The United States Environmental Protection Agency (USEPA) developed an inhalation unit risk factor (URF) of 4.3E-03 per µg/m(3) for arsenic in 1984 for excess lung cancer mortality based on epidemiological studies of workers at two smelters: the Asarco smelter in Tacoma, Washington and the Anaconda smelter in Montana. Since the USEPA assessment, new studies have been published and exposure estimates were updated at the Asarco and Anaconda smelters and additional years of follow-up evaluated. The Texas Commission on Environmental Quality (TCEQ) has developed an inhalation URF for lung cancer mortality from exposures to arsenic and inorganic arsenic compounds based on a newer epidemiology study of Swedish workers and the updates of the Asarco and Anaconda epidemiology studies. Using a combined analysis approach, the TCEQ weighted the individual URFs from these three epidemiology cohort studies, to calculate a final inhalation URF of 1.5E-04 per µg/m(3). In addition, the TCEQ also conducted a sensitivity analysis, in which they calculated a URF based on a type of meta-analysis, and these results compared well with the results of the combined analysis. The no significant concentration level (i.e., air concentration at 1 in 100,000 excess lung cancer mortality) is 0.067µg/m(3). This value will be used to evaluate ambient air monitoring data so the general public in Texas is protected against adverse health effects from chronic exposure to arsenic.
The risk of neoplastic disease, primarily lung cancer, induced by occupational, inhalation exposure to nonorganic arsenic was assessed. In order to identify individual risk in the linear dose-response relationship which would serve as a basis for the risk assessment among persons exposed occupationally, the author also analysed the latest epidemiological studies performed in Sweden, as well as repeated analyses of American studies. This allowed to diminish individual risk by several times. It is thought that a diminished value of individual risk is, in the light of the most up-to-date epidemiological studies, closer to the reality than the value proposed by the Environmental Protection Agency (EPA). Having the value of individual risk related to occupational exposure, equal 1.79 x 10(-4), lung cancer risk after forty years of employment under the exposure level within the range of currently binding MAC values for arsenic (0.05 mg/m3) accounts for 8.95 x 10(-3), thus slightly exceeding the adopted value of 1 x 10(3). Whereas a new value, proposed by the Expert Group for Chemical Factors of the International Commission for Updating the list of MAC and MAI values in 1996, equals 0.01, so the risk for a forty-year employment accounts for 1.79 x 10(-3), in fact the value corresponding to that already approved. In addition, the assessment indicated that smoking increases by 4-6 times the risk of lung cancer induced by exposure to arsenic.
One prospective epidemiologic study of asbestos cement workers with radiological small opacities has been cited as a rationale for attributing excess lung cancer to asbestosis. This approach could have considerable practical value for disease attribution in an era of decreasing exposure. However, a recent International Agency for Research on Cancer review concludes that the mechanism of production of asbestos-related lung cancer are unknown. Asbestosis, therefore, cannot be a biologically effective dose marker of lung cancer susceptibility. Asbestosis nonetheless would be useful in identifying asbestos-attributable lung cancer cases if it could be proven an infallible exposure indicator. In this study, we tested this hypothesis in the chrysotile miners and millers of Quebec, Canada. We examined exposure histories, autopsy records, and lung fiber content for 111 Quebec chrysotile miners and millers. If the hypothesis of an asbestosis requirement for lung cancer attribution were accurate, we would expect as asbestosis diagnosis to separate those with lung cancer and high levels of exposure from those with lower levels of exposure in a specific and sensitive manner. This is the first such study in which historical job-based individual estimates based on environmental measurements, lung fiber content, exposure timing, and complete pathology records including autopsies were available for review. We found significant excesses of lung tremolite and chrysotile and estimated cumulative exposure in those with lung cancer and asbestosis compared to those with lung cancer without asbestosis. However, when the latter were directly compared on a case-by-case basis, there was a marked overlap between lung cancer cases with and without asbestosis regardless of the measure of exposure. Smoking habits did not differ between lung cancer cases with and without asbestosis. In regression models, smoking pack-years discriminated between those with the without lung cancer, regardless of asbestosis status. Most seriously, the pathologic diagnosis of asbestosis itself seemed arbitrary in many cases. We conclude that although the presence of pathologically diagnosed asbestosis is a useful marker of exposure, the absence of this disease must be regarded as one of many factors in determining individual exposure status and disease causation.
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OBJECTIVES: The aim of the study was, on the basis of new information on nickel species and exposure levels, to generate a specific exposure matrix for epidemiologic analyses in a cohort of Norwegian nickel-refinery workers with a known excess of respiratory cancer. METHODS: A department-time-exposure matrix was constructed with average exposure to total nickel estimated as the arithmetic mean of personal measurements for periods between 1973 and 1994. From 1972 back to the start of production in 1910, exposure concentrations were estimated through retrograde calculation with multiplication factors developed on the basis of reported changes in the metallurgical process and work environment. The relative distribution of water-soluble nickel salts (sulfates and chlorides), metallic nickel, and particulates with limited solubility (sulfides and oxides) was mainly derived from speciation analyses conducted in the 1990s. RESULTS: The average concentration of nickel in the breathing zone was
In a population-based case-referent study of lung cancer we wanted to estimate the over-all influence on the lung cancer incidence from several occupational exposures. Standard methods to do this are based on addition of separately estimated attributable fractions (AFs) by rather complex formulas. Although a simple and valid method for direct estimation of summary effects was published in 1990, it is not well known and has rarely been used. We here describe the method and apply it to the data from the case-referent study. The AF for withdrawal of occupational exposure to both asbestos and combustion products were nearly identical regardless of if it was calculated by an algorithm for summation of AF for the exposure factors separately (6.90%), by a bootstrap method (6.89%, 95% confidence interval, CI: 3.69, 10.04), or by the simple 'dichotomization'-method (6.88%, 95%CI: 3.81, 9.84). The method is very easy to apply to population-based case-referent studies analyzed by logistic regression.
Despite international efforts to block Canada's export of asbestos, the Canadian federal government continues to defend the economic interests of the asbestos industry. Ironically, Canadian asbestos miners, mill workers, and those engaged in a wide range of other occupations continue to suffer asbestos-related disease and premature death. Although there is an employer-funded compensation system in each province, many workers with mesothelioma and other asbestos-related diseases remain uncompensated. The export of Canadian asbestos to developing countries sets the stage for another preventable occupational disease epidemic that will manifest over the coming decades. There is growing support from the Canadian labor movement for an end to asbestos exportation and for a just transition strategy for the asbestos workers and their communities.
Comment In: Int J Occup Environ Health. 2007 Oct-Dec;13(4):45118085060
Comment In: Int J Occup Environ Health. 2008 Apr-Jun;14(2):157-818507297
Long-term exposure to elevated indoor radon concentrations has been determined to be the second leading cause of lung cancer in adults after tobacco smoking. With the establishment of a National Radon Program in Canada in 2007 thousands of homes across the country have been tested for radon. Although the vast majority of people are exposed to low or moderate radon concentrations; from time to time; there are homes found with very high concentrations of radon. Among those living in homes with very high radon concentrations, it is typically parents of young children that demonstrate a great deal of concern. They want to know the equivalent risk in terms of the lifetime relative risk of developing lung cancer when a child has lived in a home with high radon for a few years. An answer to this question of risk equivalency is proposed in this paper. The results demonstrate clearly that the higher the radon concentration; the sooner remedial measures should be undertaken; as recommended by Health Canada in the Canadian radon guideline.
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