Table 22.
Inhalation exposures to aluminium in the workplace – case studies.
| Exposure conditions | Subjects described in the report | Outcomes | Comments | References |
|---|---|---|---|---|
| Cases of severe lung fibrosis due to aluminium exposure in Germany in the 1930s & 1940s | Cited by others as reporting the first case of pulmonary fibrosis in an aluminium worker. | Doese (1938) | ||
| Aluminium powder factory: ~ 4 billion particles/g dust (an explosive concentration of aluminium dust). | 700 workers making aluminium powder (98% metallic aluminium) by a stamping process just before and during World War II. | Dry cough, dyspnoea, lymphocytosis X-rays similar to those seen in silicosis, rapid spread of diffuse hyaline degeneration, spontaneous pneumothorax was common, loss of elastic tissue. 26% of 628 workers judged to be uncomplicated cases of pulmonary aluminosis. 4 men with 1.5 to 16 years exposure had spontaneous pneumothorax. One fatal case had collagenous fibres enclosing phagocytes which contained particles. | Goralewski (1941) stated: “ aluminium lung is a specific disease entity.” Paraffin-like substances were used due to a shortage of stearine in war-time Germany. The author believed the increase of serious cases of aluminium dust disease was due to omission of stearine. | Goralewski (1939; 1940; 1941; 1943; 1948) (most of the information was obtained from Perry (1947)) |
| Cases of severe lung fibrosis due to aluminium exposure in Germany in the 1930s & 1940s. | Koelsch (1942) | |||
| 28 cases of aluminium dust poisoning | Severe fibrosis of the lung due to aluminium exposure. | The action of the dust is partly mechanical, partly chemical. | Meyer & Kasper (1942a; 1942b) | |
| Aluminum Company of America - Pittsburg plant - making aluminium powder. | 125 with 6 to 23, an average of 12, years of exposure. | Health better than 3,000 workers in other parts of the plant in New Kensington. | Concluded inhalation of finely particulate aluminium powder is not harmful to human lung. | Crombie et al. (1944) |
| Grinding duralumin (95% aluminium, 3.5 to 4.5% copper, traces of other metals, ≤0.7 % silicon) and in a factory making aluminium powder. | 92 of 97 workers exposed to aluminium dust. Grinding process: Average aluminium concentration 3 to 5 mg l/m3, 1/3 was 2 to 7 μm diameter, 2/3 was ≥7 μm. Alumina particles mostly < 1 μm diameter. Polishing process: Average aluminium concentration 50 to 100 mg /m3, 95 mg/ m3 of 7 to 40 μm, 1.4 mg/ m3 of 2 to 7 μm, 2.7 mg/ m3 of < 0.4 to 2 μm diameter. | X-rays in 7 showed shadows in peripheral parts of their lungs. 27 claimed to have some cough, 10 were somewhat short of breath. | X-ray changes and reported symptoms were not thought to be significant because they worked without obvious effects on their health. There was no evidence that the dust caused any disease of the trachea, bronchi or lungs. It was noted by Mitchell et al. (1961) that nearly all respirable particles were alundum abrasive and that the aluminium particles were generally > 7 μm diameter. | Hunter et al. (1944) |
| Mostly furnace feeding, with some crane operations, in the manufacture of an abrasive, corundum, an aluminium oxide, from bauxite. Most fume particles were amorphous and < 0.5 μm in diameter. | 23 cases 23 months to 15 years employment | X-rays showed shadows accompanied by pneumothorax, dyspnoea, and sudden attacks of extreme breathlessness. Some cases showed diffuse non-nodular, interstitial fibrosis. Some were fatal. | Has features resembling the condition attributed to dust inhalation by Goralewski (1943). The hypothesis is that intense exposure to amorphous aluminium dust may play a dominant role. Stated by McLaughlin et al. (1962) that they were also exposed to fumes of amorphous silica. |
Riddell (1948); Shaver & Riddell (1947); Wyatt & Riddell (1949) |
| Aluminium smelting | 97 workers were studied. | Heavy damage to the lungs of 18 operators in smelting and alloying departments who had been employed an average of 6 years. | Aluminosis in 8, 1 with fibrosis, and other changes caused by aluminium compounds in 4. | Mödder and Schmitt (1951) |
| Aluminium pulverizing | A single case report | Died 3 years after terminating 3 years employment. | Death attributed to aluminium dust | Ueda et al.(1958) |
| Stamping of aluminium powder. Average dust concentration 4 to 50 mg/m3, most < 4 μm diameter. | 5 cases among a group of 35 workers. | Breathlessness after 2 to 4 years, and 13 years exposure in one worker. Exposure was terminated; 3 recovered, 2 did not, 1 died, showing non-specific lung inflammation, fibrosis and emphysema. | Edling (1961) | |
| Flash filler (filling fireworks with aluminium powder [many particles < 5 μm] and potassium perchlorate by hand). | A case report of a 26 year old female who had 5 years exposure. | Dyspnoea and gross pulmonary fibrosis were seen. She appeared to have had tuberculosis. |
Similar to cases reported by Goralewski (1947), Shaver (1948) and Mitchell (1959) | Jordan (1961) |
