a detection limit of 0.005 mg/m3. Workplace, 8-hour concentrations
ranged from below the detection limit to 1.84 mg PAA/m3. The majority (60%) of
employees had readings below 0.1 mg/m3, 95% were below 1 mg/m3 (Schaffernicht
and Müller, 1998).
5.2.4 Hygiene standards
No country has adopted an Occupational Exposure Limit Value (OEL) for PAA.
An internal OEL of 0.15 ppm PAA (0.45 mg/m3) for an 8-h time-weighted average (TWA)
concentration has been developed by Solvay (2000).
The following table gives examples of national OEL values for the three principal
components of PAA formulations (Table 14).
Table 14: Examples of OEL Values for Components of PAA Formulations
TWAa Ceiling Limit STELb Reference

Country (ppm) (mg/m3) (ppm) (mg/m3) (ppm) (mg/m3)
PAA - - - - - -
H2O2
Germany 1 1.4 2c 2.8c - - DFG, 1999a
UK 1 1.4 2 2.8 HSE, 2000
USA 1 1.4d - - - - ACGIH, 2000
HOAc
Germany 10 25 20c 50c - - DFG, 1999a
UK 10 25 15 37 HSE, 2000
USA 10 25d - - 15 37d ACGIH, 2000
a Time-weighted average concentration (8-h working period)

b Short-term exposure limit (15 min, unless specified otherwise)
c 5 min, maximum 8 times per shift
d Not reported as such
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6. EFFECTS ON ORGANISMS IN THE ENVIRONMENT
6.1 Micro-Organisms
PAA formulations are fast-acting oxidising biocides that are effective against a broad
spectrum of micro-organisms including bacteria, yeasts and moulds, protozoa, algae
and viruses. Spores, bacteriophages and enteroviruses are also susceptible.
PAA is effective against micro-organisms over a wide range of conditions (Block, 1991).
PAA is most active at pH values below the pKa (8.2) and also displays biocidal activity
under mildly alkaline conditions up to pH 9. PAA remains efficacious even at low
temperatures (5°C) (Schliesser and Wiest, 1979; Baldry, 1983; Block, 1991). The activity
of PAA is relatively unaffected by organic matter compared to other oxidising biocides
(Block, 1991).
Concentrations of > 300 mg PAA/l (as diluted equilibrium products) were highly effective
against vegetative bacteria and yeasts in suspension tests where a 99.999% reduction
was achieved within 5 minutes. More diluted concentrations of 30 mg/l were still effective
against vegetative bacteria. Higher concentrations and longer exposure times were
needed to inactivate spores formed by bacteria and moulds (Baldry, 1983; Bloomfield
et al, 1991; Setlow et al, 1997).
Lensing and Oei (1985) reported 2,500 mg PAA/l to be effective against Bacillus subtilis
and B. cereus within 30 minutes. Krzywicka (1970) reported 2,000 mg/l being effective
against B. subtilis in 10 minutes. For moulds, the PAA dose required was variable. Some
mould spores were inactivated at 500 mg PAA/l in 5 minutes, while others were affected
at > 1,000 mg PAA/l for longer exposure periods.
PAA is effective against bacteriophages and enteroviruses such as the poliovirus, rotavirus
and Coxsackie virus. Concentrations in the range 400 - 2,250 mg PAA/l for a 5 or 10
minute contact period were reported. Lower concentrations were effective over longer
contact times (Kline and Hull, 1960; Harakeh, 1984; Baldry et al, 1990).
The effect of PAA (2 mg/l) on the microbial respiration or sewage sludge, measured
as conversion of 14C-glucose to 14CO2, has been studied at sludge concentrations of
2.5 to 50 mg (dry weight)/l (Thus et al, 1997). Independent of the sludge concentration,
conversion of 14C-glucose to 14CO2 was reduced to 10% of expected in the first 24 hours.
When after 24 hours fresh sludge was added the respiration was comparable to controls
again, indicating that no PAA toxicity remained.
6.2 Aquatic Organims

The results of toxicity tests with aquatic organisms are summarised in Table 15.
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38
Table 15: Toxicity of PAA to Aquatic Organisms
Species Duration Composition (%) Endpoint, result Reference CoRa

(h) PAA H2O2 HOAc EC50 or LC50 NOEC
Algae Growth inhibition
EC50
Selenastrum capricornutumb 120 5.2 20 NS 0.18 0.13 Hicks et al, 1996 2b
Selenastrum capricornutum 72 18.0 0.3 NS < 1.0 < 1.0 Petit-Poulsen et al, 1997c 2b
Scenedesmus subspicatus 72 0.35 7 NS 0.035 - 0.35 0.035 Licata-Messana, 1995a 2b
Invertebrates Immobility
EC50
Daphnia magna 48 15 14 28 0.50 0.15 Douglas and Pell, 1986a 2b
Daphnia magna 48 4.5 27.5 NS 1.1 0.45 Burgess and Forbis, 1983 2b
Daphnia magna 48 15.5 22 15 0.69 0.16 Terrell, 1987a 2b
Daphnia magna 48 5.2 20 NS 0.73 0.56 Gardner and Bucksath, 1996a 2b
Daphnia magna 48 18.0 0.3 NS < 1.0 < 1.0 Lamy et al, 1997 2b
Daphnia magna 48 0.35 7 NS 0.035 - 0.350 > 0.035 Licata-Messana, 1995b 2b
Lethality
LC50
Crangon crangond 96 12 20 8 15 6.7 Tinsley and Sims, 1987a 2e
Mytilus edulisd embryo 48 12.5 19 18 0.27 0.13 Fairhurst, 1987 2e
Crassostrea gigasd embryo 48 12.5 19 18 0.28 0.13 Butler, 1987 2e
ECETOC JACC No.40
39
Table 15 continued
Species Duration Composition (%) Endpoint, result Reference CoRa

(h) PAA H2O2 HOAc EC50 or LC50 NOEC
Fish
Oncorhynchus mykisse 96 15 14 28 2.0 1.5 Douglas and Pell, 1986b 2b
Oncorhynchus mykiss 96 15.5 22 15 0.91 0.16 Terrell, 1987b 2b
Oncorhynchus mykiss 96 4.5 27.5 NS 1.0 0.45 Cohle and McAllister, 1983 2b
Oncorhynchus mykiss 96 5.2 20 NS 1.6 0.82 Gardner and Bucksath, 1996b 2b
Lepomis macrochirus 96 4.5 27.5 NS 1.2 0.45 McAllister and Cohle, 1983 2b
Lepomis macrochirus 96 15.5 22 15 3.3 2.7 Terrell, 1987b 2b
Lepomis macrochirus 96 5.2 20 NS 1.1 0.47 Gardner and Bucksath, 1996c 2b
Brachydanio rerio 96 18.0 0.3 NS 1.0 < 1.0 Bazzon et al, 1997c 2b
Brachydanio rerio 96 0.35 7 NS ≈ 0.35 > 0.035 Licata-Messana, 1995c 2b
Pleuronectes platessad 96 12 20 8 11 6.7 Tinsley and Sims, 1987b 2e
a Code of reliability (Appendix B)

b Presently known as Pseudokirchneriella subcapitata or Rhaphidocelis subcapitata
c Analytical methods following Gouges and Teral, 1997

d Saltwater species
e Previous name: Salmo gairdneri
NS Not Stated
6.2.1 Algae
A study with a freshwater green alga (Selenastrum capricornutum) and equilibrium PAA
(5.2%) has been reported. The study was performed to good laboratory practice (GLP)
guidelines. The test concentrations were 0, 0.065, 0.13, 0.25, 0.50 and 1.0 mg PAA/l.
Growth was determined by algal cell counts. The concentration of H2O2 was measured
in the test solutions. At the start of the test, the H2O2 content of all test solutions was
close to the nominal concentration. At the end of the test, the measured concentration
was lower than the detection limit except for concentrations of 0.50 and 1.0 mg PAA/l
where the remaining measured H2O2 concentrations were 84% and 110% of the nominal
values, respectively. At a concentration of 0.13 mg PAA/l an initial, statistically significant,
inhibition of growth was found between 0 and 72 hours. Growth had recovered at the
end of the test probably due to decreased exposure. Based on the cell count at the end
of the test, a concentration of 0.13 mg/l was considered to be an NOEC. At a concentration
of 0.25 mg/l the cell count at the end of the test was 3% of the control value. The
120-hour EC50 value was estimated to be 0.18 mg/l (Hicks et al, 1996). This indicates a
remarkably steep dose-response curve.
In another GLP study with the alga Selenastrum capricornutum, distilled PAA (18%) was
used to prepare test solutions with concentrations of 0, 1.0 and 10 mg PAA/l (Petit-
Poulsen et al, 1997). The solutions were renewed every 4 hours. The algal suspensions
were centrifuged followed by re-suspension of the algae in freshly prepared test solutions.
Concentrations of PAA were analytically determined before and after renewal of the
test solutions without algae. The mean decrease in concentration in the 4-hour periods
was 14.3 and 6.5% at concentrations of 1.0 and 10 mg/l, respectively. Although the algae
were centrifuged and resuspended 17 times during the test, the control cell density of
the algae increased 20-fold during the 72-hour test period, which was higher than the
minimum value of 16-fold (validity criterion). The growth of the algae was completely
inhibited at 1.0 and 10 mg PAA/l.
A GLP study with Scenedesmus subspicatus and diluted equilibrium PAA (0.35%) was
performed at nominal, static test concentrations of 0.035, 0.35 and 0.88 mg PAA/l. No
analytical concentration measurements were made. At the end of the test, at a
concentration of 0.035 mg/l, the growth rate was inhibited by 3% and total biomass
by 11% of controls, but the inhibition of biomass was not statistically significant. At
concentrations of 0.35 and 0.88 mg/l the growth of the algae was completely inhibited
(Licata-Messana, 1995a). A concentration of 0.035 mg PAA/l can be considered as a
NOEC. The H2O2 content of the product was 20 times higher than the PAA content and
therefore the effect on the algae could be due to H2O2.
The effect of diluted equilibrium PAA (5%, 20% H2O2, 10% HOAc) on cyanobacteria
(Anabaena variabilis and Synecococcus leopoliensis) and green algae (Chlamydomonas
eugametos and Scenedesmus quadricauda) was studied using microtitre plates. In many
tests an initial effect on algal growth was found at various concentrations, but growth
recovered, probably due to a decrease in PAA concentration during the tests. The results
were strongly dependent on the initial density of algal cells. A high cell density resulted
in a strong decrease of the PAA concentration and a small effect on algal growth.
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ECETOC JACC No.40
Cyanobacteria appeared to be more sensitive to than green algae. NOEC and EC50 values
were not reported (Rodgers, 1991). This study is not reliable due to the use of a non-
standard test methodology and reporting of insufficient detail. It is not clear whether
the concentrations are expressed on the basis of the product PAA or the component PAA.
Evaluation
Three well-designed algal tests were performed in accordance with GLP guidelines. The
study reported by Petit-Poulsen et al (1997) did not include a full concentration range,
but the concentration of PAA was measured and maintained due to regular renewal
of the test solutions. The study by Hicks et al (1996) was performed with a representative
product, including a full concentration range, but only the concentration of H2O2 was
determined analytically, and the PAA concentration calculated. The study of Hicks et al
showed a decrease of the H2O2 concentration and a recovery of algal growth at relatively
low concentrations. If concentrations are sufficiently low, an initial effect on the algae
is expected but the algae will be able to degrade the product and growth may fully
recover. At high concentrations algal growth will be completely inhibited and the product
not degraded. Therefore recovery of the growth does not occur.
A test with H2O2 in the green alga Chlorella vulgaris according to a modified OECD
Guideline 201 revealed EC50 and NOEC values of 2.5 and 0.1 mg H2O2/l, respectively
(Degussa, 1991). Based on these values and the relatively high H2O2 (compared to PAA)
content of the tested solutions, H2O2 could have contributed significantly to the observed
toxicity. In particular, Hicks et al (1996) used a product with a relatively high content
of H2O2.
6.2.2 Invertebrates
Daphnia magna
Three toxicity tests with diluted equilibrium PAA (4.5-15.5%) in the fresh water flea
Daphnia magna have been reported, without analysis of the PAA, active oxygen or H2O2
concentrations in the test solutions (Douglas and Pell, 1986a; Burgess and Forbis, 1983;
Terrell, 1987a,b) (Table 15). A GLP toxicity test with equilibrium PAA (5.2%) in Daphnia
magna and was reported. During this study the H2O2 content of the test solutions was
determined spectrophotometrically, based on titration with potassium permanganate,
and the PAA concentrations calculated accordingly. During the test the decrease in H2O2
concentration ranged between 19 and 35%. Nominal test concentrations were 0, 0.19,
0.32, 0.54, 0.90 and 1.5 mg PAA/l (Gardner and Bucksath, 1996a).
A test with distilled PAA (18%) in Daphnia magna was performed at test concentrations
of 0, 1.0 and 10 mg PAA/l. At the highest concentration all daphnids were immobilised
after 4 hours. At 1.0 mg/l the daphnids were transferred to fresh solutions each
4-hour period and PAA concentrations were measured spectrophotometrically, using
titration with potassium iodide, before and after each renewal. The mean decrease in
concentration over the 4-hour periods was 21%. At the end of the test the immobility of
the daphnids was 75% at 1.0 mg/l (Lamy et al, 1997).
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ECETOC JACC No.40
Exposure of Daphnia magna to concentrations of 0, 0.0035, 0.035 and 0.35 mg PAA/l

(dilutions of equilibrium PAA 0.35%) for 48 hours resulted in immobilisation rates of
5%, 5%, 5% and 100%, respectively. The EC50 value was 0.035 - 0.35 mg PAA/l (Licata-
Messana, 1995b). It should be noted that the H2O2 content of the product, and test
solutions, was relatively high. At the highest concentration the H2O2 concentration was
equivalent to 7 mg/l, while the 24-h EC50 is 2.3 mg H2O2 (reported as 7.7 mg/l for a 30%
solution) (Bringmann and Kühn, 1982). Thus, the low EC50 value, expressed as PAA
concentration, can be explained by the high concentration of H2O2. However, also during
the studies of Burgess and Forbis (1983) and Gardner and Bucksath (1996a) an effect
of H2O2 on the observed toxicity cannot be excluded if the results are compared with
the 24-h EC50 value of 2.3 mg H2O2/l reported by Bringmann and Kühn (1982).
The EC50 values of four tests with Daphnia magna ranged between 0.50 and 1.1 mg PAA/l,
which shows a good reproducibility. In another test (Lamy et al, 1997) the immobility
was 75% at 1.0 mg/l and, although only two concentrations were tested, the results of
this test do not conflict with the previous four Daphnia magna test results. The test of
Licata-Messana (1995b) is not so representative of PAA products because of the relatively
high H2O2 content.
Other invertebrates
The study with equilibrium PAA (12%) in brown shrimp (Crangon crangon) revealed an
96-h LC50 value of 15 mg PAA/l. The medium was renewed daily during the study but
analytical concentration measurements were not made. The mean weight of these
saltwater crustaceans was 1.25 g (Tinsley and Sims, 1987a). The larger size of the organism
compared to daphnids may explain the lower sensitivity of the shrimp. The high LC50
value could also be related to the rapid degradation of PAA in seawater (Section 4.2.3)
Two embryo-larval assays were carried out on marine oysters with nominal
concentrations of equilibrium PAA (12.5%) dissolved in seawater, to determine any
effects during their first 48 hours of their development from embryo to larva. In this
period a protective D-shaped shell was formed. Without a shell the embryos were
extremely sensitive to reduced water quality. Both tests were conducted under static
conditions. In the first test with embryos of the pacific oyster (Crassostrea gigas), a
48-hour EC50 of 0.28 mg PAA/l was obtained (Butler, 1987). Another test with embryos
of the common mussel (Mytilus edulis) resulted in an EC50 value of 0.27 mg PAA/l
(Fairhurst, 1987).
The effect of PAA on the fertilisation rate of a marine tubeworm (Pomatoceros triqueter)
was reported. Eggs and sperm were mixed with the test compound and then left for
3.5 hours. The reported EC50 value was 0.12 - 0.24 mg/l. Abnormal embryos were also
recorded at concentrations of 0.06 and 0.13 mg/l, but further data, which could have
enabled quantification of the effects at these concentrations, were not presented
(Dixon,1988; CoR 2c). For this reason a reliable NOEC cannot be derived from this study.
Ageing of the test solutions for 24 hours (as a 12 mg/l stock in seawater) resulted in a
marked reduction of the toxicity, probably due to decomposition of the test solution.
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ECETOC JACC No.40
In conclusion, the PAA toxicity studies with other aquatic invertebrates showed a
relatively low toxicity for the large brown shrimp but consistent EC50 values of 0.1 to
0.3 mg/l were found when small and young organisms were used.
6.2.3 Fish
Four acute studies with rainbow trout (Oncorhynchus mykiss) have been reported (Table
15). The studies with this cold-water species were conducted at temperatures of 12-14°C.
Only during the study of Douglas and Pell (1986b) were the test solutions renewed daily.
Gardner and Bucksath (1996b) made analytical measurements of H2O2 in the test
solutions. Between the start (0-hour) and the end of the test (96-hour) the decrease in
the concentration of H2O2 ranged between 14 and 26%. The LC50 values of these toxicity
tests show a good reproducibility.
Three acute studies with the warm-water bluegill sunfish (Lepomis macrochirus) have
been performed (McAllister and Cohle, 1983; Terrell, 1987b; Gardner and Bucksath,
1996c). During the first two studies the test solutions were not renewed and chemical
analysis were not conducted. Gardner and Bucksath (1996c), in a preliminary test using
concentrations of 0.32; 0.54; 0.90; 1.5 and 2.5 mg PAA/l, measured concentrations of
H2O2 after 96 hours to be less than 5% of the nominal concentrations. Therefore the test
solutions were renewed daily during the final test. The mean decrease in the H2O2
concentration over a 24-hour period was 12% and the decrease ranged between 0 and
36%.
A semi-static acute toxicity test was conducted with distilled PAA (18%) in zebra fish
(Brachydanio rerio); the tested concentrations were 0, 1.0 and 10 mg PAA/l. The zebra
fish were exposed for 96 hours and they were transferred to fresh solutions each 4-hour
period. The PAA concentrations were measured before and after each renewal using a
titration with potassium iodide followed by a spectrophometry. In this case the mean
decrease in concentration in the 4-hour period was 7.5% (Bazzon et al, 1997).
Another toxicity test in Brachydanio rerio was conducted with equilibrium PAA (0.35%)
at concentrations of 0, 0.0035, 0.035 and 0.35 mg PAA/l. After 96 hours the percentage
mortality was 0, 10, 0 and 60, respectively. This showed that the calculated LC50 was
slightly lower than 0.35 mg/l (Licata-Messana, 1995c). The low LC50 value may have
been partly due to the relatively high H2O2 concentration (7 mg/l) of the test solution,
although LC50 values for fish are generally higher than 7 mg H2O2 (ECETOC 1993). For
the other fish tests with PAA there is no indication of a contribution of H 2O2 to the
observed toxicity of PAA based on the LC50 of H2O2.
In the study of Tinsley and Sims (1987b), plaice (Pleuronectes platessa), a saltwater fish
species, with a mean weight of 8.5 g was used. Test solutions were renewed daily during
this semi-static test. The high LC50 could be due to the rapid degradation of PAA in
seawater. The half-life in seawater is less than 1 hour and therefore the exposure during
the fish test could have been low (Section 4.2.3).
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6.2.4 Birds
When quails were given a commercial mash diet containing 750 ppm PAA for 5 days,
no signs of toxicity were observed (Terrel, 1986b; CoR 4a). The diet was not analysed
for PAA and because the substance was probably unstable in the diet the actual exposure
to PAA is unknown.
6.3 Summary and Evaluation

PAA is an active bactericide, fungicide and sporicide. Spores are generally more resistant,
as well as viruses. Many studies are available which describe the effect of PAA solutions
on these target organisms, but these studies are in general conducted at relatively
high concentrations and few concentrations per study, and are therefore not very useful
for an environmental hazard assessment.
Toxicity tests with PAA and wildlife species, plants or other terrestrial organisms are
not available.
Many different toxicity tests with aquatic organisms have been reviewed in the previous
sections. Full reports were in general available allowing critical evaluation of the data.
Although analytical measurements were conducted for only a few studies, those without
analytical measurements provide useful information about the acute toxicity of PAA
solutions.
For several standard species, e.g. Selenastrum capricornutum, Daphnia magna, Oncorhynchus
mykiss and Lepomis macrochirus, more than one toxicity test was performed. The toxicity
tests were reproducible if concentrations were expressed as PAA concentrations
irrespective of the concentrations of H 2O2 and HOAc. This indicates that the PAA
concentration explains the toxicity of PAA formulations and therefore the concentration
of H2O2 and HOAc are less relevant in this respect. However, for algae and daphnids
the absolute concentrations of H2O2, at the effect concentrations of PAA, were close to
the effect concentrations of studies with H2O2 alone. For fish the absolute concentrations
of H2O2, at the effect concentrations of PAA, were not close to the effect concentrations
of studies with H2O2 alone. In conclusion, it can be stated that for algae and daphnids
there could be a contribution of H2O2 to the toxicity of the PAA formulations, while
for fish there is not always evidence for an effect of H2O2 on the toxicity of PAA. If the
product contains 0.35% PAA and 7% H2O2 then evidence for a contribution of H2O2
to the toxicity of the product for fish was found. Apart from this one example the data
for fish did not evidence than effect of H2O2 content on the toxicity of the PAA
formulation.
The results of the toxicity studies indicate a relationship between the size and sensitivity
of the organisms. Small test organisms, like unicellular algae and mussel and oyster
embryos, seemed to be relatively sensitive while larger test organisms such as brown
shrimp and fish seemed to be less susceptible. This phenomenon could be related to the
relatively unspecific mode of action of the compound. The mode of action of PAA is
based on the oxidising properties that are relevant for all organisms. Small organisms
are probably more sensitive because their body-surface to body-weight ratio is relatively
high, which results in a relatively high uptake (per gram body weight).
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The lowest endpoint was reported for an algal study with Scenedesmus subspicatus which
revealed a NOEC of 0.035 mg PAA/l (Licata-Messana, 1995a). However, this study
employed an atypical product composition (0.35% PAA, 7% H2O2). Based on the
remaining standard toxicity tests, the lowest reported NOEC is 0.13 mg PAA/l.
A NOEC of 0.13 mg PAA/l was found for the algal study with Selenastrum capricornutum
(Hicks et al, 1996). Although, an initial effect on growth was observed at this concentration
a recovery of growth was found during the last part of the test. Probably the algae are
able to degrade PAA if the initial concentration is sufficiently low. At higher initial
concentrations the algae are killed and in this case PAA is more stable. No initial effect
on the growth of Selenastrum capricornutum was found at a concentration of 0.061 mg
PAA/l.
It can be concluded that small organisms are relatively sensitive to PAA. Taking account
of the large number of standard toxicity test with algae, invertebrates and fish, the lowest
NOEC was 0.13 mg PAA/l. At such a low concentration, the organisms were apparently
able to promote the degradation of PAA.
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7. KINETICS AND METABOLISM
7.1 Absorption and Distribution

An in vitro skin penetration test with freshly prepared pig skin was described by Krüger
and Jancke (1976). A solution of 0.8% PAA (110 ml) (diluted from 40% PAA containing
5% H2O2 and 40% HOAc) was incubated with pig skin (5 cm surface area) in a diffusion
cell at 37°C for 24 hours. The receptor fluid, physiological saline (110 ml) was analysed
every 2 hours for active oxygen using photometric detection after reaction with potassium
iodide solution with a detection limit of 2 µg. No PAA could be detected in the receptor
fluid when intact skin was used (7 samples). Only in one experiment with a damaged
skin sample in which the deeper layers were affected 2.6 mg active oxygen (calculated
as PAA) was detected.
Phillips (1994a) studied the fate of 14C-labelled PAA solution after dermal application
to 4 male Sprague-Dawley rats. As the skin of the animals was severely damaged due
to the corrosive effects of the applied solution, the results of this study cannot be used
to assess absorption of PAA through intact skin.
Details of the preparation of the sample and test solution are given in Table 16.
Table 16: Protocol Used by Phillips (1994a)
PAA test solution Control PAA-free solution

Chemical composition Distilled water 0.35 ml None
HOAc (glacial) 0.13 ml HOAc (glacial) 0.1 ml
[1-14C]-HOAc, Na salt [1-14C]-HOAc, Na salt
(≈ 130 µCi) 0.12 ml (≈ 130 µCi) 0.61 ml
H2O2 solution 70% (v/v) 0.286 ml H2O2 solution 70% (v/v) 0.28 ml
Dequest 2010 (stabiliser) 10 µl None
Dipicolinic acid 2 µl None
Preparation method Heated to 50°C for 3 days in Mixed immediately before use
Sovirel tube
Final concentration PAA 5.02%a, H2O2 22.3%a PAA < 0.04%b
Distribution of 14C: 14.39 µCi/100 µl attributable to 14C: 13.10 µCi/100 µlc wholly
radioactivity HOAc (74%) and PAA (24%)cd attributable to HOAccd
a Determined by cerimetric titration

b Determined by iodometric titration
c Determined by liquid scintillation counting
d Ratio determined by HPLC analysis and liquid scintillation of the appropriate fractions
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ECETOC JACC No.40
A volume of 100 µl of the test and control solutions were applied to an area of 2.5 cm2
of the clipped rat skin using a acrylic glass ring glued to the skin of the animals. Medical
gauze was glued to the top surface of the plastic ring and the animals were then
immediately placed in a metabolic cage for 72 hours. Water-soluble vapours (i.e.
evaporating HOAc and PAA), exhaled CO2, urine and faeces were collected and analysed
at regular intervals. After 72 hours the animals were killed and the total radioactivity
content was determined of the following organs: liver, kidneys, heart, lungs, testes, brain,
stomach, small intestines, caecum/large intestines, muscle and perirenal fat samples,
residual carcass. In a pre-experiment quantitative recovery of radioactivity due to
volatilisation of HOAc and PAA from the test solution and of HOAc from the control
solution in the metabolic cage had been demonstrated after placing samples of the
solutions in the cage.
Body weight gain was not significantly different in the two groups. The skin of the
test group animals was severely damaged after the 3-day exposure period and revealed
substantial areas of scar tissue whereas that of the positive control animals appeared
undamaged. The main results with regard to recovery of radioactivity are summarised
in Tables 17 to 19.
Table 17: Percenta radioactivity recovered after 72 hours (Phillips, 1994a)
PAA test solution Control solution

Evaporated from skin 0.44 ± 0.1 19 ± 11.42
14CO 35.68 ± 7.24 26.97 ± 5.33
2
Urine 10.47 ± 3.02 16.67 ± 3.85

Faeces 2.64 ± 1.2 3.37 ± 1.26
Cumulative total 49.24 66.01
a Values represent the mean % ± SD from 4 rats given a single dermal dose of 100 µl solution
Table 18: Distributiona of radioactivity recovered after 72 hours (modified from Phillips,
1994a)

Evaporated from skin 0.71 ± 0.14 25.86 ± 15.73b
14CO 57.82 ± 4.16 37.10 ± 7.63
2
Urine 17.16 ± 5.16 22.82 ± 4.76

Faeces 4.40 ± 2.31 4.68 ± 1.92
Tissues, carcass 19.91 ± 3.99 9.54 ± 2.79
b Includes one low value of 1 animal
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Table 19: Distributiona of absorbedb radioactivity (%) recovered after 72 hours (Phillips,
1994a)

14CO 58.3 ± 4.2 50.2 ± 2.5
2
Urine 17.3 ± 5.2 30.8 ± 2.5

Faeces 4.4 ± 2.4 6.3 ± 2.4
Tissues, carcass 20.0 ± 4.0 12.8 ± 1.3
b Total recovered minus part that evaporated from skin
Total recovery of radioactivity in air evaporated from skin, expired air, urine and faeces
was about 49% in the test group and 66% in the control group (Table 17). Evaporation
of radioactivity from the rat skin during the treatment (captured in a water trap) was
less than 1% of the applied radioactivity for the test group and 29 to 41% for 3 control
group animals in the first 24 hours. In one control group animal only 2.5% of the total
radioactivity was detected in the water trap within 24 hours.
When the recovered radioactivity is presented as a percentage of the absorbed dose

(dose minus part that evaporated) significant differences between the test and control
animals were obtained, in particular with regard to the amount eliminated in urine (31%
in controls versus 17% in test group animals) and exhaled as 14CO2 (50% in controls,
58% in test group animals). Recovery in the tissues and carcass was 13% in controls and
20% in test group animals.
In the test group 14CO2 exhalation was rapid up to 8 hours following administration
(including initial lag phase of 1 - 2 h), and then continued at a lower rate up to 72 hours.
In the first 24 hours, 5 to 10% of the total recovered radioactivity was excreted in urine.
On day 2 and 3, 1 to 3% was recovered in urine. Excretion of radioactivity in the faeces
of the test group animals varied between 0.4 and 3% of the total recovered radioactivity
per day. About 20% of the total recovered radioactivity was found in the tissues and
carcass of the test animals. Highest tissue levels of radioactivity were observed in the
residual carcass, the liver, the gastro-intestinal tract and the skin. Recovery of radioactivity
was significantly higher than in controls in a number of tissues including kidney, liver,
testes and gastro-intestinal tract.
In 3 of the control animals, 14CO2 exhalation started immediately after application of

the control solution and a substantial proportion of the radioactivity was recovered after
the first 3 hours, thereafter the rate was much lower. Urine recovery of radioactivity was
approximately 5% of the total recovered radioactivity after 24, 48 and 72 hours for all
control animals. Excretion of radioactivity in the faeces of the control group animals
varied between 0.4 and 3% of the total recovered radioactivity per day and was thus
similar to that of the test group animals. In the controls about 9.5% of the total recovered
radioactivity was found in tissues and the carcass. Highest tissue levels of radioactivity
were observed in the residual carcass, the liver, the gastro-intestinal tract and the skin.
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The authors concluded that the metabolic fate of the absorbed [1-14C]acetic acid in the
control animals was consistent with the known fate of HOAc in mammals. Free acetate
is known to be metabolised by extra-hepatic tissues such as muscle and gut and is
incorporated into carbohydrates, fatty acids, glycogen, cholesterol and protein. Acetate
carbon atoms are mainly excreted as CO2 and urea. An exhalation of 50% of the dose as
CO2 is consistent with literature data on acetate. The main differences observed between
the PAA solution and the acetate control treatment were the lower amount evaporating
from the skin within 24 hours and the apparent lag phase in exhalation of radioactive
CO2, the lower excretion in urine and a higher retention of radioactivity in tissues.
The higher dermal absorption could be due to the severe damage of the barrier of the
skin observed after application of the PAA solution, resulting in an enhanced absorption
rate. This would be consistent with the in vitro data of Krüger and Jancke (1976). The
other differences observed could, according to the authors, suggest a different metabolic
fate of the PAA/HOAc mixture compared to HOAc alone. However, the difference in
absorption rate between intact and damaged skin could also explain these differences.
It is possible that the lag phase is due to a lower blood flow in skin capillaries and a
slower distribution due to the formation of micro-emboli from oxygen formation from
H2O2 and/or PAA after a higher absorption rate through damaged skin.
No toxicokinetic data are available for other routes of exposure.
7.2 Evaluation
Although only limited experimental data are available on the absorption and distribution
of PAA, some general assumptions can be derived from the physico-chemical data.
All components of the equilibrium are of low molecular weight, high water solubility,
low fat solubility and have no tendency to bioaccumulate (Section 4.2.5). For the PAA
molecule itself an octanol/water partition coefficient of log Pow = 0.3 was determined
(Table 1). For H2O2, a log Pow < 1 can also be estimated, while for HOAc a log Pow of
-0.31 to -0.17 has been reported (Verschueren, 1983). It can be assumed that absorption
of PAA through skin and mucous membranes is possible, but limited by the high water
solubility and low partition coefficients of the equilibrium compounds. Degradation of
PAA itself and in particular H2O2 at the site of entry may further limit absorption due
to capillary microembolism (Hauschild et al, 1958), detachment of epithelium and
mechanical rupture of tissues close to the port of entry (Sheehan and Brynjolfson, 1960;
Ludewig, 1965; Urschel, 1967). However, a considerable intake of radioactivity (from
PAA and/or HOAc) was observed in damaged skin, once the skin barrier is destroyed
by the corrosive effects of PAA solutions (Phillips, 1994a). In the stomach at pH 2 the
undissociated acid is the predominant species (from the pKa-value of 8.2 a ratio
acid/anion 107/1 can be calculated) which can penetrate into the cells. At a cellular pH
7.4 the ratio of the acid to the anion is smaller (6/1). It is possible that the diffusion
into the cells may be enhanced by the concentration gradient for the undissociated acid.
However, in the stomach fluid and inside the cells enzyme-catalysed degradation is
to be expected. Once absorbed, PAA is expected to be distributed in the body fluid
and metabolised; it can be anticipated that no accumulation in organs or body fat occurs.
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ECETOC JACC No.40
The study of Phillips (1994a) seems to support those assumptions as it was shown
that radioactivity of [1-14C] labelled HOAc and PAA in a PAA solution was mainly
exhaled as 14CO2 and excreted in the urine. Radioactivity recovered in other organs and
tissues is most probably due to the metabolism of HOAc in physiological pathways and
synthesis of biomolecules.
7.3 Metabolism
7.3.1 Enzymatic reactions in vitro
In vitro experiments with a number of different enzymes and peroxo acids showed that
there were no significant degradations of PAA by different lipases, proteases and
butylcholinesterase. Rates of degradation were generally below 0.05 µmol/min/ml
(concentration of the acid 0.02 mM, enzyme concentration 0.3 mM, phosphate buffer
pH 8, 25oC, 15 min). A slightly higher rate of decomposition was observed with pig liver
esterase (2.3 µmol/min/ml) and acetylcholinesterase 0.48 µmol/min/ml under the same
experimental conditions. Generation of PAA was observed when 25 mM acetylcholine
was incubated with acetylcholinesterase 25 Ua /ml and 10 mM of H2O2 at pH 7. H2O2
was consumed within 5 minutes and PAA generated which was then degraded slowly
with a half-life of about 25 min (Kirk et al, 1994).
Several authors have shown that PAA is a substrate of catalases.
In vitro activity of beef liver catalase on PAA was evaluated by Ferri (1990). Beef liver
catalase was dissolved in sodium phosphate buffer (70 mM, pH 7.0). Stock solutions
of PAA (composition not stated) 5 mM in phosphate buffer were pre-treated with 8
nM catalase for 20 min at 20°C. Thereafter the stock solutions were diluted to the final
concentrations. Spectrophotometry was performed using a double beamed
spectrophotometer and thermostatically controlled cell. The difference in the molar
absorption coefficients of the various oxidation states of the haem at 405 and 435 nm
was used to quantify the kinetics of the inter-conversion of the different steps of the
reaction. An amount of 1 nmol PAA corresponded to 5 x 10-3 absorbency units at 505
nm. Samples (70 µl) of the PAA solutions were added to a freshly prepared reaction
mixture of phosphate buffer (0.1 M, pH 7.0), phenol (30 mM), 4-aminoantipyrine (6 mM),
and horseradish peroxidase (2 U/ml). Under these conditions the peroxidase activity
of catalase did not interfere with the assay. Catalase activity on H2O2 was assayed
separately. The catalase reaction followed the summary equation:
a Activity Unit
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Figure 1: Metabolism of PAA (adapted from Ferri, 1990)
[] Theoretical intermediate
a Compound I
b Compound II
PAA Peracetic acid
HOAc Acetic acid
O2 Oxygen
The first step is a first order reaction of catalase with substrate leading to immediate
conversion of the enzyme-substrate complex to the oxidised state (Compound I) and
the release of HOAc. Compound I is spectroscopically identifiable as a stable intermediate.
The second step, first order with regard to Compound II and independent of the PAA
concentration, regenerates the free catalase in a reduction reaction (kinetic constant
k4 = 2 x 10-4 s-1). Oxygen and a second molecule of HOAc are released in that step which
is the rate limiting reaction. The author showed that the catalytic cycle rate for PAA is
independent of the substrate concentration and the rate determining step is the electron
rearrangement inside the cycle rather than the adduct formation. This is different
from the reaction of catalase with H2O2 or alkyl peroxide which is dependent on the
substrate concentration.
Under steady-state conditions the PAA consumption was independent of the PAA
concentration and the zero order rate constant was calculated to be 4 x 10-7 s-1.
Another reaction was catalysed by catalase when the enzyme solution was supplemented
with an excess of ethanol (103 to 104 times the enzyme concentration) prior to addition
of PAA. Under these conditions ethanol was oxidised to acetaldehyde. In this reaction
PAA was used as the source of oxygen for the oxidation reaction of ethanol. Because
of the large excess of ethanol the reaction was only dependent on the PAA concentration
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and the first order rate constant was determined to be 1.1 x 104 mol/l/s. During the
reaction the enzyme spectrum was that of the resting state.
Jones and Middlemiss (1972) determined reaction rates of PAA (36 to 40%, no further
data) with bacterial catalase (from Micrococcus lysodeictikus) or ox liver catalase. The PAA
solutions used in the experiment were pre-treated with a small amount of catalase (2
nM) incubated for 30 min; the absence of H2O2 was assured by cerimetric titration. The
PAA concentrations were determined iodometrically. The formation of Compound I
was followed spectrophotometrically and was much slower than with H2O2. The reaction
was more rapid with the ox catalase than with bacterial catalase. The pseudo first order
rate constants were directly proportional to the PAA concentration, but the second order
rate constants decreased with increasing pH. At pH 7 the first order rate constants for
the formation of Compound I were respectively 1.44 x kHA/mol/s with ox catalase and
5.72 x 10-2 x kHA/mol/s with bacterial catalase. The rate constant apparently depended
on the degree of dissociation and could be described as:
ko = a (kA- - kHA) + kHA (Eq. 10)
where A- is the peroxoacetate ion, HA the undissociated PAA and a the degree of
dissociation.
Different buffer systems showed similar results. From the results at different pH values
the authors concluded that the reaction occurs predominantly with the undissociated
acid. Compound I in this study was remarkably stable with the bacterial catalase, but
less with the ox liver enzyme although a slow regeneration of free catalase eventually
occurred. When ethanol or formate was added to a steady-state concentration of
Compound I, the reaction rate with those substrates greatly exceeded the reformation
of Compound I. The regeneration curves were first order and the pseudo first order rate
constants were proportional to the substrate concentrations.
The reaction with human erythrocyte catalase in vitro confirmed that Compound I
formation is a pH-dependent process. From pH 5.8 to 6.5 the rates were in the same
range, but slowed down as PAA was deprotonated (pKa = 8.2). At pH 5.8 to 6.5 the
apparent 2nd order rate constant for the formation of Compound I was 2.7x104/mol/s
(Palcic and Dunford, 1980). Under the same conditions the rate constant is 6x106/mol/sec
for H2O2 (Schonbaum and Chance, 1976). Below pH 5.8 Compound I was not stable and
decomposed before steady state was achieved.
Addition of PAA to calf serum at a concentration of 0.05% at 4°C resulted in a degradation

