American Journal of Epidemiology

About the journal

Publisher: Oxford University Press
Published: 1965 to the present, United States
Language: English
ISSN: 0002-9262 (print), 1476-6256 (electronic)
Continues: American Journal of Hygiene
Its record in the NLM Catalog

2020s

Impact of interventions to prevent asbestos-related respiratory disease in an exposed worker registry using a simplified G-computation. N.L. DeBono, L. Everest, D.B. Richardson, et al. 2026;195(1):92-101. PubMed · Publisher · Free full text

Abstract

The Ontario Asbestos Workers Registry is a regulatory exposure registry obligating employers to report the number of work hours with asbestos-containing materials for each of their workers. Currently, each worker is notified of the need for a medical examination once they have accrued 2000 reported hours of work with asbestos. We sought to evaluate the impact on disease prevention of alternative policies limiting asbestos work hours among registry participants. A cohort of 26 164 asbestos workers were followed for cancer and nonmalignant disease diagnoses between 1986 and 2019. Analyses of the association between cumulative asbestos work hours and respiratory disease incidence rates showed substantially elevated disease rates well before reaching 2000 asbestos work hours. Using a simplified application of parametric G-computation (G-POSH), limiting cumulative asbestos work hours to 100 h would have prevented 76 asbestosis, 36 pulmonary fibrosis, 27 mesothelioma, and 79 lung cancer cases at the end of follow-up compared to the observed risk in the cohort. Limiting exposure to 2000 asbestos work hours had a smaller but still substantial impact on disease prevention, particularly among workers in the construction industry. Regulatory agencies should intervene sooner to prevent respiratory disease among workers in the registry.

© The Author(s) 2025. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health.
Occupational exposures and kidney cancer among 25 000 male offshore petroleum industry workers: relative risks and healthy worker survivor bias. N.K. Shala, M.B. Veierød, R. Babigumira, et al. 2026;195(1):81-91. PubMed · Publisher · Free full text

Abstract

Kidney cancer has been a suspected occupational disease in petroleum workers. Health conditions that are linked to kidney cancer may prompt termination or change of work and thereby restrict occupational exposures in high-risk individuals, creating a healthy worker survivor bias (HWSB). We examined associations between occupational exposures and kidney cancer among males in the Norwegian offshore petroleum workers cohort using a case-cohort design, with 169 incident cancers identified by linkage to national registry data (1999-2021) and a subcohort of 2090 noncases, all employed between 1965 and 1998. Relative risks (hazard ratios [HRs]) by cumulative exposure to benzene, crude oil, chlorinated degreasing agents (CDA), asbestos, welding fumes, or surface treatment (priming, painting) were estimated by weighted Cox regression. Inverse exposure-response trends suggested HWSB, reinforced by analyses of necessary components of HWSB. Bias was partly alleviated by adjustment for total employment duration and by 20-year lagging of cumulative exposure to benzene, crude oil, or CDA. Workers in surface treatment (ever vs never) showed increased HR = 2.22, 95% confidence interval [CI], 1.04-4.72 (9 cases, only). For asbestos and welding fumes, the initial inverse trends largely remained after adjustment. In sum, we could neither confirm nor exclude an occupational impact on kidney cancer.

© The Author(s) 2025. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health.
Advancing health equity metrics: estimating the burden of lung cancer attributed to known carcinogens by socioeconomic position. E. Counil, W. Ismail, A. Roblin, et al. 2025;194(8):2174-2183. PubMed · Publisher

Abstract

Attributable burden of disease estimates reported population-wide do not reflect social disparities in exposures and outcomes. This makes one of the influential scientific tools in public health decision-making insensitive to the distribution of health impacts between socioeconomic groups. Our aim was to use the often-overlooked distributive property of the population attributable fraction (PAF) to quantitatively partition the population burden attributed to known risk factors into subgroups defined by their socioeconomic position (SEP). To illustrate our approach, we focus on lung cancer risk in relation to smoking and exposure to three occupational carcinogens: asbestos, silica dust, and diesel motor exhaust. We directly estimate PAFs from a large, population-based, case-control study using multiple unconditional logistic regression, mutually adjusting for available known risk factors. We partition the PAFs of occupational exposures and smoking according to different SEP indicators: occupational class, prestige and trajectory, and education. Our results show that workplace exposures, smoking, and their population health impacts concentrate among lower-SEP groups, a long-known reality that had never been measured through a PAF approach, to our knowledge. When attempting to quantify the avoidable burden of diseases, it is useful to partition population-wide into SEP-specific metrics, because the modifiable exposures (eg, behavioral, work-related, environmental) are socially stratified. This article is part of a Special Collection on Methods in Social Epidemiology.

© The Author(s) 2024. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: [email protected].
Environmental and occupational exposures and prognosis in patients with non-muscle-invasive bladder cancer in the Be-Well Study. Z. Wang, M.L. Kwan, R. Haque, et al. 2024;193(6):863-873. PubMed · Publisher · Free full text

Abstract

Bladder cancer is primarily diagnosed as non-muscle-invasive bladder cancer (NMIBC), with high recurrence and progression rates. Environmental and occupational exposures to carcinogens are well-known risk factors for developing bladder cancer, yet their effects on prognosis remain unknown. In the Be-Well Study, a population-based prospective cohort study of 1472 Kaiser Permanente patients newly diagnosed with NMIBC in California from 2015 to 2019, we examined history of environmental and occupational exposures in relation to tumor stage and grade at initial diagnosis by multivariable logistic regression, and subsequent recurrence and progression by Cox proportional hazards regression. Exposure to environmental and occupational carcinogens was significantly associated with increased risk of progression (hazard ratio (HR) = 1.79; 95% CI, 1.04-3.09), specifically with increased progression to muscle-invasive disease (HR = 2.28; 95% CI, 1.16-4.50). Exposures to asbestos and arsenic were associated with increased odds of advanced stage at diagnosis (asbestos: odds ratio (OR) = 1.43 [95% CI, 1.11-1.84]; arsenic: OR = 1.27 [95% CI, 1.01-1.63]), and formaldehyde exposure was associated with increased risk of recurrence (HR = 1.38; 95% CI, 1.12-1.69). Our findings suggest that considering a patient's history of these exposures may benefit current risk stratification systems in better tailoring clinical care and improving prognosis among patients with NMIBC.

© The Author(s) 2023. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: [email protected].

