Tyler asbestos workers: mortality experience in a cohort exposed to amosite.

Levin, Jeff; McLarty, Jerry; Hurst, George A.; Smith, Angela N.; Frank, Arthur L.

doi:10.1136/oem.55.3.155

Cited by 59 publications

(25 citation statements)

References 16 publications

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“…Thus, F2 was assigned a value of 1 for this study. Levin et al (1998) studied the mortality experience of 1,121 men who formerly worked at a plant in Tyler, TX, that manufactured asbestos pipe insulation. The plant operated from 1954 through February 1972.…”

Section: Paterson Nj Insulation Factorymentioning

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: Paterson Nj Insulation Factorymentioning

confidence: 99%

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

Berman¹,

Crump

2008

Critical Reviews in Toxicology

155

125

View full text Add to dashboard Cite

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“…Furthermore, concomitant asbestos and tobacco exposure have a multiplicative effect on lung cancer development, translating to as much as a 50-fold higher lung cancer risk in comparison with non-smoking individuals in the general population (8)(9)(10). This association between exposure to asbestos and excess death from lung cancer was documented in a study on former workers of a plant in Tyler, TX that used amosite to manufacture pipe insulation material (11). In this study, we performed surface-enhanced laser desorption ionization time-of-flight mass spectrometry (SELDI-TOF MS) (12,13) on the stored plasma samples of lung cancer patients and disease-free controls from the Tyler, TX cohort to identify lung cancer-specific biomarkers.…”

Section: Introductionmentioning

confidence: 91%

“…The Tyler, TX cohort was unique in several respects; namely, the workers of the pipe insulation material manufacturing plant were exposed to high levels of pure amosite for an extended period of time resulting in excess death from lung cancer (11,14). Although not prospectively designed, the availability of sequential plasma samples in this cohort, especially in some lung cancer patients, allowed meaningful molecular studies to search for diagnostic and potential early detection markers.…”

Section: Discussionmentioning

confidence: 99%

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Plasma proteomic profiling: Search for lung cancer diagnostic and early detection markers

Ali

Xiao²,

Malone³

et al. 2006

Oncol Rep

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Abstract. Environmental and occupational exposure to asbestos is among the established risk factors for lung cancer, the leading cause of cancer-related deaths in the United States. This link between exposure to asbestos and the excessive death rate from lung cancer was evident in a study of former workers of an asbestos pipe insulation manufacturing plant in Tyler, TX. We performed comparative proteomic profiling of plasma samples that were collected from nine patients within 12 months before death and their age-, raceand exposure-matched disease-free controls on strong anion exchange chips using surface-enhanced laser desorption ionization time-of-flight mass spectrometry. A distancedependent K-nearest neighbor (KNN) classification algorithm identified spectral features of m/z values 7558.9 and 15103.0 that were able to distinguish lung cancer patients from disease-free individuals with high sensitivity and specificity. The high correlation between the intensities of these two peaks (r=0.987) strongly suggests that they are the doubly and singly charged ions of the same protein product. Examination of these proteomic markers in the plasma samples of subjects from >5 years before death from lung cancer suggested that they are related to the early development of lung cancer. Validation of these biomarkers would have significant implications for the early detection of lung cancer and better management of high-risk patients.

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“…Latency of asbestos related diseases is reported to range between 15 and more than 40 years after the 1st exposure [24,33,34]. Starting between 1997 and 2001 and ending in 2012 our follow-up was conducted in the midst of the epidemic of asbestos related diseases in Germany, which was provoked by excessive use of asbestos between 1955 and 1980 (West Germany) e.g., (East Germany) [35].…”

Section: Latency Period Of Asbestos-related Diseasesmentioning

confidence: 99%

Occupational exposure to asbestos is associated with increased mortality in men recruited for a population-based study in Germany

Repp

Lorbeer

Ittermann

et al. 2015

Int J Occup Med Environ Health

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Objectives: Occupational exposure to asbestos is associated with increased mortality which, however, has not been thoroughly validated in a general population. We have aimed at exploring whether this association may be confirmed within a population-based setting after adjustment for confounders. Furthermore, the impact of tobacco consumption on the association between occupational exposure to asbestos and mortality is assessed. Material and Methods: We used data from 2072 (224 exposed) male participants of the Study of Health in Pomerania. Information on exposure to asbestos is based on a selfreport. Median follow-up time was 11.3 years. All-cause mortality and cause-specific mortality of exposed and non-exposed men were compared using mortality rate ratios, Kaplan-Meier analyses and multivariable Cox regression. Results: During the follow-up, 52 (23.2%) exposed and 320 (17.3%) non-exposed participants deceased. Exposed subjects had increased hazard ratios (HR) for all-cause mortality (HR=1.48, 95% CI: 1.1-2), benign lung disease mortality (HR=3, 95% CI: 1.18-7.62) and stomach cancer mortality (HR=4.59, 95% CI: 1.53-13.76). The duration of exposure (per 10 years) was associated with all-cause (HR=1.21, 95% CI: 1.07-1.36) and benign lung disease mortality (HR=1.68, 95% CI: 1.26-2.22). Smokers occupationally exposed to asbestos had the highest risk for all-cause (HR=3.70, 95% CI: 2.19-6.27) and cancer mortality (HR=4.56, 95% CI: 1.99-10.48) as compared to non-asbestos exposed non-smokers. Conclusion: Our results confirm associations of occupational exposure to asbestos with all-cause, benign lung disease, and stomach cancer mortality and underline the impact of joint effects of asbestos and smoking on mortality.

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Tyler asbestos workers: mortality experience in a cohort exposed to amosite.

Cited by 59 publications

References 16 publications

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

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

Plasma proteomic profiling: Search for lung cancer diagnostic and early detection markers

Occupational exposure to asbestos is associated with increased mortality in men recruited for a population-based study in Germany

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