of PAA within 4 hours. Degradation is increased in whole blood owing to the presence
of erythrocytes (Mücke, 1977).
One or 0.5 ml, respectively, of a 10% or 20% suspension of rat stomach fluid was added
to 5 or 2.5 ml of aqueous solutions of PAA (5 to 200 mg/l) and PAA concentrations
measured immediately after mixing. The PAA content was reduced by 28 to 76%
depending on the concentrations. Addition of 100 µl of human saliva to 5 ml or 2.5 ml
of PAA solutions containing 5 to 200 mg/l reduced the PAA content by 2 to 42 percent
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immediately after addition of the saliva. These experiments indicate a catalytic

degradation by catalases present in saliva and stomach fluid (Juhr et al, 1978).
The importance of the catalase reaction for the metabolism of PAA can be illustrated by
looking at the distribution of catalases in the mammalian organism.
Catalases are present at a wide range of concentrations in nearly all mammalian cells;
the enzymes are particularly efficient in metabolising large amounts of H2O2 (Chance
et al, 1979). Catalases are located in sub-cellular compartments, mainly in peroxisomes
(De Duve and Bauduin, 1966). Soluble catalases were found in erythrocytes (Saito et
al, 1984).
The highest catalase content is observed in cells of the duodenum, liver, spleen, kidney,
blood, mucous membranes and other highly vascularised tissues; the lowest catalase
activity occurs in brain, thyroid, testes and connective tissue cells (Matkovics and Novak,
1977).
For a more detailed discussion of catalase activity, inter- and intra-species differences,
the reader is referred to an ECETOC assessment of hydrogen peroxide (ECETOC, 1993,
1996).
7.3.2 Non-enzymatic degradation
In the absence of metal ions, diluted PAA solutions may undergo a pH-dependent
hydrolysis yielding HOAc and H2O2. In the presence of metal ions, PAA may also
decompose via the dismutation reaction to oxygen and HOAc (Mücke, 1977, see also
Sections 2 and 3). While PAA is relatively stable at pH values around pH 2 it rapidly
degrades to HOAc and oxygen at pH values at or above 7. PAA is stable at the pH of
the stomach (pH 2) but will probably be degraded in the intestinal tract and locally after
absorption in the cells. These reactions may play a role under physiological conditions.
Reaction of PAA with reducing agents such as cysteine or gluthathione leads to a rapid
reduction of PAA to HOAc (Mücke, 1977). This is likely to be important for the metabolic
detoxification of PAA.
7.4 Elimination
Due to its rapid metabolism it can be assumed that PAA will not be excreted unchanged
in urine, but will be degraded to oxygen and HOAc, the latter being further metabolised
via normal physiologic pathways, ultimately to CO2 and water. After dermal absorption
of a PAA solution containing [1-14C]-labelled PAA and HOAc it has been shown that
the 58% of the absorbed radioactivity was exhaled as 14CO2 and 17% was excreted in
the urine (Philips, 1994a) (Section 7.1).
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7.5 Summary and Conclusions

Only limited data are available on the kinetic properties of PAA. Due to the high water
solubility and the low octanol water partition coefficients and possibly limited absorption
by the formation of micro-bubbles of oxygen in the capillaries and tissues surrounding
the exposed tissues, absorption into the circulation is assumed to be limited (ECETOC,
1993, 1996). However, skin damaged due to the corrosivity of PAA solutions can enhance
the absorption of the components PAA and HOAc. In the stomach at pH 2 the
undissociated acid is the predominant species (ratio acid/anion 10 7/1) which can
penetrate into the cells. At a cellular pH 7.4 the ratio of the acid to the anion is smaller
(6/1). However, in the stomach fluid and inside the cells enzyme catalysed degradation
is to be expected. Distribution is only likely in the body fluids and limited by the
degradation of PAA. PAA may be degraded in the organism either non-enzymatically
by hydrolysis, dismutation or reaction with reducing agents (cysteine, GSH), or
enzymatically by the catalase reaction. The catalase reaction with PAA is independent
of PAA concentration and may therefore be saturated. H2O2 is degraded rapidly by
peroxidases, catalases and a number of other enzymes and antioxidants. As re-
equilibration is probably slow, the influence of the withdrawal of H 2O2 from the
equilibrium on the degradation of PAA cannot be predicted from the available data.
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8. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO TEST SYSTEMS
8.1 Acute Toxicity
8.1.1 Oral
A number of oral acute toxicity studies have been carried out in rats using aqueous
solutions with different concentrations of PAA ranging from 0.89 to 40%. Details of these
studies including the composition of the PAA solutions tested are shown in Table 20.
Some studies were carried out keeping the volume constant and changing the PAA
concentration according to the dose. Other studies were carried out using a constant
concentration of PAA and changing the volume of administration according to the dose
(indicated by a footnote in Table 20). In the older studies, the test concentrations were
nominal, calculated from the basic PAA grade. In the most recent studies the PAA quality
was analysed and the concentration of components measured. The more recent studies
were carried out in accordance with standard OECD/EU/US-EPA and international
GLP guidelines.
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Table 20: Acute Oral Toxicity in Rats
Strain Sex Composition (%) pH LD50a LD50a Effects observed Reference CoR
PAA H2O2 HOAc (mg/kgbw) (mg PAA/kgbw)
Sprague-Dawley M+F 0.15 0.64c NS NS > 5,000 > 7.5 None Freeman, 1991a 1a
Wistar M 0.89 7.27 10.85 NS > 2,000 > 17.8 Severe inflammation of gastro-intestinal tract Den Besten, 1994 1a
F 1,663 14.8
M+F > 2,000 > 17.8
Wistar M 2 7 19 < 0.7 1,175 23.5 No gross alterations at necropsy Joakimson da Silva and 3a
Keiko s. Coimbra, 1990a
Sprague-Dawley, M 4.89 19.72 10d NS 316 15.5 Local irritation in gastro-intestinal tract, nose, eyes Kuhn, 1996a; 1a
F 118 5.8 and respiratory tract, diarrhoea Loera, 1996e
M+F 185 9.0
Sprague-Dawley M 5f 22f 10f NS 1,993 99.7 Abdominal gripping and distension, loss of muscle Freeman, 1998 1a
F 1,859 93 control, gait disturbances, eye irritation, whitening
M+F 1,922 96.1 of tissues and blood in gastro-intestinal tract
Sprague-Dawley M 5.6 26.9 7.6 0.1 3,271 183.2 Soft faeces, reduced activity, irritation of Haynes and Brightwell, 1a
F 4,217 236.2 gastro-intestinal tract 1998ae
M+F 3,622 202.8
Sprague-Dawley M 10 NS NS NS 2,540g 254 Sedation, local irritation of Degussa, 1977a 1d
F 2,390g 239 gastro-intestinal tract
Sprague-Dawley M+F 10.85 17.19 19 NS 200h - 1,000 21.7 - 325.5 Congestion of different organs, adherence Gomond, 1998 2e
of stomach, liver and gastro-intestinal tract
Sprague-Dawley M 11.69 18.05 20i NS 846 98.9 Kuhn, 1996b; 1a
F 314 36.7 Loera, 1996

M+F 652 76.2
Wistar M 14j 23j 16j 0.5 330j 23.1 No gross alterations at necropsy Joakimson da Silva and 3a
Keiko s. Coimbra, 1990b
ECETOC JACC No.40
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Table 20 continued
Strain Sex Composition (%) pH LD50a LD50a Effects observed Reference CoR
PAA H2O2 HOAc (mg/kgbw) (mg PAA/kgbw)
Wistar M 15 21k 16k < 2k 1,026 153.9 Local irritation of gastro-intestinal tract, Degussa, 1982ae 1b
F 1,015 152.3 respiratory tract and eyes
Sprague-Dawley M 17 22.9 NS 4 > 1,000 - < 1,260 > 170 - < 214.2 Cascieri and Freeman, 2b
F < 397 < 67.5 1983a
Sprague-Dawley M+F 35 7.3 NS NS 50 - 500 17.5 - 175 Local irritation of respiratory tract and gastro Freeman, 1987 1a
intestinal tract (blood-filled stomach and intestines)
Albino F 36 - 40 5 30 NS 263 95 - 105 Restlessness, increased respiration and cyanosis, Busch and Werner, 1974e 2e
hyperaemia and oedema of the gastro-intestinal
tract, necrosis of kidney tubules
Albino F 100 NA NA NS 314.8 314.8 Restlessness, increased respiration and cyanosis, Busch and Werner, 1974e 2e
hyperaemia and oedema of the gastro-intestinal
tract,necrosis of kidney tubules
a Median dose expected to cause the death of 50% of the test animals after a 14 day observation period, except for the studies by Busch and Werner, who observed
the rats for 3 days
b Code of reliability (Appendix B)
c Assumed value
d From Solvay, 1997a
e Dosage by constant volume
f Before dosing diluted to 1.25% PAA, 5.5% H2O2 and 2.5% HOAc
g Reported as 3.00, 3.00, 2.21 and 2.08 ml/kgbw; converted to mg/kgbw assuming a relative density of 1.15 (Table 2)
h Diluted to increase the dosed volume to 2.5 ml/kgbw

i From Solvay, 1997b
j Dispersed (1:1) in vegetable oil
k From Degussa, 1996b
F Female
M Male
NA Not applicable
NS Not stated
In the study of Den Besten (1994), 1 male rat and 4 females at the two highest dose groups
were killed in extremis within 5 days of dosing. Clinical signs consisted of abnormal
posture and gait, decreased locomotion, sniffeling, respiratory difficulties, ptosis and
distended abdomen. Recovery became apparent from 2 days post dosing onwards,
although surviving females at the highest dose level did not fully recover after
14 days of observation. Gross alteration in the female animals that were killed in extremis
revealed severe inflammatory changes in the gastro-intestinal tract. No changes were
seen in the survivors sacrificed at the end of the observation period.
Kuhn (1996a,b) administered two different concentrations of PAA (4.89 and 11.69%) to
rats. Both concentrations caused overall the same clinical signs: decrease of activity as
well as diarrhoea, nasal and ocular discharge, piloerection, gasping, polyuria, ptosis,
staining of muzzle and back, salivation and respiratory chirp. In the vast majority of the
animals, the signs were no longer evident at the end of the observation period of
14 days. The necropsy of the dead animals revealed gas in the gastro-intestinal tract and
discoloured stomach, intestine, lungs, liver and spleen. The majority of the findings are
indicative of the local irritant effect of the product; the authors did not explain the
observed discoloration of the lungs and the spleen. No abnormalities were seen in
survivors at the end of the observation period.
In the study of Freeman (1998), the most significant clinical signs observed were
abdominal gripping and distension, loss of muscle control, squinting eyes, staggered
gait, tremors, walking on toes, hypersensivity to touch, splayed hind limbs and
hypothermia. Recovery was essentially complete after 7 days of dosing even if some
signs persisted for up to 13 days. Examination of the animals that died revealed blanched
stomachs and intestines, mottled and blanched livers, distended stomachs with thin
linings, darkened red adrenals and white tracheas. Blood was found in the stomach and
intestines. In the animals killed at the end of the observation period, only thinning of
the stomach wall was seen at necropsy.
Haynes and Brightwell (1988a) reported general clinical signs, such as soft or mucoid
faeces, reduced activity and piloerection, at all dose levels. Surviving animals generally
recovered within 3 days. Macroscopic examination of the dead animals revealed
abnormalities in the liver, stomach and regions of the gastro-intestinal tract. The stomach
was commonly distended and white in colour. The intestines were dark red in colour.
The liver either appeared dark or exhibited multiple pale areas. No significant
abnormalities were found on necropsy of the survivors at the end of the observation
period. The macroscopic findings in the dead animals are indicative of a local irritant
effect of the product.
In the Degussa (1977a) study, clinical signs consisted of sedation, bloody discharge from
the nose, ataxia and dyspnoea. Pathological findings were adhesion between the stomach
and adjacent organs, perforation of the stomach in the animals found dead and
haemorrhagic erosions of the stomach wall and oesophagus indicative of a severe
irritation.
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In the study of Gomond (1998), there were no deaths at the low dose level, while the
mortality at the higher doses was between 60 to 100%, but without dose-response
relationship. The autoptic examination of the descendants showed alterations to the
stomach and congestion of different organs. The gross alteration of the survivors at
the end of the observation revealed adhesion of different organs such as stomach,
liver and gastro intestinal tract. No findings were see at the lowest dose level. The signs
consisted of piloerection, abdominal constriction, hypoactivity and lessened muscular
tone. These signs were evident a few hours after the administration and lasted up to 5
to 7 days following treatment. The method of administration of the low dose (dilution
with distilled water) makes interpretation of the results difficult. This is also confirmed
by the lack of a dose-response relationship at the higher dosages, supporting the
hypothesis that all doses tested without dilution were severely irritant to the gastro-
intestinal tract.
In the Degussa (1982a) study, signs indicative of irritation of the gastro-intestinal tract
(writhing syndrome, stilted gait, and tremor), laboured breathing and bloody
lachrymation were observed. Red coloured urine was also observed in females of the
highest dose group. At necropsy adhesions were observed between the viscera and the
peritoneum. The gastro-intestinal mucosa and parts of the liver close to the stomach
appeared white or greyish in animals of the high dose group. In the lowest dose group
no clinical signs indicating irritation were observed. This dose corresponded to a
concentration of about 3% PAA, 4.5% H2O2 and 4% HOAc.
Cascieri and Freeman (1983a) observed mortality at all dose levels in males and in all
but the 250 and 630 mg/kgbw doses in females. These data were not in accordance with
the dose-response relationship and they were considered by the authors as indicative
of the instability of the test material. The latter dose groups were tested at a later date
than the preceding dose groups. The predominant clinical signs were decreased
locomotion, rales, haematuria, abdominal distension, abdomino-genital staining,
unthriftiness recumbacy, oral and nasal discharge. Gross necropsy of the decedents and
the survivors included gross alteration of the stomach, liver and intestines.
Freeman (1987) reported that all animals died at 500 mg PAA/kgbw and one animal
at 50 mg/kgbw. Predominant clinical signs were dyspnoea, oral discharge,
chromorhinorrea and decreased locomotion. Gross lesions among descendants included
mainly blood-filled stomachs and intestines. There were no gross internal alterations in
any surviving rats.
A preliminary test with undiluted 40% PAA in Sprague-Dawley rats was aborted since
all animals died from perforating ulcerations in the oesophagus and stomach at
0.5 ml/kgbw (226 mg/kgbw), the lowest dose tested (Degussa, 1977b; CoR 3a).
Several other studies are reported in the literature. Different values of LD50 (median
dose expected to cause the death of 50% of the test animals) are cited but with a poor
level of detail regarding the concentration and formulation of PAA used and the design
of the study. This reduces their value for the toxicological evaluation of PAA (Tichácek
1972; Busch and Werner 1974; Merka and Urban, 1976; Reagan et al, 1983; all CoR 3a).
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Evaluation
The acute oral toxicity data on the different PAA solutions tested do not show a consistent
pattern that can be related to PAA dose or concentration, even when the composition
appears to be similar. The test results also seem not related to the H2O2 concentration,
but rather to the total composition of the tested formulation. The fact that the volume
of administration was fixed or variable did not help to explain the differences seen in
the results of the studies. Symptoms and pathological findings were similar in all studies
and are consistent with the irritant/corrosive properties of the test material. Formulations
containing less than 10% PAA seem to possess a low oral toxicity.
8.1.2 Dermal
Several dermal toxicity studies have been carried out in rats and rabbits with aqueous
solutions of PAA at concentrations ranging from 0.89 to 11.6%. The most reliable dermal
toxicity studies are summarised in Table 21. When indicated by the protocol, the PAA
solutions were administered undiluted, adjusting the volume of administration according
to the dose. The test concentrations were nominal, calculated from the basic PAA grade.
In the most recent studies, the PAA quality was analysed and the concentration of
components measured. The more recent studies were carried out in accordance with
standard OECD/EU/US-EPA and international GLP guidelines.
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Table 21: Acute Dermal Toxicity
Species Sex Composition (%) pH Exposure LD50a LD50a Effects Reference CoRb
(strain) PAA H2O2 HOAc conditions (mg/kgbw) (mg PAA/kgbw)
Rat
Sprague-Dawley M+F 0.15 0.64c NS NS 24 h, occluded > 2,000 >3 No signs of toxicity, no pathological Freeman, 1991b 1a
organ findings, no changes at site of
contact
Wistar F 0.89 7.27 10.85 NS 24 h, occluded > 2,000 > 17.8 No signs of toxicity, no pathological Koopman, 1994 1a
findings, white and red spots at the
application site, encrustation in some
animals 1 week after administration
Wistar M 2 7 19 0.7 NS, > 12,000 > 240 No signs of toxicity, no pathological Joakimson da Silva 3a
presumably changes and Keiko s. Coimbra,
non-occlusive 1990d
patch
Wistar M 14d 23d 16d 0.5 > 12,000 > 1,680 No signs of toxicity, no pathological Joakimson da Silva 3a
changes and Keiko s. Coimbra,
1990c
Rabbit
New Zealand M 4.89 19.72 10e NS 24 h, 1,280 62.6 Decreased activity, diarrhoea, nasal Kuhn, 1996c; 1a
Albino F semi-occlusive 1,040 50.9 discharge, ptosis, salivation andslow Loera, 1996
M+F 1,147 56.1 gazing. No pathological changes
attributable to the test substance. Local
effects: moderate to severe erythema,
slight to severe oedema, eschar
formation
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Table 21 continued
Species Sex Composition (%) pH Exposure LD50a LD50a Effects Reference CoRb
(strain) PAA H2O2 HOAc conditions (mg/kgbw) (mg PAA/kgbw)
Rabbit
New Zealand M 11.69 18.05 20f NS 24 h, occlusive 1,912 223.5 Decreased activity, diarrhoea, nasal Kuhn, 1996d; 1a
Albino F 1,990 232.6 discharge, ptosis, salivation, slow Loera, 1996
M+F 1,957 228.8 gazing. No pathological changes
attributable to the test substance. Local
effects: moderate to severe erythema,
slight to severe oedema, eschar
formation
New Zealand M+F 17 22.9 NS 24 h, occlusive > 200 > 34 No signs of toxicity. No pathological Cascieri and 1b
White changes attributable to the test Freeman, 1983b
substance. Local effects: severe
erythema, blanching of skin, eschar
formation, exfoliation in 3 animals
a Observation period: 14 days

c Assumed value
d Dispersed (1:1) in vegetable oil
e From Solvay, 1997a
f From Solvay, 1997b
F Female
M Male
NS Not stated
Several other studies carried out in rats and mice are reported in the literature. Different
values of LD50 are cited but with a poor level of details regarding the concentration and
formulation of the PAA solution tested and the study design. The toxicological relevance
of these studies is therefore questionable (Reagan and Becci, 1983; CoR 3a; Benes et al,
1966; CoR 4d; Kramer et al, 1987a; CoR 3a).
Evaluation
Overall, the dermal toxicity depends on the degree of skin damage caused by the different
PAA solutions. Only Kuhn (1996c) reported signs of toxicity (nasal discharge) that could
be attributed to systemic effects at the high dose levels. However, it is likely that these
signs were caused by additional inhalation exposure in this particular study.
8.1.3 Inhalation
Various inhalation toxicity studies have been carried out in rats and mice with solutions
containing up to 40% PAA. Details of the studies and the composition of the PAA solution
are shown in Table 22. PAA was tested as vapour or aerosol. In most studies, no morbidity
or mortality was seen.
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Table 22: Acute Inhalation Toxicity
Species Sex Composition (%) pH Duration LC50 LC50 Reference CoRa

(strain) PAA H2O2 HOAc (h) (mg/m3) (mg PAA/m3)
Rat Aerosol
Wistar M+F 15 NS NS NS 4 505 - 1,263 76 - 189 Terrell, 1986a 4a
Wistar M 5.4 ≥ 19 10 NS 4 NS 213b Janssen and Van Doorn, 1994 1a
F NS 186b
M+F 4,080 204b
Sprague-Dawley M+F 4.5 27 16.7 NS 4 > 5,350 > 241 Dudek, 1984 1a
Sprague-Dawley M+F 0.15c 0.67c 0.30c NS 4 > 7,669 > 117d Whitman, 1991 1d
Rat Vapour
Sprague-Dawley M 35.5 6.8 39.3 NS 4 ≈ 490def Hutt and Kinney, 1985 1a
Wistar M+F 5 20g 10g NS 4 > 5,000 > 200h Biffi, 1992a 2e
Wistar M+F 5 20g 10g NS 4 > 50,000 > 2,000h Biffi, 1995 2e
Mouse
CBA, NS 36-40i NSi NSi NS 1 NS 1,334 - 5,404f Krüger and Kruschinski, 1982 2a
0.5 NS 4,171f
a Code of reliability (Appendix B) f Vapour/aerosol

b Nominal concentrations calculated by the authors from g From Solvay, 1997a
aerosol composition, assuming 5% PAA content h Calculated from partial vapour pressure of PAA in a 5% solution (Table 2)
c i
PAA 5%, diluted (1:33) in distilled water; H2O2 and HOAc Inferred from other publications on the same compound
concentrations from FMC, 1998a F Female
d Measured concentrations M Male
e Approximate Lethal Concentration NS Not stated
Aerosol studies
Terrel (1986a) exposed rats to aerosol (or vapour, not clearly stated in the report )
concentrations of PAA ranging from 18 to 2,138 mg/m3. The animals were kept under
observation for 14 days after the exposure. During the exposure the animals showed a
range of clinical signs which consisted of blinking, foaming, gasping, nasal discharge,
salivation, lachrymation, ptosis, laboured respiration, twitching, chewing motion,
convulsions, staggering, cornea opacity or death depending on the concentration. Post-
exposure clinical signs were laboured respiration, nasal discharge, gasping, lachrymation,
haemorrhage from the eye, cornea opacity, blindness, staggering, loss of righting reflex,
crusty appearance, piloerection or death depending on the dose. Gross necropsy of
the animals that died during the observation period revealed alterations to the lungs
and thymus, enteritis, swollen nose, congested nasal cavity and trachea, thickening of
the oesophagus and larynx. Animals that were killed at the end of the observation period
showed similar alterations. A more detailed evaluation of the study is not possible since
only the summary is available.
Janssen and Van Doorn (1994) tested a 4.7 - 5.4% solution of PAA in rats exposed nose-
only to aerosols containing measured concentrations of 87, 163, 185 and 267 mg PAA/m3.
The animals were observed for 14 days after exposure. Mortalities were observed only
in the two highest dose groups. Clinical signs consisted of apathy, respiratory distress,
reduced respiratory rates, decreased fear reaction, freezing and reduced locomotion
activity. A number of clinical signs indicative of irritant effects of the product were noted.
Surviving animals suffered from a temporary loss of body-weight. Animals that died
during the observation period revealed increased lung weight and pulmonary oedema.
No macroscopic alterations were seen at necropsy carried out at the end of the observation
period.
In the study of Dudek (1984), none of the rats died during the study. All the animals
showed irregular breathing and damp fur during the exposure. No macroscopic
alterations were found at necropsy.
Whitman (1991) exposed rats whole-body to an aerosol / vapour (nominal concentration

66,171 mg/m3, actually 7,669 mg/m3) containing 117 mg PAA/m3 and observed them
for 14 days. A particle size analysis was attempted, but did not produce any valid results
due to the extremely high (> 99%) water content of the test atmosphere and the volatility
of the test material. No rats died during the study. Clinical signs observed during the
exposure were decreased activity and closed eyes. After the exposure some animals
showed ocular discharge that lasted for up to 8 days. At necropsy all animals appeared
free from any test-related macroscopic alterations.
Janssen (1989a,b) exposed rats (Wistar, M and F) nose-only for 0.5, 1 and 1.5 hours to an
aerosol nebulised from a solution containing 15% PAA (14% H2O2 and 28% HOAc). Two
separate tests were carried out. In the first test, the animals were exposed for 15, 30 and
60 minutes (5 male rats per exposure period); in the second test another group was
exposed for up to 90 minutes. The mean measured concentration of PAA in the first test
ranged from 0.13 to 1.45 mg/l (130 - 1,450 mg/m3), in the second test the measured
concentration varied from 0.17 to 0.59 mg/l (170 - 590 mg/m3). The animals were kept
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under observation for 14 days after exposure. At necropsy, the organs of the respiratory
tract as well as the head of the animal were removed and preserved for histopathological
examination (the nasal cavities were also flushed with fixative). Two animals exposed
to 590 mg/m3 for 60 minutes were killed in extremis 24 hours after the exposure; mortality
was also observed in the highest dose group exposed for 60 minutes in the first test.
Clinical signs consisted of noisy breathing, sniffing, sneezing, nasal discharge and
intensified grooming. The severity and time of disappearance of the clinical signs
increased with the exposure level and duration. No clinical signs persisted until the end
of the observation period. Macroscopic examination of animals that died or were killed
in extremis during the observation period revealed alteration to the respiratory tract (red
mucosa of internal nares and trachea, blood in trachea and red lungs), while gas was
found in the gastro-intestinal tract; the latter was attributed to air swallowed during the
exposure. Histopathology of the upper respiratory tract revealed tissue damage limited
to the anterior parts of the nasal cavity in the area where the epithelial lining changes
from respiratory to olfactory epithelium. Histopathology of the lungs revealed blood
and alveolar macrophages in one animal and hyperplasia and metaplasia in two others.
No alterations were found in the animals that were killed at the end of the observation
period. No LC50 values were calculated in this study.
Benes et al (1966; CoR 4b as cited by Heinze et al, 1982) performed acute inhalation
studies in rats (strain and sex not stated). Exposure to aerosols containing 7.2, 72, or
237.6 mg PAA /m3 for 4 hours resulted in signs of restlessness in the low dose group.
Additional signs in the mid-dose group consisted of lachrymation and laboured breathing.
In the high dose group lung oedema was observed and one animal died (group size not
reported).
Vapour / aerosol studies

Hutt and Kinney (1985) administered a vapour/aerosol atmosphere to groups of 6 male
Sprague-Dawley rats. The animals were exposed nose-only for 4 hours to PAA
concentrations varying from 260 to 670 mg/m3. The test atmosphere was sampled
and PAA concentrations analysed by iodometric titration. After the exposure the animals
were kept under observation for 14 days. During the exposure the animals showed
moderate red nasal discharge and did not exhibit a normal startle response. Rats exposed
to 490 mg/m3 had laboured breathing. Two rats exposed to 490 mg/m3 and one rat
exposed to 670 mg/m3 died, 1 and 2 days respectively after the exposure. One to 4 days
after cessation of exposure all animals showed lung noise, laboured breathing or gasping
and nasal and ocular discharge. At lethal concentrations some rats had diarrhoea, hunched
posture, wet or stained perineum and discoloured fur.
Biffi (1992a, 1995) carried out two different acute inhalation toxicity studies with a
solution of 5% PAA containing 20% H2O2 and 10% HOAc. (Assuming the vapour phase
contained 2% H2O2, 4% PAA and 9% HOAc, the respective partial pressures were 0.4,
0.3 and 0.8 hPa). Rats were exposed whole-body to a vapour with a nominal concentration
of 5,000 mg/m3 (limit test) and 50,000 mg/m3. No mortality was seen. Clinical signs
consisted of dyspnoea, piloerection and hyperaemia of nasal mucosa. Body weight gain
was not affected. No alterations were found at necropsy after the 14-day observation
period.
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Krüger and Kruschinski (1982) studied the influence of fog density, i.e. the amount of
liquid in 1 m3 of air, on the concentration of PAA aerosol and vapour when aerosols
were generated from solutions of different concentrations. Aerosols with droplet size
ranging from 0.6 to 4 µm diameter, the majority between 1.5 and 2 µm (i.e. in the respirable
range), were generated in a volume of 0.138 m3. Groups of 10 CBA mice (sex not stated)
were exposed to aerosols generated from diluted PAA solutions (1 to 23%; content of
H2O2 and HOAc not stated) yielding fog densities of 7.25, 14.5, 29, 58 and 116 ml/m3
for 1 hour. The post-exposure observation period lasted 47 hours. When the exposure
time was held constant the lethal concentration was dependent on the fog density. A
50% death rate was reported for a 3.6% PAA solution (corresponding to a LC50 of
1,334 mg PAA/m3) at a fog density of 116 ml/m3 and an 18.5% PAA solution
(corresponding to an LC50 of 5,404 mg PAA/m3) at a fog density of 7.25 ml/m3. In a
second experiment, a 30-min LC50 of 4,171 mg/m3 was obtained with aerosols created
from 4, 5, and 8% PAA solutions with a fog density of 116 ml/m3. According to the
authors the LC50 was not related to the concentration of PAA expressed in mg/m3.
Furthermore, the aerosol was probably not stable over the experimental period and
some PAA may have volatilised into the vapour phase, which would have complicated
the determination of the actual concentration of PAA in the aerosols.
The same authors (Krüger and Kruschinski, 1982) exposed groups of 3 CBA mice (sex
not stated) in closed chambers to atmospheres saturated with vapour/aerosol from PAA
solutions of 5, 17, 20 and 40% PAA. The concentrations of PAA in the vapour phase were
calculated using an equation derived from experimental determinations of PAA vapour
equilibrium concentrations over open PAA solutions of different concentrations at
different temperatures. Death of the animals occurred after inhalation of 3,800 mg PAA
/m3 for 1 hour or 260 mg/m3 for 20 hours.
Other acute inhalation studies are reported in the literature. The lack of details regarding
the study protocol and the experimental conditions prevents their use in a meaningful
evaluation of the inhalation toxicity of PAA in experimental animals (Tichácek, 1972;
Merka and Urban, 1976; Spiegelberger et al, 1984; all CoR 3a).
Evaluation
The available acute inhalation studies with aerosols and vapour derived from different
PAA solutions suffered from the difficulty of generating and maintaining a stable
atmosphere of PAA, and accurate measurement of the composition of the test atmosphere
and particle size of the aerosol. The resulting LC50 values should therefore be treated
with circumspection.
A common finding of those studies was local irritation of the respiratory tract, which
seems more pronounced with PAA aerosols than vapours.
8.1.4 Intravenous
In mice, an intravenous LD50 of 17.86 mg/kgbw was reported (composition and

concentration of PAA solution not specified) (Li et al, 1988; CoR 4). Gloxhuber and Kästner
(1983; CoR 2c), testing a formulation containing 4.6% PAA, 29.4% H2O2 and 7.4% HOAc
in CF1 mice, determined an LD50 value of 212 mg PAA/kgbw.
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8.1.5 Summary and evaluation
The acute toxicity of PAA has been studied in experimental animals. The oral, dermal
and inhalation routes are the most relevant routes of administration for health hazard
assessment.
PAA is of moderate acute toxicity via the oral route. The acute oral toxicity of PAA
formulations is dependent on the composition (i.e. the content of PAA, H2O2 and HOAc)
and the concentration of the applied test solution. PAA formulations containing less
than 10% of PAA are usually of low oral toxicity.
The acute dermal toxicity of PAA formulations is relatively low, depending on the applied
concentration and presence of local irritation.
The available acute inhalation toxicity studies in rats and mice with aerosols and vapours
derived from different PAA formulations suffer from difficulties in achieving and
measuring constant concentrations due to the instability of the test substance itself and
the aerosol droplets. Consequently LC50 values derived from such studies show a wide
variation. The main effect in all studies was local irritation of the respiratory tract.
The predominant effect of PAA in all acute toxicity studies is local irritation at the site
of contact, the extent of which depends on the concentration and the composition of the
applied test solution.
8.2 Skin, Respiratory Tract and Eye Irritation, Sensitisation
8.2.1 Skin irritation
Rabbits
An overview of the available skin irritation studies in rabbits and composition of the
PAA formulation tested is presented in Table 23.
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Table 23: Skin Irritation Studies in Rabbits
Concentration Composition (%) Dilution Exposure Result Reference CoRb

applieda duration
(% PAA) PAA H2O2 HOAc
40 36-40 < 5 45 None 4h Corrosive Janssen and Pot, 1987 2b
17 17 23 16 None 4h Corrosive Cascieri and Freeman, 1983c 1a
15 15 15 30 None 4h Corrosive Janssen and Pot, 1987 2b
15 14-15 22-23 16 None 4h Corrosive Degussa, 1982b 1b
15 14-15 22-23 16 None 3 min Corrosive Degussa, 1990b 1a
10 10 <5 25 None 3 min Corrosive Degussa, 1988a 1a
5 20c 10c NS 1:4 24 h Corrosive Biffi, 1992b 2b
5 5 20 10 None 4h Corrosive Janssen and Pot, 1987 2b
5 5 24-25 4-5 None 45 min Corrosive Degussa, 1988b 1a
5 5 24-25 4-5 None 3 min Moderate to Degussa, 1988b 1a

severe irritant
3.87 15.5 22 15 1:4 1h Corrosive Van Beek, 1980 2e
3.87 15.5 22 15 1:4 3 min Not irritant Van Beek, 1980 2e
3.4 34 7.5 40 1:10 24 h Corrosive Duprat et al, 1974 2e
0.35 14 23 16 1:40 24 h Not irritant Joakimson da Silva and 2e