2010s

Extended Mortality Follow-up of a Cohort of 25,460 Workers Exposed to Acrylonitrile. S. Koutros, J.H. Lubin, B.I. Graubard, et al. 2019;188(8):1484-1492. PubMed · Publisher · Free full text

Abstract

We extended the mortality follow-up of a cohort of 25,460 workers employed at 8 acrylonitrile (AN)-producing facilities in the United States by 21 years. Using 8,124 deaths and 1,023,922 person-years of follow-up, we evaluated the relationship between occupational AN exposure and death. Standardized mortality ratios (SMRs) based on deaths through December 31, 2011, were calculated. Work histories and monitoring data were used to develop quantitative estimates of AN exposure. Hazard ratios were estimated by Cox proportional hazards regression. All-cause mortality and death from total cancer were less than expected compared with the US population. We observed an excess of death due to mesothelioma (SMR = 2.24, 95% confidence interval (CI): 1.39, 3.42); no other SMRs were elevated overall. Cox regression analyses revealed an elevated risk of lung and bronchial cancer (n = 808 deaths; for >12.1 ppm-year vs. unexposed, hazard ratio (HR) = 1.43, 95% CI: 1.13, 1.81; P for trend = 0.05), lagged 10 years, that was robust in sensitivity analyses adjusted for smoking and co-exposures including asbestos. Death resulting from bladder cancer (for >2.56 ppm vs. unexposed, lagged 10-year HR = 2.96, 95% CI: 1.38, 6.34; P for trend = 0.02) and pneumonitis (for >3.12 ppm-year vs. unexposed, HR = 4.73, 95% CI: 1.42, 15.76; P for trend = 0.007) was also associated with AN exposure. We provide additional evidence of an association between AN exposure and lung cancer, as well as possible increased risk for death due to bladder cancer and pneumonitis.

Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health 2019.
Modeling Variables With a Spike at Zero: Examples and Practical Recommendations. E. Lorenz, C. Jenkner, W. Sauerbrei, et al. 2017;185(8):650-660. PubMed · Publisher

Abstract

In most epidemiologic studies and in clinical research generally, there are variables with a spike at zero, namely variables for which a proportion of individuals have zero exposure (e.g., never smokers) and among those exposed the variable has a continuous distribution. Different options exist for modeling such variables, such as categorization where the nonexposed form the reference group, or ignoring the spike by including the variable in the regression model with or without some transformation or modeling procedures. It has been shown that such situations can be analyzed by adding a binary indicator (exposed/nonexposed) to the regression model, and a method based on fractional polynomials with which to estimate a suitable functional form for the positive portion of the spike-at-zero variable distribution has been developed. In this paper, we compare different approaches using data from 3 case-control studies carried out in Germany: the Mammary Carcinoma Risk Factor Investigation (MARIE), a breast cancer study conducted in 2002-2005 (Flesch-Janys et al., Int J Cancer. 2008;123(4):933-941); the Rhein-Neckar Larynx Study, a study of laryngeal cancer conducted in 1998-2000 (Dietz et al., Int J Cancer. 2004;108(6):907-911); and a lung cancer study conducted in 1988-1993 (Jöckel et al., Int J Epidemiol. 1998;27(4):549-560). Strengths and limitations of different procedures are demonstrated, and some recommendations for practical use are given.

© The Author 2017. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: [email protected].
Accounting for outcome misclassification in estimates of the effect of occupational asbestos exposure on lung cancer death. J.K. Edwards, S.R. Cole, H. Chu, et al. 2014;179(5):641-7. PubMed · Publisher · Free full text

Abstract

In studies of the health effects of asbestos, lung cancer death is subject to misclassification. We used modified maximum likelihood to explore the effects of outcome misclassification on the rate ratio of lung cancer death per 100 fiber-years per milliliter of cumulative asbestos exposure in a cohort study of textile workers in Charleston, South Carolina, followed from 1940 to 2001. The standard covariate-adjusted estimate of the rate ratio was 1.94 (95% confidence interval: 1.55, 2.44), and modified maximum likelihood produced similar results when we assumed that the specificity of outcome classification was 0.98. With sensitivity assumed to be 0.80 and specificity assumed to be 0.95, estimated rate ratios were further from the null and less precise (rate ratio = 2.17; 95% confidence interval: 1.59, 2.98). In the present context, standard estimates for the effect of asbestos on lung cancer death were similar to estimates accounting for the limited misclassification. However, sensitivity analysis using modified maximum likelihood was needed to verify the robustness of standard estimates, and this approach will provide unbiased estimates in settings with more misclassification.
Analysis of occupational asbestos exposure and lung cancer mortality using the g formula. S.R. Cole, D.B. Richardson, H. Chu, et al. 2013;177(9):989-96. PubMed · Publisher · Free full text

Abstract

We employed the parametric G formula to analyze lung cancer mortality in a cohort of textile manufacturing workers who were occupationally exposed to asbestos in South Carolina. A total of 3,002 adults with a median age of 24 years at enrollment (58% male, 81% Caucasian) were followed for 117,471 person-years between 1940 and 2001, and 195 lung cancer deaths were observed. Chrysotile asbestos exposure was measured in fiber-years per milliliter of air, and annual occupational exposures were estimated on the basis of detailed work histories. Sixteen percent of person-years involved exposure to asbestos, with a median exposure of 3.30 fiber-years/mL among those exposed. Lung cancer mortality by age 90 years under the observed asbestos exposure was 9.44%. In comparison with observed asbestos exposure, if the facility had operated under the current Occupational Safety and Health Administration asbestos exposure standard of <0.1 fibers/mL, we estimate that the cohort would have experienced 24% less lung cancer mortality by age 90 years (mortality ratio = 0.76, 95% confidence interval: 0.62, 0.94). A further reduction in asbestos exposure to a standard of <0.05 fibers/mL was estimated to have resulted in a minimal additional reduction in lung cancer mortality by age 90 years (mortality ratio = 0.75, 95% confidence interval: 0.61, 0.92).
Welding and lung cancer in Central and Eastern Europe and the United Kingdom. A. 't Mannetje, P. Brennan, D. Zaridze, et al. 2012;175(7):706-14. PubMed · Publisher

