Fiberglass or silica exposure and increased nephritis or ESRD (end-stage renal disease)

We conducted a case-control study of 325 men ages 30-69 who were diagnosed with end-stage renal disease (ESRD) between 1976 and 1984, and resided in four urban areas of Michigan in 1984. Cases were selected from the Michigan Kidney Registry and excluded men with diabetic, congenital, and obstructive nephropathies. Controls were selected by random-digit dialing and were pair-matched to cases for age, race, and area of residence. Telephone interviews were conducted with 69 percent of eligible cases and 79 percent of eligible controls. Risk of ESRD was significantly related to phenacetin or acetaminophen consumption (odds ratio(OR) = 2.66), moonshine consumption (OR = 2.43), a family history of renal disease (OR = 9.30); and regular occupational exposures to solvents (OR = 1.51) or silica (OR = 1.67). Particular occupational exposures with elevated risk were solvents used as cleaning agents and degreasers (OR = 2.50) silica exposure in foundries or brick factories (OR = 1.92), and silica exposure during sandblasting (OR = 3.83). Little or no trend of increased risk with duration of exposure was found for these occupational exposures, with the exception of silica in sandblasting. Limitations of these data include representativeness of cases, possible overreporting by cases, and misclassification of exposures inherent in self-reports.

Fibrous glass and mineral wool workers exposed to airborne man-made mineral fibers prior to 1964 were identified and followed for deaths caused by respiratory disease. Fiber exposure levels were estimated for each worker. Average fiber concentrations were very low in relation to a National Institute of Occupational Safety and Health recommendation that exposure to man-made mineral fibers less than 3.5 microns in diameter be limited to 3 fibers per cubic centimeter of air. Fibrous glass workers were exposed to about one hundredth and mineral wool workers to about one tenth of that amount. Respiratory cancer death rates were not excessive for the fibrous glass workers, but they were significantly elevated for the mineral wool workers. When respiratory cancer deaths were compared with fiber exposure levels, however, there was in no instance a strong positive correlation. There was a significant excess in nonmalignant respiratory disease deaths (excluding influenza and pneumonia) for fibrous glass workers and for the total cohort. When these nonmalignant respiratory disease deaths were compared with fiber exposure levels, however, there was in no instance a strong positive association. A special study was made of workers exposed to small diameter fibers. Respiratory cancer deaths were not in excess; however, there was an excess in nonmalignant respiratory disease deaths. This study provided no consistent evidence of a respiratory disease hazard related to exposure to man-made mineral fibers among the workers who produce these fibers. Results must be interpreted in relation to the relatively low exposure levels for these workers.

Silica is not generally considered to be a carcinogen, however, occupations characterized by high exposure to crystalline silica have excessive rates of lung cancer mortality. Respiratory cancer excesses have been reported from North America and from Europe for the following dusty trades in which exposure to silica is a common factor: iron and steel foundry workers, steel casting workers, sand blasters, metal molders, non-uranium miners, and ceramic workers. These findings have been reinforced by two reports from the Swedish Pneumoconiosis Register and the Ontario Ministry of Labor indicating that silicotics have statistically significant risks of lung cancer mortality. Animal studies suggest that silica can be an initiating carcinogen or can act as a cocarcinogen or promoter when combined with benzo(a)pyrene. We propose three candidate hypotheses and two pathways for silicocarcinogenesis.