(slight erythema) Keiko s. Coimbra, 1990e
0.34 34 7.5 40 1:100 24 h Slight irritant Duprat et al, 1974 2e
0.20 2 7 19 1:9 24 h Not irritant Joakimson da Silva and 2e

(slight erythema) Keiko s. Coimbra, 1990f
0.17 34 7.5 40 1:200 24 h Slight irritant Duprat et al, 1974 1d
0.15 5-6 22-23 10-11 1:33 4h Not irritant Freeman, 1991c 1a
0.034 34 7.5 40 1:1,000 24 h Not irritant Duprat et al, 1974 1d
a Sample volume for all tests: 0.5 ml

b Code of Reliability (Appendix B)
c From Solvay, 1997a
NS Not Stated
PAA solutions of 40% (Janssen and Pot, 1987), 17% (Cascieri and Freeman, 1983c),
15% (Degussa, 1982b; Janssen and Pot, 1987) and 5% (Janssen and Pot, 1987; Biffi, 1992b)
were found to be corrosive to rabbit skin. The test solutions were applied at a volume
of 0.5 ml for 4 hours using standard skin irritation protocols (Draize Test).
Exposure of the skin of one animal to 0.5 ml PAA 15% for 3 minutes under occlusive
conditions resulted in white to yellowish discoloration of the application site and
deepening of the treated skin area. Severe erythema was observed at the border of the
application site and slight oedema was reported. Microscopic examination revealed
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complete coagulation necrosis of the epidermis and upper third of the corium including
skin adnexae. The damage developed within 1 hour. It was concluded that 15% PAA
was corrosive after 3 minutes of occlusive exposure (Degussa, 1990b).
After exposure of 3 rabbits to 10% PAA for 3 minutes under occlusive conditions
whitening of the skin was observed 1 hour after removal of the patch. After 24 hours
severe damage of the skin developed with necrosis up to 5 mm in depth (Degussa, 1988a).
Groups of 6 male New Zealand white rabbits were exposed to PAA 5% for 24 hours
under occlusive conditions. The patches were removed 24 hours after the application
and the skin was washed using saline solution. The alterations were scored using the
Draize method, from 1 to 7 days after exposure. The medium score was 4.00, i.e. PAA
was extremely irritant (Biffi, 1992b).
Groups of 3 rabbits were exposed to PAA 5% for 3 or 45 minutes under occlusive

conditions. After the 3 minutes exposure period, moderate to severe erythema and very
slight to slight oedema (primary irritation index 3.3) were observed. The effects were
completely reversible within 14 days. Exposure for 45 minutes resulted in corrosive
effects. For humane reasons the animals were killed after two days (Degussa, 1988b).
An in vitro skin corrosion study using Corrositex Continuous Time Monitor Assay
was also conducted with 5% PAA. The results indicate that a 5% solution is corrosive
according to the US Department of Transport (DOT) Packing Group II classification
system (Nims, 1996a).
A 3.4% test solution (from 3.4% PAA, diluted 1: 10) was corrosive when applied to rabbit
skin for 24 hours in a volume of 0.5 ml (Duprat et al, 1974). A 3.87% (diluted) PAA solution
was placed in contact with the skin of rabbits for 3 minutes (4 animals) or 60 minutes (6
animals). There was no skin reaction other than slight erythema following the 3-min
exposure. Severe skin reactions were noted in animals exposed for 60 minutes to the
final concentration of 3.87% PAA, indicating a corrosive response (Van Beek, 1980).
Duprat et al (1974) reported slight irritation after exposure of rabbit skin to 0.34% or
0.17% test solutions for 24 hours. Joakimson da Silva and Keiko s. Coimbra (1990e,f)
found no skin irritation after exposure to a 0.20% solution or 0.35% solution for 24 hours
under an occlusive patch.
PAA was evaluated in rabbits in the Draize test. Solutions of 0.15% PAA were in contact
with the skin for 4 hours under occlusive wrap. No irritation was noted at any site
(Freeman, 1991c). Exposure of rabbits to 0.034% had no effect on the skin other than
reversible enlargement of scars in scarified skin areas (Duprat et al, 1974).
Guinea pigs
Bulnes et al (1982a; CoR 3c) exposed the depilated skin of 20 guinea pigs to dressings
impregnated with 1 or 3% PAA (further composition not stated) solutions for up to
5 hours. Animals exposed to 3% for 2 hours or more developed an acute dermatitis. No
irritation was noted after exposure to 1% for up to 5 hours under the conditions of the
experiment. In another study, Bulnes et al (1982b; CoR 3c) exposed guinea pigs via cage
humidification to 1% or 3% PAA solution for a single exposure. Skin tissue was saved
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24, 48 and 72 hours after exposure for histopathological evaluation. Animals exposed
to 1% or 3% solutions had no changes to skin sections compared to untreated control
animals. Neither of these studies (Bulnes et al, 1982a,b) are appropriate for evaluation
of skin irritation because the study design is not a standard protocol for this end point.
Kramer et al (1987a; CoR 2c) attempted simulation of skin disinfection with PAA in
surgical hand disinfection, using guinea pigs. They found no irritation in guinea pigs
after 5 consecutive applications (presumably 5 minutes each time) of 0.5% PAA (diluted
from equilibrium PAA 40%, 14% H2O2 and 27% HOAc). Moderate erythema was noted
when 0.5% PAA was applied for 5 minutes after soaping, brushing and washing of
the animal skin (3 x 3 min). Focal necrosis and eschar formation was observed after
soaping, brushing and washing (2 x 3 min) and subsequent application of 0.5% PAA for
5 minutes. Soaping, brushing and washing alone led to mild erythema after 3 x 3 min
and moderate to severe erythema after 2 x 3 min.
8.2.2 Eye irritation
An overview of the available eye irritation studies in rabbits and composition of the
PAA formulation tested is presented in Table 24.
Table 24: Eye Irritation Studies in Rabbits
Concentration Composition (%) Dilution Exposure Result Reference CoRb

applieda PAA H2O2 HOAc duration
(% PAA) (h)
17 17 23 16 4 Corrosive Cascieri and Freeman, 1b

1983d
5 20c 10c NS 24 Corrosive Biffi, 1992c 2b
3.4 34 7.5 40 1:10 24 Corrosive Duprat et al, 1974 2e
0.35 14 23 16 1:40 24 Corrosive Joakimson da Silva and 2e

Keiko s. Coimbra, 1990g
0.34 34 7.5 40 1:100 24 Severe irritation Duprat et al, 1974 2e
0.22 2 7 19 1:9 24 Severe irritation Joakimson da Silva and 2e

Keiko s. Coimbra, 1990h
0.15 5-6 22-23 10-11 1:33 4 Mild irritation Freeman, 1991d 1a
0.034 34 7.5 40 1:1,000 24 Very slight irritation Duprat et al, 1974 2e
a Sample volume for all tests: 0.1 ml

c From Solvay, 1997a
NS Not Stated
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PAA was corrosive or severely irritant to the rabbit eye at concentrations of 0.2% and
higher (Duprat et al, 1974; Joakimson da Silva and Keiko s. Coimbra, 1990g,h).
Cascieri and Freeman (1983d) tested 17% PAA in rabbit eyes and found that it was
extremely irritant to washed and unwashed eyes. An in vitro test was performed with
5% PAA using the Bovine Corneal Opacity and Permeability test. A classification of
severe irritant was determined (Nims, 1996b).
Groups of 6 male New Zealand white rabbits were exposed to PAA 5%. The product
was instilled into the conjunctival sac at the dose of 0.1 ml/animal. The eyes were
then observed from 1 hour to 7 days after exposure. The alterations to the cornea, iris
and conjunctiva were scored using the Draize method. The index of ocular irritation
was 75.00 at 1 hour and 90.00 from 24 hours up to 7 days. The alterations had not resolved
after 7 days. Based on the Draize scale the author concluded that PAA was irritant (Biffi,
1992c). A more appropriate evaluation would be to consider this solution as corrosive.
Duprat et al (1974) found maximal irritation at 3.4% PAA and extreme irritation at 0.34%,
both with severe irreversible corneal opacity (at 0.34% only 2 of 6 animals) and severe
conjunctivitis, ulceration and iritis. A diluted solution of 0.35% PAA was maximally
irritant (Joakimson da Silva and Keiko s. Coimbra, 1990g). A diluted solution of 0.2%
was severely irritant to rabbit eyes (Joakimson da Silva and Keiko s. Coimbra, 1990h).
When a solution of 0.15% PAA was evaluated in rabbit eyes it was found to be mildly
irritant (Freeman, 1991d; CoR 1a). Similarly, a 0.034% solution caused no effects other
than slight conjunctivitis during the first 24 hours after exposure (Duprat et al, 1974).
8.2.3 Respiratory tract irritation
Janssen (1989c; CoR 1a) nebulised a 15% PAA (14% H2O2, 28% HOAc) solution into
an exposure chamber for 25 minutes. Male Wistar rats were exposed (nose-only) to
the aerosol at concentrations ranging from 9.5 to 40.3 mg PAA/m3 (3.7 to 14.3 mg
H2O2/m3; HOAc not measured) and their respiration rate was monitored. The RD50,
referring to a concentration of PAA inducing a 50% reduction of respiratory rate, was
calculated to be 21.5 to 24.1 mg/m3. Reduction of respiratory rate occurred at levels
from 5 to 10 mg PAA/m3. After termination of exposure the respiratory rates returned
to normal and the animals recovered fully within 3 days. No other clinical signs and no
histopathological changes were observed.
The same author (Janssen, 1990; CoR 1a) exposed male Wistar rats to aerosol
concentrations ranging from 221 to 487.5 mg PAA/m3 (8.45 to 63.05 mg H2O2/m3; HOAc
not measured), generated from a 15% PAA (14% H2O2, 28% HOAc) formulation. Recovery
was complete in the lowest dose group while respiratory rates were still depressed after
24 hours in one animal of the mid-dose (299 to 331.5 mg PAA/m3) and 2 animals of
the high dose group (435.5 to 487.5 mg PAA/m3). Microscopic examination of the nose,
trachea and lungs revealed necrosis in the anterior part of the nose while no treatment-
related effects were observed in the trachea and lungs. The RD50 in this study was
determined to be less than 299 mg PAA/m3.
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Guinea pigs exposed by inhalation to aerosol atmospheres (concentration not reported),

generated from 1 to 3% PAA formulations (further composition not stated), for 3 days
showed eye irritation and coughing. Histopathological examination of the animals 24,
48 or 72 hours after exposure to the 3% solution showed indications of irritation of the
respiratory tract mucosa. No effects were noted following exposure to the 1% solution
(Bulnes et al, 1982b; CoR 3a). This study did not include sufficient detail for further
evaluation to be made.
Spraying cattle in closed stables with 0.4 - 1.6% PAA solutions induced coughing and
moderate lachrymation and salivation (Zrunek, 1966; CoR 4c as cited in Kretzschmar et
al, 1972).
8.2.4 Skin sensitisation
In skin sensitisation tests performed with diluted solutions of 14% PAA (23% H2O2 and
16% HOAc) and 2% PAA (containing 2% PAA, 7% H2O2 and 19% HOAc) administered
intradermallly to guinea pigs, no evidence of sensitisation was found (Joakimson da
Silva and Keiko s. Coimbra, 1990i,j; CoR 3a). However, PAA was diluted (1 : 1,000) in
saline and probably degraded during the test.
A skin sensitisation study using the Bühler method was conducted on short-haired
albino guinea pigs to determine if a 5% PAA (20% H2O2 and 10% HOAc) formulation
could induce dermal sensitisation (Kuhn, 1996e; CoR 1a). The animals were treated
(1 x /wk) with 0.4 ml of a 10% solution of the test compound in deionised water for
3 weeks. After a 2-wk rest period, the animals were challenged at a virgin test site
with an application of 0.4 ml of a 7% solution of the test substance. After the challenge,
a very faint erythema was observed in both the control and the treated group and,
therefore, 5% PAA was not considered to have elicited a sensitising reaction in guinea
pigs.
A similar study was conducted with 12% PAA (20% H2O2 and 20% HOAc) (Kuhn, 1996f;
CoR 1a). In this case the animals were challenged with 0.4 ml of a 0.5% solution of the
test substance in deionised water. The results showed that 12% PAA did not elicit a
sensitising reaction in guinea pigs.
The Bühler method for skin sensitisation was also used with 0.15% PAA (5-6% PAA,
22-23% H2O2, 10-11% HOAc) (Freeman, 1991e; CoR 1a). Groups of 10 male and 10 female
guinea pigs were treated with 0.3 ml of a diluted (1 : 33) test solution of PAA in contact
with the skin for 6 hours. This treatment was repeated once a week for 3 weeks. Fourteen
days after the third treatment the animals were challenged at a virgin site. No irritation
or sensitisation reactions were noted.
A solution of 5% PAA (20% PAA, 10% H2O2, HOAc not stated; diluted with distilled
water) was tested in guinea pigs (20 females) using the Magnusson and Kligman protocol
to investigate the ability of the test material to produce skin sensitisation. The test solution
(5% PAA) was administered during the induction phase by intradermal injection
(0.1 ml/animal) and topical application (0.5 ml/animal). Twenty-one days after induction,
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the test solution was administered by percutaneous injection (0.5 ml/animal) to challenge
the animals. A second group of control animals was treated with the vehicle alone during
the induction phase and then challenged with the test material by the same procedure
above (Biffi, 1992d; CoR 3b). The authors considered the test material to be moderately
sensitising. The study is, however, poorly reported and does not follow GLP guidelines.
In particular, the results were not divided into control and treated animals. There were
3/10 animals responding with grade 1 reported in the first table and 5/10 responding
with grade 1 reported in the second table. Not knowing which corresponds to the control
and which to the treated animals makes it difficult to understand the author's conclusion
of moderately sensitising. This study is deficient and does not allow a valid conclusion
to be drawn on the sensitising potential of PAA.
PAA should be considered as corrosive at concentrations of 10% and higher when applied
to the skin of rabbits. PAA was also corrosive to rabbit skin at concentrations of 3-5%
if contact lasted 1 hour or longer; contact for 3 minutes resulted in less severe responses.
Concentrations of less than 1% PAA were only slightly irritant or not irritant, depending
on the length of exposure of the skin.
PAA was corrosive at concentrations of 0.35% and greater when tested in the rabbit eye.
Slight or no eye irritation was found at concentrations of 0.15% or less PAA. Evidence
of respiratory irritation could be detected above 5 mg/m3 in rats. The RD50 for respiratory
irritation is 21-24 mg/m3.
No skin sensitisation was observed in two Bühler tests in guinea pigs with different
formulations of PAA. In one guinea pig maximisation test a positive result was claimed,
but the report does not permit critical evaluation of the results.
8.3 Repeated Dose Toxicity
8.3.1 Oral
The available oral toxicity studies with PAA are summarised in Table 25. PAA was
administered in the diet or drinking water of the animals.
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75
Table 25: Toxicity following Repeated Oral Dosage
Route of Number Composition (%) Concentration Dose Results Main effects Remarks Reference CoRb
administration, of PAA H2O2 HOAc (mg PAA/kgbw/d) LOAEL NOAELa
species, animals/ (mg/kgbw/d)
strain group,
Duration (d)
sex
Diet (mg PAA/kg food)
Rat, Wistar 10 M 38 14c 27c 0, 429, 859, 0, 60, 120, 240, 5 NS 960 From 480 mg/kgbw, Dose levels questionable Krüger et al, 3
1,718, 3,435 480, 960 statistically non- because of gas formation 1977
and 6,870 significant reduction in in food, indicating instability
food consumption and of PAA in the diet
body-weight gain
Rat, Wistar 20 M 38 14c 27c NS 0, 6, 21, 420 28 21 6 Decrease of serum Dose levels questionable Krüger et al, 3
alkaline phosphatase because of gas formation 1977
levels. Unclear if truly in food, indicating instability
treatment related. of PAA in the diet .No
histopathology performe
Pig, "Läufer" NS 38 14c 27c NS, presumably NS 5 NS NS No effects Dose levels uncertain. Krüger et al, 3
1,400d (behavioural, No histopathology 1977
clinical signs) performed
Drinking water (mg PAA/l water)

Rat, BD IX 10 M 40 14c 27c 0, 3.1, 6.2, NS 7 NS NS Reduced water Reportedly 200 mg/l was Juhr et al, 2
12.5, 25, 50, consumption, but no without effects, but due to 1978
100, 200 influence on body instability of the test
weight, growth, compound, concentrations were
reproduction, reduced by 50 - 60% after
histopathology of liver, 1 day and 75% after 4 days
lung, spleen, kidney
and gastro-intestinal tract
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Table 25 continued
Route of Number Composition (%) Concentration Dose Results Main effects Remarks Reference CoRb
administration, of PAA H2O2 HOAc (mg PAA/kgbw/d) LOAEL NOAELa
species, animals/ (mg/kgbw/d)
strain group,
Duration (d)
sex
Rat , BD IX NS, M 40 14c 27c 200 NS 10 NS NS No influence on body Reportedly 200 mg/l was Juhr et al, 3
months weight, growth, without effects, but due to 1977, 1978
reproduction, instability of the test compound,
histopathology of liver, concentrations were reduced by
lung, spleen, kidney and 50 - 60% after 1 day and 75%
gastro-intestinal tract. after 4 days
Mouse, NMRI NS, M, F 40 14c 27c 200 NS 10 NS NS No influence on body Reportedly 200 mg/l was Juhr et al, 3
and C3Hf months weight, growth, without effects, but due to 1977, 1978
Gerbil reproduction, instability of the test compound,
Guinea pig, histopathology of liver, concentrations were reduced by
Pirbright white lung, spleen, kidney and 50 - 60% after 1 day and 75%
Golden hamster, gastro-intestinal tract. after 4 days
Ha: AURA
Rat, Wistar 12, M 36-40 NS NS 0, 1, 10, 0.13 - 0.15, 28 0.13 NS Elevated haemoglobin levels, Veger et al, 2
50 1.3 - 1.5, - 0.15 increased spleen weights, 1977
6.5 - 7.6e increase in haemosiderin
in spleen. At 0.13 - 0.15
mg/kgbw/d: cloudy swelling of

liver, congestion of kidney medulla.
a No-observed adverse effect level e Based on reported average body weight of 217 g and water consumption between 28 and 33 ml
b Code of reliability (Appendix B) F Female
c From other publications by the same authors M Male
d Highest concentration in the diet was 10 x that NS Not Stated
used for disinfection of pigpens. Food changed daily
Dietary studies
In none of the dietary studies of Krüger et al (1977) were details given concerning the
stability of PAA in the diet, apart from the observation of an increased feed volume and
oxygen formation indicating decomposition of the test substance. The authors performed
some further testing in order to evaluate the degradation of PAA under specific conditions.
When 1,400 mg PAA was added to 1 kg of feed, only 10% of the amount of PAA could
be detected in the feed directly after mixing with PAA. The stability of PAA was dependent
on the water content of the diet. The higher the water content in the food, the less rapid
was PAA degradation. PAA stability was greater in water than in food. Based on this
indication of decomposition, the doses that the rats or pigs received should be regarded
as nominal only and the results should not be used for hazard assessment.
Drinking water
Rats received drinking water containing 3.1 to 200 mg PAA/l for one week. The
concentration was determined daily by photometric analysis after reaction with potassium
iodide. At higher dilutions yielding concentrations of 12.5 mg/l or lower, the PAA
had almost disappeared within 2 days. Contamination by saliva to aqueous PAA solutions
may have further reduced the PAA content. Animal water consumption was reduced
by 12-19% at 200 mg/l and by 4% at 6.2 mg PAA/l. No effect on water consumption
was found at 3.1 mg/l (Juhr et al, 1978).
The same authors briefly reported on the toxic effects of PAA administered in the drinking
water of rats, mice, hamsters, gerbils and guinea pigs at a single concentration of 200
mg PAA/l for 10 months. The tests were designed to evaluate possible adverse effects
of a concentration of PAA that would be used in disinfection of drinking water of farm
animals. Water bottles were changed every week. The breeding capacity and health
status of the animals were observed continuously. At regular intervals (not specified)
interim kills were performed, the animals were autopsied and underwent pathological
and histopathological examination. No changes were seen on growth, reproduction and
histology of liver, kidney, spleen, lung and intestines. No further details were given (Juhr
et al, 1977, 1978).
Drinking water containing 0.1% PAA administered to rats for 7 weeks did not results in
any toxicological change (Benes et al, 1966; CoR 4b as cited in Kramer, 1982).
Rats received 1, 10 and 50 mg PAA/l in distilled water for 4 weeks (Veger et al, 1977).
Three control groups were included in the study, one received distilled water only;
the other two groups received distilled water with chlorine in concentrations of 1 and
10 mg/l respectively. Fresh test solutions were prepared daily and water consumption
was recorded. Six animals per group were killed immediately after the end of the exposure
period while the other half was kept for a recovery period of another 4 weeks. Clinical
signs were recorded twice a week. Haematology and organ weight data (lungs, heart,
liver, kidneys, adrenals, and stomach) were obtained from all animals after termination
of the study. In the recovery group organ histopathology of the low- and mid-dose group
animals was evaluated. Water consumption was significantly reduced in all dose groups
compared to the water only control group. In the chlorinated water groups, water
consumption was also lower than in the water only control group, but the difference
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was not statistically significant. No differences in body weight and body-weight gain
were observed between the groups. Haemoglobin levels were elevated in all dose groups
compared to water only controls. An increase in haemoglobin levels was also reported
in the high chlorine control group. In the lower-chlorinated water group a decrease in
haemoglobin levels was observed. The number of leukocytes and differential blood
counts were not different between the groups. In the PAA dose groups and the lower-
chlorinated water rats, spleen weights were increased significantly compared to controls.
All other organ weights (heart, liver, adrenals, stomach, and lungs) were not different
from controls. Histopathology at week 8 did not reveal any significant differences from
controls in the low dose group. In all dose groups treated with PAA an increase of
haemosiderin in the red matter of the spleen was reported. In the 10 mg/l dose groups
of both PAA and chlorine, changes in spleen (cloudy swelling of the white pulp), the
liver (cloudy swelling) and congestion of the kidney medulla were observed in the
majority of the treated animals. The increase in blood haemoglobin levels and
haemosiderin in spleen of the animals treated with PAA (low doses only) were considered
to be related to an increased absorption of iron due to acidic pH of the drinking water.
(This conclusion is not supported by experience with other acids. As the iron uptake
is receptor-regulated it seems doubtful that it could be substantially influenced by the
pH. It is possible that the haematological changes could be related to the decreased
drinking water consumption of the animals.) The LOAEL with regard to haematological
changes was 1 mg PAA/l (0.13-0.15 mg/kgbw). Liver and kidney changes were observed
in the 10 mg/l (1.3 to 1.5 mg/kgbw) and higher dose groups, thus a no-observed adverse
effect level (NOAEL) for liver and kidney effects of 0.13 - 0.15 mg PAA/kgbw could
be derived from this study. In the opinion of the Task Force the effects on liver and kidney
could well be an artefact of the experimental procedures and hence should be viewed
with caution.
8.3.2 Dermal
The available dermal toxicity studies on PAA are summarised in Table 26, including
details of the study protocol and results.
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Table 26: Toxicity following Repeated Open Dermal Application
Number of Composition (%) Concentration Dose Frequency, Main Effects Remarks Reference CoRa
animals/ PAA H2O2 HOAc (%) (mg PAA/l) (mg PAA/kgbw) duration
group, sex
Guinea pig
20, M, F 40 14 27 0.3 1,200 0, 3.84b 2 x /d, Skin: slight skin irritation reduced body- Control and treated animals Kramer et al, 2e
5 d/wk, weight gain from day 20, slight evelvation had pneumonia, more 1982
28 d of liver enzymes and LDHc, slight severe in treated
decrease of liver weights, no
histopathological findings.
20, M, F 40 14 27 0.3 1,200 0, 3.84b 2 x /d, Slight skin irritation and reduced body- Control and treated animals Kramer et al, 2e
5 d/wk, weight gain from day 44, white blood cell had pneumonia, more 1982
90 d count increased, slight elevation of liver severe in treated
enzymes and LDH, increased relative
kidney and spleen weights,
histopathological changes in liver and
kidneys
Rabbit
28, F 40 14 27 0.5 2,000 1d 3 x /wk, Skin: atrophy and vacuolar degeneration Only skin was examined (1 Müller et al, 2e
12 months of hair follicles animal after 1d, 1,2,3 wk, 1988
2 animals every month from
month 1 to 12)
Pig
5, F 40 14 27 NS 15,000 113.6e 1 x / 2 d, Skin: inflammation, hair loss, and Busch and 4e
NSf 15,000f 120 d hyper-parakeratosis. No systemic effects Werner, 1974
a Code of reliability (Appendix B) e Reported as 250 ml/33 kgbw, assuming a density of the test solution of
b Applied as 0.16 ml/100 gbw = 1.92 mg/kgbw, assuming 1 mg/ml
a density of 1 mg/ml f Pure (distilled) PAA
c Lactate dehydrogenase F Female
d 1 ml of the test solution was applied; the dose was calculated assuming M Male
an adult rabbit of 2 kgbw and density of the test solution 1 mg/ml NS Not Stated
In the 28-day study of Kramer et al (1982) with dermal application of diluted PAA in
guinea pigs, water consumption and clinical signs were recorded daily. Body weight
and heart action were checked twice weekly at the beginning of the experiment and
weekly thereafter. At the end of the study haematological and clinical chemistry
parameters were determined and organ weights recorded. The following organs were
examined macroscopically and microscopically: liver, lungs, kidneys, adrenals, pancreas,
heart, brain, spleen and skin. Fourteen animals showed slight skin irritation with reduced
intensity from day 25 of dosing. A number of animals of the control group also showed
transient slight erythema. No differences in water intake were observed between treated
and control animals. A reduction in body-weight gain was observed in the treated animals
compared to controls from day 20. Body weight gain returned to normal in the post-
exposure observation period (40 days) within 10 days. Heart rate was elevated in both
control and exposed animals, but to a slightly greater extent in the exposure group.
Relative liver weights were slightly decreased. Liver enzyme levels and lactate
dehydrogenase (LDH) levels were slightly elevated in the treated animals. No macroscopic
changes were seen. No characteristic histopathological findings were observed.
Pneumonia was observed in all animals including controls with an increased severity
in the treated animals. According to the authors this could be due to an infection that
was possibly aggravated by inhalation of PAA vapours originating from the treated
skin. As the animals in this study were suffering from infection, observed effects could
have been secondary to the infectious disease. It follows that no reliable conclusions on
possible systemic effects of PAA after dermal application can be drawn from this study.
Kramer et al (1982) performed a 90-day study in guinea pigs using an otherwise identical
protocol to that described above. The clinical findings were identical to those of the
28-day study, except that the reduction in body-weight gain began later, from day 44.
Relative liver weights were not reduced, but an increase in kidney and spleen weights
relative to body weight was observed in treated animals compared to controls.
Haematological effects were confined to an increase in white blood cells of the treated
animals. Liver enzyme levels and LDH levels were slightly elevated in the treated
animals. In 7 of 9 animals some greyish yellow areas were reported on the liver surface.
A number of animals showed focal liver cell necrosis (periportal) and fatty hepatocytes
in the liver. Cell infiltration was seen in the Glisson triangle and swelling and slight
sectional proliferation of the Kupffer cells. Pneumonia was observed in all animals
including controls with an increased severity in the treated animals. According to the
authors this could be due to an infection that was possibly aggravated by inhalation
of PAA vapours originating from the treated skin. In the kidneys of the test animals, but
not of controls, interstitial lymphocyte infiltration were observed in the glomeruli (Kramer
et al, 1982). As all the animals in this study were infected, the observed effects could have
been secondary to the infectious disease. Accordingly, no reliable conclusions on possible
systemic effects of PAA after dermal application can be drawn from this study.
Busch and Werner (1974) applied a 1.5% PAA solution to the skin of pigs. The solution
was applied to the whole back of the animals using a sponge. Clinical signs were recorded
daily. Body weight determinations and haematological examinations were performed
every 20 days. The animals showed signs of salivation, lachrymation and increased
respiratory rate within 10 to 15 min after application, probably due to inhalation of PAA
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that evaporated from the skin. Transient skin irritation was observed immediately after
application of the test substance but was reversible within 10 to 15 min. After 20 days
the skin showed signs of hyperkeratosis, parakeratosis, hair loss and signs of inflammation
(cellular infiltration up to the corium). Gains in body weight were comparable to controls
throughout the observation period. Haematological and clinical chemistry examinations
did not reveal any treatment-related effect. The kidney function of the treated animals
(phenol red test) was similar to that of controls.
8.3.3 Inhalation
The available studies on possible toxic effects of repeated exposure to PAA by inhalation
are summarised in Table 27. The test compounds was administered as a vapour or aerosol.
No analytical determination of the concentration of PAA in the test atmosphere was
performed in any of the studies. The nominal concentration of the test atmosphere was
calculated from the amount of PAA used for aerosol or vapour generation and the
chamber volume. In some cases aerosol droplet sizes were measured.
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Table 27: Repeated Dose Studies in Mice and Guinea Pigs by Inhalation
Number of Composition (%) Concentration Vapour or Frequency, Results (mg/m3) Main effects Remarks Reference CoRb
animals/ PAA H2O2 HOAc Solution Atmosphere aerosol, duration LOAEC NOAECa
group, sex (%) (mg PAA/m3) particle size
Mousec
40, F 40d 14d 27d 0.39, 1.56, 0, 70, 281, Aerosol, 5, 10, 1,125 281 Acute effects during and No analytical Heinze et al, 2e
6.25 1,125 0.5-8 µm 15 min/d immediately after exposure: determination of 1981
for 29 d respiratory distress, eye atmospheric
irritation. Decreased body- concentration of PAA
weight gain, increased mortality
(15 min exposure group),
increased red/white blood cell
count, haemoglobin, haematocrit,
lung inflammation (pneumonia)
40, NS 40d 14d 27d 2.06, 7.8, 0, 280, 1,125, Vapour, 5, 10, 2,250 1,125 Laboured breathing, eye No analytical Heinze et al, 2e
16.1 2,250 NS 15 min/d irritation, increased mortality, determination of 1982
for 29 d decreased body-weight gain. atmospheric
Increased red/white blood cell concentration
count, haemoglobin, of PAA
haematocrit, inflammation
of the lung
40, NS 40d 14d 27d 0.39, 1.56, 0, 70, 280, Aerosol, 5, 10, 1,125 280 Laboured breathing, eye No analytical Heinze et al, 2e
6.25 1,125 0.5-8 µm 15 min/d irritation, increased mortality, determination of 1982
for 29 d decreased body-weight gain. atmospheric