Abstract

Occupation as a welder has been associated with a 25%-40% increase in lung cancer risk. This study aims to elucidate to what extent confounding by smoking and asbestos drives this association and to evaluate the role of welding-related exposures such as chromium. The study included 2,197 male incident lung cancer cases and 2,295 controls from Romania, Hungary, Poland, Russia, Slovakia, the Czech Republic, and the United Kingdom from 1998 to 2001. Information on risk factors was collected through face-to-face interviews. Experts assessed exposure to 70 agents, and risk estimates were adjusted for smoking and occupational exposures. Occupation as a welder/flame cutter (prevalence controls: 3.7%) was associated with an odds ratio of 1.36 (95% confidence interval (CI): 1.00, 1.86) after adjustment for smoking and occupational exposures including asbestos. An odds ratio of 1.18 (95% CI: 1.01, 1.38) was found for welding fumes (prevalence controls: 22.8%), increasing to 1.38 for more than 25 exposure years (95% CI: 1.09, 1.75). A duration-response association was also observed for mild steel welding without chromium exposure. In this population, occupational exposure to welding fumes accounted for approximately 4% of lung cancer cases, to which both stainless and mild steel welding contributed equally. Given that welding remains a common task for many workers, exposure to welding fumes represents an important risk factor for lung cancer.
Hierarchical latency models for dose-time-response associations. D.B. Richardson, R.F. MacLehose, B. Langholz, et al. 2011;173(6):695-702. PubMed · Publisher · Free full text

Abstract

Exposure lagging and exposure-time window analysis are 2 widely used approaches to allow for induction and latency periods in analyses of exposure-disease associations. Exposure lagging implies a strong parametric assumption about the temporal evolution of the exposure-disease association. An exposure-time window analysis allows for a more flexible description of temporal variation in exposure effects but may result in unstable risk estimates that are sensitive to how windows are defined. The authors describe a hierarchical regression approach that combines time window analysis with a parametric latency model. They illustrate this approach using data from 2 occupational cohort studies: studies of lung cancer mortality among 1) asbestos textile workers and 2) uranium miners. For each cohort, an exposure-time window analysis was compared with a hierarchical regression analysis with shrinkage toward a simpler, second-stage parametric latency model. In each cohort analysis, there is substantial stability gained in time window-specific estimates of association by using a hierarchical regression approach. The proposed hierarchical regression model couples a time window analysis with a parametric latency model; this approach provides a way to stabilize risk estimates derived from a time window analysis and a way to reduce bias arising from misspecification of a parametric latency model.

© The Author 2011. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved.
Lagging exposure information in cumulative exposure-response analyses. D.B. Richardson, S.R. Cole, H. Chu, et al. 2011;174(12):1416-22. PubMed · Publisher · Free full text

Abstract

Lagging exposure information is often undertaken to allow for a latency period in cumulative exposure-disease analyses. The authors first consider bias and confidence interval coverage when using the standard approaches of fitting models under several lag assumptions and selecting the lag that maximizes either the effect estimate or model goodness of fit. Next, they consider bias that occurs when the assumption that the latency period is a fixed constant does not hold. Expressions were derived for bias due to misspecification of lag assumptions, and simulations were conducted. Finally, the authors describe a method for joint estimation of parameters describing an exposure-response association and the latency distribution. Analyses of associations between cumulative asbestos exposure and lung cancer mortality among textile workers illustrate this approach. Selecting the lag that maximizes the effect estimate may lead to bias away from the null; selecting the lag that maximizes model goodness of fit may lead to confidence intervals that are too narrow. These problems tend to increase as the within-person exposure variation diminishes. Lagging exposure assignment by a constant will lead to bias toward the null if the distribution of latency periods is not a fixed constant. Direct estimation of latency periods can minimize bias and improve confidence interval coverage.

2000s

A simple approach for fitting linear relative rate models in SAS. D.B. Richardson. 2008;168(11):1333-8. PubMed · Publisher

Abstract

The linear relative rate model has been employed in epidemiologic analyses of a variety of environmental and occupational exposures. In contrast to an exponential rate model, the linear relative rate model implies that the excess relative rate of disease changes in an additive fashion with exposure. The linear relative rate model may be fitted using EPICURE (HiroSoft International Corporation, Seattle, Washington), a specialized statistical software package widely used for such analyses. In this paper, the author presents a simple approach to fitting the linear relative rate model to epidemiologic data using PROC NLMIXED in the SAS statistical software package (SAS Institute Inc., Cary, North Carolina). This approach is illustrated via analyses of data from a study of mortality in a cohort of South Carolina asbestos textile workers (1940-2001).
Occupational exposure and laryngeal and hypopharyngeal cancer risk in central and eastern Europe. O. Shangina, P. Brennan, N. Szeszenia-Dabrowska, et al. 2006;164(4):367-75. PubMed · Publisher

Abstract

A multicenter case-control study was conducted during 1999-2002 in four European countries (Poland, Romania, Russia, and Slovakia) to evaluate the role of occupational exposures in risk of laryngeal/hypopharyngeal cancer. Male cancer cases (34 hypopharyngeal, 316 laryngeal) with full data on occupational history and nonoccupational factors were compared with 728 hospital controls for occupational exposure to 73 suspected carcinogens. Occupational history was evaluated by industrial hygienists blinded to case/control status. Elevated risks for ever exposure to coal dust were found for both hypopharyngeal (odds ratio (OR) = 4.19, 95% confidence interval (CI): 1.18, 14.89) and laryngeal (OR = 1.81, 95% CI: 0.94, 3.47) cancer, with clear dose-response patterns. Inclusion of a 20-year lag in the analysis strengthened these associations. Hypopharyngeal cancer risk was also significantly associated with exposure to mild steel dust (OR = 3.04, 95% CI: 1.39, 6.64) and iron compounds and fumes (OR = 2.74, 95% CI: 1.29, 5.84), without clear dose-response relations. Laryngeal cancer was significantly associated with exposure to hard-alloys dust (OR = 2.23, 95% CI: 1.08, 4.57) and chlorinated solvents (OR = 2.18, 95% CI: 1.03, 4.61), without dose-response relations. A possible link between high formaldehyde exposure and laryngeal cancer was suggested. No association was found for exposure to asbestos or inorganic acid mists. These data indicate that occupational exposure to coal dust may play a role in laryngeal and hypopharyngeal cancer. Other possible relations need further evaluation.
Vapor, dust, and smoke exposure in relation to adult-onset asthma and chronic respiratory symptoms: the Singapore Chinese Health Study. T.D. LeVan, W.P. Koh, H.P. Lee, et al. 2006;163(12):1118-28. PubMed · Publisher · Free full text