| Pyro stamping. Total dust concentration (means of 5 & 7 samples): 615 & 685 mg/m3. Respirable dust: 51 & 52 mg/m3. Stamping, screening and weighing room mean respirable dust concentration: 19 to 114 mg/m3; mean daily exposure time to dusty work: 3.5 hr. 70% of particles < 5 μm diameter. 81% free aluminium, 17% aluminium oxides and hydroxides, 0.5% stearine (½ palmitic, ½ stearic acid), 0.5% silicon. | Examined 27 of 30 workers at risk. 12 were exposed to fine aluminium powder (2 died, 2 were affected). 15 worked with coarser powder (2 had radiological symptoms). | 6 had pulmonary fibrosis. There were 2 fatal cases where pulmonary fibrosis was conclusive, in 3 cases it was sufficient and in 1 suggestive. | A follow-up of Mitchell (1959), case report. Concluded that finely divided aluminium was responsible for the lung damage. |
Mitchell et al. (1961) |
| A ball mill operator in an aluminium flake powder factory that incorporated 1.5 to 5 % stearic acid. Average concentrations from 2 sites: total dust 0.94 and 1.46 mg/m3 (60 & 71% aluminium) Respirable dust concentration: 0.24 and 0.38 mg/m3 (42 & 48% aluminium) | A case report of 49 year old male with 13.5 years exposure. | Lung shadows, adhesions in pleural cavities, diffuse fibrosis of upper lobes. 20 μm aluminium flakes were seen in his lungs, which had 340 & 430 mg Al/kg lung (wet weight). | Histological picture similar to that described by Mitchell et al. (1961) | McLaughlin et al. (1962) |
| Aluminium welder | Case report | Diffuse interstitial infiltrate and mild dyspnoea. Microscopic examination of material from lung biopsy showed extensive interstitial granulomas composed of macrophages, foreign body giant cells and crystals containing Al. | Chen et al. (1978) | |
| Aluminium welding | Case report | Desquamative interstitial pneumonia Lung biopsy showed large amounts of particles containing Al, particularly in alveolar macrophages. |
A nonspecific response to inhaled particles. | Herbert et al. (1982) |
| Welding with exposure exclusively to aerosols of oxidized aluminium | A case report of a 35 year old male with 17 years exposure who was a 60 pack per year smoker. | Shortness of breath. X-ray showed ill-defined nodular, infiltrative lesions, especially in the upper airway. Fibrous pleural adhesions were present. |
Vallyathan et al. (1982) | |
| Aluminium rail grinding, often in an extremely dusty work environment | Case report of a 44 year old with 6 years exposure. | Shortness of breath X-ray showed diffuse infiltrates and restrictive lung disease. Lung tissue contained > 342,000,000 particles/g dry weight, of which 94.8% were pure aluminium. | Concluded the inhaled aluminium particles caused this pulmonary alveolar proteinosis. | Miller et al. (1984) |
| Exposure to aluminium dust | A case report. Developed first symptoms of cough, sputum after 3 years exposure, diagnosis of pneumoconiosis made 13 years after initiation of exposure at age 33. | Pneumoconiosis, characterized by intensive lung fibrosis with an hyperelastogenic reaction X-ray showed extensive, defacing fibrosis in both lungs and pseudo-tumoral shadows. Dyspnoea, which was attributed to fibrosis, which led to fatal chronic cor pulmonale. |
Aluminium concentration 50 to 70 mg/kg in mediastinal lymph nodes and 0.4 to 2.2 mg/kg in lung parenchyma | Freour et al. (1966) |
| Metal polishing | A case report of a 61 year old male with 20 years exposure who was a 45 pack per year smoker. | Shortness of breath, dry cough, and dyspnoea. X-ray showed dense, diffuse interstitial infiltrate, which was denser in upper lung. Bronchoalveolar lavage, lung & lymph node particles ~ 1/3 aluminium, ~ ¼ silicon. Large amount of 0.5 to 5 μm particles in lung. |
Diagnosis of pneumoconiosis based on severe, diffuse, fibrosis; massive dust deposits and no specific sign of other lung disease. No silicotic nodules were seen. |
De Vuyst et al. (1986) |
| Bauxite refining for aluminium oxide production (8 cases), cold grinding of aluminium (3 cases), other occupations (2 cases) | 13 males, mean 53 years old. Awarded compensation by Turin branch of INAIL (National Institute for Insurance against Occupational Accidents) | X-ray showed irregular opacities and nodular fibrosis. | Relatively benign character of modern aluminium lung. | Avolio et al. (1989) |
| 19 males, mean 54.7 years old, mean 16 year dust inhalation. Awarded compensation by Venice branch of INAIL. | X-ray showed 10 cases had signs of fibrosis, 9 cases of chronic obstructive pulmonary disease. | Confirmation of aluminium pneumoconiosis with moderate functional alterations. | Lorusso et al. (1992) | |
| Aluminium production | A case report of a 62 year old male industrial engineer with 23 years exposure. | Exertional dyspnoea. X-ray showed bilateral interstitial infiltrates. Pulmonary function tests were consistent with severe restrictive ventilatory defect. | Al-Masalkhi & Walton (1994) |