Increased red/white blood cell concentration
count, haemoglobin, of PAA
haematocrit, inflammation
of the lung
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83
Table 27 continued
Number of Composition (%) Concentration Vapour or Frequency, Results (mg/m3) Main effects Remarks Reference CoRb
animals/ PAA H2O2 HOAc Solution Atmosphere aerosol, duration LOAEC NOAECa
group, sex (%) (mg PAA/m3) particle size
10, NS 36-40d NS NS NS 0, 70, 140 Aerosol, 3 x 1 h/wk 70 Respiratory distress during No data on Merka and 3a
0.5 µm for 28 d exposure, small inflammatory analytical Urban, 1976
(MMADe foci in the lungs. determination of
1.6 µm) PAA, limited
reporting
20 or 60, 40d 14d 27d 1, 1.5 0, 186, 280 Aerosol, 2 x 30 186 Inflammatory changes in the No analytical Heinze and 2e
NS NS min/d for lung, liver granuloma and determination of Nattermann,
90 d lymphocyte infiltration. atmospheric 1984
concentration of PAA,
liver granuloma could
be related to infection
Guinea pigc
20, NS 40d 14d 27d 1, 1.5 0, 186, 280 Aerosol, 2 x 30 186 Decreased body-weight No analytical Heinze and 2e
NS min/d for gain, increased ALATf levels, determination of Nattermann,
90 d inflammatory changes in the atmospheric 1984
lung, granuloma, lymphocyte concentration of
infiltration and increased PAA, liver granuloma
amount of lipid droplets in the could be related
liver. to infection
a No observed adverse effect concentration f Alanine aminotransferase

b Code of reliability (Appendix B) F Female
c Strain not stated M Male
d Inferred from other publications on the same product NS Not Stated
e Mass median aerodynamic diameter
Heinze et al (1981) exposed mice to PAA aerosols by whole-body exposure; control groups
received either no treatment or water aerosol for 10 min/d. Interim kills were performed
on days 1, 2, 3, 4, 5, 8, 16, and 22. In all PAA-treated groups, excitement followed by
lethargy was observed during exposure, an effect that was dose-related. After exposure,
signs of respiratory distress were observed for several hours in the highest dose group.
These effects were independent of the daily duration of exposure. Signs of eye irritation
were also observed in some animals. Compared to both control groups, mortality and
decreased body-weight gain was noted in the 1,125 mg/m3 group exposed for 15 min/d.
A significant decrease in body weight was also observed in the active (water aerosol)
control group compared to the passive control (no treatment) group. Increased erythrocyte
count, haematocrit, haemoglobin content and white blood cells were observed at the
high dose group, but no exposure-duration relationship was evident. Changes in
leukocyte and lymphocyte counts did not follow a consistent pattern and were not clearly
attributable to treatment. Histopathological changes in the lungs (pneumonia) were
noted mainly at the 1,125 mg PAA/m3 dose and related to the duration of exposure.
Other organs were not examined. The changes in blood parameters were attributed to
the lung damage (compensatory changes). A NOAEL for inflammatory changes in the
lung of 281 mg PAA/m3 can be derived from this study.
In two other studies (Heinze et al, 1982) mice were exposed (with different frequency)
to PAA vapours or aerosols by whole-body exposure; passive (no aerosol) and active
(water aerosol) controls were also used. Deaths occurred in the high-dose groups at
2,250 mg PAA/m3 as vapour and 1,125 mg PAA/m3 as aerosol respectively. In all treated
groups, there was excitement followed by lethargy during the inhalation period, while
lethargy persisted after exposure in the high-dose groups (vapour and aerosol). Evidence
of respiratory distress and marked inflammation of the eye were noted in many animals
of the high-dose aerosol group. Decreased body-weight gain was noted in the high-dose
vapour/aerosol groups for all treatment durations. The observed increases in erythrocyte
count, haemoglobin content, haematocrit and white blood cell count were considered
to be related to exposure at 1,125 mg PAA/m3 aerosol and 2,250 mg/m3 vapour, but
in this latter group changes were less severe. In the high-dose aerosol exposure group
the gastro-intestinal tract was found to be distended and had a foamy appearance.
Inflammatory changes in the lungs were found to be significant at the high-dose
vapour/aerosol groups; these changes increased with duration of exposure. No
histopathological changes were observed in the liver and kidneys. The authors concluded
that all effects observed were due to the irritant effect of PAA as similar findings were
reported following exposure to lactic acid, HOAc aerosols or sulphur dioxide gas.
The overall NOAEL based on irritant responses was 1,125 mg PAA/m3 vapour or
280 mg PAA/m3 aerosol, both for exposures of up to 15 min/d.
In the study of Merka and Urban (1976) in mice, signs of respiratory distress were
observed in the animals during exposure; these effects disappeared after cessation of
exposure. Gains in body weight of exposed animals were reduced compared to untreated
controls. In mice killed after 14 days of exposure the only histopathological findings
were mild morphological changes in the lung. No other organs (unspecified, but
presumed to be heart, liver, spleen, kidneys as for an acute study reported in the same
paper) were affected. Isolated small foci of inflammation in the lungs were seen after
4 weeks of exposure.
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Heinze and Nattermann (1984) exposed mice to PAA aerosols and included additional
groups of animals that were treated with different drugs in order to study their influence
on PAA toxicity. Control groups received no treatment or water aerosol with and without
drugs. Body-weight gain in all groups was similar to controls. Haematology and clinical
serum chemistry parameters also did not differ significantly between the groups.
Histopathological examination of the lungs revealed an increased incidence and severity
of inflammatory changes (thickening of alveolar walls, epithelial cell proliferation,
infiltration by eosinophils and neutrophils) in treated animals compared to controls.
Epithelial cell tumours were observed in the lungs of 3 test animals of the low dose
group only and one control mouse. Since these tumours were not observed in the higher
dose group, they were not considered to be due to PAA treatment. In addition the number
of control animals in which lungs were examined was less than the number of test
animals examined. Examination of the livers of the test animals after 30 and 90 days
of treatment revealed an increase in lymphocyte infiltration and granuloma compared
to controls. The size of the granuloma increased after 90 days of treatment. Follow up
studies of the livers of the animals indicated that bacterial infection could have been the
reason for the observed changes. It is not clear from the report if the histopathology of
organs other than lungs, liver and kidneys was examined.
In a similar study (Heinze and Nattermann, 1984) guinea pigs were exposed to PAA
aerosols, as well as additional groups of animals treated with different drugs to study
their influence on PAA toxicity. Control groups received no treatment or water aerosol
with and without drugs. Body-weight gain in the treated groups was decreased compared
with controls. Haematology studies revealed no significant treatment-related differences
in white blood cell count, erythrocyte count, haemoglobin and serum proteins, except
for a slight increase in γ-globulin in treated compared with control animals. Serum liver
enzyme values of asparagine aminotransferase (ASAT) were not different from controls,
but alanine aminotransferase (ALAT) levels were significantly higher in the treated
animals compared to controls. Histopathological examination of the lungs revealed
an increased incidence and severity of inflammatory changes (thickening of alveolar
walls, epithelial cell proliferation, infiltration by eosinophils and neutrophils) in treated
animals compared with controls. Examination of the livers of the test animals revealed
a slight increase in lymphocyte infiltration and granuloma compared to controls from
day 60 of treatment as well as an increase in lipid droplets. Changes in the liver and in
γ-globulin were possibly related to bacterial infections in the animals. It is not clear from
the report if the histopathology of organs other than lungs, liver and kidneys was
examined.
One of 10 rats died after inhalation for 4 days of vapours from a 3% PAA solution
(Polakova, 1968; CoR 4c as quoted in Krüger and Kruschinski, 1982). No deaths were
observed after exposure of rats for 28 days to PAA vapours from a 1% solution. The only
sign noted was transient restlessness at the beginning of the treatment (Benes et al, 1966;
CoR 4b as cited in Krüger and Kruschinski, 1982).
Benes et al (1966; CoR 4b as cited in Heinze et al, 1982 and Krüger and Kruschinski, 1982)
exposed rats to 0, 7.2 and 72 mg/m3 PAA aerosol for 1 h/d, during 24 exposures in 28
days. Reduced body weight and clinical signs (restlessness, eye discharge and respiratory
distress) were reported in the 72 mg/m 3 group. In the 7.2 mg/m 3 group signs of
excitement, but not irritation or other clinical signs, were observed.
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8.3.4 Other studies
Pigs (5) and calves (15) were exposed for 1 h/d to 0 and 50 mg PAA/m3 aerosol for 14
days. The aerosol (droplet size 0.5 to 6 µm) consisted of 2 ml/m3 of diluted (6.25%)
equilibrium PAA 40% (14% H2O2 and 27% HOAc). Simultaneously, animals infected
with Chamydiae were treated to study the effect of PAA aerosols on bacterial infections.
In the context of this report, only the results for non-infected animals are of relevance.
Clinical observations in pigs and calves consisted of increased lachrymation, salivation,
nasal discharge and cough in the first 3 to 5 days. Additionally, pigs showed signs of
laboured breathing and vomiting. The effects were less pronounced after further
exposures. At the end of the 86-day test period, treated pigs had decreased body-weight
gain compared to untreated controls. In calves no effect on body-weight gain was
observed. An increased pulse and respiratory rate was observed in exposed calves.
Haematological changes (decreased red blood cell counts and haemoglobin levels) were
noted. These effects were transient and adaptation occurred during treatment. Acute
lung inflammation was also reported to affect both control and treated calves (Heinze
et al, 1979).
Groups of 5 mice were exposed (1 h/d) to 50 mg PAA/m3 aerosol (droplet size 0.5 to
6 µm) for 14 days. Some animals were immunised, while others were infected with a
virus. PAA exposure did not influence the immune reaction and generation of antibodies
(Heinze et al, 1979).
A number of publications on the toxicity of PAA after repeated oral, dermal or inhalation
exposure in different animal species have been reviewed.
There are deficiencies in the reporting of the available repeat-dose toxicity studies,
including uncertainties regarding the nature, concentration and the stability of the
test substance, the limited amount of doses tested and limited reporting on histopathology.
Furthermore in a number of studies the test animals suffered from infectious diseases
and it remains unclear to what extent the reported effects can be attributed only to the
administration of PAA. In spite of those limitations, a number of conclusions may be
drawn from the studies.
The reduced food or water consumption observed in some of the oral studies may well
be related to the unpalatability due to the odour and irritant properties of PAA. No
treatment-related changes were observed in a drinking water study in rats, mice, golden
hamsters, gerbils and guinea pigs receiving up to 200 mg PAA/l water for 10 months.
However, the stability of PAA in drinking water varied and was not sufficient during
these studies to inspire confidence in the lack of findings.
Only one study reported an increase in haemoglobin levels and haemosiderin deposition
in the spleen of rats receiving PAA in drinking water for 28 days from 1 mg PAA/l
corresponding to a dose of about 0.15 mg/kgbw. As these effects have not been reported
in other studies even at higher dose levels and as the methodology was not sufficiently
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described, these results may not be related to the test substance. In the same study, effects
on kidney, liver and spleen were reported at doses from 10 mg PAA/l (1.5 mg/kgbw);
these could well be an artefact of the experimental procedures and should thus be treated
with circumspection.
Repeated dermal exposure of pigs to a 1.5% PAA solution for 120 days resulted in irritant
effects to the skin including hair loss, hyper- and parakeratosis as well as signs of
inflammation. No systemic effects were observed. In guinea pigs exposed to a 0.3%
solution of PAA (corresponding to 3.84 mg/kgbw/d) twice daily for 90 days, transient
slight skin erythema was observed. A reversible reduction of body-weight gain was also
reported. A slight increase in numbers of white blood cells and of liver enzyme levels
were reported in the treated group. An increase in relative kidney and spleen weights
and changes in liver (focal liver cell necrosis) and kidneys (lymphocyte infiltration) were
observed in the treated animals. As pneumonia was reported for both treated and control
animals the effects observed could be a consequence of the infectious disease, rather
than treatment with PAA.
Effects seen in repeated-dose inhalation studies are mostly attributable to the irritant
properties of the test substance. The single exposure periods however, were relatively
short (5 min to a maximum of 1 hour per exposure).
A NOAEL of 280 mg PAA/m3 for aerosols or 1,125 mg/m3 for PAA vapours was derived
for mice exposed up to 15 min/d for 29 days.
Subchronic inhalation studies using PAA aerosols in different species (pigs, calves
and mice exposed for 1 h/d) showed restlessness, irritation of the respiratory tract, lung
damage and related transient blood parameter changes from 50 mg PAA/m3. No effect
or very slight irritation only was found at 7.2 mg PAA/m3.
Inflammatory changes of the lung and the liver were reported in mice and guinea
pigs exposed (2 x 30 min/d) to PAA aerosols of 186 or 280 mg/m3 for 90 days. It remains
unclear if these effects were treatment related or attributable to an infection in the animals.
In all, the predominant effects arising from oral, dermal or inhalation exposure to
PAA seem to be related to local irritation at the site of contact. However, systemic effects
on liver, kidney and perhaps spleen cannot be ruled out from the limited studies available.
Clear no-adverse effect levels cannot be derived from the available studies.
8.4 Genetic Toxicity
8.4.1 Gene mutation in vitro
The available studies on possible gene mutation activity of PAA in vitro are presented
in Table 28.
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Table 28: In Vitro Genetic Toxicity Assays
Test system Test organism, strain Composition (%) Dose Metabolic Resulta Reference CoRb
PAA H2O2 HOAc (PAA) activation
Spot-test Salmonella typhimurium TA 1535, 35-37 8-9 36-38 10 µg/plate No -vec Agnet et al, 1977 3a
TA 1536, TA 1537,TA 1538
Wild strain LT-2 36 8.5 37 10 µg/plate No +ved Agnet et al, 1977 3a
Wild strain LT-2 36 8.5 37 10 µg/plate No -vee Agnet et al, 1977 3a
TA 1978 36f 8.5f 37f 6 µg/plate No +ved Dorange et al, 1974 3a
TA 1978 36f 8.5f 37f 6 µg/plate No -vee Dorange et al, 1974 3a
Gene conversion/ Saccharomyces cerevisiae 36g 8.5g 37g 0 - 40 µg/ml No -ve Dorange et al, 1974 3a
mitotic recombination Strain D7
Reversion-assay S. typhimurium TA 1978 36 8.5 37 0 - 40 µg/ml No +veg Agnet et al, 1977 3a
(Ames test) TA 98, TA 100 9 NS NS 50 µg/plate Yes -veg Yamaguchi and Yamashita, 1980 4e
TA 98, TA 100, TA 102, TA 1535, 4.5 25.5 6.7 7 - 4,576 Yes / No -veg Wallat, 1984a 1d
TA 1537, TA 1538 µg/plate
TA 97, TA 98, TA 100, TA 1535 40 NS NS 0.3 - 200 Yes / No -veg Zeiger et al, 1988 2e
µg/plate
Unscheduled DNAh Human lung fibroblasts, 31i 4.7 NS 0.2 - 32 mg/ml No -veg Coppinger et al, 1983 1d
synthesis WI-38 CCL75 42i 5.5 NS
DNA repair assay Human lung fibroblasts, 4 - 32 µg/ml No -veg Coppinger et al, 1983 1d
WI-38 CCL75
Chromosomal Human lymphocytes 5.17 20j 10j 0.25 - 5 mg/ml Yes / No -ve Phillips, 1994b 1b
aberration +vek
a -ve, negative; +ve, positive g Test was conducted up to cytotoxic concentration

b Code of reliability (Appendix B) h Deoxyribonucleic acid
c His-reversion i Measured
d Resistance towards potassium chlorate (with LT-2 combined with j Inferred from Blowers, 1994a, 1995
resistance towards 2-desoxy-D-galactoside) k At highest, cytotoxic doses
e Resistance towards ethionine NS Not Stated
f Inferred from Agnet et al, 1977 ND Not Determined
In bacteria and yeast

Several studies on bacterial gene mutation tests in which PAA was assayed using the
Ames method have been reported. In a number of tests possible toxic or detoxifying
effects were investigated in the presence and absence of the so-called S9 metabolic
activation system (supernatant of centrifuged 9,000 x g liver homogenate) containing
the microsome and cytosol fractions usually derived from rats previously treated with
microsomal enzyme inducing compounds such as phenobarbital or Aroclor.
A diluted equilibrium PAA solution was tested in the spot test using different strains of
Salmonella typhimurium and different selection for mutants. No mutagenic effects were
observed using the strains TA 1535, TA 1536, TA 1537, TA 1538. With strain TA 1978 and
the wild strain LT-2, respectively, resistance towards ethionine was not found. When
selecting the two strains for mutants resistant to potassium chlorate and 2-deoxy-D-
galactose, the authors claimed to have observed an induction of mutants after treatment
with PAA at 6-10 µg PAA/plate, compared to the untreated control (Dorange et al, 1974;
Agnet et al, 1977). Judging from the limited data presented in the reports the effect is
quite small (not quantified).
The same authors also tested PAA in the Ames test with S. typhimurium strain TA 1978
up to 40 µg PAA/ml without metabolic activation. An increase in mutation frequency
above threefold appears to have been seen only in concentrations that reduced bacterial
survival far below 50% (> 15 µg PAA/ml) (Agnet et al, 1977). Detailed information on
the induced mutation frequencies of treated and untreated samples is not given.
Dorange et al (1974) also reported that treatment of the yeast Saccharomyces cerevisiae
strain D7 with diluted equilibrium PAA, failed to stimulate mitotic recombination, gene
conversion or homo-allelic reversion in yeast strain D7. No details of the results were
reported.
When a solution of 9% PAA in HOAc (not further specified) was tested in S. typhimurium
TA 98 and TA 100 in the presence of S9 mix, no mutagenic activity was found. Data on
the results without S9 mix were not explicitly given (Yamaguchi and Yamashita, 1980).
An evaluation of the concentration-activity relationship is not possible, as only one
concentration, 50 µg/plate (probably of the formulation) was tested.
It is generally known that peroxides are highly toxic especially to repair-deficient S.

typhimurium strains. S. typhimurium TA 102 that is not repair-deficient has been suggested
as the strain of choice for this type of test substance (Berglin and Carlson, 1986). Therefore,
strain TA 102 was included in another reversion-assay with PAA. In strain TA 102, PAA
up to cytotoxic concentrations produced only a slight increase of reverted colonies
(up to 30%) and the test substance was judged to be non-mutagenic. Total inhibition
was achieved in concentrations exceeding 183 and 915 µg PAA/plate (depending on
the strain and activation system). With regard to cytotoxicity no marked differences, i.e.
reduced sensitivity, were observed in strain TA 102 (Wallat, 1984a). The concentrations
that were reached in this assay were relatively high compared with the results presented
by other authors.
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Equilibrium PAA (40%) proved to be negative in the standard S. typhimurium reversion

assay at concentrations of 0.3 to 200 µg PAA/plate. The highest concentration was chosen
after toxicity testing prior to the actual test and represents the dose that elicited toxicity
or a dose immediately below (half-log dose intervals). In addition to rat liver S9 mix,
material from hamster tissues was also used as a metabolic system. With both protocols
PAA was found to be devoid of mutagenic activity (Zeiger et al, 1988).
DNA repair in cultured mammalian cells

The possible induction of UDS by PAA (40% nominal) was investigated in human diploid
foetal lung cells. Ethyl methane sulphonate, N-methyl-N'-nitro-N-nitrosoguanidine
(MNNG), and 4-nitroquinoline-1-oxide were used in preliminary experiments to assure
the appropriateness of the test system to show UDS and DNA repair. MNNG was used
as positive control in both the UDS and DNA repair assay (Table 28). Cells incubated
with PAA for 4 hours did not reveal a consistent dose-related increase of UDS using
liquid scintillation counting (duplicate experiments). Slightly, but statistically significantly
elevated rates of UDS were reported at 8 and 16 µg PAA/l in the first experiment and
at 16 and 32 µg/l in the second experiment. The increase never exceeded 1.6 times the
solvent control, which were reported to be within the variability of the test system.
Therefore, the results did not meet the criteria for a positive response, i.e. 2-fold increase
above controls. The authors explained the slight increase by a possible oxidation of
hydroxyurea, which is used in this test system. No statistically significant increase of
UDS compared to solvent (water) controls was detected in a second (triplicate)
experimental series using autoradiography (a more sensitive technique that does not
require hydroxyurea). In this assay 32 µg PAA/ml was clearly cytotoxic (50% survival).
Conflicting results were obtained; the first experiment with PAA indicated a possible
positive response. However, repeated testing with the same lot of PAA showed negative
results (Coppinger et al, 1983).
Using the same test system and controls, a DNA repair assay (three independent
experiments) was conducted. Cells incubated with PAA were assessed by equilibrium
ultra-centrifugation of density-labelled DNA. The assay was negative at all dose levels.
At the highest concentration normal DNA replication was considerably reduced
(Coppinger et al, 1983).
In conclusion, PAA was negative in UDS and DNA repair assays in human lung fibroblasts
when tested up to cytotoxic concentrations.
Chromosomal aberrations in cultured mammalian cells

Two independent experiments on the potential of PAA to induce structural chromosomal
aberrations in human lymphocytes were conducted with equilibrium PAA (5.17%). Cells
were treated at 0.25, 0.5, 1.0, 2.0 and 4.0 mg PAA/ml for 20 hours in the first experiment
and with 0.25, 0.5, 0.75, 1.0 and 1.5 mg/ml in the second experiment. Treatment in the
presence of S9 mix was carried out at 0.31, 0.63, 1.25, 2.5 and 5 mg/ml in both experiments
and was limited to 3 hours. Cells were arrested in metaphase and harvested 20 and 44
hours after the start of treatment. Two hundred metaphases at each dose level were
examined for structural chromosome aberrations. Cyclophosphamide (with activation)
and Mitomycin C (without activation) served as positive controls (Table 28).
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In the absence of S9 mix, 4 and 2 mg PAA/ml reduced the mitotic index of the cells to
below 25% of the control in the test, chromosome analysis was conducted at the next three
lowest concentrations and in the control. In the test with S9 mix, the highest concentration
of PAA reduced the mitotic index to 69% and chromosome analysis was therefore conducted
on the three highest concentrations and the controls. Without S9 mix there was a statistically
significant and reproducible increase in the number of aberrant metaphases at 1.0 and 1.5
mg/ml. With metabolic activation, a concentration of 5 mg/ml was clastogenic. Effects
observed were mainly deletions. Both in the 1.5 mg/ml (without S9) and 5 mg/ml (with
S9) replicate, one single chromatid exchange was observed. Under the conditions employed,
S9 mix reduced both cytotoxicity and mutagenicity. In summary, PAA revealed positive
results only in the highest, moderately cytotoxic doses, which reduced the mitotic index
to 44.5 - 63% without S9 mix and to 61 - 69% with S9 mix. The author concluded that PAA
caused chromosomal damage in cultured human lymphocytes (Phillips, 1994b). It is
speculated that the cytotoxicity and genotoxicity exerted by PAA is a result of the same
mechanism at the cellular level, e.g. production of reactive oxygen species which are
not detoxified at higher concentrations.
8.4.2 Gene mutation in vivo
The available in vivo studies on possible gene mutation of PAA are summarised in
Table 29.
Table 29: In Vivo Genetic Toxicity Assays
Test Route of Composition (%) Dose Resulta Reference CoR

application PAA H2O2 HOAc (mg PAA/kgbw)
Chromosomal Topical 40 5b 45b 0, 5c +veb Paldy et al, 1984 3b
aberration, Intraperitoneal 0, 50d
mouse Intraperitoneal 0, 5e
Micronucleus Oral, gavage 4.5 26.7 6.7 0, 400 -1,600 -ve Wallat, 1984b 1b
test, mouse
Micronucleus Oral, gavage 5.17f 20 10 0, 8 - 150 -ve Blowers, 1994a 1b
test, mouse
Unscheduled Oral, gavage 5.17 20 0 0, 330, 1,000 -ve Blowers, 1994b 1b
DNA synthesis,
rat
a -ve, negative; +ve, positive

b Assumed value
c 0.1 ml equilibrium PAA 40%
d 2 ml of 0.5% solution in distilled water
e 1 ml of 0.1% solution in distilled water
f Blowers (1995) confirmed that 15.17% was a typing error
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Chromosomal aberration and micronucleus induction in mammals

In a bone marrow chromosome aberration test in mice (male and female, unspecified
strain), PAA was found to cause chromosome mutations after topical or intraperitoneal
(i.p.) application. The authors recommend further in-depth investigations (Paldy et al,
1984) (Table 29). Insufficient detail was reported in this study and the chromosome
analysis conducted does not comply with the relevant OECD guideline 475. Only 200
mitoses/group were evaluated compared to the evaluation of at least 100 metaphases
per animal required by the OECD guideline and the data are not specified separately
for each animal. No information is given on cytotoxicity to the bone marrow. Given the
small number of analysed metaphases per animal and dose group, the numbers of
aberrations recorded do not show a convincing dose dependency in the i.p. treated
groups. Only one dose was applied epicutaneously and only two by i.p. administration.
The results obtained are surprisingly similar, independent of the treatment regime
and dose.
In a micronucleus test conducted with equilibrium PAA (4.5%), the test solution was
administered by gavage to groups of 7 male and 7 female CF21/W68 mice. The animals
received two doses of 200, 400, and 800 mg PAA/kgbw/d at 0 and 24 hours. Six hours
after the second administration the animals were killed. Cyclophosphamide served as
a positive control. The femoral bone marrow was removed and examined for the incidence
of micronuclei in polychromatic erythrocytes, the proportion of polychromatic
erythrocytes in the erythrocyte population and the incidence of micronuclei in
normochromatic erythrocytes. Dose-dependent clinical signs of toxicity were observed
in all groups. No mortalities were recorded within the time frame of the investigation
and no increased incidences of micronuclei were found. General bone marrow toxicity
was detected as the inhibition of proliferation in the erythropoiesis since the ratio of
normochromatic versus polychromatic erythrocytes was increased in the highest dose
group (Wallat, 1984b). The samples were collected 6 hours after the last or 30 hours after
the first administration, whereas current standard guidelines require the samples to
be collected once within time interval of 18 to 24 hours.
In a mouse micronucleus test with equilibrium PAA (5.17%), groups of 15 male and
15 female CD-1 mice were given single oral doses by gavage. Positive control groups of
males and females were given a single oral dose of 100 mg/kgbw cyclophosphamide
to confirm that the system was capable of detecting the effects of a known genotoxin.
Five males and 5 females from each group were killed at 24, 48 or 72 hours after treatment
and bone-marrow smears prepared for each time point. There were no significant
differences in the frequency of micronuclei in polychromatic or normochromatic
erythrocytes between mice treated with PAA and the untreated controls. This was
true for all doses of PAA tested, all three sampling times and both sexes of mice. PAA
did not induce a dose-related decrease in the proportion of polychromatic erythrocytes,
indicating a lack of toxicity to the bone marrow. No clinical signs were reported (Blowers,
1994a, 1995). It is not clear from this study whether PAA actually reached the target
organ. In the light of this, the significance of the negative results obtained are questionable.
In preliminary studies the highest dose tested (150 mg/kgbw) had been found to be the
maximum tolerated dose in both sexes of mice. In the main study the highest dose of
PAA had no effect on body-weight gain.
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Primary DNA repair after in vivo treatment

An in vivo / ex vivo UDS assay (Table 29) was conducted in groups of 6 male F344 rats
receiving doses of equilibrium PAA (5.17%) at 330 or 1,000 mg PAA/kgbw by gavage,
the maximum dose causing no observable toxicity as determined in a preliminary toxicity
study. A positive response with controls receiving 2-acetylaminofluorene and
nitrosodimethylamine confirmed the validity of the assay. From each treatment group,
2 animals were killed after 2 hours and 4 animals were killed after 16 hours, and
hepatocytes were isolated. No significant increases in UDS (measured as net grain
increase) were observed in both treated groups at either time. It was concluded that the
tested PAA formulation was not genotoxic under the conditions of the study (Blowers,
1994b). Information on the type of toxicity observed at higher doses, which could confirm
bioavailability, is not given in the report.
Limited information is available on effects of PAA on DNA and its potential to induce
gene and chromosome mutations both in vitro and in vivo. Considering the paucity of
reliable data, a final reliable evaluation of the mutagenic potential of PAA can hardly be
achieved (DFG, 1999b). Several bacterial tests are available, but these are of limited value
because PAA is a biocide and exerts its cytotoxic effects in these systems at low
concentrations. Cytotoxicity in most cases was diminished by the addition of an
exogenous metabolic system. In the strain TA 102, considered to be most sensitive
with regard to mutagenicity, only a slight response was detected, that was not statistically
significant.
The results of two DNA repair tests in human foetal lung cells did not indicate that PAA
had a genotoxic potential. In the in vitro chromosome aberration test, positive findings
were obtained only in concentrations that produced cytotoxicity. A common mechanism
for cytotoxicity and genotoxicity could be at play, e.g. relating to insufficient detoxification
of developing reactive oxygen species at high doses.
In one adequate in vivo study, PAA did not produce micronuclei. Another study failed
to prove that PAA had actually reached the target organ. In this study the doses may
have been too low to produce clinical signs of toxicity and cytotoxicity in the target
organ.
In an in vivo / ex vivo UDS assay in rats, PAA did not show genotoxic potential. The
highest dose was chosen to produce no toxicity and, as in the micronucleus tests,
bioavailability of PAA at the target organ was not verified. However, after oral treatment
it is more likely that a considerable amount of PAA reaches the liver after absorption
in the gastro-intestinal tract via the portal vein.
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8.5 Chronic Toxicity and Carcinogenicity
8.5.1 Chronic toxicity
8.5.2 Carcinogenicity
8.5.3 Tumour initiation-promotion
Bock et al (1975) reported diluted equilibrium PAA 40% (5% H2O2, 40% HOAc) to be a
skin tumour promoter and a weak initiator in mice. The results of the experiments are
summarised in Table 30.
Table 30: Initiation- Promotion Study with PAA (40%) on the Skin of Mice
(Bock et al, 1975)
Initiation Concentrationb Solvent Duration Incidence

with DMBAa of
treatment Skin tumour Skin cancer
(wk) (non-invasive) (invasive)
Yes 3% Water 66 24/30 5/30
Yes 1% Water 66 8/30 1/30
Yes 0.3% Water 66 2/30 0/30
Yes 0% None 66 0/30 0/30
Yes 2%c Water 56 2/30 0/30
Yes 1%c Acetone 56 2/30 0/30
No 2% Water 52 3/30d 0/30d
No 2% Acetone 52 NAe NAe
No 1% Acetone 52 0/30 0/30
No 0% None 66 0/30 0/30
a 7,12-Dimethylbenz[a]anthracene, 1 x 125 µg in 0.25 ml acetone, 3 weeks prior to treatment

b Related to formulation or active substance (not stated)
c “Decomposed”
d After first 26 weeks of treatment
e Not applicable, because all animals died early in the experiment
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The clipped dorsal skin of 3 groups of 30 female ICR Swiss mice was painted once with
7,12-dimethylbenz[a]anthracene (DMBA) in acetone. After 3 weeks, the mice were treated
(5 x 0.2 ml/wk) with 0.3%, 1% or 3% PAA solutions for 66 weeks. The authors reported
that a pilot study had indicated that 4% “aqueous PAA” would be excessively lethal. (It
is not clearly stated in the paper if the given concentrations relate to the formulation
or active substance. If the latter were so, the test solutions contained 1,200, 4,000 or
12,000 mg PAA/l). Two other groups of 30 mice pre-treated with DMBA were painted
(5 x 0.2 ml/wk) with “decomposed PAA” solutions (2% in water and 1% in acetone) for
56 weeks. PAA was “decomposed” by passing the product through a screen made of
a precious metal acting as catalyst. After this procedure, peroxy compounds could not
be detected iodometrically in the solution (detection limit not specified). Three additional
groups of 30 mice each were not treated with DMBA, but received (5 x 0.2 ml/wk) 2%
PAA in water or 1-2% PAA in acetone for 52 weeks. The mice were examined weekly
and the number and distribution of tumours were noted. A lesion was classified as a
skin tumour if it was at least 1 mm in diameter and if it persisted on the skin for at least
3 successive weeks.
After initiation with DMBA, a solution of PAA in water exhibited a dose-dependent

tumour-promoting activity at concentrations of 3% and 1%, respectively, but not at 0.3%
(Table 30). After DMBA pre-treatment both the 2% “decomposed PAA” in water and
the 1% “decomposed PAA” in acetone produced 2/30 tumours (7%) after 56 weeks.
Without DMBA pre-treatment, application of 2% PAA in water produced tumours in
3/30 (10%) of the animals after 26 weeks. Subsequent treatment for another 26 weeks
failed to increase the tumour rate. No tumours were recorded after treatment with PAA
in acetone. With regard to toxicity of PAA in acetone, an extraordinarily steep dose-
response curve was obtained. At 2% PAA all animals died early in the experiment,
whereas 1% was reported to be well-tolerated, as were PAA solutions of up to 3% in
water. Skin irritation resulting from the treatment with PAA was mentioned but not
specified as to the extent and expected differences between the dose and control groups.
The observed tumours were further classified by the authors as “skin cancers” if they
were capable of invading tissues below the panniculus carnosus. The tumours induced
by PAA in water alone were classified as non-invasive, but not explicitly specified as
benign. It should be noted that the applied tumour classification does not correspond
to current standards of tumour classification (Greaves and Barsoum, 1990).
This initiation-promotion study suffers from deficiencies in experimental design and

reporting of results. An irritation threshold was not determined and the concentration
of PAA used was apparently irritant. As only one dose of PAA in water was used, no
dose-response analysis can be made. Furthermore, the negative control mice do not
appear to have been treated in the same manner as the other groups. In particular, in
the negative controls, the two solvents (water and acetone) do not seem to have been
applied and it is not clear whether the hair was clipped.
Tumour generation ceased in the second phase of the experiment with PAA in water
only; after the first 26 weeks 3/30 (10%) tumours were found, but this number did not
increase over the next 26 weeks of treatment. With regard to historical data on tumour
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incidence in Swiss mice, Bock et al claim that only one skin tumour was found in
thousands of negative controls painted with acetone for up to 1.5 years. After treatment
with DMBA followed by acetone or water only, the authors reported a historical incidence
of 5.4% tumours in this strain. According to Ingram and Grasso (1991) the general
scientific consensus is that up to an incidence of 10%, there is no carcinogenic activity
induced in mouse skin by irritant substances. The effect is thought to be due to an
enhancement of spontaneous tumour incidence. In this context it is difficult to evaluate
the relevance of the observed 10% incidence of skin tumours with vehicle alone in a
single dose group.
No chronic toxicity or carcinogenicity studies have been conducted with PAA.
In one study, PAA acted as a tumour promoter in mouse skin after DMBA initiation. It
is likely that this is due to chronic irritation caused by PAA treatment. The data are
insufficient to identify PAA as an initiator, i.e. a complete carcinogen.
The German MAK Commissiona has classified PAA in category 3 for its carcinogenicity
(i.e. substances which give rise to concern because of possible carcinogenic effects in
humans, but which cannot be finally evaluated because of insufficient information), and
states that a 40% PAA solution causes very severe inflammation and corrosion of the
skin (DFG, 1999b). However, the “Ausschuß für Gefahrstoffe (AGS)”, the official OEL
setting committee in Germany, concluded that the available data on PAA do not allow
for a final conclusion to be made with regard to its carcinogenicity, mutagenicity or
toxicity to reproduction. Therefore, the AGS considered classification of PAA for those
endpoints inappropriate; an OEL was not established (TRGS, 1997).
In conclusion, in the only available initiation-promotion study, which suffers from a

number of experimental and reporting deficiencies, the observed effects represent an
effect secondary to local irritation, rather than indicating a carcinogenic potential for
PAA.
8.6 Reproductive Toxicity and Teratogenicity
8.6.1 Fertility
The breeding data from a specific-pathogen-free BD IX rat colony (77 animals, 67 controls)
receiving PAA in their drinking water (200 PAA mg/l) over several generations (not
specified) did not differ from those of the control group. Litter sizes and weights at
weaning were similar to controls. No further details are given in the publication (Juhr
et al, 1978) (CoR 4e).
Breeding pairs of NMRI and C3Hf mice, gerbils and Pirbright white guinea pigs were
given drinking water containing 200 mg PAA/l ad libitum for 10 months. Drinking water
a Sentatskomission zur Prüfung gesundheitsschädlicher Arbeitsstoffe
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was renewed every week. Breeding capacity was observed continuously. Growth and
outcome of breeding was similar to known historical stock data. No further details
are given (Juhr et al, 1978; CoR 4e).
Sperm head morphology

