Occupational exposure aluminum

One case study was identified where a man who had been occupationally exposed to hexachloroethane was treated for a liver tumor (Selden et al. 1989). Exposure had occurred over a period of 6 years as a result of the presence of hexachloroethane in a degassing agent used during aluminum smelting. However, the hexachloroethane reacted at the 700 C use-temperature, releasing a gas that was 96% hexachlorobenzene with small amounts of other chlorinated compounds. Because there was occupational exposure to a mixture of chlorinated compounds rather than just hexachloroethane, it is highly unlikely that the tumor was the result of hexachloroethane exposure alone. Occupational exposure to mineral oil mists for 20 years was also part of the subject s employment history. 

In general, these occupational exposure studies poorly characterize aluminum exposure. Some of the studies reported aluminum air concentrations for a single time period (Dick et al. 1997 Sim et al. 1997 Sjogren et al. 1996 White et al. 1992), but did not have earlier monitoring data when aluminum exposures were higher. The lack of adequate exposure monitoring data and the different types of aluminum exposure makes it difficult to compare these studies and draw conclusions regarding the neurotoxic potential of inhaled aluminum in workers. 

A case control study by Salib and Hillier (1996) examined the possible relationship between the risk of Alzheimer s disease and occupational exposure to airborne aluminum. The occupation histories of patients with a clinical diagnosis of Alzheimer s disease (198 cases) were compared with two control groups patients with dementia other than Alzheimer s disease (164 cases) and patients with diagnoses other than dementia. Occupational histories were obtained from the patients via a questionnaire. No significant association between occupational exposure to aluminum dust or fumes and the risk of Alzheimer s disease were found (the odds ratio for the comparison with all controls was 0.98, 95% confidence interval of 0.53-1.75). 

Six volunteers had urinary levels of 14-414 g/L aluminum compared to concentrations of <3 g/L prior to a 1-day exposure to 0.3-10.2 mg Al/m3 in welding fumes (Sjogren et al. 1985). The urinary aluminum levels of 7 welders exposed occupationally to aluminum fumes or dust for 6 months were increased 3-fold after an 8-hour workshift compared to concentrations at the beginning of the day (Mussi et al. 1984). In another occupational study, workers exposed to 1.5 mg/m3 for 0.3-21 years eliminated the highest levels of urinary aluminum concentrations (82 g/L) immediately after exposure (Sjogren et al. 1988). After an exposure-free period of 16-37-days, levels decreased to a mean concentration of 29 g/L. These studies indicate that urinary levels were related to exposure concentration however, quantitative correlations, as well as elimination of aluminum in the feces, were not reported. 

Comparative Toxicokinetics. The animal data indicate that the nervous system is a sensitive target of toxicity for aluminum following oral exposure, as summarized in the Data Needs sections on Neurotoxicity. Although the interpretation of the human data is limited by poor exposure characterization, the occupational exposure studies suggest that neurotoxicity is also a sensitive end point following inhalation exposure (Hanninen et al. 1974 Hosovski et al. 1990 Rifat et al. 1990 Sim et al. 1997 Sjogren et al. 1996 White et al. 1992). The toxicokinetic properties of aluminum have been extensively studied in human and animals. The results of these studies suggest that the absorption, distribution, and excretion properties of aluminum are similar across species. 

The most recent National Occupational Exposure Study (NOES) conducted by NIOSH from 1981 to 1983, estimated the number of workers potentially exposed to aluminum and aluminum compounds (NIOSH 1991). Results of this survey are summarized in Table 5-8. The NOES was based on observational field surveys of 4,490 facilities and was designed as a nationwide survey based on a statistical sample of virtually all workplace environments, except mining and agriculture, in the United States where eight or more persons are employed and only provides estimates of the numbers of workers... 

Al-Masalkhi A, Walton SP. 1994. Pulmonary fibrosis and occupational exposure to aluminum. J Ky Med Assoc 92 59-61. 

Dehm B, Letzel S, Raithel HJ, et al. 1996. [Pulmonary fibrosis following occupational exposure to aluminum dust]. Arbeitsmed Sozialmed Umweltmed 31 161-164. (German). 

Musk AW, Greeville HW, Tribe AE. 1980. Pulmonary disease from occupational exposure to an artificial aluminum silicate used for cat litter. Br J Ind Med 37 367-372. 

Valkonen S, Aitio A. 1997. Analysis of aluminum in serum and urine for the biomonitoring of occupational exposure. Sci Total Environ 199 103-110. 

Observe normal precautions appropriate to the circumstances and quantity of the material handled. In the UK, the occupational exposure limits for aluminum oxide are lOmg/m long-term (8-hour TWA) for total inhalable dust and 4 mg/m for respirable dust. ... 