Abstract

Occupational factors contribute to a significant fraction of respiratory disease and symptoms. The authors evaluated the role of occupational exposures in asthma, chronic bronchitis, and respiratory symptoms in the Singapore Chinese Health Study, a population-based cohort of adults aged 45-74 years at enrollment in 1993-1998. Information on occupations and occupational exposures was collected at enrollment for 52,325 subjects for whom respiratory outcomes were obtained via follow-up interviews in 1999-2004. Exposure to dusts from cotton, wood, metal, minerals, and/or asbestos was associated with nonchronic cough and/or phlegm (odds ratio (OR) = 1.19, 95% confidence interval (CI): 1.08, 1.30), chronic bronchitis (OR = 1.26, 95% CI: 1.01, 1.57), and adult-onset asthma (OR = 1.14, 95% CI: 1.00, 1.30). Cotton dust was the major contributor to respiratory symptoms. Vapor exposure from chemical solvents, dyes, cooling oils, paints, wood preservatives, and/or pesticides was associated with nonchronic cough or phlegm (OR = 1.14, 95% CI: 1.03, 1.27), chronic dry cough (OR = 1.55, 95% CI: 1.19, 2.01), and adult-onset asthma (OR = 1.34, 95% CI: 1.15, 1.56). Chemical solvents, cooling oils, and pesticides were the major contributors to respiratory symptoms. These data support the role of occupational exposures in the etiology of respiratory illness in a population-based cohort in Singapore with a low prevalence of atopic illness.
Evidence for excess colorectal cancer incidence among asbestos-exposed men in the Beta-Carotene and Retinol Efficacy Trial. O.A. Aliyu, M.R. Cullen, M.J. Barnett, et al. 2005;162(9):868-78. PubMed · Publisher

Abstract

The relation between asbestos exposure and colorectal cancer remains controversial. The authors of this 1984-2004 US study examined the association among 3,897 occupationally exposed participants in the Beta-Carotene and Retinol Efficacy Trial (CARET) for chemoprevention of lung cancer, followed prospectively for 10-18 years. When a Cox stratified proportional hazards model was used, risks of colorectal cancer were elevated among male heavy smokers exposed to asbestos. Their relative risk was 1.36 (95% confidence interval: 0.96, 1.93) when compared with that for CARET heavy smokers not exposed to asbestos, after adjusting for age, smoking history, and intervention arm. The presence of asbestos-induced pleural plaques at baseline was associated with a relative risk of 1.54 (95% confidence interval: 0.99, 2.40); colorectal cancer risk also increased with worsening pulmonary asbestosis (p = 0.03 for trend). A dose-response trend based on years of asbestos exposure was less evident. Nonetheless, these data suggest that colorectal cancer risk is elevated among men occupationally exposed to asbestos, especially those with evidence of nonmalignant asbestos-associated radiographic changes.
Predictors of lung cancer among asbestos-exposed men in the {beta}-carotene and retinol efficacy trial. M.R. Cullen, M.J. Barnett, J.R. Balmes, et al. 2005;161(3):260-70. Randomized trial PubMed · Publisher

Abstract

Despite numerous published studies, debate continues regarding the risk of developing lung cancer among men exposed occupationally to asbestos, particularly those without radiographic or functional evidence of asbestosis. The beta-Carotene and Retinol Efficacy Trial (CARET), a study of vitamin supplementation for chemoprevention of lung cancer, has followed 4,060 heavily exposed US men for 9-17 years. Lung cancer incidence for 1989-2002 was analyzed using a stratified proportional hazards model. The study confirmed excessive rates of lung cancer among men with radiographic asbestosis. Comparison of study arms revealed a strong, unanticipated synergy between radiographic profusion category and the active intervention. In the large subgroup of men with normal lung parenchyma on chest radiograph at baseline, there was evidence of exposure-related lung cancer risk: Men with more than 40 years' exposure in high-risk trades had a risk approximately fivefold higher than men with 5-10 years, after adjustment for covariates. The effect in these men was independent of study intervention arm, but pleural plaques on the baseline radiograph and abnormal baseline flow rate were strong independent predictors of subsequent lung cancer. Residual confounding by subclinical asbestosis, exposure to unmeasured lung carcinogens, or differences in smoking are unlikely to explain these observations better than a carcinogenic effect of asbestos per se.
Lung cancer and internal lung doses among plutonium workers at the Rocky Flats Plant: a case-control study. S.C. Brown, M.F. Schonbeck, D. McClure, et al. 2004;160(2):163-72. PubMed · Publisher

Abstract

The authors conducted a nested case-control study of the association between lung cancer mortality and cumulative internal lung doses among a cohort of workers employed at the Rocky Flats Plant in Colorado from 1951 to 1989. Cases (n = 180) were individually matched with controls (n = 720) on age, sex, and birth year. Annual doses to the lung from plutonium, americium, and uranium isotopes were calculated for each worker with an internal dosimetry model. Lung cancer risk was elevated among workers with cumulative internal lung doses of more than 400 mSv in several different analytical models. The dose-response relation was not consistent at high doses. Restricting analysis to those employed for 15-25 years produced a statistically significant linear trend with dose (chi-square = 67.2, p < 0.001), suggesting a strong healthy worker survivor effect. The association between age at first internal lung dose and lung cancer mortality was statistically significant (odds ratio = 1.05, 95% confidence interval: 1.01, 1.10). No associations were found between lung cancer mortality and cumulative external penetrating radiation dose or cumulative exposures to asbestos, beryllium, hexavalent chromium, or nickel.
Mesothelioma trends in the United States: an update based on Surveillance, Epidemiology, and End Results Program data for 1973 through 2003. B. Price, A. Ware. 2004;159(2):107-12. PubMed · Publisher

Abstract

Using 1973-2000 mesothelioma incidence data released by the Surveillance, Epidemiology, and End Results Program in April 2003, the authors estimated the parameters of a birth-cohort and age model to determine whether previously reported patterns of mesothelioma in the United States have changed. Compared with analyses based on data through 1992, a slower decline was found in male cases immediately after a peak in 2000-2004, but no other notable changes in the time pattern were detected. Analysis confirmed that the annual number of male mesothelioma cases, which increased steeply from the 1970s through the mid-1990s, has leveled off in terms of both the age-adjusted rate and the absolute numbers of cases. After a peak of approximately 2,000 cases, a return to background levels is expected by 2055. The total projected number of male mesothelioma cases in 2003-2054 is approximately 71,000. The maximum lifetime risk for males, which occurs for the 1925-1929 birth cohort, is 1.8 x 10(-3). The age-adjusted rate for females is constant, as are the female lifetime mesothelioma risk across birth cohorts (3.6 x 10(-4)) and the annual risk (3.9 x 10(-6)). The time pattern of cases for females supports the existence of a threshold exposure for mesothelioma and a quantifiable background rate.
Re: "Mesothelioma trends in the United States: an update based on surveillance, epidemiology, and end results program data for 1973 through 2003". J.H. Lange. 2004;160(8):823. Comment · Letter · Review PubMed · Publisher