The sperm head morphology test is an in vivo test for evaluating the potential of a chemical
to induce abnormalities to the heads of sperm. The test has the potential to identify
chemicals that induce spermatogenic dysfunction and, possibly, heritable mutations.
The relationship of positive results in this test to carcinogenic or mutagenic potential
is not clear. No clear evidence is obtained from the test model whether alterations in
sperm morphology are due to cytotoxicity or to a clastogenic effect. In addition, the
validity of this test in assessing reproductive toxicity has not been established. The
genetic consequences of fertilisation by sperm affected by chemical treatment during
spermatogenesis remain unclear; embryonic death or transmission of genetic aberrations
to live-born progeny are possibilities (Wyrobek et al, 1983). These authors found that all
murine germ-cell mutagens tested also induce sperm-shape abnormalities in mice.
Therefore, it is critical that the sperm head morphology test be stringently conducted
so that the results can be properly interpreted.
A sperm head morphology test was conducted with PAA (40%, 14% H2O2, 27% HOAc),
applied as a 0.1% solution of the formulation in distilled water. ICR mice
(10 animals/group) were administered (0.2 ml i.p.) a dose of 2.6 mg PAA/kgbw/d
for 5 days. Positive and negative controls were included in the study. Animals were
killed 36 days after the first treatment, and spermatozoa were collected from the left and
right epididymis of each animal. Spermatozoa (200/animal) were examined for
abnormalities. The results showed that a dose of 2.6 mg PAA/kgbw doubled the incidence
of sperm head abnormalities. When the dose was reduced to 1.3 mg/kgbw, no increase
in anomalies was seen (Koch et al, 1989; CoR 3b). This study is deficient with regard
to the proper conduct of the test in that a pure, colony bred mice strain was used, whereas
hybrid strains are recommended (Wyrobek et al, 1983). Hybrid strains have a lower and
more stable spontaneous incidence of abnormal sperm than pure inbred strains. The
paper does not state that the epidydimes were minced, washed and filtered before sperm
smears were prepared, steps necessary to ensure good quality sperm for evaluation. It
is also not stated whether the smears were read “blind” to ensure lack of bias. The results
of the test do not meet the criteria for a positive response of PAA because statistically
significant results were not found at two consecutive dose levels. Thus, insufficient
evidence was provided to conclude that PAA caused abnormal sperm heads. In addition,
the i.p. route of exposure is not a route relevant to human exposure of PAA.
Subsequent to the i.p. study, the same group of investigators conducted a sperm head
test following dermal exposure to PAA, a route more relevant to human exposure. Groups
of ICR mice received twice daily dermal applications of 0.1 ml of 0.5% or 5.0% PAA
(formulation above) dissolved in distilled water, for 28 days. Controls received water
only. (The corresponding doses are estimated to be 0, 11.8 and 118 mg/kgbw/d). The
backs of the mice were depilated prior to application. The mice were killed 36 days after
the first application, the epididymides removed and smears of sperm prepared. The
skin of animals exposed to 5.0% PAA had marked necrosis after 3 days. The results of
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this test were positive, i.e. PAA caused abnormalities at both doses (Kramer et al, 1991;
CoR 3b). The study has the same deficiencies as that of Koch et al (1989) in using inbred
mice and in preparation and reading of sperm samples. In addition, a positive control
was omitted.
The relevance of the findings in the two sperm head anomaly tests (Koch et al, 1989;
Kramer et al, 1991) to the potential mutagenicity and clastogenicity of PAA is not clear.
The two tests did not meet the scientific criteria for valid assays (Wyrobek et al, 1983).
8.6.2 Developmental toxicity
In a teratogenicity study with ICR mice, the animals (5-10/group) were exposed (2 x/d)
by inhalation to nominal concentrations of 20 and 100 mg PAA/m3 throughout gestation.
The atmospheres were generated from a 1% or 5% dilution of PAA (40%, H2O2 14%,
HOAc 27%). The authors reported a statistically significant retardation of foetal growth
(body length and weight) at 100 mg PAA/m3, but no retardation at 20 mg/m3. No
exposure related skeletal anomalies were observed. The health status of the dams was
not reported (Kramer et al 1990; CoR 3a,b). Exposure to a level of 100 mg PAA/m3 would
have been expected also to produce maternal toxicity. Because of uncertainty about the
exposure levels and limited reporting, a reliable conclusion cannot be drawn from
this study.
8.6.3 Evaluation
No reliable conclusion can be drawn from the data regarding reproductive and
developmental toxicity of PAA because the available studies are inadequate, poorly
conducted or not relevant to these endpoints.
8.7 Other Studies

Laub et al (1990) studied the effects of PAA-containing disinfectants on Langerhans cells
of the epidermis of guinea pigs. Equilibrium PAA (formulation presumably 40% PAA,
14% H2O2 and 27% HOAc) and a mixture of 10% PAA and 75% glyceroltriacetate were
diluted with water yielding test solutions of 0.2% (2,000 mg PAA/l) of the formulation
and 0.1% (1,000 mg PAA/l) of the mixture. The pH (5.6) was adjusted with acetate buffer.
The test solutions were applied (1 x 50 µl/d) to the right ears of groups of 3 white guinea
pigs (inbred strain) for 1, 7 or 14 days. The animals were killed and the epidermis of
both ears (the left one was untreated and served as control) was isolated, fixed and
cut into ultra-fine slices and mounted on slides. Langerhans cells were counted after
staining with adenosine-triphosphatase (ATPase) stain. A time-dependent decrease in
Langerhans cells was observed in the treated ears compared to the control ears for both
preparations. When acetate buffered solutions were used the reduction of Langerhans
cells was less pronounced. The authors speculated that the reduction of Langerhans
cells in the epidermis after topical application of PAA solutions could alter the
immunological defence capacity of the treated skin.
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The effect on oral mucosa of long-term exposure to PAA was studied in a group of 8
rabbits exposed (1 - 8 h/d, 4 d/wk) via an “oral tank” to a 0.2% PAA solution (2,000 mg
PAA/l) prepared from 40% PAA (formulation above) for 11 months. The oral tanks,
made of Piacryl, were modelled to fit the oral cavity of the individual animals and slowly
released the test substance into the animal’s mouth (see Müller et al, 1978 for details).
One control group of 16 animals received water via the oral tank, while another group
of 10 rabbits remained untreated. The animals were regularly monitored for alterations
of the oral mucosa over the whole test period. Histopathological evaluation of the
oral mucosa was performed at the end of the study. Results indicated only epithelial
thickening (free from dysplasia and reversible at the end of the exposure period) and
inflammation of the oral mucosa. This effect was more pronounced in the PAA treated
group compared with the water treated group (Müller et al, 1980). The test conditions
are highly artificial and could have resulted in mechanical irritation of the mucous
membranes of the mouth and in forced drinking.
One ml of a 0.2% PAA solution (2,000 mg PAA/l), freshly prepared from 40% PAA
(formulation above) was applied (3 x/wk) to the oral or vaginal mucosa of groups of
1 or 2 rabbits for up to 12 months. Histology of the oral mucosa revealed isolated nuclear
oedema in the mucosal epithelium and increased epithelial desquamation of the
superficial layers of the epithelium beginning with the eighth month. No increase in
mitotic rate or dysplasia was observed in animals treated for up to 12 months. In the
vaginal mucosa slight focal oedema with circumscribed nuclear oedema and slight sub-
epithelial fibrosis was observed after 12 months. The mucosal epithelium was unaffected
(Müller et al, 1988).
8.7.1 Neurotoxicity
Possible neurotoxic effects of PAA vapours (nominal concentration 10 mg PAA/m3)

were studied in two behavioural tests (open field and maze trials) with mice and rats.
In the first test, male and female ICR mice (10 animals/group) were exposed (10 min/d,
whole-body) for 28 days to vapours evolving from 1 ml of equilibrium PAA 36-40%
(containing 14% H2O2 and 27% HOAc) in a 23 litres desiccator. Water served as the
control substance. The open field test was conducted for 10 minutes at the same time of
day prior to the first exposure and after 18 and 28 days of exposure. The test was
conducted immediately after exposure to the test substance. At day 18, an increase in
activity was observed in the treated mice compared to controls with regard to field
changeover, erect posture and jumping. No increase in tail drumming or grooming was
observed. After 28 days of exposure, activity was significantly depressed compared with
controls in respect of field changeover, erect posture and jumping, but there was increased
grooming, probably to remove PAA from the fur. Body-weight gain was initially retarded,
but subsequently recovered fully (Kramer et al, 1993; CoR 3b). It is likely that the observed
effects were secondary to irritation.
In the second test, following a 5-day training phase in a maze, Wistar rats (number
and sex not stated) were exposed using the same test conditions as for mice above. Four
separate test series were conducted. The maze trial was conducted on days 7, 14, 21, and
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28 with exposure taking place after passage through the maze on these days. For the
control animals the arrival time was shortened and the number of errors reduced
proportional to the length of the experiment. This was considered an expression of
the learning capacity of the animals. In the animals exposed to PAA, arrival times were
extended and did not get shorter with time. The number of errors did not decrease
significantly in the tests. (No individual data were given in the paper.) The authors
concluded that the effects observed in the animals were indicative of a possible neurotoxic
effect of PAA (Kramer et al, 1993; CoR 3b). However, as the exposures were scheduled
after the behavioural test it is possible that the delay of the animals was due to a learning
effect associated with avoidance of the discomfort of exposure to an irritant vapour.
Evaluation
The protocols do not meet the standards for neurotoxicity evaluation by various
regulatory authorities and hence the two experiments are not sufficiently standardised
to enable firm conclusions to be drawn. The behavioural effects reported in the publication
are likely to be secondary to the irritant properties of PAA. Clarification of the findings
could only be obtained from studies which included appropriate control exposures with
another known irritant using standard methods.
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9. EFFECTS ON HUMANS
9.1 Acute and Subchronic Toxicity

9.2 Irritation
9.2.1 Skin irritation
The available data on skin irritation in humans related to PAA are presented below (Table
31).
Table 31: Skin Tolerance Testing in Humans with PAA Solutions
Concentration Composition Dilution Effects Reference

(% PAA) PAA H2O2 HOAc (%)
0.5 40 14 27 1.25 Dermatosis when used Kramer et al, 1987a
with soap and water for
7 days
0.5 40 14 27 1.25 Irritation Mücke, 1970
< 0.5 40 14 27 1.25 No effects Kretzschmar et al, 1972
0.4 NS NS NS NS No effects Schröder, 1982
0.35 Irritationa French, 1993
0.2 40 14 27 0.5 No effects Mücke, 1970
0.2 No effects Pazdiora and
Kubiček, 1967
0.2 40 14 27 0.5 Rough skin and Kretzschmar et al, 1972
slippery feel for
1-2 days
0.1 1 7 10 10 No effectsa Baldry, 1992
a In eczema-prone patients
Kramer et al (1987a) reported immediate erythema formation in 3 of 15 surgeons using

0.5% PAA solution for hand disinfection repeatedly over a day. The procedure involved
soaping, brushing, washing for 3 minutes followed by hand disinfection for 5 minutes
and approximately 5 further hand disinfections of 5 minutes during the working day
between different operations. In 6 of 15 surgeons, hand dermatosis developed after 7
days of using PAA disinfecting solutions.
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Subjects using a wash solution of 0.5% PAA to disinfect hands reported irritation to the
skin, whereas those using a more dilute solution (0.2% PAA) did not. Long-term use
of 0.2% PAA solution for disinfection of hands did not result in any adverse effects on
skin (Mücke, 1970).
Tolerance to 0.4% PAA was found in humans. This article provides no further information
(Schröder, 1982).
Surgeons using 0.2% PAA for 3 minutes, followed by washing with soap, did not
experience intolerance. A burning sensation was experienced only when small wounds
were present. Concentrations of up to 0.5% PAA did not damage the skin of the hand
(Pazdiora and Kubiček, 1967).
Skin desquamation was noted for 1 to 2 days after hand disinfection with 0.2% PAA.
Rough skin was reported the day after treatment in 2 of 10 subjects. The roughness
disappeared during continued treatment. Subjects also reported a slightly slippery feeling
for 1 to 2 days when hands were washed with 0.2% PAA (Kretzschmar et al, 1972).
At concentrations of 0.35% PAA, 7 out of 56 eczema-prone patients showed irritation

responses (French, 1993). Use of lower concentrations (0.1% PAA and less) under occlusive
wrap was not associated with significant irritation in 122 eczema-prone patients in a
clinical skin irritation study (Baldry, 1992). Higher concentration levels were not tested.
A double-blind primary skin irritation study was conducted with various concentrations
of PAA in petrolatum on 10 subjects. The test material was prepared in petrolatum
and 0.2 ml applied under a band aid for 24 hours. The goal of the study was to determine
the concentration of PAA that could be tolerated for 4 days (continuous exposure) without
causing substantial skin damage. The criteria for a positive finding was a grade of
less than 2 on a scale of 0 to 5 (highest) in 5 of 10 subjects. A grade 2 response corresponded
to “intense redness/erythema”. A concentration of 2% PAA in petrolatum was found
to be the maximum concentration tested which met these criteria (Robinson, 1984).
9.2.2 Eye irritation
A solution of 0.1% PAA was applied with compresses to the eyelids for 5 to 10 minutes
in 4 subjects. A slight burning sensation was felt which disappeared during the application
(Kretzschmar, 1972). Ocular irritation was not reported, probably because PAA was
applied to the eyelid.
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9.2.3 Respiratory irritation
Respiratory effects or symptoms reported at different atmospheric concentrations of

PAA are given in Table 32.
Table 32: Atmospheric PAA Concentrations and Reported Effects or Symptoms
Concentration Effects or symptoms Reference

(mg/m3)
7.0 H2O2a Lachrymation, extreme discomfort and irritation Fraser and Thorbinson, 1986
of nasal membranes
2.8 - 4.2 H2O2b Extreme discomfort
1.4 - 2.8 H2O2c Tolerable discomfort
0.7 H2O2d No discomfort
0.9 - 1.2e Not immediately irritant, but unpleasant for an McDonagh, 1997
extended period.
0.4 - 0.5f Tolerable and not unpleasant
< 0.7 PAA No appreciable odour was detected Harvey, 1992
< 0.3 PAAg No symptoms of runny eyes or nose Simms, 1995
< 0.15 PAA Odour threshold lower than, but probably Ancker and Zetterberg, 1997
not much lower than, 0.15 mg/m3
a Reported as 5 ppm H2O2 (Section 5.2.2)

b Reported as 2.0 - 3.0 ppm H2O2
c Reported as 1.0 - 2.0 ppm H2O2
d Reported as 0.5 ppm H2O2
e Reported as 0.3 - 0.4 ppm
f Reported as 0.13 - 0.17 ppm
g Reported as < 0.15 mg/m3 H2O2
Fraser and Thorbinson (1986) reported lachrymation and extreme discomfort following
exposure to 7.0 mg/m3 total active oxygen compounds in an aerosol consisting of PAA
and H2O2 (Section 5.2.2) for only 3 minutes. Extreme discomfort, but no lachrymation
was reported for exposures of 3.5 - 4.2 mg/m3 for about 5 minutes and for 2.8 mg/m3
for up to 10 minutes. Exposure to 2.8 mg/m3 for 4 minutes caused unbearable irritation,
but was tolerated for 2 minutes of a 5-minute exposure.
McDonagh (1997) reported that exposure to PAA vapour at 0.9 - 1.2 mg/m3 (0.28 -
0.38 ppm) was not immediately irritant, but would have been considered “unpleasant”
for an extended time period. A vapour concentration of 0.4 - 0.5 mg PAA/m3 (0.13 - 0.16
ppm) was tolerable and not unpleasant for up to 3 hours.
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Exposure to PAA aerosols at a concentration of 1.5 ppm (4.74 mg/m3) for 15 to 20 minutes
caused discomfort to mucous membranes. Lower respiratory effects were not reported
even after exposure to 5 ppm PAA, although upper respiratory effects were reported
(Fraser and Thorbinson, 1986).
Schaffernicht and Müller (1998) conducted an investigation of 45 workplaces (150 workers)

at a university hospital (Section 5.2.2). For an 8-hour time period the concentrations
ranged from less than 0.005 mg PAA/m3 (detection limit) up to 1.84 mg/m3. Of the
measured values recorded, 60% were less than 0.1 mg/m3 and 5% exceeded 1.0 mg/m3.
The employees reported irritation around the eyes and of the nasal and pharyngeal
mucous membranes, as well as reddening and itching of the skin on the hands and face.
In the same study, Müller and Schaffernicht (1998) investigated whether the concentrations
observed in the 45 workplaces in the university hospital were likely to result in damage
of the teeth and gingivae. The dental status of the persons exposed to a workplace
concentration of > 0.4 mg PAA/m3 was examined. The study included a test group and
a control group of 26 females of the same age group with approximately the same oral
hygiene status. The findings were based on three criteria: oral hygiene, condition of the
gingivae, and the condition of the dental enamel. The only significant difference between
the test and control groups was in the sulcus bleeding index according to Mühlemann
and Son, indicating gingivitis in the front teeth area. Otherwise, no significant differences
were found between the test and the control groups. The authors concluded that a
damaging effect of PAA fumes on the gingivae probably could arise from low levels
of exposure.
A concentration of 4.6 mg PAA/m3 was used in intensive care rooms for short-term
disinfection purposes. No symptoms were reported by clinical staff or patients other
than a slight acidic odour (Dworschak and Linde, 1976).
Tichácek (1966 as cited in Kretzschmar, 1972) described irritant effects in humans exposed
to aerosol application of 0.8% PAA solution in a closed room. Effects included
lachrymation, increased nasal secretions, mucous membrane irritation and temporary
loss of smell. No further details were provided.
9.3 Sensitisation
There are no cases of skin sensitisation reported by the German network of dermatological
clinics (Informationsverbund Dermatologischer Kliniken) (IVDK, 1999).
9.4 Evaluation
When used as a hand wash solution, concentrations of 0.5% PAA caused skin irritation
in humans, but not if the concentration of the wash solution was 0.2% PAA or lower.
A solution of 0.1% PAA applied to the eyelids caused only a slight burning sensation.
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Data from topical skin applications or ocular exposure in humans are in agreement with
the information from animal studies (Section 8.2). Although the concentrations tested
were not identical, both humans and rabbits showed similar sensitivity in that < 0.2%
PAA was not irritant to skin and < 0.1% was not irritant to the eyes.
Exposure to atmospheric concentrations of 0.5 mg PAA/m3 (0.16 ppm) or lower seem

to be well tolerated by humans. Concentrations up to 1.2 mg/m3 (0.38 ppm) were not
immediately irritant but unpleasant after exposure for an extended time period.
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10. FIRST AID AND SAFE HANDLING ADVICE
10.1 First Aid

Liquid and mist are corrosive and can cause burns, direct contact could cause irreversible
damage to the eyes including blindness and/or irreversible destruction of skin tissue.
Vapour / mist will irritate the nose, throat and lungs, but will usually subside when
exposure ceases. The severity of the effects depends on the concentration and dose.
10.1.1 Skin and eye injuries
Eye contact: Immediately flush with water for at least 15 minutes, lifting the upper and
lower eyelids intermittently. Continue flushing until further treatment.
See medical doctor or ophthalmologist immediately.
Skin contact: Immediately flush with plenty of water while removing contaminated
clothing and /or shoes. Thoroughly wash with water. See medical doctor
if there is persistant irritation or if there are burns.
10.1.2 Inhalation
• The patient should be taken into fresh air and should rest in a seated posture.
• If breathing discomfort occurs and persists after cessation of exposure, see a medical
doctor.
• If breathing has stopped, artificial respiration should be administered until qualified
medical personnel are able to take over.
10.1.3 Ingestion
• Do not induce vomiting.

• If the subject is conscious, flush mouth with water, give 1 to 2 glasses of water to drink.
• Never give anything by mouth to an unconscious person but provide classical
resuscitation measures.
• See a medical doctor immediately or take subject to a hospital.
10.2 Safe Handling
10.2.1 Handling and safety at work
• Operate in well ventilated area, do not breathe vapours

• Provide mechanical local exhaust ventilation
• No eating, drinking, smoking in work area
• Use adequate personal protective equipment (PPE) (below)
• Never return unused material to original container
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• Avoid contamination of product

• Avoid contact with skin, eyes and clothing
• Wash face and hands after handling product
• Provide emergency showers and eye wash stations
Personal protective equipment

• Respiratory protection :
• In case of emissions of vapours and aerosols, use suitable respiratory protection.
• In case of large uncontrolled emissions, positive pressure self-contained breathing
apparatus should be used.
• Hands - Wear suitable gloves made from materials with acceptable penetration times,
e.g. butylrubber, polychloroprene, fluororubber
• Eyes - Use chemical proof goggles, full face shield or full face mask
• Body - Wear acid proof protective clothing., e.g. apron and boots made of butylrubber
if risk of splashing.
10.2.2 Storage
• Store in vented containers in a clean, cool, dry, well-ventilated area

• Store away from reducing agents, fuels, non-compatible materials e.g., alkalis, reducing
agents, metallic salts, combustibles and other oxidising agents.
• Keep away from direct sun light, heat sources and sources of ignition
• Keep in original package, keep closed, Use first in first out
10.3 Management of Spillage and Waste
10.3.1 Spills and waste
• Evacuate and isolate the hazard area, approach release from upwind
• Use adequate PPE (Section 10.2.1)
• Stop leak / contain spill (if this can be done safely)
• Dilute spilled material with large quantities of water or mix with an inert material
such as sand or earth
• Do not seal waste material, do not use textiles, tissues, saw dust or combustible materials
to clean spill
• Remove endangered containers to safe place, if this can be done safely
• Never return spilled material to original container
• Keep non-compatible materials away from spill
• Dispose of spilled material in accordance with all country, state and local regulations
• Immediately notify appropriate authorities
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10.3.2 Fire-fighting measures
During a fire, PAA could begin to decompose releasing oxygen gas, which can support
combustion of flammable materials. If decomposition occurs, a pressure burst may occur
if the container is not properly vented. To fight the fire:
• Approach from upwind

• Use proper personal protective equipment such as an acid resistant over suit and a
positive pressure self contained breathing apparatus
• Bring persons to safety, evacuate all non-essential personnel
• Use large quantities of water spray to fight the fire and to keep fire-exposed containers
cool
Refer to the local authorities for disposal of PAA. For further and more detailed safety
instructions, contact your PAA supplier.
For bulk storage spillage, an emergency plan should be worked out in conjunction with
the supplier and the competent authority, if applicable.
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11. BIBLIOGRAPHY
11.1 Databases Consulted

HSDB - Hazardous Substances Data Bank (CD Rom Search)
Chemical Abstracts Database
DIALOG
RTECS - Registry of Toxic Effects of Chemical Substances (CD Rom Search)
CA SEARCH 1998 American Chemical Society
Toxline format only 1998 The Dialog Corporation
BIOSIS PREVIEWS 1998 BIOSIS
AGRICOLA format only 1998 The Dialog Corporation
CAB Abstracts 1998 CAB International
Enviroline 1997 Congressional Information Service
Pollution Abs 1998 Cambridge Scientific Abstracts
Aquatic Sci&Fish Abs 1998 FAO (for ASFA Adv Brd)
Env.Bib. 1998 Internl Academy at Santa Barbara
SEDBASE
EMBASE
MEDLINE
TOXLINE
Chemical Safety News Base
NIOSH
Food Science and Technology Abstracts
International Pharmaceutical Abstracts
Life Sciences Collection
Drug Information Fulltext
Agrochemicals Handbook
Chemical Safety Newsbase
American Medical Association Journals Online
New England Journal of Medicine Online
11.2 References Quoted

ACGIH (American Conference of Governmental Industrial Hygienists). 2000. 2000 TLVs and
BEIs, threshold limit values for chemical substances and physical agents and biological
exposure indices. ACGIH, Cincinnati, OH, USA, pp 15, 42.
Agnet Y, Dorange JL, Dupuy P. 1977. Mutagenicity of peracetic acid on Salmonella typhimurium.
Unpublished report, Annex 2. Institut National de la Recherche Agronomique, Station de
Technologie des Produits Végétaux, Dijon, France.
AISE (Association Internationale de la Savonnerie, de la Détergence et des Produits

d'Entretien). 2000. Peracetic acid, data for ECETOC JACC report [on peracetic acid from
TAED]. Personal communication by Poelloth C, 28 March. AISE, Brussels, Belgium.
Akzo Nobel. 1998. SDS safety data sheet, peracetic acid (PAA) 38%, revised October 1998.
Akzo Nobel, Eka Chemicals, Bohus, Sweden.
109
ECETOC JACC No.40
Ancker K, Zetterberg L. 1997. Mätning av perättiksyra vid Eka Chemicals AB i Bohus

[Measurement of peracetic acid at Eka Chemicals AB, Bohus]. Unpublished report A97329,
IVL (Institutet för Vatten- och Luftvårdsforskning), Stockholm, Sweden. Eka Chemicals,
Bohus, Sweden [Swedish; English translation].
Ausimont. 1997a. Oxystrong 5%, scheda di sicurezza. Ausimont, Bollate, MI, Italy.
Ausimont. 1997b. Oxystrong 15%, scheda di sicurezza. Ausimont, Bollate MI, Italy.
Ausimont. 1999. Campagna de rilevamento igienico ambientale, risultati monitoraggio di

area, reparto H2O2. Personal communication to Malinverno G, April 1999. Ausimont, Bussi,
Italy.
Ausimont. 2000. Campagna de rilevamento igienico ambientale, risultati monitoraggio di

area, reparto infusamento PAA. Personal communication to Malinverno G, March 2000.
Ausimont, Bussi, Italy.
Bactria. 1995. Sicherheitsdatenblatt gemäß 91/155/EWG, Bactrozon 5/23, Austellungsdatum

30.03.95. Bactria, Kircheimbolanden, Germany.
Bactria. 1997. Sicherheitsdatenblatt gemäß 91/155/EWG, Bactrozon 15/23, Austellungsdatum

17.09.97. Bactria, Kircheimbolanden, Germany.
Baldry MGC. 1983. The bactericidal, fungicidal and sporicidal properties of hydrogen peroxide
and peracetic acid. J Appl Bact 54:417-423.
Baldry MGC. 1992. Irritancy of peracetic acid to skin. Personal communication, memorandum
MGCB/SB/M-4-92. Solvay Interox, Widnes, Cheshhire, UK.
Baldry MGC, Fraser JAL. 1988. Disinfection with peroxygens. In Payne KR, ed, Industrial
Biocides, Wiley, Chichester, UK, pp 91-116.
Baldry MGC, French MS, Slater D, Desprez F. 1990. Désinfection par l'acide peracétique des
effluents urbains, l'expérience anglaise. L'eau, L'industrie, Les Nuisances 137:42-44.
Baldry MGC, French MS, Slater DS. 1991. The activity of peracetic acid on sewage indicator
bacteria and viruses. Wat Sci Tech 24:353-357.
Baldry MGC, Cavadore A, French MS, Massa G, Rodrigues LM, Schirch PFT, Threadgold
TL. 1995. Effluent disinfection in warm climates with peracetic acid. Wat Sci Tech 13:161-164.
BAM (Bundesanstalt für Materialforschung und -prüfung). 1999. Verpackungen und IBC
zur Beförderung von Salpetersäure, Ergebnisvermerks der Besprechung am 16. Dezember
1998 in der BAM, Berlin. Personal communication by Wieser KE. BAM, Berlin, Germany.
Basta J, Holtinger L, Ludgren P, Persson C. 1995. Emerging technologies in TCF bleaching.

In TAPPI pulping conference. TAPPI, Technology Park, Atlanta GA, USA, pp 53-57.
Battelle. 1999. Personal communication of 14 December [on the consumption of TAED] by

Dallé J to Leonhardt W, Degussa Hüls. Batelle, Darouge, Genève, Switzerland.
110
ECETOC JACC No.40
Bazzon M, Chauvire L, Giacalone J, Gondelle F, Lamy MH, Petit-Poulsen V, Bailleul S,

Rose M. 1997. Toxicité aiguë vis-à-vis des poissons Brachydanio rerio. Substance d'essai:
solution aqueuse d'acide peracétique. Unpublished report, study Ba567a, INERIS (Institut
National de l'Environnement Industriel et des Risques), Verneuil-en-Halatte, France. Air
Liquide, Chemoxal, Jouy en Josas, France.
Benes V, Tichácek B, Veger J. 1966. Toxicita kyseliny peroctové [Die Toxizität der Peressigsäure].
In Tichácek B et al, ed. Kyselina peroctová a moznosti jejího využití v dežinfekci [Peressigsäure
und die Möglichkeiten ihrer Verwendung in der Desinfektion]. Zdrav. aktuality 163, Stát.
Zdrav. Nakl. Praha [Staatsverlag für das Gesundheitswesen der CSSR, Prague,
Czechoslovakia], pp 100-107 [Only title translated].
Berglin EH, Carlson J. 1986. Effect of hydrogen sulfide on the mutagenicity of hydogen
peroxide in Salmonella typhimurium strain TA102. Mutation Res 175:5-9.
BG Chemie (Berufsgenossenschaft der chemischen Industrie). 1993. Unfallverhütungsverschrift

58, Organische Peroxide. BG Chemie, Heidelberg, Germany.
Biffi E. 1992a. Tossicita’ inalatoria nel ratto (dose limite). Unpublished report 92/14445, Biolab
SGS, Vimodrone, Milano, Italy. Solvay Interox, Milano. [Italian; English translation].
Biffi E. 1992b. Irritazione cutanea nel coniglio, acido peracetico 5 %. Unpublished report
92/14443, Biolab SGS, Vimodrone, Milano, Italy. Solvay Interox, Milano. [Italian; English
translation].
Biffi E. 1992c. Irritazione oculare nel coniglio, acido peracetico 5 %. Unpublished report
92/14444, Biolab SGS, Vimodrone, Milano, Italy. Solvay Interox, Milano. [Italian; English
translation].
Biffi E. 1992d. Sensibilizzazione allergica nella cavia, acido peracetico 5 %. Unpublished

report 92/14446, Biolab SGS, Vimodrone, Milano, Italy. Solvay Interox, Milano. [Italian;
English translation].
Biffi E. 1995. Tossicita’ inalatoria acuta, acido peracetico 5 %. Unpublished report 95/01665,
Biolab SGS, Vimodrone, Milano, Italy. Solvay Interox, Rosignano Solvay, Livorno, Italy.
[Italian; English translation].
Bioxal. 1999. Bactipal 5/14, stabilité après dilution à 100 et 1000 ppm. Unpublished report.
Bioxal, Chalon sur Saône, France.
Bioxal. 2000a. Produits chimiques à usage industriel, fiche de données de sécurité, Bactipal
5-14. Seppic-Air Liquide, Paris, France.
Bioxal. 2000b. Produits chimiques à usage industriel, fiche de données de sécurité, Bactipal
15-23. Seppic-Air Liquide, Paris, France.
Blakistone B, Chuyate R, Kautter D, Charbonneau J, Suit K. 1999. Efficacy of oxonia active

against selected spore formers. J Food Prot 62:262-267.
Block SS. 1991. Peroxygen compounds. In Block SS, ed, Disinfection, sterilization, and preservation,
4th ed. Lea and Felbinger, Philadelphia PA, USA, pp 167-181.
111
ECETOC JACC No.40
Bloomfield SF, Arthur M, Looney E, Begun K, Patel H. 1991. Comparative testing of

disinfectant and antispetic products using proposed European suspension testing methods.
Letters in Applied Biology 13:233-237.
Blowers SD. 1994a. A micronucleus test with Proxitane-0510. Unpublished report 1324/1/2/94,
BIBRA Toxicology International, Carshalton, Surrey, UK. Johnson & Johnson Medical, Skipton,
N. Yorkshire, UK.
Blowers SD. 1994b. An in vivo unscheduled DNA synthesis assay with Proxitane-0510.
Unpublished report 1334/1/2/94, BIBRA Toxicology International, Carshalton, Surrey, UK.
Johnson & Johnson Medical, Skipton, N. Yorkshire, UK.
Blowers SD. 1995. A micronucleus test with Proxitane-0510. Unpublished report 1324/1/2/94,
addendum 1, BIBRA Toxicology International, Carshalton, Surrey, UK. Johnson & Johnson
Medical, Skipton, N. Yorkshire, UK.
Bock FG, Myers HK, Fox HW. 1975. Cocarcinogenic activity of peroxy compounds. J Natl
Cancer Inst 55:1359-1361.
Bowler G, Malone J, Pehrsson R. 1996. Recent advances in the application of peracetic acid
formulations in the European sugar beet industry. Zuckerind 121:414-416.
Bringmann G, Kühn R. 1982. Ergebnisse der Schadwirkung wassergefährdender Stoffe gegen

Daphnia magna in einem weiterentwickelten standardisierten Testverfahren. Z Wasser Abwasser
Forsch 15:1-6.
Bulnes C, Garcia MG, Tablada L. 1982a. Efectos toxicos del acido peracetico II, estudio
morfopatologico en la piel de cobayos en condiciones de contacto directo. Rev Salud Anim
4:59-65.
Bulnes C, Garcia MG, Tablada L. 1982b. Efectos toxicos del acido peracetico I, estudio
morfopatologico en la piel y las mucosas de cobayos sometidos a condiciones forzadas de
inhalacion. Rev Salud Anim 4:75-84.
Bundesminister (für Umwelt, Naturschutz und Reaktorsicherheit). 1999. Allgemeine

Verwaltungs-vorschrift zum Wasserhaushaltsgesetz über die Einstufung wassergefährdender
Stoffe in Wassergefährdungsklassen (Verwaltungsvoschrift wassergefährndder Stoffe,
VwVwS) vom 17.05.99. Bundesanzeiger 98a:1-31.
Burgess D, Forbis AD. 1983. Acute toxicity of Oxonia Active to Daphnia magna. Unpublished
report report 30724, Analytical Bio-Chemistry Laboratories, Columbia MO, USA. Bonewitz
Chemical Services, Burlington, Iowa, USA.
Busch A, Werner E. 1974. Zur Problematik der Tierverträglichkeit von Peressigsäure I. Mitt.,
Untersuchungsergebnisse nach Applikation von Peressigsäure. Mh. Vet. Med. 29:494-498.
Butler R. 1987. Determination of the 48 hour median effect concentration (EC50) of Oxymaster
to the pacific oyster (Crassostrea gigas) in terms of larval survival and development.
Unpublished report CO1643-M/EV8687, WRc Environment. Interox Chemicals, Widnes,
Cheshire, UK.
112
ECETOC JACC No.40
Byers L. 1998. Octanol-water partition coefficient for peracetic acid and hydrogen peroxide.
Personal communication to Caropreso F, February 5. FMC, Princeton PA, USA.
Calvert JG, Lazrus A, Kok GL, Heikes BG, Walega JG, Lind J, Cantrell CA. 1985. Chemical
mechanisms of acid generation in the troposphere. Nature 317:27-35.
Caropreso FE. 2000. Calculation of peracetic acid vapor compositions using ideal solutions.
Personal communication, 25 April. FMC, Princeton PA, USA.
Cascieri T, Freeman C. 1983a. Acute oral toxicity of dilute peracetic acid in rats. Unpublished
report, study I83-718. FMC Corporation, Somerville NJ, USA.
Cascieri T, Freeman C. 1983b. Acute dermal toxicity of dilute peracetic acid in rabbits.
Unpublished report, study I83-721. FMC, Somerville NJ, USA.
Cascieri T, Freeman C. 1983c. Primary skin irritation and skin corrosion study of dilute
peracetic acid in rabbits. Unpublished report, study I83-720. FMC, Somerville NJ, USA.
Cascieri T, Freeman C. 1983d. Primary eye irritation study of dilute peracetic acid in rabbits.
Unpublished report, study I83-719. FMC, Somerville NJ, USA.
CEFIC (European Chemical Industry Council). 2000a. Peracetic acid production in Europe.
Personal communication by Le Doré L, Peroxygens Sector Group, 10 April. CEFIC, Brussels,
Belgium.
CEFIC (European Chemical Industry Council). 2000b. Peracetic acid production and
consumption data. Personal communication by Le Doré L, Peroxygens Sector Group, 20
June. CEFIC, Brussels, Belgium.
Cerne O, Ancker K, Palokangas P. 1999. Arbetsmiljö och miljöeffekter av massaindustrins

miljöanpassning, perättiksyra som blekkemikalie samt förstudie av slutning av
processvattenströmmar [Occupational and environmental effects of the environmental
approach in the pulp industry, and a pre-study of effluent closure]. Report B 1326. IVL
(Institutet för Vatten- och Luftvårdsforskning), Stockholm, Sweden [English translation].
Chalkley NJ. 1991a. Degradation of peracetic acid, investigation of the depth of penetration
of peracetic acid into soil. Personal communication 20th March 1991. Solvay Interox, Widnes,
Cheshire, UK.
Chalkley NJ. 1991b. Degradation of peracetic acid in pond and stream waters. Personal
communication 15th May 1991. Solvay Interox, Widnes, Cheshire, UK.
Chalkley NJ. 1991c. Degradation of peracetic acid in soil, potato and Brussels sprouts. Personal
communication 6th February 1991. Solvay Interox, Widnes, Cheshire, UK.
Chalkley NJ. 1992. Degradation of peracetic acid in contact with coir and various samples
of [tap] water. Personal communication 19th March 1992. Solvay Interox, Widnes, Cheshire,
UK.
Chance B, Sies H, Boveris A. 1979. Hydroperoxide metabolism in mammalian organs. Physiol

Rev 59:527-605.
113
ECETOC JACC No.40
Chemoxal. 1995a. Procès-verbal de la dégradation abiotique du APA 0.35%, hydrolyse en

fonction du pH, protocole paru au JO des CE L383 A/229 du 29/12/92. Unpublished report.
Air Liquide, Chemoxal, Paris, France.
Chemoxal. 1995b. Détermination de l'équation d'Arrhenius, At.Chem.95.05 suite. Unpublished

report. Air Liquide, Chemoxal, Paris, France.
Chemoxal. 1997. Safety data sheet, Bactipal 15-14. Seppic-Air Liquide Group, Chalon-sur-
Saône, France.
Chemoxal. 1999. Data about PAA 15% [Bactipal 15/23 and 15/14]. Personal communication
by Gouges Y, 5 March. Chemoxal, Air Liquide Chimie, Paris, France.
Cohle P, McAllister WA. 1983. Acute toxicity of Oxonia Active to rainbow trout (Salmo
gairdneri). Unpublished report 30723, Analytical Bio-Chemistry Laboratories, Columbia MO,
USA. Bonewitz Chemical Services, Burlington, Iowa, USA. <Henkel>
Coppinger WJ, Wong TK, Thompson ED. 1983. Unscheduled DNA synthesis and DNA repair
studies of peroxyacetic and monoperoxydecanoic acids. Environmental Mutagenesis 5:177-
192.
Cords BR. 1994. New peroxyacetic acid sanitizer. In: Proceedings of the twenty-third convention
[Reference details lacking].
Cords BR, Dychdala GR. 1993. Sanitizers, halogens, surface-active agents and peroxides.
Food Science and Technology 57:469-537.
Crow S. 1992. Peracetic acid sterilization, a timely development for a busy healthcare industry.
Infection Control and Hospital Epidemiology 13:111-113.
Dalin I. 1996. Framtida kemikalier i blekeriet [Future chemicals in the bleach plant]. Presented
at: ÅF-IPK Fibre Line Conference, Stockholm, Sweden 27 November. Akzo Nobel, Eka
Chemicals, Bohus, Sweden.
De Duve C, Bauduin P. 1966. Peroxisomes (microbodies and related particles). Physiol.