The primary routes of potential human exposure to coke oven emissions are inhalation and dermal contact. Occupational exposure to coke oven emissions may occur for those workers in the aluminum, steel, graphite, electrical, and construction industries. Coke oven emissions can have a deleterious effect on human health. Coke oven emissions contain literally several thousand compounds, several of which are known carcinogens and/or cocarcinogens including polycyclic organic matter from coal tar pitch volatiles, jS-naphthylamine, benzene, arsenic, beryllium, cadmium, chromate, lead, nickel subsulfide, nitric oxide, and sulfur dioxide. Most regulatory attention has been paid to coal tar pitch volatiles. 

Graves AB, Rosner D, Echeverria D, et al. Occupational exposures to solvents and aluminum and estimated risk of Alzheimer s disease. Occup Environ Med 1998 55(9) 627-33. 

Occupational exposure to inhaled fluoride dusts in cryolite workers during aluminum refining has resulted in severe bone abnormalities, but safety equipment now limits such exposure. No cases of skeletal fluorosis are attributed to use of controlled fluoridation of water supplies. However, skeletal fluorosis may occur in areas of the world where naturally occurring drinking water has high levels of fluoride, such as China and the Indian subcontinent. It is thought that exposure to fluoride intakes of 10 to 25mg/day for 10 years or more may result in skeletal fluorosis, but other nutritional factors may make these populations more susceptible. ... 

Becher G, Haugen A, Bjorseth A. 1984. Multimethod determination of occupational exposure to polycyclic aromatic hydrocarbons in an aluminum plant. Carcinogenesis 5 647-651. 

In the same decade, five dialysis patients developed dyspraxia and seizures at a dialysis center in Denver, Colorado (Alfrey et al. 1972). Investigators suspected a contaminant in the tap water used for dialysis but did not suspect aluminum until their second study in 1976 found increased aluminum in the gray matter of 12 subjects with dialysis dementia (DD) (Alfrey et al. 1976). Two fields of research then merged with additional data from occupational exposures to focus on aluminum s putative role as a cause of dementing illnesses. 

Table 6-2 lists the neurological and psychiatric symptoms attributed to aluminum exposure. Most references do not consider aluminum an industrial poison, but chronic inhalation of aluminum dust causes pulmonary irritation leading to lung fibrosis (Shaver s disease) and bronchopneumonia (Katz 1985). An industrial case of pulmonary fibrosis in an aluminum refiner with DD-like symptoms and increased brain aluminum showed the overlap of symptoms between occupational exposures and DD (McLaughlin et al. 1962). Aluminum poisoning from the natural environment is one of several proposed causes of parkinsonism-... 

EXPOSURE ROUTES Inhalation dermal contact (used to treat skin disorders) occupational exposure in the aluminum, steel graphite, electrical and construction industries, coking and coal tar production plants. 

The orally taken and not absorbed aluminum is excreted as aluminum phosphate in the feces. Most of the absorbed aluminum is eliminated with the urine and, according to the present state of knowledge, in amounts of less than 14 p.g/day for normal persons. Considerably higher levels can be found in cases of occupational exposure to aluminum. There are no studies on the aluminum clearance of persons without renal diseases. Results from animal experiments show that the elimination of aluminum via gallbladder, perspiration, and breast milk is negligibly low in contrast to the urine elimination. 

Increased aluminum concentrations in the bone could also be observed in aluminum welders widi an occupational exposure to aluminum over a long period of time [18]. There are, however, no unequivocal indications that occupational exposure to aluminum causes osteomalacia. 

Mark Cullen is professor of medicine and public health at Yale University School of Medicine. His research interests are in occupational and environmental medicine, including isocyanate exposure in automobile-shop workers, lung cancer in people exposed to asbestos, and lead toxicity in workers. He has published several textbooks, including Clinical Occupational Medicine and Textbook of Clinical Occupational and Environmental Medicine. Dr. Cullen received his MD from Yale University and did his residency in internal medicine. He is a member of the DuPont Epidemiology Review Board, a member of the MacArthur Foundation Network on Socioeconomic Status and Health, and a corporate medical director for the Aluminum Company of America. Dr. Cullen is a member of the Institute of Medicine and served as a member of its Board on Health Sciences. 

Hepatic Effects. No studies were located regarding hepatic effects in humans following acute- or chronic-duration inhalation exposure to various forms of aluminum. Intermediate occupational inhalation exposure to aluminum fumes, dusts, or powders did not affect liver function or hepatic microanatomy in a group of 7 workers as determined from biopsy samples (Mussi et al. 1984). 

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