Summary

In this letter, the author responded to an article by Price and Ware on mesothelioma trends in the United States, based on Surveillance, Epidemiology, and End Results program data, which had suggested that simian virus 40 may contribute to some cases of mesothelioma. The author said that simian virus 40 is not the only agent other than asbestos that has been suggested to cause mesothelioma. Citing published literature, he listed other suggested agents in a table: metals, rubber, glass dust, pleural scars, sugar cane, dietary factors, man-made mineral fibers, lung infections, zeolite minerals and ionizing radiation. He noted that the share of mesothelioma cases not caused by asbestos had not been quantified exactly. He cited one study that reported 11 percent of the cases investigated had no exposure to asbestos. When probable, unclassified and nonoccupational asbestos exposures were included, this share might be around 20 percent, and some had suggested it could be larger. He also cited reports that the disease has a familial and spontaneous basis. He cited reports that nonasbestos cases differed from asbestos cases, with shorter survival, occurrence at a younger age and a different sex ratio. He concluded that there appear to be many potential causes of mesothelioma besides asbestos. An editor's note stated that Price and Ware were invited to respond but chose not to.

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Low-dose exposure to asbestos and lung cancer: dose-response relations and interaction with smoking in a population-based case-referent study in Stockholm, Sweden. P. Gustavsson, F. Nyberg, G. Pershagen, et al. 2002;155(11):1016-22. PubMed · Publisher

Abstract

This population-based case-referent study investigated the lung cancer risk associated with occupational exposure to asbestos, focusing on dose-response relations and the interaction with tobacco smoking. Incident cases of lung cancer among males aged 40-75 years in Stockholm County, Sweden, were identified from 1985 to 1990. Referents were selected randomly within strata (age, inclusion year) of the study base. Questionnaires administered to subjects or their next of kin gave information on occupations, tobacco smoking habits, and residences. Response rates of 87% and 85% resulted in 1,038 cases and 2,359 referents, respectively. Occupational exposures were assessed by an industrial hygienist. Lung cancer risk increased almost linearly with cumulative dose of asbestos. The risk at a cumulative dose of 4 fiber-years was 1.90 (95% confidence interval (CI): 1.32, 2.74), higher than that predicted by downward linear extrapolation from highly exposed occupational cohorts. The relative risk (exp(beta)) for a transformed dose variable ln(fiber-years + 1) was 1.494 (95% CI: 1.193, 1.871) per unit of exposure. The joint effect of asbestos and smoking was estimated to be 1.15 (95% CI: 0.77, 1.72) times that predicted from the sum of their individual effects and 0.31 (95% CI: 0.11, 0.86) times that predicted from their product, indicating a joint effect between additivity and multiplicativity.
Cancer mortality among workers exposed to amphibole-free chrysotile asbestos. E. Yano, Z.M. Wang, X.R. Wang, et al. 2001;154(6):538-43. PubMed · Publisher

Abstract

The issue of whether exposure to chrysotile asbestos alone, without contamination from amphibole asbestos, causes lung cancer and mesothelioma was investigated in a 25-year longitudinal study (1972-1996) in Chongqin, China. The study cohort comprised 515 male asbestos plant workers exposed to chrysotile only; the control cohort included 650 non-dust-exposed workers. The results of analysis in which the proportional hazards model was used indicated that mortality due to all causes, all cancers, and lung cancer was related to asbestos exposure; the relative risks, adjusted for age and smoking, were 2.9, 4.3, and 6.6, respectively. Fiber concentrations in the raw material section and the textile section of the plant were 7.6 and 4.5 fibers/ml, respectively. Because of differences between the study and control plants, the authors also compared various sections of the asbestos plant that had different levels of dust exposure. The adjusted relative risk of lung cancer was 8.1 for workers exposed to high versus low levels of asbestos. Two cases of malignant mesothelioma, one pleural and the other peritoneal, were found in the asbestos cohort. These results suggest that heavy exposure to pure chrysotile asbestos alone, with negligible amphibole contamination, can cause lung cancer and malignant mesothelioma in exposed workers.
Case-control study on lung cancer and residential radon in western Germany. L. Kreienbrock, M. Kreuzer, M. Gerken, et al. 2001;153(1):42-52. PubMed · Publisher

Abstract

In a 1990-1996 case-control study in western Germany, the authors investigated lung cancer risk due to exposure to residential radon. Confirmed lung cancer cases from hospitals and a random sample of community controls were interviewed by trained interviewers regarding different risk factors. For 1 year, alpha track detectors were placed in dwellings to measure radon gas concentrations. The evaluation included 1,449 cases and 2,297 controls recruited from the entire study area and a subsample of 365 cases and 595 controls from radon-prone areas of the basic study region. Rate ratios were estimated by using conditional logistic regression adjusted for smoking and for asbestos exposure. In the entire study area, no rate ratios different from 1.0 were found; in the radon-prone areas, the adjusted rate ratios for exposure in the present dwelling were 1.59 (95% confidence interval (CI): 1.08, 2.27), 1.93 (95% CI: 1.19, 3.13), and 1.93 (95% CI: 0.99, 3.77) for 50-80, 80-140, and >140 Bq/m3, respectively, compared with 0-50 Bq/m3. The excess rate ratio for an increase of 100 Bq/m3 was 0.13 (-0.12 to 0.46). An analysis based on cumulative exposure produced similar results. The results provide additional evidence that residential radon is a risk factor for lung cancer, although a risk was detected in radon-prone areas only, not in the entire study area.
Relation of occupational exposure to respiratory symptoms and asthma in a general population sample: self-reported versus interview-based exposure data. P.S. Bakke, R. Hanoa, A. Gulsvik. 2001;154(5):477-83. PubMed · Publisher

Abstract

The objective of this study was to examine how the consistency of self-reported exposure to dust or gas, asbestos, and quartz varied between subjects with and those without respiratory symptoms and asthma in a Norwegian community sample () in 1987-1988. Exposure characterization obtained in a structured work history interview was used as the "gold standard." The authors also wanted to assess how the exposure-disease relation differed when the exposure was based on self-reported versus interview-obtained data. The prevalence of self-reported exposure to dust or gas, asbestos, and quartz was 28%, 5%, and 4%, respectively. The sensitivity of the self-reported exposure data varied from 21% to 64% and was higher in those with than in those without the respiratory disorders. The specificity varied from 78% to 100% and was lower in those with than in those without the respiratory disorders. The sex-, age-, and smoking-adjusted odds ratios of the respiratory disorders in those with exposure to dust or gas and to asbestos were only slightly reduced when misclassification was taken into account. The corresponding numbers for exposure to quartz were halved and lost their statistical significance when the misclassification was allowed for. In this general population sample, the self-reported occupational, airborne exposure data were differentially misclassified by disease status.
Environmental exposure to tremolite and respiratory cancer in New Caledonia: a case-control study. D. Luce, I. Bugel, P. Goldberg, et al. 2000;151(3):259-65. PubMed · Publisher