Rev. 46:323-353.
Degussa. 1977a. Prüfung der akuten Toxizität von Peressigsäure 10%ig bei peroraler
Applikation an Ratten. Unpublished report by Leuschner F, Laboratorium für Pharmakologie
und Toxikologie, Hamburg, Germany. Degussa, Frankfurt am Main, Germany.
Degussa. 1977b. Orientierende Prüfung der akuten Toxizität von 40%iger Peressigsäure bei
Sprague-Dawley Ratten. Unpublished report by Leuschner F, Laboratorium für Pharmakologie
Degussa. 1982a. Bericht über die toxikologische Prüfung von Peressigsäure 15% nach
einmaliger oraler Gabe an der Ratte. Ergänzende Mitteilung. Unpublished report Ind-Tox-
86-81/82, 86/1-82/83 by Zechel HJ, Toxikologisches Institut Degussa-Asta, Bielefeld, Germany.
Degussa, Frankfurt am Main, Germany.
114
ECETOC JACC No.40
Degussa. 1982b. Bericht über die Prüfung der lokalen Reizwirkung von Peressigsäure 15%
nach einmaliger Applikation an der Haut des Kaninchens (Patch-Test). Unpublished report
Ind-Tox-87-81/82 by Zechel HJ, Toxikologisches Institut Degussa-Asta, Bielefeld, Germany.
Degussa, Frankfurt am Main, Germany.
Degussa. 1988a. Peroxyacetic acid 10%, acute toxicity, testing the primary irritancy after
single application to the skin of the rabbit (patch test). Unpublished report study 864876
by Mayr W, Asta Pharma, Bielefeld, Germany. Degussa, Hanau, Germany.
Degussa. 1988b. Peroxyacetic acid 5%, acute toxicity, testing the primary irritancy after single
application to the skin of the rabbit (patch test). Unpublished report study 864865 by Mayr
W, Asta Pharma, Bielefeld, Germany. Degussa, Hanau, Germany.
Degussa. 1990a. Arbeitsplatzmessungen auf Peressigsäure in der Raumluft, Asta Pharma,

Frankfurt am Main, Germany. Personal communication 12 December. Degussa, Hanau,
Germany.
Degussa. 1990b. Peroxyacetic acid 15%, acute toxicity, testing the primary irritation/corrosion
after single application to the skin of the rabbit (patch test). Unpublished report study 864870
by Zechel HJ, Asta Pharma, Bielefeld. Degussa, Hanau, Germany.
Degussa. 1991. Prüfbericht Chlorella vulgaris, Algenwachstumshemmtest mit Wasser-

stoffperoxid 35%G. Unpublished report 91/11/01 by Geschäftsbereich Industrie- und
Feinchemikalien, Hanau, Germany. Degussa, Hanau, Germany.
Degussa. 1996a. Peracetic acid 15%, safety data sheet (93/112/EEC) valid from 06.09.1996.
Degussa, Hanau, Germany.
Degussa. 1996b. Peracetic acid 35%, safety data sheet (93/112/EEC) valid from 19.2.1996.
Degussa. 1997. Peracetic acid 5%, safety data sheet (93/112/EEC) valid from 10.04.1997.
Den Besten C. 1994. Proxitane 0103, acute oral toxicity study in the rat. Unpublished report
S.9406, Solvay Duphar, Weesp, Netherlands. Solvay Interox, Brussels, Belgium.
DFG (Deutsche Forschungsgemeinschaft). 1999a. MAK- und BAT-Werte-Liste 1999, Maximale

Arbeitsplatzkonzentrationen und biologische Arbeitsstofftoleranzwerte. Mitteilung 35.
Wiley-VCH, Weinheim, Germany, pp 12, 57, 108.
DFG (Deutsche Forschungsgemeinschaft). 1999b. MAK- und BAT-Werte-Liste 1999,

Senatskommission zur Prüfung gesundheitsschädlicher Arbeitsstoffe. Mitteilung 35. Wiley-
VCH, Weinheim, Germany, pp 90, 120-122, 166.
Dixon D. 1988. Comparative study of the toxicity and genotoxicity of Oxymaster and
hypochlorite (on reproductive stages of the marine tubeworm Pomatoceros triqueter L.). Solvay
Interox, Warrington, UK.
115
ECETOC JACC No.40
Dorange JL, Agnet Y, Dupuy P. 1974. Etude des propriétés mutagènes de l'acide peracétique.
[The mutagenic acitivity of peracetic acid, Appendix 2-5]. Unpublished report, Aide DGRST
74-7-673 et 674, Annexe 2-5. Institut National de la Recherche Agronomique, Station de
Technologie des Produits Végétaux, Dijon, France. Chemoxal, Paris, France. [French; English
translation].
Douglas MT, Pell IB. 1986a. The acute toxicity of Proxitane 1507 to Daphnia magna. Unpublished
report LPT44/851641. Huntingdon Research Centre, Huntingdon, Cambridgeshire, UK.
Laporte Industries, Widnes, Cheshire, UK.
Douglas MT, Pell IB. 1986b. The acute toxicity of Proxitane 1507 to rainbow trout (Salmo
gairdneri). Unpublished report LPT43/851643. Huntingdon Research Centre Huntingdon,
Cambridgeshire, UK. Laporte Industries, Widnes, Cheshire, UK.
Drimus J, Matasa C. 1966. Sur la décomposition spontanée de l'acide peracétique [Spontaneous

decomposition of peracetic acid]. Bulletin de la Société Chimique de France 12: 253-255 [French;
English translation].
Dudek BD. 1984. Four hour acute aerosol inhalation toxicity study in rats of P3 Oxonia Active.
Unpublished report, study 420-1467. ToxiGenics, Decatur, IL, USA. Bonewitz Chemical
Services, Burlington, Iowa, USA. <Henkel>
Duprat P, Gradiski D, Delsaut L, Lepage M. 1974. Pouvoir irritant sur la peau et l'oeil du
lapin de l'eau de Javel et de l'acide peracétique à différentes concentrations. Revue Méd Vét
125:879-895.
Dworschak D, Linde J. 1976. Raumluftdesinfektion mit Peressigsäure (PES)-Aerosolen auf

Intensivtherapiestationen unf ihre Konsequenzen für die Behandlung des Hopitalis-
musproblems. Dt. Gesundh.-Wesen 31:1622.
Dychdala GR. 1988. New hydrogen peroxide-peroxyacetic acid disinfectant/sanitizer. In:

Kutz SM et al, eds, 4th Conference on progress in chemical disinfection. Janauer G, Chairman.
Dept. of Chemistry State University of New York NY, USA, pp 315-342.
EC (European Commission). 1996. Commission regulation (EC) No 1433/96 of 23 July

1996 amending annexes II and III to Council Regulation (EEC) No 2377/90 laying down a
Community procedure for the establishment of maximum residue limits of veterinary
medicinal products in foodstuffs of animal origin. Official Journal of the European Communities
L 184:21-23.
EC (European Commission). 1998. Cas No 79-21-0, peracetic acid …%. In Annex to

Commission directive 98/98/EEC of 15 December 1998 adapting to technical progress for
the twenty-fifth time Council directive 67/548/EEC on the approximation of the laws,
regulations and administrative provisions relating to the classification, packaging and
labelling of dangerous substances. Official Journal of the European Communities L 355:275.
ECE (Economic Commmission for Europe), Inland Transport Committee. 1996. European
agreement concerning the international carrage of dangerous goods by road (ADR) and
protocol of signature, done at Geneva on 30 september 1957, volume I. Agreement, protocol
of signature, annex A and appendices to Annex A with amendments thereto up to 1 January
1997. ECE/Trans/115 (Vol.I). UN, Geneva, Switzerland.
116
ECETOC JACC No.40
ECETOC (European Centre for Ecotoxicology and Toxicology of Chemicals). 1993. Hydrogen
peroxide, CAS 7722-84-1. Joint Assessment of Commodity Chemicals 22. ECETOC, Brussels,
Belgium.
ECETOC (European Centre for Ecotoxicology and Toxicology of Chemicals). 1996. Hydrogen
peroxide OEL criteria document, CAS 7722-84-1. Special report 10. ECETOC, Brussels,
Belgium.
EEC (European Economic Community). 1990. Council regulation (EEC) 2377/90 of 26 June
1990 laying down a Community procedure for the establishment of maximum residue limits
of veterinary medicinal products in foodstuffs of animal origin. Official Journal of the European
Communities L 224:1-8.
Effkemann S, Karst U. 1998. Reagent for the high-performance liquid chromatography

determination of peroxycarboxylic acids. Analyst 123:1761-1765.
Effkemann S, Brødsgaard S, Mortensen P, Linde SA, Karst U. 1999a. Determination of gas

phase peroxyacetic acid using pre-column derivatization with organic sulfide and liquid
chromatography. J Chromatography A 855:551-561.
Effkemann S, Pinkernell U, Harms D, Karst U. 1999b. Recent techniques for the determination
of peroxycarboxylic acids. International Laboratory 29:14-19.
Effkemann S, Brødsgaard S, Mortensen P, Linde SA, Karst U. 2000. Spectrophotometric and

direct-reading methods for the analysis of gas-phase peroxyacetic acid. Fresenius J Anal Chem
366:361-364.
EU (European Union). 1998. Directive 98/8/EC of the European Parliament and of the Council
of 16 February 1998 concerning the placing of biocidal products on the market. Official Journal
of the European Communities L 123:1-63.
EU (European Union). 1999. Directive 1999/45/EC of the European Parliament and of the
Council of 31 May 1999 concerning the approximation of the laws, regulations and
administrative provisions of the Member States relating to the classification, packaging and
labelling of dangerous preparations. Official Journal of the European Communities L 200:1-68.
Europerox. 1997. New methods and instrumentation for selective peroxide monitoring in
industrial processes, a standards, measurements and testing proposal (1994-1998). Theme
1, measurements for quality European products including written standards for industry,
1.3. Measurement and testing for the control of production, proposal description, part A.
European Commission standards, measurements and testing programme project SMT4-
CT97-2153. Europerox, University of Münster, Münster, Germany.
Fairhurst F. 1987. Determination of the 48 hour median effect concentration (EC50) of

Oxymaster to the common mussel (Mytilus edulis), in terms of larval survival and
development. Unpublished report CO1644-M/EV8687, WRc Environment, Medmenham,
Marlow, Bucks, UK. Interox Chemicals, Widnes, Cheshire, UK.
Feigenbaum H. 1997. The use of peracetic acid as a chemical oxidant in pharmaceutical

synthesis. Speciality Chemicals 17:80-81.
117
ECETOC JACC No.40
Ferri A. 1990. Action of catalase on peroxoacetic acid. Kinetic studies. Biochemistry. International
21:623-631.
Fischbach LJ. 1985. Renalin, qualification as a dialyzer sterilant. AAMI 1985:15-19.
Fischer W, Arlt E, Brabäder B. 1989. Verfahren und Reagenz zur Bestimmung von Persäuren.
Merck Patent, Darmstadt. Offenlegungsschrift DE 37 43 224 A1. Deutsches Patentamt,
München, Germany.
FMC. 1998a. Material safety data sheet, peracetic acid 5%, version US/Canada. FMC, Princeton
PA, USA.
FMC. 1998b. Material safety data sheet, peracetic acid 15%, version US/Canada. FMC,
Princeton PA, USA.
FMC. 1998c. Material safety data sheet, peracetic acid 35%, version US/Canada. FMC,
Princeton PA, USA.
Fraser JAL. 1986. Peroxygens in environmental protection. Effluent and Water Treatment Journal
June 1986:186-199.
Fraser JAL, Thorbinson A. 1986. Fogging trials with Tenneco Organics Limited (30th June.
1986) at Collards Farm. Unpublished report. Solvay Interox, Warrington, UK.
Freeman C. 1987. 35% peracetic acid, preliminary oral toxicity study in rats. Unpublished
report, study I86-0935. FMC, Princeton, NJ, USA.
Freeman C. 1991a. Peracetic acid 0.15% use dilution, acute oral toxicity study in rats, guideline
81-1. Unpublished report, study I91-1192. FMC, Princeton, NJ, USA.
Freeman C. 1991b. Peracetic acid 0.15% use dilution, acute dermal toxicity study in rats,
guideline 81-2. Unpublished report, study I91-1193. FMC, Princeton, NJ, USA.
Freeman C. 1991c. Peracetic acid 0.15% use dilution, primary skin irritation study in rabbits,
Freeman C. 1991d. Peracetic acid 0.15% use dilution, primary eye irritation study in rabbits,
Freeman C. 1991e. Peracetic acid 0.15% use dilution, skin sensitisation study in guinea pigs,
Freeman C. 1998. Peracetic acid 5%, acute oral toxicity study in rats. Unpublished report,
study I97-2236. FMC, Princeton, NJ, USA.
French M. 1993. Irritancy testing of peracetic acid to skin. Personal communication, 10 March.
Solvay Interox, Widnes, Cheshire, UK.
Gaffney JS, Streit GE, Spall WD, Hall JH. 1987. Beyond acid rain. Environ Sci Technol
21:519-524.
118
ECETOC JACC No.40
Gardner C, Bucksath JD. 1996a. Static acute toxicity of 5 % peracetic acid (Vigor Ox) to Daphnia
magna. Amended final report 42349, ABC Laboratories, Columbia, MO, USA. Unpublished
report, study I95-2021. FMC, Princeton, NJ, USA.
Gardner C, Bucksath JD. 1996b. Static acute toxicity of 5 % peracetic acid (Vigor Ox) to
rainbow trout (Oncorhynchus mykiss). Final report 42348, ABC Laboratories, Columbia, MO,
USA. Unpublished report, study I95-2023. FMC, Princeton NJ, USA.
Gardner C, Bucksath JD. 1996c. Static renewal toxicity of 5 % peracetic acid (Vigor Ox) to
bleugill (Lepomis macrochirus). Final report 42347, ABC Laboratories, Columbia, MO, USA.
Unpublished report, study I95-2029. FMC, Princeton, NJ, USA.
Gerike P and Jasiak W, 1983. Biologische Abbaubarkeit der Peressigsäure. Unpublished

report 1983/2179. Henkel, Düsseldorf, Germany.
Gerike P, Gode P. 1990. The biodegradability and inhibitory threshold concentration of some
disinfectants. Chemosphere 21:799-812.
Gloxhuber C, Kästner W. 1983. Prüfung der akuten intravenösen Toxizität von P3-oxonia
aktive im Vergleich zu Formalin (37,6 Gew.% Formaldehyd in Wasser). Unpublished report
1160, ZR-FE/Toxikologie. Henkel, Düsseldorf, Germany.
Gomond P. 1998. Toxicité orale aiguë chez le rat de la préparation Bactipal D. Unpublished
report Te675/98-3904, Evic-Ceba, Bordeaux, France. Chemoxal, Chalon sur Saône, France.
Gouges Y, Teral G. 1997. Les méthodes d'analyses utilisées dans le cadre de l'étude d'écotoxicité
de l'acide peracétique. Personal communication, 15 May. Chemoxal, Jouy en Josas, France.
Greaves P and Barsoum N. 1990. Pathology of tumours in laboratory animals, tumours of

the rat, tumours of soft tissues. IARC Sci Publ 99:597-623 [Review].
Greenspan FP, MacKellar DG. 1948. Analysis of aliphatic peracids. Anal Chem 20:1061-
1063.
Groeneveld AHC, De Groot WA. 1999. Activated sludge, respiration test with hydrogen
peroxide. Unpublished report A.SOL.S.003, Solvay Pharmaceuticals, Weesp, NL. Solvay,
Brussels, Belgium.
Gunz DW, Hoffmann MR. 1990. Atmospheric chemistry of peroxides, a review. Atmospheric
Environment 24A:1601-1633.
Hanst PH, Gay BW. 1983. Atmospheric oxidation of hydrocarbons, formation of

hydroperoxides and peroxyacids. Atmospheric Environment 17:2259-2265.
Harakeh MS. 1984. Inactivation of enteroviruses, rotaviruses and bacteriophages by peracetic

acid in a municipal sewage effluent. FEMS Microbiology Letters 23:27-30.
Harvey AJ. 1992. Atmospheric test on Cidox formulation. Personal communication of 22

September 1992. Solvay Interox, Widnes, Cheshire, UK.
Harvey AJ. 1993. Atmospheric monitoring of peracetic acid. Personal communication of

25 August 1993. Solvay Interox, Widnes, Cheshire, UK.
119
ECETOC JACC No.40
Hauschild F, Ludewig R, Muelhberg H. 1958. Ueber die “aetzende” Wirkung von Wasserstoff-
peroxyd. Naunyn-Schmiedeberg's Arch Exp Pathol Pharmak 235:51-62.
Haynes G, Brightwell J. 1998a. Oxystrong 5, acute oral toxicity study in the rat, final report.
Unpublished report 6018/T/192/97, Research Toxicology Centre (RTC), Pomezia-Roma,
Italy. Ausimont, Bollate, Italy.
Haynes G, Brightwell J. 1998b. Oxystrong 5, acute dermal irritation study in the rabbit, final
report. Unpublished report 6020/T/175/97, Research Toxicology Centre (RTC), Pomezia-
Roma, Italy. Ausimont, Bollate, Italy.
Heikes BG, Miller WL, Lee M. 1991. Hydrogen peroxide and organic peroxides in the marine
environment. In: Schiff HI, ed, Measurement of atmospheric gases. SPIE Proceedings 1433. SPIE
International Society for Optical Engineering, Bellingham WA, USA, pp 253-260.
Heinze W, Nattermann H. 1984. Peressigsäure-Aerosol-Wirkung bei Langzeitanwendung

niedriger keimwirksamer Konzentrationen auf Versuchstiere [The effect of peracetic acid in
aerosol formed during long-term application in low antibacterial concentrations on test
animals]. Wissenschaftliche Zeitschrift der Humboldt-Universität zu Berlin, Math-Nat R 18:513-
517 [German; English translation].
Heinze W, Nattermann H. 1985. Zur Wirkung von Aerosolen, die aus verschieden
konzentrierten Wolfasterillösungen hergestellt wurden, auf pathogene Bakterien. Monatshefte
Vet. Med. 40:335-338.
Heinze W, Werner E, Krüger Von S, Wilsdorf G. 1979. Zur Tierverträglichkeit von

Peressigsigsäure-Aerosolen unter besonderer Berücksichtigung der Beeinträchtigung der
Abwehrleistung. Monatshefte Vet. Med. 34:212-217.
Heinze W, Werner E, Fischer AR. 1981. Wirkung und Wirkungsweise von Peressigsäure-
Aerosolen auf den tierischen Organismus. Monatshefte Vet. Med. 36:343-49.
Heinze W, Hahn T, Wrensch G, Fischer AR. 1982. Wirkungsweise und Grenzen der
Schadwirkung von Peressigsäure- (PES-), Milchsäure- und Essigsäure-Aerosolen sowie von
Peressigsäure und Schwefeldioxid-Gasen bei Säugetieren. Wiss. Z Humbolt.-Univ. Berlin,
Math.-Nat. R. 31:549-55.
Hellpointer E, Gäb S. 1989. Detection of methyl, hydroxymethyl and hydroxyethyl

hydroperoxides in air and precipitation. Nature 337:631-634.
Henkel. 1995. P3-oxonia aktiv S [15%], material safety data sheet according to 91/155/EEC,
ISO 11014-1, Classification and labelling according to GefStoffV. Henkel, Düsseldorf, Germany.
Henkel. 1997a. P3-oxonia aktiv [5%], material safety data sheet according to 91/155/EEC,
Henkel. 1997b. P3-oxonia aktiv S [30%], material safety data sheet according to 91/155/EEC,
Hicks L, Ziegler TA, Bucksath JD. 1996. Acute toxicity of 5% peracetic acid (Vigor Ox) to
Selenastrum capricornutum Printz. Unpublished report 42866, ABC Laboratories, Columbia
MO, USA. FMC, Princeton NJ, USA.
120
ECETOC JACC No.40
HSE (UK Health and Safety Executive). 2000. Occupational exposure limits 2000. EH40/98.
HSE Books, Sudbury, Suffolk, UK, pp 12, 19.
Hutt CW, Kinney LA. 1985. Inhalation approximate lethal concentration (ALC) of peroxyacetic
acid. Unpublished report 751-85, Haskell Laboratory, Newark DW, USA. Du Pont, Wilmington
DW, USA.
Ingram AJ, Grasso P. 1991. Evidence for and possible mechanisms of non-genotoxic
carcinogenesis in mouse skin. Mutation Research 248:333-340.
IVDK (Informationsverbund Dermatologischer Kliniken). 1999. Benzisothiazolinon (BIT),

Peressigsäure. Schnuch A, personal communication to Sterzel W, 21 November. IVDK,
University of Göttingen, Göttingen, Germany. Henkel, Düsseldorf, Germany.
Jacobi S. 1997. Mackay level I calculations for peracetic acid. Personal communication of
25 February. Degussa-Hüls, Hanau, Germany.
Jäger P, Püspok J. 1980. Peressigsäure als Desinfektionsmittel in Brauereien un Betrieben der

alkoholfreien Getränkeindustrie. Mitteilungen der Versuchsstation für das Gärungsgewerbe in
Wien 3/4:32-35.
Jäkärä J, Parén A, Nyman J. 1998. Production and use of different peracids in chemical pulp
bleaching. Paperi ja Puu - Paper and Timber 80:281-287.
Jakobi G, Löhr A. 1991. Detergent ingredients, bleaches, householl detergents, references. In

Gerhartz W, Yamamoto YS, Kaudy L, Pfefferkorn R, Rousaville JF, eds, Ullmann’s Encyclopedia
of Industrial Chemistry, 5th ed, Vol A8. VCH, Weinheim, Germany, pp 357-362, 373-375,
438-448.
Janssen PJM. 1989a. Acute inhalation toxicity studies of Proxitane 1507 in male rats I.
Unpublished report S.8906, Duphar, Weesp, Netherlands. Solvay, Brussels, Belgium.
Janssen PJM. 1989b. Acute inhalation toxicity studies of Proxitane 1507 in male rats II.
Unpublished report S.8908, Duphar, Weesp, Netherlands. Solvay, Brussels, Belgium.
Janssen PJM. 1989c. Acute inhalation study to investigate the respiratory irritating properties
of Proxitane 1507 in male rats. Unpublished report S.8912, Duphar, Weesp, Netherlands.
Solvay, Brussels, Belgium.
Janssen PJM. 1990. Preliminary acute inhalation study to investigate the respiratory irritating
properties of Proxitane 1507 in male rats. Unpublished report S.9003, Duphar, Weesp,
Netherlands. Solvay, Brussels, Belgium.
Janssen PJM, Pot TE. 1987. Primary irritation study of Proxitane 0512, Proxitane 1507 and
Proxitane 4002 to the skin of the male rabbit. Unpublished report S.8706, Duphar, Weesp,
Netherlands. Solvay, Brussels, Belgium.
Janssen PJM, Van Doorn WM. 1994. Acute inhalation toxicity study with Proxitane AHC
in male and female rats. Unpublished report S.9408, Duphar, Weesp, Netherlands. Solvay,
Brussels, Belgium.
121
ECETOC JACC No.40
Joakimson da Silva E, Keiko s Coimbra I. 1990a. Determinação da DL50, por via oral, Proxitane
RFA. Unpublished report 97976, Instituto de Tecnologia do Paraná, Curitiba, Parana, Brasil.
Peroxidos do Brasil LTDA, Sao Paulo, Brazil.
Joakimson da Silva E, Keiko s Coimbra I. 1990b. Determinação da DL50, por via oral, Proxitane
1512. Unpublished report 97975, Instituto de Tecnologia do Paraná, Curitiba, Parana, Brazil.
Peroxidos do Brasil LTDA, Sao Paulo, Brazil.
Joakimson da Silva E, Keiko s Coimbra I. 1990c. Determinação da DL50, por via dérmica,
Proxitane RFA. Unpublished report 43041-A, Instituto de Tecnologia do Paraná, Curitiba,
Parana, Brazil. Peroxidos do Brasil LTDA, Sao Paulo, Brazil.
Joakimson da Silva E, Keiko s Coimbra I. 1990d. Determinação da DL50, por via dérmica,
Proxitane 1512. Unpublished report 43040-A, Instituto de Tecnologia do Paraná, Curitiba,
Parana, Brazil. Peroxidos do Brasil LTDA, Sao Paulo, Brazil.
Joakimson da Silva E, Keiko s Coimbra I. 1990e. Teste de irritabilidade dérmica, Proxitane

1512. Unpublished report 46552-A, Instituto de Tecnologia do Paraná, Curitiba, Parana,
Brazil. Peroxidos do Brasil LTDA, Sao Paulo, Brazil.
Joakimson da Silva E, Keiko s Coimbra I. 1990f. Teste de irritabilidade dérmica, Proxitane

RFA. Unpublished report 46553-A, Instituto de Tecnologia do Paraná, Curitiba, Parana,
Joakimson da Silva E, Keiko s Coimbra I. 1990g. Teste de irritabilidade ocular, Proxitane

Joakimson da Silva E, Keiko s Coimbra I. 1990h. Teste de irritabilidade ocular, Proxitane

RFA. Unpublished report 48398-A, Instituto de Tecnologia do Paraná, Curitiba, Parana,
Joakimson da Silva E, Keiko s Coimbra I. 1990i. Teste de sensibilização dérmica, Proxitane

Joakimson da Silva E, Keiko s Coimbra I. 1990j. Teste de sensibilização dérmica, Proxitane

RFA. Unpublished report 44121-A. Peroxidos do Brasil LTDA, Sao Paulo, Brazil.
Johnson WK. 1995. CEH product review, acetaldehyde. In SRI International, ed, Chemicals
Economic Handbook 601.5000A. SRI International, Menlo Park, CA, USA.
Jones P, Middlemiss DN. 1972. Formation of compound I by the reaction of catalase with
peroxoacetic acid. Biochem J 130:411-415.
Juhr NC, Spranger A, Haas A. 1977. Erhaltung der Tränkwasserqualität beim Verbrauch,
Versuche zur Tränkwasserkonservierung. Z Versuchstierk 19, 147-154.
Juhr NC, Klomburg S, Haas A. 1978. Tränkwassersterilisation mit Peressigsäure [Drinking

water sterilization with peracetic acid]. Z Versuchstierk 20:65-72 [German; English translation].
122
ECETOC JACC No.40
Junkermann W, Fels M, Pietruk P, Slemr F, Hahn J. 1993. Peroxide measurements at remote

mountain field sites (Wank - 1780 m. and 1175 m.), seasonal and diurnal variations of hydrogen
peroxide and organic peroxides. In: Borell PM et al, eds, Proceedings of EUROTRAC
Symposium '92. SPB Academic, The Hague, Netherlands, pp 180-184.
Kelly TJ, Daum PH, Schwartz SE. 1985. Measurements of peroxides in cloudwater and rain.
Journal of Geophysical Research 90:7861-7871.
Kirk O, Damhus T, Christensen MW. 1992. Determination of peroxycarboxylic acids by high-

performance liquid chromatography with electrochemical detection. J Chromatogr
606:49-53.
Kirk O, Christensen MW, Damhus T, Godtfredsen SE. 1994. Enzyme catalyzed degradation
and formation of peroxycarboxylic acids. Biocatalysis 11:65-77.
Klahre J, Lustenberger M, Fleming HC. 1996a. Microbielle Probleme in der Papierfabrikation,

Teil 1, Schäden, Ursachen, Kosten, Grundlagen. Das Papier 2:47-53.
Klahre J, Heim T, Flemming HC. 1996b. Environmental compatibility of peracetic acid and
conventional biocides in paper industry applications. DECHEMA Monographs
133:501-506.
Klenk H, Götz PH, Siegmeier R, Mayr W. 1991. Peroxy compounds, organic. In Gerhartz W,
Yamamoto YS, Kaudy L, Pfefferkorn R, Rousaville JF, eds, Ullmann's Encyclopedia of Industrial
Chemistry. 5th ed, Vol A19. VCH, Weinheim, Germany, pp 206-211:224-233.
Kline LB, Hull RN. 1960. The virucidal properties of peracetic acid. American Journal of Clinical
pathology 33:30-33.
Koch S, Kramer A, Stein J, Adrian V, Weuffen W. 1989. Mutagenitätsprüfung im Spermakopf-

Test/Maus und mutagene Potenz von 2 Desinfektionsmitteln auf Basis von Peressigsäure
bzw Phenolen [Investigation into the mutagenicity in the sperm head test on mice and the
mutagenic potency of two disinfectants based on peracetic acid and phenols]. Zbl Hyg 188:391-
Koopman TSM. 1994. Proxitane 0103, acute dermal toxicity study in the rat. Unpublished
report S.9405, Solvay Duphar, Weesp, Netherlands. Solvay Interox, Brussels, Belgium.
Kramer A. 1989. Hinweise / Empfehlungen zur Herabsetzung einer Gesundheitsgefährdung

durch peressigsäurehaltige Desinfektionsmittel im Gesundheits- und Sozialwesen. Zent. Bl.
Chir. 114:619-625.
Kramer JF. 1997. Peracetic acid, a new biocide for industrial water applications. MP (Materials
Performance) 36:42-50.
Kramer A, Weuffen W, Bauer M, Heinze W, Werner E, Lorenz G, Grimm U, Brachmann K,

Schroeder H, Spiegelberger E, Fehrmann P, Wegner H. 1982. Subakute und subchronische
percutane Verträglichkeitsprüfung im 28- und 90-Tage-Test von Desinfektionsmitteln bei
epicutaner Applikation, dargestellt am Beispiel von Peroxyethansäure [Investigation into
subacute and subchronic percutaneous tolerance of disinfectants in the 28 and 90 day test
following epicutaneous application using the example of peroxyethanoic acid]. Pharmazie
37:41 [German; English translation].
123
ECETOC JACC No.40
Kramer A, Weuffen W, Merka V, Tichácek B. 1983. Toxizität von Peroxyethansäure

(Peressigsäure). In Weuffen W, ed, Handbuch der Antiseptik.Vol II/2. Volk und Gesundheit,
Berlin, Germany, pp 177-187.
Kramer A, Weuffen W, Adrian V. 1987. Toxische Risiken bei der Anwendung von
Desinfektionsmitteln auf der Haut. Hyg Med 12:134-142 [German; English translation].
Kramer A, Koch S, Adrian V. 1990. Teratogene Potenz von Wofasteril® bei der ICR-Maus.
Hyg Med 15:371-372.
Kramer A, Koch S, Adrian V, Stein J, Weuffen W. 1991. Mutagenitätsprüfung ausgewählter

