Exposure-response analysis of risk of respiratory disease associated with occupational exposure to chrysotile asbestos.

Stayner, Leslie T.; Smith, Randall J.; Bailer, A. John; Gilbert, Stephen J.; Steenland, Kyle; Dement, John M.; Brown, David P.; Lemen, Richard A.

doi:10.1136/oem.54.9.646

Cited by 112 publications

(96 citation statements)

References 20 publications

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“…There have been a number of investigations of a cohort of workers exposed primarily to chrysotile at a textile plant in South Carolina (Dement et al, 1982(Dement et al, , 1983a(Dement et al, , 1983b(Dement et al, , 1994Stayner et al, 1997Stayner et al, , 2007 Brown, 1998, Hein et al, 2007). The present analysis is based upon follow-up though 2001 of 3072 workers (1256 white men, 1.5% lost to follow-up; 1265 mostly white females, 17% lost to follow-up; and 551 nonwhite males, 7% lost to follow-up) who worked for at least one month between 1940 and 1965.…”

Section: The South Carolina Cohortmentioning

confidence: 99%

Update of Potency Factors for Asbestos-Related Lung Cancer and Mesothelioma

Berman¹,

Crump

2008

Critical Reviews in Toxicology

155

125

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The most recent update of the U.S. Environmental Protection Agency (EPA) health assessment document for asbestos (Nicholson, 1986, referred to as "the EPA 1986 update") is now 20 years old. That document contains estimates of "potency factors" for asbestos in causing lung cancer (K L 's) and mesothelioma (K M 's) derived by fitting mathematical models to data from studies of occupational cohorts. The present paper provides a parallel analysis that incorporates data from studies published since the EPA 1986 update.The EPA lung cancer model assumes that the relative risk varies linearly with cumulative exposure lagged 10 years. This implies that the relative risk remains constant after 10 years from last exposure. The EPA mesothelioma model predicts that the mortality rate from mesothelioma increases linearly with the intensity of exposure and, for a given intensity, increases indefinitely after exposure ceases, approximately as the square of time since first exposure lagged 10 years. These assumptions were evaluated using raw data from cohorts where exposures were principally to chrysotile (South Carolina Although the linear EPA model generally provided a good description of exposure response for lung cancer, in some cases it did so only by estimating a large background risk relative to the comparison population. Some of these relative risks seem too large to be due to differences in smoking rates and are probably due at least in part to errors in exposure estimates. There was some equivocal evidence that the relative risk decreased with increasing time since last exposure in the Wittenoom cohort, but none either in the South Carolina cohort up to 50 years from last exposure or in the New Jersey cohort up to 35 years from last exposure.textileThe mesothelioma model provided good descriptions of the observed patterns of mortality after exposure ends, with no evidence that risk increases with long times since last exposure at rates that vary from that predicted by the model (i.e., with the square of time). In particular, the model adequately described the mortality rate in Quebec chrysotile miners and millers up through >50 years from last exposure. There was statistically significant evidence in both the Wittenoom and Quebec cohorts that the exposure intensity-response is supralinear 1 rather than linear. The best-fitting models predicted that the mortality rate varies as [intensity] 0.47 for Wittenoom and as [intensity] 0.19 for Quebec and, in both cases, the exponent was significantly less than 1 ( p < .0001).Using the EPA models, K L 's and K M 's were estimated from the three sets of raw data and also from published data covering a broader range of environments than those originally addressed in the EPA 1986 update. Uncertainty in these estimates was quantified using "uncertainty bounds" that reflect both statistical and nonstatistical uncertainties. Lung cancer potency factors (K L 's) were developed from 20 studies from 18 locations, compared to 13 locations covered in the EPA 1986 update. Mesothelioma p...

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Section: The South Carolina Cohortmentioning

confidence: 99%

Update of Potency Factors for Asbestos-Related Lung Cancer and Mesothelioma

Berman¹,

Crump

2008

Critical Reviews in Toxicology

155

125

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“…Lesage advanced the concept of "controlled use" of asbestos, "safe" practices that are a fiction in the developing countries where regulations is seldom enforced and voluntary standards are almost never implemented or monitored (Castleman 2003;Egilman and Roberts 2004). The strictest occupational exposure limit in the world for chrysotile asbestos (0.1 fiber/cc) is estimated to be associated with lifetime risks of 5/1,000 for lung cancer and 2/1,000 for asbestosis (Stayner et al 1997). This exposure limit can be technically achieved in the United States and in a few other highly industrialized countries, but the residual risks still are too high to be acceptable.…”

Section: Asbestos Bansmentioning

confidence: 99%

The asbestos cancer epidemic.

LaDou

2004

Environ Health Perspect

179

106

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The asbestos cancer epidemic may take as many as 10 million lives before asbestos is banned worldwide and exposures are brought to an end. In many developed countries, in the most affected age groups, mesothelioma may account for 1% of all deaths. In addition to mesotheliomas, 5-7% of all lung cancers can be attributed to occupational exposures to asbestos. The asbestos cancer epidemic would have been largely preventable if the World Health Organization (WHO) and the International Labor Organization (ILO) had responded early and responsibly. The WHO was late in recognizing the epidemic and failed to act decisively after it was well under way. The WHO and the ILO continue to fail to address the problem of asbestos mining, manufacturing, and use and world trade of a known human carcinogen. Part of the problem is that the WHO and the ILO have allowed organizations such as the International Commission on Occupational Health (ICOH) and other asbestos industry advocates to manipulate them and to distort scientific evidence. The global asbestos cancer epidemic is a story of monumental failure to protect the public health.

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“…The 2014 Helsinki report (1) states on pages 6 and 7: "Using an estimate of 4% increase of risk for each fibres per cubic centimeter per year (fibre year) of cumulative exposure: 'A cumulative exposure of 25 fibre-years is estimated to increase the risk of lung cancer 2-fold, clinical cases of asbestosis may occur at comparable cumulative exposures." Setting aside the fact that published studies support a linear dose-response relationship without a threshold (24)(25)(26)(27), the 2014 consensus statement ignores its previously acknowledged range of risk estimates and chooses the upper end of the range without comment or explanation. This compounds the error of its failure to acknowledge and reference studies indicating a linear dose-response relationship and instead embraces a statement that implicates a specific threshold.…”

Section: Letter To the Editormentioning

confidence: 99%