Abstract

A case-control study on respiratory cancers was conducted in New Caledonia (South Pacific), where a high incidence of malignant pleural mesothelioma had been observed. The disease pattern suggested an environmental exposure to asbestos. The first results showed that, in some areas, tremolite asbestos derived from local outcroppings was used as whitewash (locally named "pö"). All cases diagnosed between 1993 and 1995 (including 15 pleural mesotheliomas, 228 lung cancers, and 23 laryngeal cancers) and 305 controls were included in the study. Detailed information on past or present use of the whitewash, residential history, smoking, diet, and occupation was collected. The risk of mesothelioma was strongly associated with the use of the whitewash (odds ratio (OR) = 40.9; 95% confidence interval (CI): 5.15, 325). All Melanesian cases had been exposed. Among Melanesian women, exposure to the whitewash was associated with an increased risk of lung cancer (OR = 4.89; 95% CI: 1.13, 21.2), and smokers exposed to po had an approximately ninefold risk (OR = 9.26; 95% CI: 1.72, 49.7) compared with women who never smoked and had never used the whitewash. In contrast, no association was noted between exposure to pö and lung cancer risk among Melanesian men, probably because of lower exposure levels. Among non-Melanesians, the numbers of exposed subjects were too small to assess the effect of exposure to po. There was no indication of elevated risks for the other cancer sites.
Exposure to nitrosamines, carbon black, asbestos, and talc and mortality from stomach, lung, and laryngeal cancer in a cohort of rubber workers. K. Straif, U. Keil, D. Taeger, et al. 2000;152(4):297-306. PubMed · Publisher

Abstract

There is sufficient evidence for an excess occurrence of stomach and lung cancer among rubber workers. However, evidence for causal associations with specific exposures is still limited. A cohort of 8,933 male German rubber workers was followed for mortality from January 1, 1981 through December 31, 1991. Work histories were reconstructed using routinely documented cost center codes. For each cost center code, calendar time-and plant-specific levels of exposure to nitrosamines, asbestos, talc (low, medium (m), and high (h)), and carbon black (two levels) were estimated by industrial hygienists. Rate ratios (RR) and 95% confidence intervals (CI) were calculated using Cox proportional hazards models, with the lowest exposure level used as the reference category. Exposure was lagged 10 years to account for latency. Exposure-response relations between exposure to asbestos and lung cancer mortality (RRm = 1.3, 95% CI: 0.9, 1.9; RRh = 2.0, 95% CI: 0.9, 4.1) and between exposure to dust (talc and asbestos combined) and stomach cancer mortality (RRm = 1.8, 95% CI: 0.9, 3.8; RRh = 2.7, 95% CI: 1.0, 7.1) were observed. Exposure to nitrosamines was not associated with mortality from stomach or lung cancer. These results suggest that the increased mortality from lung and stomach cancer among rubber workers is associated with exposure to asbestos and dust, respectively.
Occupational exposure and lung cancer risk: a population-based case-referent study in Sweden. P. Gustavsson, R. Jakobsson, F. Nyberg, et al. 2000;152(1):32-40. PubMed · Publisher

Abstract

This case-referent study investigated the lung cancer risk from occupational exposure to diesel exhaust, mixed motor exhaust, other combustion products, asbestos, metals, oil mist, and welding fumes. All cases of lung cancer in males aged 40-75 years among stable residents of Stockholm County, Sweden, were identified from 1985 to 1990. Referents were selected as a stratified (age, inclusion year) random sample. Information on lifetime occupational history, residency, and tobacco smoking was obtained from the study subjects or from next of kin. Response rates of 87% and 85% resulted in 1,042 cases and 2,364 referents, respectively. Occupational exposures were assessed by an occupational hygienist who coded the intensity and probability of each exposure. Risk estimates were adjusted for tobacco smoking, other occupational exposures, residential radon, and environmental exposure to traffic-related air pollution. For the highest quartile of cumulative exposure versus no exposure, the relative risk was 1.63 (95% confidence interval (CI): 1.14, 2.33) for diesel exhaust, 1.60 (95% CI: 1.09, 2.34) for combustion products, and 1.68 (95% CI: 1.15, 2.46) for asbestos. Dose-response analyses indicated an increase in lung cancer risk of 14% per fiber-year/ml for asbestos exposure. No increased risk was found for the other exposure factors. An overall attributable proportion of 9.5% (95% CI: 5.5, 13.9) was estimated for lung cancer related to diesel exhaust, other combustion products, and asbestos.
Occupational lung cancer risk for men in Germany: results from a pooled case-control study. I. Brüske-Hohlfeld, M. Möhner, H. Pohlabeln, et al. 2000;151(4):384-95. PubMed · Publisher

Abstract

Occupational exposures such as crystalline silica, diesel engine exhaust, polycyclic aromatic hydrocarbons, and man-made mineral fibers are strongly suspected to increase lung cancer risk. Two case-control studies in Germany conducted between 1988 and 1996 were pooled for a joint analysis. A total of 3,498 male cases and 3,541 male population controls, frequency matched for age and region, were included in the study. The lifelong history of all jobs and industries was coded and occupational exposures were evaluated by expert rating. Odds ratios, crude and adjusted for smoking and asbestos exposure, were calculated by conditional logistic regression. Job-related evaluation showed a statistically significant increased odds ratio adjusted for smoking among farmers; forestry workers, fishermen, and livestock workers; miners and quarrymen; chemical processors; cabinet makers and related wood workers; metal producers and processors; bricklayers and carpenters; road construction workers, pipelayers and well diggers; plasterers, insulators, and upholsterers; painters and lacquerers; stationary engine and heavy equipment operators; transport workers and freight handlers; and service workers. With regard to specific occupational exposures, elevated odds ratios (OR) (95% confidence intervals (CI)) for lung cancer risk adjusted for smoking and asbestos exposure were observed for man-made mineral fibers (OR = 1.48, 95% CI 1.17, 1.88); crystalline silica (OR = 1.41, 95% CI 1.22, 1.62); diesel engine exhaust (OR = 1.43, 95% CI 1.23, 1.67); and polycyclic aromatic hydrocarbons (OR = 1.53, 95% CI 1.14, 2.04). The risk of asbestos exposure, adjusted for smoking was also increased (OR = 1.41, 95% CI 1.24, 1.60).