Desinfektionsmittel im Spermakopftest and der Maus. Investigation of mutagenicity of
selected disinfectants in sperm head test in mice. Hyg Med 16:279-286 [German and English].
Kramer A, Zwinger B, Adrian V, Jülich WD. 1993. Tierexperimentelle Untersuchungen

und Fragebogenerhebung zu neurotoxischen Risiken durch Peressigsäure. Animal studies
and results of a survey on the neurotoxic hazards of peracetic acid. Hyg Med 18:377-385.
Kretzschmar Ch, Agerth R, Bauch R, Friedrich D. 1972. Peressigsäure, nur ein neues
Desinfektionsmittel? [Peracetic acid, only a new disinfectant?]. Monatshefte Vet Med 27:324-
Krüger S, Jancke S. 1976. Zur Problematik der Tierverträglichkeit von Peressigsäure, 2. Mitt.,
Qualitäts- und Rückstandsuntersuchungen an Fleish nach Applikation von peressig-
säurehaltigen Lösungen auf die Haut von Schweinen. Monatshefte Vet Med 31:65-68.
Krüger S, Kruschinski D. 1982. Zur akuten Inhalationstoxizität von Peressigsäure-Aerosolen

bei Mäusen. Wiss Z Humboldt-Univ. Berlin, Math-Nat 31:543-548.
Krüger S, Wilsdorf G, Bebenroth M. 1977. Toxikologische Aspekte der Zwischendesinfektion

am Beispiel der Peressigsäure. Monatshefte Vet Med 32:785.
Krzywicka H. 1970. The effect of peracetic acid on the spores of bacteria. Roczniki PZH 21:595-
599 [Polish; English translation]. <ECETOC*translation only>
Kuhn JO. 1996a. Proxitane AHC, acute oral toxicity study in rats. EPA guidelines 81-1.
Unpublished report 2811-96, Stillmeadow, Sugar Land, TX, USA. Solvay Interox, Deer Park,
TX, USA.
Kuhn JO. 1996b. Proxitane WW12, acute oral toxicity study in rats, EPA guideline 81-1.
Unpublished report 2817-96, Stillmeadow, Sugar Land, TX, USA. Solvay interox, Deer Park,
TX, USA.
Kuhn JO. 1996c. Proxitane AHC, acute dermal toxicity study in rabbits, EPA guideline 81-
2. Unpublished report 2812-96, Stillmeadow, Sugar Land TX, USA. Solvay Interox, Deer Park
TX, USA.
Kuhn JO. 1996d. Proxitane WW12, acute dermal toxicity study in rabbits, EPA guideline 81-
2. Unpublished report 2818-96, Stillmeadow, Sugar Land, TX, USA. Solvay Interox, Deer
Park, TX, USA.
124
ECETOC JACC No.40
Kuhn JO. 1996e. Proxitane AHC, dermal sensitization study in guinea pigs, EPA guideline
81-6. Unpublished report 2815-96, Stillmeadow, Sugar Land, TX, USA. Solvay Interox, Deer
Park, TX, USA.
Kuhn JO. 1996f. Proxitane WW12, dermal sensitization study in guinea pigs, EPA guideline
81-6. Unpublished report 2821-96, Stillmeadow, Sugar Land, TX, USA. Solvay Interox, Deer
Park, TX, USA.
Kuhn F. 2000. Decomposition of peracetic acid in synthetic seawater. Unpublished report

69/00. Degussa-Hüls, Hanau, Germany.
Kurzweg W, Steiger A, Profé D. 1988. Ökologische Aspekte des Desinfektionsmitteleinsatzes

in der Tierproduktion [Ecological aspects of the use of disinfectants in livestock production].
Arch Exp Vet Med 42:518-527 [German; English translation].
Lamy MH, Lamy MH, Chauvire L, Gondelle F, Bazzon M, Giacalone J, Bailleul S, Rose M.
1997. Toxicité aiguë vis-à-vis des daphnies, substance d'essai: solution aqueuse d'acide
péracétique. Unpublished report, study Ba567b, INERIS (Institut National de l'Environnement
Industriel et des Risques), Verneuil-en-Halatte, France. Air Liquide, Chemoxal, Jouy en Josas,
France.
Laub R, Möhring M, Beyer C, Welsch N. 1990. Einfluß von Desinfektionsmitteln auf

epidermale Langerhanszellen, Möglichkeiten zur Verbesserung der Hautverträglichkeit.
Z gesamte Hyg 36:559-560 [German; English translation].
LaZonby J. 1997. Dramatic improvements in microbiological control using the synergistic

acivity between select organic biocides and a new non-halogenated oxidant. In TAPPI, ed,
1997 Engineering and Papermakers conference proceedings. TAPPI, Atlanta, GA, USA, pp 1107-
1113 [Abstract]
Lazrus AL, Kok GL, Lind JA, Gitlin SN, Heikes BG, Shetter RE. 1986. Automated fluorometric
method for hydrogen peroxide in air. Anal Chem 58:594-597.
Lefevre F, Audic JM, Ferrand F. 1992. Peracetic acid disinfection of secondary effluents
discharged off coastal seawater. Wat Sci Tech 25:155-164.
Lenahan RJ. 1992. Peroxyacetic acid: the new generation sanitizer. MBAA Technical Quarterly
29:53-56.
Lensing HH, Oei HL. 1985. Investigations on the sporicidal and fungicidal activity of
disinfectants. Zbl Bakt Hyg I. Abt Orig B 181:487-495.
Lever Industrial (Development and Application Centre). 1987. Reiniging en desinfectie,

SU 338, CIP-desinfectie met perazijnzuur. VMT (Voedingsmiddelentechnologie) 10:22-26.
Li C, Ye Y, Deng J. 1988. Pharmacological actions of peracetic acid. Yaoxue Tongbao 23:345-

348 [Chinese; English abstract].
Liberti L, Notarnicola M. 1999. Advanced treatment and disinfection for municipal wastewater
reuse in agriculture. Wat Sci Technol 40:235-245.
125
ECETOC JACC No.40
Liberti L, Lopez A, Notarnicola M. 1998. Disinfection with peracetic acid for municipal
wastewater reuse in agriculture. In Proceedings of Innovations 2000, joint conference of the
European Water Pollution Control Association (EWPCA), the Water Environment Federation
(WEF), 7-10 July 1998, Cambridge, UK. EWPCA Hennef, Germany and WEF, Alexandria,
VA, USA.
Licata-Messana L. 1995a. Inhibition test (72 hours) in freshwater unicellular algae, semi-
static system (1, 10 and 100 mg/l), test substance Dialox. Unpublished report F227, SEPC,
Sarcey, France. SEPPIC, Paris, France.
Licata-Messana L. 1995b. Test to evaluate acute toxicity (48 hours) in Daphnia, semi-static
system (1, 10 and 100 mg/l), test substance Dialox. Unpublished report F237, SEPC, Sarcey,
France. SEPPIC, Paris, France.
Licata-Messana L. 1995c. Test to evaluate acute toxicity (96 hours) in freshwater fish
(Brachydanio rerio), semi-static system (1, 10 and 100 mg/l), test substance Dialox. Unpublished
report F236, SEPC, Sarcey, France. SEPPIC, Paris, France.
Lind JA, Kok JL. 1986. Henry’s Law deteminations for aqueous solutions of hydrogen peroxide,
methylhydroperoxide, and peroxyacetic acid. Journal of Geophysical Research
91:7889-7895.
Loera BS. 1996. Chemical characterization of test sample to determine amount of active
ingredient. Unpublished report, study 2816-96, Stillmeadow, Sugar Land, TX, USA. Solvay
Interox, Deer Park, TX, USA.
Ludewig R. 1965. Nachweis von 180 in Exspirationsluft und Blut waehrend sublingualer
Einwirkung 180-markierten Wasserstoffperoxids. Abhandl. Deutsch Akad Wiss Berlin, Kl Chem
Geol Biol 7:549-552.
McAllister WA, Cohle P. 1983. Acute toxicity of Oxonia Active to bluegill sunfish (Lepomis
macrochirus). Unpublished report 30722, Analytical Bio-Chemistry Laboratories, Columbia,
MO, USA. Bonewitz Chemical Services, Burlington, IO, USA.
McDonagh J. 1997. Atmospheric monitoring of peracetic acid on the existing caprolactone

plant distillation houses A & B, assessment of results. Personal communication. Solvay
Interox, Warrington.
Mackay D, Paterson S, Shiu WY. 1992. Generic models for evaluating the regional fate of
chemicals. Chemosphere 24:695-717.
Malchesky PS. 1993. Peracetic acid and its application to medical intrument sterilization.
Artificial Organs 17:147-152.
Matkovics B, Novák R. 1977. The effects of chronic peroxide intake on the peroxide metabolism
enzyme activities of rat organs. Experientia 33:1574-1575.
Merck. 1994. Réflectomètre RQflex Merck. Laboratoires Merck-Clévenot, Nogent-sur Marne,

France.
126
ECETOC JACC No.40
Merck. 1995. Peracetic acid. In: Merckoquant, chemical microchips for analysis you take in your
stride. Merck, Darmstadt, Germany, p 27.
Merck. 1998. Merckoquant, peracetic acid test 1.10084.0001, RQ-flex en Reflectoquant,

analytical test kit 115975. Merck, Darmstadt, Germany.
Merka V, Urban R. 1976. Study of inhalation toxicity of performic, peracetic and perpropionic
acid in mice. Journal of Hygiene, Epidemiology, Microbiology and Immunologynm 20:54-60.
Meyer E. 1976. Abwasserdesinfektion in Tierkörperbeseitigungsanstalten mit Hifle der

Peressigsäure. Journal of Hygiene, Epidemiology, Microbiology and Immunology 20:266-273.
Mielke H, Hopp H. 1982. Untersuchungen über den Einfluß der Peressigsäure auf
Fußkrankheiten des Getreides. Zeitschrift für Pflanzenkrankheiten und Pflanzenschutz
89:282-290.
Mrazek H. 1996. Desinfektionsmittel. In Wildbrett G, ed, Reinigung und Desinfektion in der

Lebensmittelindustrie, 1st ed. Behr, Hamburg, Germany, pp 65-67.
Mücke H. 1970. Die Eigenschaften der Peressigsäure [The properties of peracetic acid, excerpts
relating to the bactericidal, sporicidal, viricidal and fungicidal effect of peracetic acid].
Zeitschrift der Universität Rostock 3:267-270 [German; English translation].
Mücke H. 1977. Untersuchungen über Einflüsse auf die Zersetzung von verdünnter
Peressigsäure [Studies on effects on the decomposition of dilute peracetic acid]. Pharmazie
32:32:613-9 [German; English translation].
Mücke H, Sprössig M. 1967. Über die antimikrobielle Wirkung der Peressigsäure, 2. Mitteiliun:
unetersuchingen zur Stabilität der Peressigsäure. Pharmazie 22:446-447 [Evaluates stability
of PAA solutions; covered by Mücke, 1977].
Mücke H, Sprössig M. 1969. Die Eigenschaften der Peressigsäure. Wissenschaftliche Zeitschrift

der Humboldt-Universität zu Berlin, Math-Nat Reihe B 18:1167-1170 [Reviews properties of
PAA solutions; covered by Mücke, 1977].
Müller U, Schaffernicht H. 1998. Schädigung der Zähne und des Zahnfleisches durch
Peressigsäuredämpfe [Damage of teeth and gingiva caused by fumes of peracetic acid].
Zbl Arbeitsmed 48:109-111 [German; English translation].
Müller P, Raabe G, Schumann D. 1978. Leukoplakia induced by repeated deposition of

formalin in rabbit oral mucosa. Exp Path 16:36-42.
Müller P, Raabe G, Schumann D, Müller R, Schwabe L. 1980. Action of chronic peracetic acid
(Wofasteril) administration on the rabbit oral mucosa. Exp Path 18:80-85.
Müller P, Raabe G, Hörold J, Juretzek U. 1988. Action of chronic peracetic acid (Wofasteril)
administration on the rabbit oral mucosa, vaginal mucosa and skin. Exp Pathol 34:223-228.
Nims RW. 1996a. Corrositex continuous time monitor assay, test article VigorOx. Unpublished
report I95-2035, Microbiological Associates, Rockville, ML, USA. FMC, Princeton, PA, USA.
127
ECETOC JACC No.40
Nims RW. 1996b. Bovine corneal opacity and permeability assay with histological evaluation,
test article VigorOx. Unpublished report I95-2036, Microbiological Associates, Rockville,
ML, USA. FMC, Princeton, PA, USA.
Nystrand R. 1985. Disinfectants in beet sugar extraction. Zuckerind 110:693-698 [Efficacy tests
of PAA]
Palcic MN, Dunford HB. 1980. The reaction of human erythrocyte catalase with
hydroperoxides to form compound I. J Biol Chem 255:6128-6132.
Paldy A, Berencsi G, Kramer A, Weuffen W, Spiegelberger E. 1984. Mutagene Potenz von

Wofasteril, Wofasept, Formaldehyd, Chlorhexidin und Bronopol im Knochenmarkstest an
der Maus. In Kramer A, Wigert H, Kemter B, eds, Aspekte der Prophylaxe und Bekämpfung
des infektiösen Hospitalismus. In Horn H, Weuffen W, Wigert H, series eds, Mikrobielle Umwelt
und antimikrobielle Maßnahmen. Barth, Leipzig, Germany, pp 349-352.
Pazdiora A, Kubiček V. 1967. Rapid pre-operative preparation of the hand with Persteril.
Vojenské Zdravotnické Listy 36:116-117 [Polish; English translation].
Pehrsson R, Malone JWG, Simms RA. 1995. Verwendung von Peressigsäure für die
Desinfektion in Rübenextraktionsanlagen. The use of peracetic acid formulations in the
disinfection of beet sugar extraction plants. Zuckerind 120:S593-597 [German; English].
Petit-Poulsen V, Lamy MH, Chauvire L, Gondelle F, Bazzon M, Giacalone J, Bailleul S,

Rose M. 1997. Essai d'inhibition de la croissance de l'algue d'eau douce Pseudokirchneriella
subcapitata. Substance d'essai: solution aqueuse d'acide peracétique. Unpublished report
BA567c, INERIS (Institut National de l'Environnement Industriel et des Risques), Verneuil-
en-Halatte, France. Air Liquide, Chemoxal, Jouy en Josas, France.
Phillips JC. 1994a. Pharmacokinetic studies on peroxyacetic acid as a component of Proxitane

0510 in the rat. Unpublished report 1304/4/2/94, BIBRA Toxicology International, Carshalton,
Surrey, UK. Johnson and Johnson Medical, Skipton, N. Yorkshire, UK.
Phillips JC. 1994b. The effects of Proxitane-0510 on the chromosomes of cultured human
lymphocytes. Unpublisehd report 1295/1/3/94, BIBRA Toxicology International, Carshalton,
Surrey, UK. Johnson and Johnson Medical, Skipton, N. Yorkshire, UK.
Pierre MP, Desmures MJ, Gamet JC. 2000. Procès verbal de la dégradation abiotique de l'acide
peracétique, hydrolyse en fonction du pH, protocole paru au Journal Officiel des
Communautés européennes L 383 A/228 du 29/12/92. Unpublished report 04/00. Bioxal-
Air Liquide, Châlon sur Saône, France.
Pinkernell U, Karst U, Cammann K. 1994. Determination of peroxyacetic acid using high-

performance liquid chromatography with external calibration. Anal. Chem. 66:2599-2602.
Pinkernell U, Effkemann S, Karst U. 1997a. Simultaneous HPLC determination of peroxyacetic

acid and hydrogen peroxide. Anal. Chem. 69:3623-3627.
Pinkernell U, Luke JJ, Karst U. 1997b. Selective photometric determination of peroxycarboxylic

acids in the presence of hydrogen peroxide. Analyst 122:567-571.
128
ECETOC JACC No.40
Pinkowski A. 1995. Verfahren zur Bestimmung von Persäuren. Patentschrift DE 42 23 228

C2. Prominent Dosiertechnik, Heidelberg, Germany.
Poffé R, De Burggrave A, Houtmeyers J, Verachtert H. 1978. Disinfection of effluents from

municipal sewage treatment plant with peroxy acids. Zbl Bakt Hyg I. Abt Orig B 167:337-346
[Evaluation bactericidal efficacy].
Potokar M, Banduhn N, Bechstedt W, Gode, Stenzel W. 1996. Beitrag zur toxikologischen

Bewertung der Peressigsäure als Desinfektionsmittel für die chemothermische
Wäschedesinfektion. Dermatosen 44:23-28.
Price D, Worsfold PJ, Mantoura RFC. 1992. Hydrogen peroxide in the marine environment,
cycling and methods of analysis. Trends in Analytical Chemistry 11:379-384.
Profaizer M, Massone A, Nurrizzo C, Banderta F. 1997. The Behaviour of Peracetic Acid as

a Water Disinfectant. Med Fac Landbouww Univ Gent 62,1785-1792.
Prominent. 1997 Dulcometer D1C Perox , measurement and control of H2O2 or PAA (AL
DM 002 4/97 GB). Prominent Dosiertechnik, Heidelberg, Germany.
Qi X, Baldwin RP. 1993. Liquid chromatography and electrochemical detection of organic

peroxides by reduction at an iron phthalocyanine chemically modified electrode. Electroanalysis
5:547-554.
Reagan EL, Becci PJ. 1983. Acute oral LD50 in albino rabbits of Divosan Forte disinfectant.
Unpublished report, study 7586A, Food and Drug Research Laboratories, Waverly, NY, USA.
Diversey Wyandotte, Wyandotte, MI, USA [Summary].
Reagan EL, Davidson TJ, Becci PJ. 1983. Acute dermal LD50 assay in rats, test article Divosan
Forte disinfectant. Unpublished report, study 7586A, Food and Drug Research Laboratories,
Waverly, NY, USA. Diversey Wyandotte, Wyandotte, MI, USA [Summary].
Reinold A. 2000. Re-equilibrium of peracetic acid (PAA). Unpublished report 87/00. Degussa-
Hüls, Hanau, Germany.
Richterich K, Gode P. 1986. Abbauprüfung toxischer Stoffe, Vermeidung störender toxischer

Selbsthemmung durch gestufte Prüfmusterzugabe (AT-test). Unpublished report 1986/2418,
TFB-Ökologie. Henkel, Düsseldorf, Germany.
Robinson EC. 1984. Titration of the capacity of the [human] skin to tolerate primary irritating
effects of peracetic acid. Unpublished report PI-3196. Monsanto, St. Louis, MO, USA.
Rodgers ML. 1991. Effects of peracetic acid and hydrogen peroxide on the growth of some
cyanobacteria and micro-algae. MSc thesis. University of Bath, Bath, UK.
Rowbottom KT. 1996a. Atmospheric monitoring during filling of IBC's with peracetic acid
at Ellis and Everard on the 27th March 1996. Personal communication of 28 March. Solvay
Interox, Widnes, Cheshire, UK.
Rowbottom KT. 1996b. Atmospheric monitoring at North Devon District Hospital in

Barnstaple, 2nd December 1996. Personal communication of 4 December. Solvay Interox,
Widnes, Cheshire, UK.
129
ECETOC JACC No.40
Rudd T, Hopkinson LM. 1989. Comparison of disinfection techniques for sewage and sewage
effluents. J IWEM 3:612-618.
Ruohoniemi K, Heiko J, Laakso I, Martikainen S, Väryrynen V, Jäkärä J. 1998. Experience

in the use to peracetic acid in ECF and TCF bleaching. In KCL (The Finnish Pulp and Paper
Research Institute), ed, Proceedings from international pulp bleaching conference, June 1-5, 1998,
Helsinki, Finland, Vol 1. KCL, Helsinki, Finland, pp 145-150 [ISBN 951-97513-3-5].
Saito T, Kurasaki M, Kaji M, Saito K. 1984. Deficiency of erythrocyte superoxide dismutase

and catalase activities in patients with malignant lymphoma and acute myeloid leukemia.
Cancer Lett. 24:141-146.
Sandström DA, Cederborg SE, Malmström E. 1999. Utvecklingen av ECF fortsätter medan
TCF planar ut. Svensk Papperstidning 4:38-40.
Schaffernicht H, Müller U. 1998. Zur Exposition gegenüber Peressigsäure von Beschäftigten

eines Universitätsklinikums [Regarding the exposure to peracetic acid in university hospital
employees]. Zbl Arbeitsmed 48:106-108 [German; English translation].
Schliesser TH, Wiest JM. 1979. About the temperature dependence of the bactericidal effect
of some chemical disinfectants. Zbl Bakt Hyg I. Abt Orig B 169:560-566.
Schonbaum GR, Chance B. 1976. Catalase-mediated redox reactions. In Doyer PB, ed, The
enzymes, oxydation-reduction, dehydrogenases (II), oxidases (II), hydrogen peroxide cleavage, 3rd
ed, Vol XIII Part C. Academic Press, New York, NY, USA, pp 389-395.
Schröder W. 1982. Peressigsäure (PES) als Desinfektionswirkstoff für die Lebens-

mittelindustrie. Confructa 26:139-147.
Senf HJ. 1984. Eine modifizierte Methode zur titrimetrischen Peressigsäurebestimmung. Zbl
Pharma 123:77-79.
Setlow B, Setlow CA, Setlow P. 1997. Killing of bacterial spores by organic peroxides. J Ind
Micro and Biotech 18:384-388.
Shapilov OD, Kostyukovskii YL, Gramenitskaya VG. 1972. Preparation and properties of an
oxidizing system based on acetic acid and hydrogen peroxide. Zh Prikladnoi Khimii 45:2062-
2066 [Russian; English translation] [Evaluates sporicidal effectiveness of PAA solutions].
Sheehan JF, Brynjolfsson G. 1960. Ulcerative colitis following hydrogen peroxide enema:
Case report and experimental production with transient emphysema of colonic wall and gas
embolism. Lab Invest 9:150-168.
Simms RA. 1995. Peroxygen atmospheric monitoring, Glan Clwyd Hospital Bodelwyddan.
Personal communication of 25 September. Solvay Interox Warrington, Cheshire, UK.
Solvay. 1997a. Proxitane AHC 5%, material safety data sheet, date prepared 22.09.1997. Solvay
Interox, Houston, TX, USA.
Solvay. 1997b. Proxitane 5%, material safety data sheet, date prepared 16.01.98. Solvay Interox,
Houston, TX,USA.
130
ECETOC JACC No.40
Solvay. 1997c. Proxitane WW-12, material safety data sheet, effective date September 9, 1997.
Solvay Interox, Houston, TX, USA.
Solvay. 1997d. Proxitane 15%, material safety data sheet, date prepared 22.09.1999. Solvay
Interox, Houston, TX, USA.
Solvay. 1999. Overview of existing peraceticacid (PAA) monitoring methods. Personal

communication of 12 January by Smit J, Olthof H. Solvay, Expertise Centre for Industrial
Hygiene Monitoring. Solvay, Weesp, Netherlands.
Solvay. 2000. Solvay acceptable exposure limits (SAEL), January 2000. Solvay, Brussels,
Belgium.
Spiegelberger A, Kramer A, Weuffen W, Burmeister C. 1984. Akute epicutane bzw. Subcutane

LD50 der Desinfektionsmittel der Liste der DDR, geprüft an der ICR-Mause. In Kramer A,
Wigert H, Kemter B, eds, Aspekte der Prophylaxe und Bekämpfung des infektiösen Hospitalismus.
In Horn H, Weuffen W, Wigert H (series eds), Mikrobielle Umwelt und antimikrobielle Maßnahmen.
Barth, Leipzig, Germany, pp 342-343.
Steiner N. 1995. Nontoxic bleaching, evaluation of peracetic acid as an environmentally safe

alternative for hypochlorite. J. AATCC 27:29-32.
Steiner N. 2000. Composition of Degussa-Huels peracetic acid. Personal communication

of 4 July. Degussa-Hüls, Frankfurt am Main, Germany.
Swern D. 1970. Organic peroxides Vol 1. Wiley Interscience, New York, NY, USA, pp 340-
369, 461-474.
Tanner RL, Schorran DE. 1995. Measurements of gaseous peroxides near the Grand Canyon,
implication for summertime visibility impairment from aqueous-phase secondary sulfate
formation, Atmospheric Environment 29,1113-1122.
Tecnon Consulting. 1999. Analysen, Prognosen, Nachrichten, Fakten, Zwischenprodukte,

Markt für Acetaldehyde Märkte. Europa Chemie 99:8.
Teral G, Hamon C. 1995. Détermination de faibles teneurs en acide peracétique [seawater].

Unpublished report AT.Chem 95.05. Air Liquide, Chemoxal, Les Loges, France.
Teral G, Gouges Y. 1997. La courbe de stabilité de l'APA en fonction de la température. Personal

communication of 26 May. Chemoxal, Air Liquide Chimie, Paris, France.
Terrell Y. 1986a. Acute inhalation toxicity of Divosan Forte in rats. American Standards
Biosciences Corporation project 86-635. Diversey Wyandotte, Wyandotte, MI, USA [Summary].
Terrell Y. 1986b. Avian dietary quail study (limit test) of Diversey Wyandotte Divosan Forte
Sanitizer 15 % peroxyacetic acid in bobwhite quail. Unpublished report, project 86-636,
American Standards Biosciences Corporation, Reading, PA, USA. Diversey Wyandotte,
Wyandotte, MI [Summary].
Terrell Y. 1987a. Acute toxicity bioassay of Divosan Forte on Daphnia magna. Unpublished
report, project 86-718, American Standards Biosciences Corporation, Reading, PA, USA.
Diversey Wyandotte, Wyandotte, MI USA [Summary].
131
ECETOC JACC No.40
Terrell Y. 1987b. Acute toxicity bioassay of Divosan Forte on rainbow trout and bluegill
sunfish. Unpublished report, project 86-719/720 American Standards Biosciences Corporation,
Reading, PA, USA. Diversey Wyandotte, Wyandotte, MI, USA [Summary].
Thomasfolk H, Myhrman LE, Strandell B. 1996. Mill experience with hydrogen peroxide
(PO) and peracetic acid (PAA). Presented at: International Non-Chlorine Bleaching Conference,
Orlando, USA, paper 13-3. Rottneros AB, Vallviks Bruk, Sweden. Miller Freeman, San
Francisco, CA, USA.
Thompson AM. 1994. Oxidants in the unpolluted marine atmosphere. In Nriagu JO, Simmons
MS, eds, Environmental oxidants. John Wiley and Sons, New York, NY, USA, pp 31-61. [ISBN
0-471-57928-9].
Thus JLG. 1994. Calculation of the octanol/water partition coefficient of peracetic acid.
Personal communication of 16 May. Solvay Duphar, Weesp, Netherlands.
Thus JLF, Allan E, Feenstra AFM. 1996. The development of an analytical method for the
selective determination of peracetic acid and hydrogen peroxyde in air samples. Unpublished
report 56834/77/95. Solvay Duphar, Weesp, Netherlands.
Thus JLG, Groeneveld AHC, Van der Laan-Straathof JMT. 1997. Possible biodegradation
of peracetic acid (preliminary experiment). Unpublished report 56834/16/97. Solvay Duphar,
Weesp, Netherlands.
Tichácek B. 1972. Persteril. Avenicum, Praha [Czech; title only translated].
Tinsley D, Sims I. 1987a. The acute toxicity of Oxymaster to plaice (Pleuronectes platessa) under
semi-static conditions. Unpublished report CO1650-M/EV8687, WRc Environment,
Medmenham, UK. Interox Chemicals, Widnes, Cheshire, UK.
Tinsley D, Sims I. 1987b. The acute toxicity of Oxymaster to brown shrimp (Crangon crangon)
under semi-static conditions. Unpublished report CO1649-M/EV8687, WRc Environment,
Medmenham, UK. Interox Chemicals, Widnes, Cheshire, UK.
TRGS (Technische Richtlinie Gefahrstoffe). 1997. Peroxyessigsäure, CAS-Nr. 79-21-0. In TRGS

906, Begründungen zur Bewertungen der TRGS 905, Verzeichnis krebserzeugender,
erbgutverändernder oder fortpflanzungsgefährdernder Stoffe. In Kühn R, Birett K, series
eds, Merkblätter Gefährliche Arbeitsstoffe, Vol 100, ed 7/97. Ecomed, Landsberg, Germany.
Umweltbundesamt. 2000. Peroxyessigsäure. In Umweltbundesamt, ed, Katalog

wassergefährdender Stoffe, Stand 31. Oktober 2000. Einstufung aufgrund der
Verwaltungsvorschrift wassergefährdender Stoffe (VwVwS). Umweltbundesamt, Berlin,
Germany [http://www.umweltbundesamt.de/wgs/wgs-index.htm].
UN (United Nations). 1995. Tests and criteria for the classification of organic peroxides. In
Recommendations on the transport of dangerous goods, manual of tests and criteria, 2nd ed, Part
II, UN, New York, NY, USA, pp 185-304.
Urschel HC. 1967. Progress in cardiovascular surgery; Cardiovascular effects of hydrogen

peroxide: current status. Dis Chest 51:180-192.
132
ECETOC JACC No.40
US-DOT (US Department of Transportation). 1995. Product designation, UN proper shipping

name and number. Personal communication by Jones JE, October 25, 1995. FMC, Philadelphia,
PA, USA.
US-EPA (Environmental Protection Agency). 1999a. TRI chemicals in waste, by chemical.

1997. In Toxics release inventory (TRI). 1997 public data release, chapter 2. EPA, Washington,
DC, USA, pp 79 [http://www.epa.gov/opptintr/tri/tri97/pdf/chap2.pdf].
US-EPA (Environmental Protection Agency). 1999b. Technology transfer network, Chief

clearing house for inventories and emission factors. EPA, Washington, DC, USA
[http://www.epa.gov/ttn/chief].
Van Beek L. 1980. Primary dermal corrosion test with Divosan Forte in albino rabbits. Personal
communication, Centraal Instituut voor Voedingsonderzoek TNO, Zeist, Netherlands.
Diversey, Woerden, Netherlands.
Veger J, Svihovcova P, Benesova O, Nejedly K. 1977. Toxicité subchronique du Persteril

par voie buccale. Cesk Hyg 22:59-63 [Czech; English and French translations].
Verschueren. 1983. Handbook of environmental data on organic chemicals, 2nd ed. Van Nostrand
Reinhold, New York, NY, USA, pp 143-144.
Veschetti E, Cutilli D, Bonadonna L, Della Libera S, Ottaviani M. 1998. Preliminary results

on the possibility of using peracetic acid as disinfectant of wastewater. Presented at: AWT98
Advanced wastewater treatment, recycling and reuse, Milano 14-16 September (No further
publication details] Evaluation of microbial efficacy].
Wallat S. 1984a. P3-oxonia aktiv, Prüfung auf Mutagenität im Ames-Test. Wallat S, Institut
für Toxikologie. Unpublished report 840154. Henkel, Düsseldorf, Germany.
Wallat S. 1984b. P3-oxonia aktiv, Prüfung auf Mutagenität in vivo., Institut für Toxikologie.
Unpublished report 840242. Henkel, Düsseldorf, Germany.
Wayne RP. 1991. Oxidation and transformation. In Wayne RP, ed, Chemistry of atmospheres,
2nd ed. Clarendon, Oxford, UK, pp214-225.
Werner. 1988. Disinfectants in dialysis: dangers, drawbacks and disinformation. Nephron

49:1-8.
Whitman FT. 1991. Acute inhalation toxicity study of peracetic acid 0.15 use dilution (MRD-
91-004) in the rat, guideline 81-3. Unpublished report I91-1199, Exxon Biomedical Sciencies,
East Millstone, NJ, USA. FMC Princeton, NJ, USA.
Wurster P. 1992. Die Peressigsäurebleiche, eine Alternative zu Bleichverfahren mit

halogenhaltigen Oxidationsmitteln. Textil Praxis 47:960-965.
Wutzler P, Mücke H, Battke H, Goebel P, Schreiber D. 1987. Tierexperimentelle

Untersuchungen über den Einfluß der Peressigsäure auf das Harnblasenurothel. Z Urol
Nephrol 80:105-110.
Wyrobek, AJ, Gordon LA, Burkhaart JG et al. 1983. An evaluation of the mouse sperm
morphology test and other sperm tests in nonhuman mammals. A report of the U.S.
Environmental Protection Agency Gene-Tox Program. Mutation Research 115:1-72.
133
ECETOC JACC No.40
Yamaguchi T, Yamashita Y. 1980. Mutagenicity of hydroperoxides of fatty acids and some

hydrocarbons. Agric Biol Chem 44:1675-1678.
Yuan Z, Ni Y, Van Heiningen ARP. 1977a. Kinetics of peracetic acid decomposition, part II:
pH effect and alkaline hydrolysis. Can J Chem Eng 75:42-47.
Yuan Z, Ni Y, Van Heiningen ARP. 1977b. Kinetics of peracetic acid decomposition, part I:
Spontaneous decomposition at typical pulp bleaching conditions. Can J Chem Eng 75:37-
41.
Zeiger E, Anderson B, Haworth S, Lawlor T, Mortelmans K. 1988. Salmonella mutagenicity

tests IV, results from the testing of 300 chemicals. Env Mol Mut 11:1-158.
11.3 References Not Quoted

The following references were consulted by the Task Force, but not quoted for the specific
reasons indicated. Several references are beyond the scope of this report because they are
concerned with the biocidal efficacy of PAA used as an antiseptic or disinfectant.
Agnet Y, Dorange JL, Dupuy P. 1976. Mutagenicity of peracetic acid on Salmonella typhimurium.
Mutation Research 38:119 [CoR 4a; abstract covered by Agnet et al, 1977].
Allen DW, Newman, LM, Okazaki, IJ. 1991. Inhibition of arachidonic acid incorporation into
erythrocyte phospholipids by peracetic and other peroxides. Role of arachidonyl-CoA, 1
palimotyl-sn-glycero-3-phosphocholine acyl transferase. Biochimica et Biophysica Acta 1081:267-
273 [Study on enzyme, not on PAA].
Anonymous. 1982. Description of a method for a European suspension test for the evaluation
of the efficacy of disinfectants in food hygiene. Unpublished report, restricted CD-P-SP
(82 32), appendix B. [Efficacy].
Arturo-Schaan M, Suavager F, Mamez C, Gougeon A, Cornier M. 1996. Use of peracetic acid

as a disinfectant in a water-treatment plant: effect of plasmid content of Escherichia coli strains.
Current Microbiology 32:43-47 [Efficacy].
Baldry MGC. 1994. Peracetic acid residuals. Technical memo M-12-94, Solvay Interox, Widnes,
Cheshire, UK [Covered by Chalkley, 1991a,b,c].
Booth RA, Lester JN. 1995. The potential formation of halogenated by-products during
peracetic acid treatment of final sewage effluent. Wat. Res. 29:1793-1801 [Disinfection].
Brázdová K, Dluhoπ M, Veleck˝ R, Sekaninová G, Táborsk˝ I, Zajícova V. 1970. Tissue tolerance

and peracetic acid toxicity in relation to plastics. Scripta medica 43:323-327 [Effect of PAA
residues on tissue cultures; CoR 3a].
Brown GE, Schubert TS. 1987. Use of Xanthomonas campestris pv. vesicatoria to evaluate surface
disinfectants for canker quarantine treatment of citrus fruit. Plant Disease 71:319-323 [Efficacy].
Busch A. 1973. Untersuchungen zur Toxizität PES-haltiger Desinfektionsmittel beim Auftragen

auf die Haut des Schweines. Diss. Vet.-Med., Humboldt University, Berlin, Germany [Thesis
covered by Busch and Werner, 1974].
134
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Cechova L. 1969. Die Peressigsäure als Desinfektionsmittel in der Stomatologie. Wirksamkeit

und Entwicklungsstand. Wissenschaftliche Zeitschrift der Humboldt-Universität zu Berlin, Math-
Nat Reihe B 18:1179-1181 [Efficacy in disinfection of mouth protheses].
Chalkley NJ. 1992a. Degradation of peracetic acid in contact with various samples of water.
Personal communication of 1 April 1992. Solvay Interox, Widnes, Cheshire, UK [Repeated
experiments of Chalkley 1992; no additional information].
Chalkley NJ. 1992b. Degradation of peracetic acid in contact with various samples of water,
tomato plant washing project. Personal communication of 22 April 1992. Solvay Interox,
Widnes, Cheshire, UK [No aditional information].
Chanratchakool P. 1994a. Minimum bactericidal concentration of Proxitane 1507 against

various shrimp pathogen. Unpublished draft report, Aquatic Animal Health Research Institute,
Bangkok, Thailand. Peroxythai, Bangkok, Thailand [Efficacy, draft report].
Chanratchakool P. 1994b. Toxicity of Proxitane on shrimp, microflora and plankton.

