Documents Stayner, Leslie 7 results

Background Approximately one-third (32%) of U.S. workers are employed in small business industries (those with 80% of workers in establishments with fewer than 100 employees), and approximately 53 million persons in private industry work in small business establishments. This study was performed to identify small business industries at high risk for occupational injuries, illnesses, and fatalities. Methods Small business industries were identified from among all three- and four-digit Standard Industrial Classification (SIC) codes and ranked using Bureau of Labor Statistics (BLS) data by rates and numbers of occupational injuries, illnesses, and fatalities. Both incidence rates and number of injury, illness, and fatality cases were evaluated. Results The 253 small business industries identified accounted for 1,568 work-related fatalities (34% of all private industry). Transportation incidents and violent acts were the leading causes of these fatalities. Detailed injury and illness data were available for 105 small business industries, that accounted for 1,476,400 work-related injuries, and 55,850 occupational illnesses. Many of the small business industries had morbidity and mortality rates exceeding the average rates for all private industry. The highest risk small business industries, based on a combined morbidity and mortality index, included logging, cut stone and stone products, truck terminals, and roofing, siding, and sheet metal work. Conclusions Identification of high-risk small business industries indicates priorities for those interested in developing targeted prevention programs.

"Objectives The purpose of this study was to evaluate empirically the relevance of animal-bioassay-based models for predicting human risks from exposure to 1,3-butadiene (BD) using epidemiologic data.Methods Relative-risk results obtained with a regression model in a recent epidemiologic study were used to estimate leukemia risk for occupational and environmental exposures to BD and to compare these estimates with those previously derived from an analysis of animal bioassay data.Results The estimates of risk were found to be highly dependent on the model used when low levels of exposure were evaluated that are of environmental concern, but not at the levels of occupational concern. For example, at the level (1 part per million) of the recently revised standard of the Occupational Safety and Health Administration in the United States the estimates of lifetime excess risk ranged from 1 to 8 per 1000 workers. The range of the risk estimates derived from the epidemiologic models was remarkably similar to the range of risk estimates for occupational exposures (1 to 9 per thousand) previously developed by Dankovic et al in 1993 from an analysis of a mouse bioassay study for lymphocytic lymphoma.Conclusions Results for BD seem to provide another example of a high degree of concordance between the risk predictions from models of toxicologic and epidemiologic data, particularly at occupational levels of exposure."

Background Diesel exhaust is considered a probable human carcinogen by the International Agency for Research on Cancer (IARC). The epidemiologic evidence rests on studies of lung cancer among truck drivers, bus drivers, shipyard workers, and railroad workers. The general public is exposed to diesel exhaust in ambient air. Two regulatory agencies are now considering regulating levels of diesel exhaust: the California EPA (ambient levels) and the Mine Safety Health Administration (MSHA) (occupational levels). To date, there have been few quantitative exposure-response analyses of diesel exhaust and lung cancer based on human data. Methods We conducted exposure-response analyses among workers in the trucking industry, adjusted for smoking. Diesel exhaust exposure was estimated based on a 1990 industrial hygiene survey. Past exposures were estimated assuming that they were a function of 1) the number of heavy duty trucks on the road, 2) the particulate emissions (grams/mile) of diesel engines over time, and 3) leaks from trucks' exhaust systems for long-haul drivers. Results Regardless of assumptions about past exposure, all analyses resulted in significant positive trends in lung cancer risk with increasing cumulative exposure. A male truck driver exposed to 5 g/m3 of elemental carbon (a typical exposure in 1990, approximately five times urban background levels) would have a lifetime excess risk of lung cancer of 1-2%, above a background risk of 5%. Conclusions We found a lifetime excess risk ten times higher than the 1 per 1,000 excess risk allowed by OSHA in setting regulations. There are about 2.8 million truck drivers in the U.S. Our results depend on estimates about unknown past exposures, and should be viewed as exploratory. They conform reasonably well to recent estimates for diesel-exposed railroad workers done by the California EPA, although those results themselves have been disputed.