1990s

Invited commentary: Is it possible to investigate the quantitative relation between asbestos and mesothelioma in a community-based study?. J. Siemiatycki, P. Boffetta. 1998;148(2):143-7. Comment PubMed · Publisher
Summary

This invited commentary discussed whether a community-based study can measure the quantitative relation between asbestos exposure and mesothelioma. It responded to a study by Iwatsubo et al. in the same journal issue, a community-based case-control study in selected areas of France. In that study, a panel of industrial hygiene experts assessed asbestos exposure from interview-based job descriptions. The study reported elevated mesothelioma risk at very low cumulative exposure (fourfold risk at 0.5 fiber/ml-years).

The authors described three problems that they considered specific to asbestos and mesothelioma:
- **Diagnostic bias:** Physicians who knew of a patient's asbestos work history may have been more likely to diagnose mesothelioma.
- **Information bias:** Cases may recall asbestos exposure more readily than controls. They cited a study by Spirtas et al. in which the relative risk among men was 27 when based on next-of-kin reports, compared with 11 when based on an occupation list.
- **Exposure assessment bias:** Experts may have underestimated the higher exposure levels before 1970, which would inflate the estimated risk per unit dose.
The authors stated that all three biases would exaggerate risk per unit dose, while nondifferential random exposure error would act in the opposite direction. They also raised selection bias and possible differences in potency between amphibole and chrysotile fibers.

They concluded that the association between asbestos and mesothelioma is incontrovertible. They called the French study a valiant effort that deserves replication under conditions that reduce these problems, and they considered direct data from low- or intermediate-exposure populations important.

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Mortality from amyotrophic lateral sclerosis, other chronic disorders, and electric shocks among utility workers. C. Johansen, J.H. Olsen. 1998;148(4):362-8. PubMed · Publisher

Abstract

Above-average exposure to electromagnetic fields has been associated with certain nonmalignant medical conditions such as amyotrophic lateral sclerosis, other neurologic diseases, depressive symptoms, and suicide. The authors conducted a nationwide mortality study in Denmark of 21,236 men employed in utility companies between 1900 and 1993. The causes of death were ascertained for January 1, 1974, through December 31, 1993, and cause-specific mortality was analyzed by latency and estimated levels of exposure to 50-Hz electromagnetic fields. Overall, 3,540 deaths were observed as compared with 3,709 expected from national mortality rates, yielding a standardized mortality ratio of 0.96 (95% confidence interval 0.93-0.99). A slight excess in mortality from cancer was due to deaths from cancers of the lung and pleural cavity, probably because of exposure to asbestos. A twofold increase in mortality from amyotrophic lateral sclerosis and a tenfold increase in mortality from electrical accidents were seen on the basis of 14 and 10 deaths, respectively, the former increasing with time since first employment in a utility company. The excess mortality from amyotrophic lateral sclerosis seems to be associated with above-average levels of exposure to electromagnetic fields and may be due to repeated episodes with electric shocks.
Pleural mesothelioma: dose-response relation at low levels of asbestos exposure in a French population-based case-control study. Y. Iwatsubo, J.C. Pairon, C. Boutin, et al. 1998;148(2):133-42. PubMed · Publisher

Abstract

A hospital-based case-control study of the association between past occupational exposure to asbestos and pleural mesothelioma was carried out in five regions of France. Between 1987 and 1993, 405 cases and 387 controls were interviewed. The job histories of these subjects were evaluated by a group of experts for exposure to asbestos fibers according to probability, intensity, and frequency. A cumulative exposure index was calculated as the product of these three parameters and the duration of the exposed job, summed over the entire working life. Among men, the odds ratio increased with the probability of exposure and was 1.2 (95% confidence interval (CI) 0.8-1.9) for possible exposure and 3.6 (95% CI 2.4-5.3) for definite exposure. A dose-response relation was observed with the cumulative exposure index: The odds ratio increased from 1.2 (95% CI 0.8-1.8) for the lowest exposure category to 8.7 (95% CI 4.1-18.5) for the highest. Among women, the odds ratio for possible or definite exposure was 18.8 (95% CI 4.1-86.2). We found a clear dose-response relation between cumulative asbestos exposure and pleural mesothelioma in a population-based case-control study with retrospective assessment of exposure. A significant excess of mesothelioma was observed for levels of cumulative exposure that were probably far below the limits adopted in most industrial countries during the 1980s.
Re: "Dose-response associations of silica with nonmalignant respiratory disease and lung cancer mortality in the diatomaceous earth industry". M.J. Mirliss. 1998;148(3):307-9. Comment · Letter PubMed · Publisher
Re: "Dose-response associations of silica with nonmalignant respiratory disease and lung cancer mortality in the diatomaceous earth industry". G.W. Gibbs. 1998;148(3):307; author reply 308-9. Comment · Letter PubMed · Publisher

Summary

In this letter, the author commented on an updated mortality study of diatomaceous earth workers by Checkoway et al. (Am J Epidemiol 1997). He argued that misclassification of asbestos exposure and asbestos-silica interactions may have influenced its results and interpretation. An earlier reanalysis had excluded workers employed before 1930, because asbestos was definitely used in the facility then but specific jobs and exposure levels could not be identified. The update included these workers and extrapolated 1930 job-specific estimates to earlier years. The author stated that no asbestos was used in the facility in 1930 and that asbestos exposure was assigned only to maintenance workers. As a result, pre-1930 production workers were treated as nonexposed, although some may have had high asbestos exposure, which carries its own lung cancer risk. He noted that the only non-asbestos-exposed group with a rate ratio above 1.00 was the highest silica category (13 deaths, rate ratio 2.03). He asked how much of this excess was due to the five lung cancer deaths among pre-1930 hires. Citing the reanalysis, he reported standardized mortality ratios from 1.34 in non-asbestos-exposed silica workers to 4.4 (CI 1.20-11.3) with more than 6.8 fibers/ml-years of asbestos, and 8.32 (CI 1.71-24.3) for the highest asbestos and silica category. He concluded that the update's asbestos categories (>0-1.2 and >1.2 fibers/ml-years) may have diluted effects at higher asbestos levels and influenced the conclusion of no asbestos effect.