Unpublished draft report, Aquatic Animal Health Research Institute, Bangkok, Thailand.
Peroxythai, Bangkok, Thailand [CoR 4e, draft report].
Christiansen B, Eggers H-J, Exner M, Gundermann K-O, Heeg P, Hingst V, Höffler U, Krämer
J, Mar H, Rüden H, Schliesser Th, Schubert R, Sonntag H-G, Spicher G, Steinmann J, Thofern
E, Thraenhart O, Werner H-P. 1991. Richtlinie für die Prüfung und Bewertung von
Hautdesinfektionsmitteln. Zbl Hyg 192:99-103 [Efficacy in (hand) skin disinfection].
CPR (Commissie Preventie van Rampen door gevaarlijke stoffen [Dutch Committee for the
Prevention of Disasters caused by dangerous substances]). 1997. Storage of organic peroxides.
Report CPR 3E, 2nd ed. Sdu, Den Haag, Netherlands [National guidance on safe handling
following UN and EU directives].
Davenport L. 1990. Oxymaster treated samples received 4th October 1989, conclusion of the
report on the mutagenic potential detectable in sewage effluents received from Interox.
Personal communication 3 April with continuation of report 5 December 1989, Severn-Trent
Laboratories, Finham, Coventry, UK. Solvay Interox, Widnes, Cheshire, UK [Efficacy; non-
standard test].
Davidson KA, McClanahan MA, Rodgers G, Morawetz J. 1998. Acute exposure guideline
levels (AEGLs) for peracetic acid, June 5. 1998. Unpublished draft report by Lockheed Martin
Energy Research/US Department of Energy to Tobin, PS, NAC/AEGL. US Environmental
Protection Agency, Washington, DC, USA [Review].
Degussa. 1977. Orientierende Prüfung der akuten Toxizität von 40%iger Peressigsäure bei
Sprague-Dawley Ratten. Unpublished report by Leuschner F, Laboratorium für Pharmakologie
Degussa. 1992a. Desodorierung von Klärschlamm mit Peressigsäure 15%. Report IC-AO-
AT/BC 106/92 by Del Grosso B and Schmidt K, Asta Pharma, Bielefeld, Germany. Degussa,
Hanau, Germany [Efficacy to remove smell from cat litter made of sewage sludge].
Degussa. 1992b. Desodorierung von Klärschlamm mit Peressigsäure 15%. Report IC-AO-
AT/BC 129/92 by Del Grosso B, Asta Pharma, Bielefeld, Germany. Degussa, Hanau, Germany
[Efficacy to remove smell from cat litter made of sewage sludge].
135
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Degussa. 1993. Stabilität von Peressigsäure-Konzentrationen im ppm-Bereich in Leitungs-

wasser und dest. Wasser. Unpublished report BC108/93 by Del Grosso B, Asta Pharma,
Bielefeld, Germany. Degussa, Hanau, Germany [Stability test in drinking/distilled water,
no additional information].
DFG (Deutsche Forschungsgemeinschaft, Senatskommission zur Prüfung gesundheits-

schädlicher Arbeitsstoffe). 1988. Peroxyessigsäure. In: Henschler D (ed), Gesundheits-
schädliche Arbeitsstoffe, toxikologish-arbeitsmedizinische Begründing von MAK-Werten,
14th ed. VCH, Weinheim, Germany [Review].
DOE (UK Department of the Environment). 1988. Review of operational and experimental
techniques for the removal of bacteria, viruses and pathogens from sewage effluents.
Unpublished report PECD 7/7260. Consultants in Environmental Sciences, DOE, London,
UK [Review, disinfection].
Euler J, Werner HP. 1978. Untersuchungen über den Einfluß von Peressigsäure auf Ehrlich-
Lettre-Mäuse-Aszitestumorzellen. Krebsgeschehen 10:30-33 [Non-standard test and cell line,
interpretation unclear].
Flemming HC. 1984. Die Peressigsäure als Desinfektionsmittel, ein Überblick. Zbl Bakt Hyg,
I. Abt Orig B 179:97-111 [Review, disinfection].
Fordham JP. 1978. Safe handling of peracetic acid in a closed environment. Laboratory Animals
12:247-248 [Safe handling in laboratory, no additional information].
Geiler W, Otto J, Mücke H. 1989. Einhaltung der arbeitshygienischen Grenzwerte in der

Raumluft bei Flächendesinfektion mit Peressigsäure durch Alkalisierung der Lösung. Z Klin
Med 44:349-352 [Disinfection, OEL/odour threshold compliance].
Gode P, Winkler J. 1982. Biologische Abbaubarkeit und Toxizität von 19 P3-Desinfektions-

mitterohstoffen. Unpublished report 1982/2088, ZR-FE-ALAB-Ökologie. Henkel, Düsseldorf,
Germany [CoR 3a; test substance and method not specified].
Gould DJ. 1989. Microbiological and biological monitoring at Southend-on-Sea, Essex 1989.
Unpublished report 50, interim draft, Marine Environmental Consultants, Baldock, Herts,
UK [Efficacy in sewage disinfection].
Greenspan FP, MacKellar DG. 1951. The application of peracetic acid germicidal washes
to mold control of tomatoes. Food Technol 5:95-97 [Efficacy].
Grussel T, Busch W. 1997. Experimental studies of the effect of peracetic acid on the
endometrium of cattle. Tierärztl. Prax. 25:28-34 [CoR 3a; no additional information].
Heinze W, Nattermann H. 1984. Zur Wirkung von Wofasteril-Aerosolen auf tierpathogene

Keime. Monatshefte Vet Med 39:776-779 [Efficacy].
Heneghan JB, Gates DF. 1966. Effects of peracetic acid used in gnotobiotics on experimental
animals. Laboratory Animal Care 16:96-104 [Disinfection].
Henkel. 1998. Peressigsäure-Desinfektion/COP [Collection of exposure data during use,

different applications 1994-1998]. Personal communication dated 20 January. Henkel,
Düsseldorf, Germany [MAK compliance measurements for H2O2 and HOAc during
application of undefined PAA-containing product].
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Hercik J, Dachovsky V. 1975. [Use of peracetic acid for disinfection in sugar refining]. Listy
Cukrovarnicke 91:126-132. [CoR 4d, Czech, English summary; no additional information].
James AP, Shehad NS. 1995. Peroxygen systems for consumer applications. Presented at:
86th AOCS annual meeting, American Oil Chemists’ Society, Champaign, Illinois, USA.
Solvay Interox, Widnes, Cheshire, UK and Deer Park, TX, USA [Review].
Kästner W. 1981. Desinfektion bei der Lebensmittelherstellung, Wirkstoffe und deren

toxikologische Beurteilung. Archiv für Lebensmittelhygiene 32:117-125 [Review].
Kramer A, Halle W, Weuffen W, Adrian V, Herrmann M, Bremer J, Fleck H and Steiger E.

1987b. Antimikrobielle Wirkung, Zytotoxizität und Phytotoxizität als Basisinformationen
zur Verträglichkeit von Desinfektionsmitteln bzw. Antiseptika [Antimicrobial effect,
cytotoxicity and phytotoxicity: aspects providing basic information on the compatibility
of disinfectants and antiseptics]. Z gesamte Hyg 33:610-615 [German; English translation]
[Review, efficacy].
Kühn H. 1978. Versuche zur antimikrobiellen Behandlung von dermatologischen

Zubereitungen mittels Peressigsäure, 2. Mitteilung. Pharmazie 33:292-293 [Efficacy].
Lai DY, Woo Y, Argus MF, Arcos JC. 1996. Carcinogenic potential of organic peroxides,
prediction based on structure-activity relationships (SAR), and mechanism-based short-term
tests. Environ Carcino Ecotox Revs C 14:63-80 [Review].
Lenon G, Hivert G, Escabasse JY. 1997. Effect, identification and control of catalase in deinking
plants, literature survey, 2nd part, biological aspects. Unpublished report, CTP project FR
96-18. Centre Technique du Papier, Grenoble, France [Review of enzymatic breakdown of
hydrogen peroxide; PAA briefly mentioned].
Lichtenberg F, Gutknecht J. 1987. Peressigsäure, ein universelles Desinfektionsmittel.

Anwendungstechnische Vor- und Nachteile. Brauwelt 14:586-590 [Disinfection in brewery].
Ljarskij. 1983. Caractéristique toxicologique et hygiénique des agents désinfectants à base

de peroxyde d'hydrogène et de ses dérivés. Gig. y Sanit. 48: 28-31 [CoR 4e; Russian; French
translation; report insufficient].
Lowings PH. 1956. The fungal contamination of Kentish strawberry fruits in 1955. Applied
Microbology 4:84-88 [Efficacy].
Mayr E. 1973. Wofasteril (= Peressigsäure). Zbl Pharm 112:275-280 [Review].
Merka V, Sokol D. 1972. Zum Wirkungsmechanismus von Peressigsäure, Perameisensäure

und Perpropionsäure. Z Ges Hyg 2:638-641 [Efficacy].
Monev V. 1974. L'acide peracétique comme désinfectant. Suvrem Med 25:36-39 [Bulgarian;
French translation] [Review, disinfection].
Morelli G. 1991. Disinfezione acque reflue e loro riutilizzo a scopo irriguo. IA - Ingegnena
Ambientale 20:183-192 [Disinfection of wastewater for agricultural irrigation].
Morris R. 1993. Reduction of microbial levels in sewage effluents using chlorine and peracetic
acid disinfectants. Wat Sci Tech 27:387-393 [Efficacy].
137
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Niebling, G, Aigner R, Wabner D, Menzel R. 1996. Data reduction for curve analysis. Sensors
and Actuators B 34:481-486 [Uses for example voltammetry analysis curves of PAA+H2O2
mixtures].
Rothe A, Fiss I, Wagner E. 1996. Zum Kontaktekzem durch formaldehydfreie

Desinfektionsmittel. Contact dermatitis caused by formaldehyde-free disinfectants. Hyg Med
18:167-175 [German and English; no allergies related to PAA, covered by IVDK, 1999].
Sax I, Lewis RJ. 1989. Dangerous properties of industrial materials, 7th ed. Van Nostrand
Reinhold, New York, NY, USA, pp 2693-2694 [Review, handbook].
Sosnovsky G, Zaret EH. 1970. Base-catalyzed autoxidation. In Swern D, ed, Organic peroxides
Vol 1. Wiley Interscience, New York, NY, USA, pp 517-560 [Review].
Sprössig M, Mücke H. 1969. Die Virusdesinfektion durch Peressigsäure in Gegenwart von

Alkoholen. Wissenschaftliche Zeitschrift der Humboldt-Universität zu Berlin, Math-Nat Reihe B
18:1171-1173 [Efficacy].
Sprössig M, Mücke H. 1982. Peroxide als Desinfektionsmittel - Wirksamkeit und

Entwicklungsstand. Wissenschaftliche Zeitschrift der Humboldt-Universität zu Berlin, Math-Nat
Reihe B 31:539-541 [Review].
Tichácek B et al, ed. 1966. Kyselina peroctová a možnosti jejího vyu ití v dezinfekci, Zdravotnické
aktuality 163 [Peressigsäure und die Möglichkeiten ihrer Verwendung in der Desinfektion,
Monographie 163]. Stát. Zdrav. Nakl., Praha CSSR [Staatsverlag für das Gesundheitswesen
der CSSR, Prague] [CoR 4d; Czech; review, title only translated].
Tye RJ. 1989a. Investigation of the mutagenic potential detectable in sewage effluents treated
with Oxymaster, interim report. Personal communication of 14 March, Severn Trent
Laboratories, Finham, Coventry, UK. Solvay Interox, Widnes, Cheshire, UK [Efficacy; non-
standard test].
Tye RJ. 1989b. Preliminary report on the mutagenic potential detectable in sewage effluents
received from Interox. Personal communication of 5 December, Severn Trent Laboratories,
Finham, Coventry, UK. Solvay Interox, Widnes, Cheshire, UK [Efficacy; non-standard
test].
Wallhäußer K-H. 1995. Praxis der Sterilisation, Desinfektion, Konservierung, 5th ed. Georg-
Thieme, Stuttgart, Germany, pp 397 [Efficacy; so-called 5-5-5-test for evaluation of
disinfectants].
Wiedman T. 1999. P3-oxonia aktiv and P3-oxonia aktiv 150, vapour pressure and evaporation
enthalpy. Unpublished report 98/154, VTA-Safety Technology. Henkel, Düsseldorf, Germany.
[Covered by Caropreso, 2000].
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APPENDIX A. SPECIAL ABBREVIATIONS
ABTS 2,2´-Azino-bis-(3-ethyl-benzo-thiazoline)-6-sulphonate
ADS 2-((-3(2-(4-amino-2-(methhylsulphanyl)phenyl)-1-diazenyl)phenyl)
sulphonyl)-1-ethanol
ALAT Alanine aminotransferase
ASAT Asparagine aminotransferase
DMBA 7,12-Dimethylbenz[a]anthracene
DNA Dexoyribonucleic acid
DOC Dissolved organic carbon
DOT Department of Transport
DPD N,N’-diethyl-p-phenylendiamine
EC50 Median concentration expected to have an effect in 50% of the test organisms
EINECS European inventory of existing commercial chemical substances
FTIR Fourier transform infrared (spectroscopy)
GLP (Principles of ) good laboratory practice
GSH Glutathione
H2O2 Hydrogen peroxide
HOAc Acetic acid
HPLC High performance liquid chromatography
i.p. Intraperitoneal
IBC Intermediate bulk container
IUPAC International Union of Pure and Applied Chemistry
LC50 Median concentration expected to cause the death of 50% of the test
organisms
LD50 Median dose expected to cause the death of 50% of the test animals
LDH Lactate dehydrogenase
MTS Methyl p-tolyl sulphide
MTSO Methyl p-tolyl sulphoxide
NOAEL No-observed adverse effect level
NOEC No-observed effect concentration
OEL Occupational exposure limit value
PAA Peracetic acid
ppbv Parts per billion by volume
PPE Personal protective equipment
RD50 Concentration inducing a 50% reduction of respiratory rate
RQflex Reflectometer quality flexible (test strips)
SADT Self-accelerating decomposition temperature
TAED Tetra-acetyl ethylenediamine
TCF Total chlorine free
TWA Time-weighted average
UDS Unscheduled DNA synthesis
U Activity unit (of enzymes)
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APPENDIX B. CRITERIA FOR RELIABILITY CATEGORIES
Adapted from Klimisch et al (1997)
Code of Category of reliability

reliability
(CoR)
1 Reliable without restriction
1a GLP guideline study (OECD, EC, EPA, FDA, etc.)
1b Comparable to guideline study
1c Test procedure in accordance with national standard methods (AFNOR, DIN, etc...)
1d Test procedure in accordance with generally accepted scientific standards and described
in sufficient detail
2 Reliable with restrictions
2a Guideline study without detailed documentation
2b Guideline study with acceptable restrictions
2c Comparable to guideline study with acceptable restrictions
2d Test procedure in accordance with national standard methods with acceptable
restrictions
2e Study well documented, meets generally accepted scientific principles, acceptable for
assessment
2f Accepted calculation method
2g Data from handbook or collection of data
3 Not reliable
3a Documentation insufficient for assessment
3b Significant methodological deficiencies
3c Unsuitable test system
4 Not assignable
4a Abstract
4b Secondary literature
4c Original reference not yet available
4d Original reference not translated (e.g. Russian)
4e Documentation insufficient for assessment
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MEMBERS OF THE TASK FORCE
S. Jacobi (Chair) Degussa-Hüls

D - Hanau
W. Aulmana Henkel
D - Düsseldorf
A. G. Berends Solvay
B - Brussels
F. E. Caropreso FMC
USA - Princeton, NJ
I. Dalin Eka Chemicals (Akzo Nobel)

S - Bohus
Y. Gouges Chemoxal Seppic (Air Liquide)

F - Paris
G. Malinverno Ausimont
I - Bollate
N. Steiner Degussa-Hüls
D - Hanau
M. L. Weiner FMC
USA - Princeton, NJ
F. Wiebela Henkel
D - Düsseldorf
H. Vrijhof (Secretary) ECETOC

B - Brussels
a Part-time
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MEMBERS OF THE SCIENTIFIC COMMITTEE
(Peer Review Committee)
N. Carmichael (Co-chairman) Aventis

Head, Toxicology F - Sophia Antipolis
G. Randall (Co-chairman) AstraZeneca

Director, Environmental Laboratory UK - Brixham
C. Braun Akzo Nobel

Occupational Toxicologist NL - Arnhem
E. Bomhard Bayer
Head, Industrial Toxicology D - Wuppertal
C. d’Hondt Syngenta
Head, Environmental Safety Department CH - Basel
T. Feijtel Procter & Gamble

Manager, Professional and Regulatory Services B - Brussels
B. Hildebrand BASF
Vice President, Experimental Toxicology and Ecology D - Ludwigshafen
J. Jackson Monsanto
Senior Associate, Medical Adviser B - Brussels
E. Löser Bayer
Institute of Industrial Toxicology D - Wuppertal
R. Millischera Elf Atochem

Head, Industrial Toxicology Department F - Paris
A. Sarrif DuPont
Director, Toxicology Affairs, Europe D - Bad Homburg
J. Solbéa Unilever
Head, SEAC Environment UK - Bebington
L. Smith Syngenta
Director, Central Toxicology Laboratory UK - Macclesfield
H-J. Wiegand Degussa-Hüls

Head, Product Safety Department D - Marl
a Stewards responsible for primary peer review
142
ECETOC JACC No.40
ECETOC PUBLISHED REPORTS
Monographs
No. Title
No. 1 Good Laboratory Practice

No. 2 A Contribution to Strategy for Identification and Control of Occupational Carcinogens
No. 3 Risk Assessment of Occupational Chemical Carcinogens
No. 4 Hepatocarcinogenesis in Laboratory Rodents: Relevance for Man
No. 5 Identification and Assessment of the Effects of Chemicals on Reproduction and Development
(Reproductive Toxicology)
No. 6 Acute Toxicity Tests, LD50 (LC50) Determinations and Alternatives
No. 7 Recommendations for the Harmonisation of International Guidelines for Toxicity Studies
No. 8 Structure-Activity Relationships in Toxicology and Ecotoxicology: An Assessment (Summary)
No. 9 Assessment of Mutagenicity of Industrial and Plant Protection Chemicals
No. 10 Identification of Immunotoxic Effects of Chemicals and Assessment of their Relevance to Man
No. 11 Eye Irritation Testing
No. 12 Alternative Approaches for the Assessment of Reproductive Toxicity (with emphasis on
embryotoxicity/teratogenicity)
No. 13 DNA and Protein Adducts: Evaluation of their Use in Exposure Monitoring and Risk Assessment
No. 14 Skin Sensitisation Testing
No. 15 Skin Irritation
No. 16 Early Indicators of Non-Genotoxic Carcinogenesis
No. 17 Hepatic Peroxisome Proliferation
No. 18 Evaluation of the Neurotoxic Potential of Chemicals
No. 19 Respiratory Allergy
No. 20 Percutaneous Absorption
No. 21 Immunotoxicity: Hazard Identification and Risk Characterisation
No. 22 Evaluation of Chemicals for Oculotoxicity
No. 23 Receptor Mediated Mechanisms in Chemical Carcinogenesis
No. 24 Risk Assessment for Carcinogens
No. 25 Practical Concepts for Dose Selection in Chronic Toxicity and Carcinogenicity Studies in
Rodents
No. 26 Aquatic Toxicity Testing of Sparingly Soluble Volatile and Unstable Substances
No. 27 Aneuploidy
No. 28 Threshold-Mediated Mutagens - Mutation Research Special Issue
No. 29 Skin Sensitisation Testing for the Purpose of Hazard Identification and Risk Assessment
Technical Reports
No. Title
No. 1 Assessment of Data on the Effects of Formaldehyde on Humans

No. 2 The Mutagenic and Carcinogenic Potential of Formaldehyde
No. 3 Assessment of Test Methods for Photodegradation of Chemicals in the Environment
No. 4 The Toxicology of Ethylene Glycol Monoalkyl Ethers and its Relevance to Man
No. 5 Toxicity of Ethylene Oxide and its Relevance to Man
No. 6 Formaldehyde Toxicology: An Up-Dating of ECETOC Technical Reports 1 and 2
No. 7 Experimental Assessment of the Phototransformation of Chemicals in the Atmosphere
No. 8 Biodegradation Testing: An Assessment of the Present Status
No. 9 Assessment of Reverse-Phase Chromatographic Methods for Determining Partition Coefficients
No. 10 Considerations Regarding the Extrapolation of Biological Data in Deriving Occupational
Exposure Limits
143
ECETOC JACC No.40
No. 11 Ethylene Oxide Toxicology and its Relevance to Man: An Up-Dating of ECETOC Technical
Report No. 5
No. 12 The Phototransformation of Chemicals in Water: Results of a Ring-Test
No. 13 The EEC 6th Amendment: A Guide to Risk Evaluation for Effects on the Environment
No. 14 The EEC 6th Amendment: A Guide to Risk Evaluation for Effects on Human Health
No. 15 The Use of Physical-Chemical Properties in the 6th Amendment and their Required Precision,
Accuracy and Limiting Values
No. 16 A Review of Recent Literature on the Toxicology of Benzene
No. 17 The Toxicology of Glycol Ethers and its Relevance to Man: An Up-Dating of ECETOC Technical
Report No. 4
No. 18 Harmonisation of Ready Biodegradability Tests
No. 19 An Assessment of Occurrence and Effects of Dialkyl-o-Phthalates in the Environment
No. 20 Biodegradation Tests for Poorly-Soluble Compounds
No. 21 Guide to the Classification of Carcinogens, Mutagens, and Teratogens under the 6th Amendment
No. 22 Classification of Dangerous Substances and Pesticides in the EEC Directives. A Proposed
Revision of Criteria for Inhalational Toxicity
No. 23 Evaluation of the Toxicity of Substances to be Assessed for Biodegradability
No. 24 The EEC 6th Amendment: Prolonged Fish Toxicity Tests
No. 25 Evaluation of Fish Tainting
No. 26 The Assessment of Carcinogenic Hazard for Human Beings exposed to Methylene Chloride
No. 27 Nitrate and Drinking Water
No. 28 Evaluation of Anaerobic Biodegradation
No. 29 Concentrations of Industrial Organic Chemicals Measured in the Environment: The Influence
of Physico-Chemical Properties, Tonnage and Use Patterns
No. 30 Existing Chemicals: Literature Reviews and Evaluations (Fifth Edition) (No longer available)
No. 31 The Mutagenicity and Carcinogenicity of Vinyl Chloride: A Historical Review and Assessment
No. 32 Methylene Chloride (Dichloromethane): Human Risk Assessment Using Experimental Animal
Data
No. 33 Nickel and Nickel Compounds: Review of Toxicology and Epidemiology with Special Reference
to Carcinogenesis
No. 34 Methylene Chloride (Dichloromethane): An Overview of Experimental Work Investigating
Species Differences in Carcinogenicity and their Relevance to Man
No. 35 Fate, Behaviour and Toxicity of Organic Chemicals Associated with Sediments
No. 36 Biomonitoring of Industrial Effluents
No. 37 Tetrachlorethylene: Assessment of Human Carcinogenic Hazard
No. 38 A Guide to the Classification of Preparations Containing Carcinogens, Mutagens and Teratogens
No. 39 Hazard Assessment of Floating Chemicals After an Accidental Spill at Sea
No. 40 Hazard Assessment of Chemical Contaminants in Soil
No. 41 Human Exposure to N-Nitrosamines, their Effects and a Risk Assessment for
N-Nitrosodiethanolamine in Personal Care Products
No. 42 Critical Evaluation of Methods for the Determination of N-Nitrosamines in Personal Care and
Household Products
No. 43 Emergency Exposure Indices for Industrial Chemicals
No. 44 Biodegradation Kinetics
No. 45 Nickel, Cobalt and Chromium in Consumer Products: Allergic Contact Dermatitis
No. 46 EC 7th Amendment: Role of Mammalian Toxicokinetic and Metabolic Studies in the
Toxicological Assessment of Industrial Chemicals
No. 47 EC 7th Amendment "Toxic to Reproduction": Guidance on Classification
No. 48 Eye Irritation: Reference Chemicals Data Bank (Second Edition)
No. 49 Exposure of Man to Dioxins: A Perspective on Industrial Waste Incineration
No. 50 Estimating Environmental Concentrations of Chemicals using Fate and Exposure Models
No. 51 Environmental Hazard Assessment of Substances
No. 52 Styrene Toxicology Investigation on the Potential for Carcinogenicity
No. 53 DHTDMAC: Aquatic and Terrestrial Hazard Assessment (CAS No. 61789-80-8)
144
ECETOC JACC No.40
No. 54 Assessment of the Biodegradation of Chemicals in the Marine Environment

No. 55 Pulmonary Toxicity of Polyalkylene Glycols
No. 56 Aquatic Toxicity Data Evaluation
No. 57 Polypropylene Production and Colorectal Cancer
No. 58 Assessment of Non-Occupational Exposure to Chemicals
No. 59 Testing for Worker Protection
No. 60 Trichloroethylene: Assessment of Human Carcinogenic Hazard
No. 61 Environmental Exposure Assessment
No. 62 Ammonia Emissions to Air in Western Europe
No. 63 Reproductive and General Toxicology of some Inorganic Borates and Risk Assessment for
Human Beings
No. 64 The Toxicology of Glycol Ethers and its Relevance to Man
No. 65 Formaldehyde and Human Cancer Risks
No. 66 Skin Irritation and Corrosion: Reference Chemicals Data Bank
No. 67 The Role of Bioaccumulation in Environmental Risk Assessment: The Aquatic Environment
and Related Food Webs
No. 68 Assessment Factors in Human Health Risk Assessment
No. 69 Toxicology of Man-Made Organic Fibres
No. 70 Chronic Neurotoxicity of Solvents
No. 71 Inventory of Critical Reviews on Chemicals (Only available to ECETOC members)
No. 72 Methyl tert-Butyl Ether (MTBE) Health Risk Characterisation
No. 73 The Value of Aquatic Model Ecosystem Studies in Ecotoxicology
No. 74 QSARs in the Assessment of the Environmental Fate and Effects of Chemicals
No. 75 Organophosphorus Pesticides and Long-term Effects on the Nervous System
No. 76 Monitoring and Modelling of Industrial Organic Chemicals, with Particular Reference to
Aquatic Risk Assessment
No. 77 Skin and Respiratory Sensitisers: Reference Chemicals Data Bank
No. 78 Skin Sensitisation Testing: Methodological Considerations
Joint Assessment of Commodity Chemicals (JACC) Reports

No. Title
No. 1 Melamine
No. 2 1,4-Dioxane
No. 3 Methyl Ethyl Ketone
No. 4 Methylene Chloride
No. 5 Vinylidene Chloride
No. 6 Xylenes
No. 7 Ethylbenzene
No. 8 Methyl Isobutyl Ketone
No. 9 Chlorodifluoromethane
No. 10 Isophorone
No. 11 1,2-Dichloro-1,1-Difluoroethane (HFA-132b)
No. 12 1-Chloro-1,2,2,2-Tetrafluoroethane (HFA-124)
No. 13 1,1-Dichloro-2,2,2-Trifluoroethane (HFA-123)
No. 14 1-Chloro-2,2,2-Trifluoromethane (HFA-133a)
No. 15 1-Fluoro 1,1-Dichloroethane (HFA-141B)
No. 16 Dichlorofluoromethane (HCFC-21)
No. 17 1-Chloro-1,1-Difluoroethane (HFA-142b)
No. 18 Vinyl Acetate
No. 19 Dicyclopentadiene (CAS: 77-73-6)
No. 20 Tris-/Bis-/Mono-(2 ethylhexyl) Phosphate
No. 21 Tris-(2-Butoxyethyl)-Phosphate (CAS:78-51-3)
145
ECETOC JACC No.40
No. 22 Hydrogen Peroxide (CAS: 7722-84-1)

No. 23 Polycarboxylate Polymers as Used in Detergents
No. 24 Pentafluoroethane (HFC-125) (CAS: 354-33-6)
No. 25 1-Chloro-1,2,2,2-tetrafluoroethane (HCFC 124) (CAS No. 2837-89-0)
No. 26 Linear Polydimethylsiloxanes (CAS No. 63148-62-9)
No. 27 n-Butyl Acrylate (CAS No. 141-32-2)
No. 28 Ethyl Acrylate (CAS No. 140-88-5)
No. 29 1,1-Dichloro-1-Fluoroethane (HCFC-141b) (CAS No. 1717-00-6)
No. 30 Methyl Methacrylate (CAS No. 80-62-6)
No. 31 1,1,1,2-Tetrafluoroethane (HFC-134a) (CAS No. 811-97-2)
No. 32 Difluoromethane (HFC-32) (CAS No. 75-10-5)
No. 33 1,1-Dichloro-2,2,2-Trifluoroethane (HCFC-123) (CAS No. 306-83-2)
No. 34 Acrylic Acid (CAS No. 79-10-7)
No. 35 Methacrylic Acid (CAS No. 79-41-4)
No. 36 n-Butyl Methacrylate; Isobutyl Methacrylate (CAS No. 97-88-1) (CAS No. 97-86-9)
No. 37 Methyl Acrylate (CAS No. 96-33-3)
No. 38 Monochloroacetic Acid (CAS No. 79-11-8) and its Sodium Salt (CAS No. 3926-62-3)
No. 39 Tetrachloroethylene (CAS No. 127-18-4)
No. 40 Peracetic Acid (CAS No. 79-21-0) and its Equilibrium Solutions
Special Reports
No. Title
No. 8 HAZCHEM; A Mathematical Model for Use in Risk Assessment of Substances

No. 9 Styrene Criteria Document
No. 10 Hydrogen Peroxide OEL Criteria Document (CAS No. 7722-84-1)
No. 11 Ecotoxicology of some Inorganic Borates
No. 12 1,3-Butadiene OEL Criteria Document (Second Edition) (CAS No. 106-99-0)
No. 13 Occupational Exposure Limits for Hydrocarbon Solvents
No. 14 n-Butyl Methacrylate and Isobutyl Methacrylate OEL Criteria Document
No. 15 Examination of a Proposed Skin Notation Strategy
No. 16 GREAT-ER User Manual
Documents
No. Title
No. 32 Environmental Oestrogens: Male Reproduction and Reproductive Development

No. 33 Environmental Oestrogens: A Compendium of Test Methods
No. 34 The Challenge Posed by Endocrine-disrupting Chemicals
No. 35 Exposure Assessment in the Context of the EU Technical Guidance Documents on Risk
Assessment of Substances
No. 36 Comments on OECD Draft Detailed Review Paper: Appraisal of Test Methods for Sex-Hormone
Disrupting Chemicals
No. 37 EC Classification of Eye Irritancy
No. 38 Wildlife and Endocrine Disrupters: Requirements for Hazard Identification
No. 39 Screening and Testing Methods for Ecotoxicological Effects of Potential Endocrine Disrupters:
Response to the EDSTAC Recommendations and a Proposed Alternative Approach
No. 40 Comments on Recommendation from Scientific Committee on Occupational Exposure Limits
for 1,3-Butadiene
No. 41 Persistent Organic Pollutants (POPs) Response to UNEP/INC/CEG-I Annex 1
146
ECETOC JACC No.40

Todo Acido Peracetico

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Peracetic Acid (CAS No.

ECETOC JACC No. 40

ECETOC JACC No.40

THE ECETOC SCHEME FOR THE JOINT ASSESSMENT OF COMMODITY CHEMICALS 2

1. SUMMARY AND CONCLUSIONS 3

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS 7

ECETOC JACC No.40

4.2 Environmental Fate and Biotransformation 27

ECETOC JACC No.40

8.4 Genetic Toxicity 87

APPENDIX B. CRITERIA FOR RELIABILITY CATEGORIES 140

MEMBERS OF THE TASK FORCE 141

MEMBERS OF THE SCIENTIFIC COMMITTEE 142

ECETOC JACC No.40

THE ECETOC SCHEME FOR THE JOINT ASSESSMENT OF COMMODITY

This report presents a critical evaluation of the ecotoxicology, toxicology and

a A list of special abbreviations used throughout this report is at Appendix A

1. SUMMARY AND CONCLUSIONS

PAA is produced commercially as a solution in which PAA is in equilibrium with

The production of non-equilibrium solutions involves the vacuum distillation of PAA

Possible routes of human exposure to PAA are by inhalation of vapours or aerosols

The decomposition of PAA is strongly exothermic, liberating large volumes of oxygen

The predominant effects after repeated oral, dermal or inhalation exposure of

Limited information is available on the effects of PAA on deoxyribonucleic acid (DNA)

Limited data are available on reproductive toxicity of PAA in experimental animals.

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL

IUPAC Name: Peroxyethanoic acid

Synonyms: Acetyl hydroperoxide

French: Acide peracétique

Greek: Υπεροξικó οξú

Italian: Acido peracetico

Portuguese Acido peracetico

Spanish: Acido peracético

CAS Name: Ethaneperoxoic acid

CAS Registry No. 79-21-0

Molecular Weight: 76.05

2.2 Conversion Factors

• 1 ppm = 3.162 mg/m3

In this report, converted values are given in parentheses.

2.3 EU Classification and Labelling

EC (EINECS) No. 201-186-8

Index No. 607-094-00-8

EEC classification: R 10, flammable

O, oxidising; R 7, may cause fire

EEC labelling: Symbols: O, Oxidising

R-phrases: R 10, flammable

S-phrases: S 1/2, keep locked up / keep out of the reach of

Preparations must be classified in accordance with Directive 1999/45/EC (EU, 1999).

Concentration ≥ 10% C, corrosive; R20/21/22, harmful by inhalation / in

5 ≤ Concentration < 10% C, corrosive; R34, causes burns

1 ≤ Concentration < 5% Xi, irritant; R 36/37/38, irritant to eyes / respiratory

For the classification of equilibrium PAA solutions, the concentrations of hydrogen

2.4 Commercial Formulations

2.4.1 Equilibrium PAA solutions

2.4.2 Distilled PAA solutions

2.5 Physical and Chemical Poperties

Table 1: Physical and Chemical Properties of PAA

Property Value, unit Reference

2.5.1 Equilibrium PAA grades