Several quantitative risk assessment models have been published for occupational and environmental exposures to diesel exhaust particles (DEP). These risk assessment models are reviewed and applied to predict lung cancer risks for miners exposed to DEP. The toxicologically based unit risk estimates varied widely (from 2 to 220 ? 10-6 per g/m3). The epidemiologically based unit risk estimates were less variable and suggest higher risks (from 100 to 920 ? 10-6 per g/m3). The wide range of risk estimates derived from these analyses reflects the strong assumptions and large uncertainties underlying these models. All of the models suggest relatively high risks (i.e., >1/1,000) for miners with long-term exposures greater than 1,000 g/m3. This is not surprising, given the fact that miners may be exposed to DEP concentrations similar to those that induced lung cancer in rats and mice, and substantially higher than the exposure concentrations in the positive epidemiologic studies.

The evidence for the association between occupational chrysotile (12001295) exposure and cancer was reviewed to evaluate the amphibole hypothesis which proposed that the mesotheliomas observed among workers exposed to chrysotile may actually be caused by contamination by relatively low concentrations (below 1%) of tremolite (77536686) fibers. The review considered evidence obtained in studies investigating chrysotile lung burdens, epidemiologic and laboratory animal studies investigating asbestos carcinogenicity, and mechanistic studies. Low concentrations of chrysotile fibers have been found in the lungs of asbestos workers, even those who worked primarily in chrysotile producing industries. Unexpectedly high concentrations of amphibole asbestos (1332214) forms were found. These findings provided the primary basis for the amphibole hypothesis. Most case/control studies investigating associations between asbestos lung burdens and mesothelioma risk have found clear dose response relationships with amphibole lung burdens, but not chrysotile lung burdens. Some studies, however, have found associations between mesothelioma risk and chrysotile lung burdens. Both epidemiological and experimental studies have shown that chrysotile can cause lung cancer and mesothelioma and that its carcinogenic activity was not due to contamination with tremolite. Some of the epidemiologic evidence has indicated that chrysotile may be less potent than the amphiboles in causing mesothelioma. The experimental animal evidence showed than when expressed on a per weight basis, chrysotile fibers are as at least as potent as amphibole asbestos fibers in causing lung cancer. The authors conclude that the toxicologic and epidemiologic literature strongly support the view that occupational exposure to chrysotile increases the risk of lung cancer and mesothelioma. It is considered prudent that chrysotile be treated with the same level of concern as the amphibole forms of asbestos.

"Despite the considerable efforts and funds devoted to cancer research over several decades, cancer still remains a mainly lethal disease. Cancer incidence and mortality have not declined at the same rate as other major causes of death, indicating that primary prevention remains a most valuable approach to decrease mortality. There is general agreement that environmental exposures are variously involved in the causation of the majority of cancer cases and that at least half of all cancers could be avoided by applying existing etiologic knowledge. There is disagreement, however, regarding the proportion of cancer risks attributable to specific etiological factors, including diet, occupation and pollution. Estimates of attributable risks are largely based today on unverified assumptions and the calculation of attributable risks involves taking very unequal evidence of various types of factors and treating them equally. Effective primary prevention resulting in a reduction of cancer risk can be obtained by: (i) a reduction in the number of carcinogens to which humans are exposed; or (ii) a reduction of the exposure levels to carcinogens. Exposure levels that could be seen as sufficiently low when based on single agents, may actually not be safe in the context of the many other concomitant carcinogenic and mutagenic exposures. The list of human carcinogens and of their target organs might be quite different if: (i) epidemiological data were available for a larger proportion of human exposures for which there is experimental evidence of carcinogenicity; (ii) more attention was paid to epidemiological evidence that is suggestive of an exposure-cancer association, but is less than sufficient, particularly in identifying target organs; and (iii) experimental evidence of carcinogenicity, supported by mechanistic considerations, were more fully accepted as predictions of human risk."