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Risk of cancer among Danish utility workers--a nationwide cohort study. C. Johansen, J.H. Olsen. 1998;147(6):548-55. PubMed · Publisher

Abstract

The authors report the incidence of cancer in a large cohort of employees identified from all 99 Danish utility companies. Personal data and information on employment and exposure to magnetic fields and asbestos were obtained from manual files at the companies, the Danish Supplementary Pension Fund, and the public payroll administration. A total of 32,006 individuals with more than 3 months of employment were linked with the files of the Danish Cancer Registry. The period of follow-up for cancer occurrence among the employees was from April 1968 through December 1993 in the study conducted from 1994 to 1997. Overall, 3,008 cancers were observed, with 2,825 expected, yielding a small but significantly increased risk of 1.06 (95% confidence interval 1.03-1.10) among the utility workers in comparison with the general population. No excess was observed for all leukemias or for cancers of the brain or breast among men or women. There was no association of electromagnetic field exposure with risk of these cancers, even when the level and length of exposure to magnetic fields were taken into account. Increased risks for cancers of the lung and pleural cavity were seen mainly for workers whose jobs involved exposure to asbestos. The results from this study do not support the hypothesis of an association between occupational exposures to magnetic fields in the electric utility industry and the risk for cancer.
Analysis of current trends in United States mesothelioma incidence. B. Price. 1997;145(3):211-8. PubMed · Publisher

Abstract

Mesothelioma incidence often is interpreted as an index of past exposure to airborne asbestos. The mesothelioma rate for US males exhibits an increasing trend throughout the 1970s and early 1980s. The trend has been attributed to occupational exposure in the shipbuilding industry during World War II, in manufacturing, and in building construction. Incidence data (1973-1992) from the Surveillance, Epidemiology, and End Results Program were used to investigate current trends in age-adjusted and age-specific mesothelioma rates. An age and birth-cohort model was used to project both lifetime probabilities of mesothelioma by cohort and the annual number of cases expected over the next 70 years. The current trend in female rates is flat (age-adjusted rate = 0.30 per 100,000). The estimated lifetime risk for females is 2.5 x 10(-4), independent of birth cohort. The projected average annual number of female cases is 500. For males, the age-adjusted mesothelioma rate is increasing solely due to the age group 75 years and over, albeit at a declining growth rate. Lifetime risk for males peaks at 2 x 10(-3) for the 1925-1929 birth cohort, then decreases to 5 x 10(-4) for the 1955-1959 birth cohort. The pattern of rates reflected in the age and birth-cohort model suggests a peak in the annual number of mesothelioma cases for males at 2,300 before the year 2000. The number of male cases then will drop during the next 50-60 years toward 500. These trends mirror the US trend in raw asbestos consumption and a reduction in workplace airborne asbestos levels.
Cohort mortality study of pulp and paper mill workers in British Columbia, Canada. P.R. Band, N.D. Le, R. Fang, et al. 1997;146(2):186-94. PubMed · Publisher

Abstract

The authors studied a cohort of 30,157 male pulp and paper workers in British Columbia, Canada. Of these, 20,373 worked in kraft mills only, 5,249 in sulfite mills only, and 4,535 in both kraft and sulfite mills. All workers with at least 1 year of employment on January 1, 1950, or thereafter until December 31, 1992, were studied. Standardized mortality ratios (SMRs) were used to compare the mortality rates of the cohort with those of the Canadian male population. Ninety percent confidence intervals (CIs) for the SMRs were obtained. Cancer risks significantly associated with work duration and time from first employment of 15 years or more were observed: 1) total cohort: pleura (SMR = 3.61, 90% CI 1.42-7.58); kidney (SMR = 1.69, 90% CI 1.13-2.43); brain (SMR = 1.51, 90% CI 1.03-2.16); 2) workers in kraft mills only: kidney (SMR = 1.92, 90% CI 1.04-3.26); 3) workers in sulfite mills only: Hodgkin's disease (SMR = 4.79, 90% CI 1.29-12.37); 4) workers ever employed in both kraft and sulfite mills: esophagus (SMR = 1.91, 90% CI 1.00-3.33). These malignancies have been associated with the following known or suspected carcinogens to which pulp and paper workers may have been exposed: asbestos (pleura), biocides (kidney), formaldehyde (kidney, brain, Hodgkin's disease), hypochlorite (esophagus). A nested case-control study with detailed exposure assessment is under way to help determine whether excess risks for specific cancers reflect exposure among subsets of workers.
Dose-response associations of silica with nonmalignant respiratory disease and lung cancer mortality in the diatomaceous earth industry. H. Checkoway, N.J. Heyer, N.S. Seixas, et al. 1997;145(8):680-8. PubMed · Publisher

Abstract

The potential carcinogenicity of crystalline silica to humans remains a controversial issue. The authors conducted an historical cohort mortality study of 2,342 male workers exposed to crystalline silica, predominantly cristobalite, in a diatomaceous earth mining and processing facility in California. During the years 1942-1994, mortality excesses were detected for nonmalignant respiratory diseases (NMRD) (standardized mortality ratio = 2.01, 95% confidence interval (CI) 1.56-2.55) and lung cancer (standardized mortality ratio = 1.29, 95% CI 1.01-1.61). NMRD mortality rose sharply with cumulative exposure to respirable crystalline silica; allowing for a 15-year latency, the rate ratio for the highest exposure stratum (> or = 5.0 mg/m3-years) was 5.35 (95% CI 2.23-12.8). The rate ratio for lung cancer reached 2.15 (95% CI 1.08-4.28) in the highest exposure category. These associations were unlikely to have been confounded by smoking or asbestos exposure. The findings indicate a strong dose-response relation for crystalline silica and NMRD mortality. The lung cancer results, although less convincing, add further support to an etiologic role for crystalline silica.
Silicosis among foundry workers. Implication for the need to revise the OSHA standard. K.D. Rosenman, M.J. Reilly, C. Rice, et al. 1996;144(9):890-900. PubMed · Publisher

Abstract

To evaluate the risk of pneumoconiosis among workers in a Midwestern automotive foundry, medical records and silica sand exposure data were analyzed for 1,072 current and retired employees with at least 5 years of employment as of June 1991. Approximately half of these employees had worked at the foundry for 20 or more years. Sixty workers were found to have radiographic evidence of pneumoconiosis. Twenty-eight workers had radiographs consistent with silicosis, of which 25 were consistent with simple silicosis and three with progressive massive fibrosis. The prevalence of radiographic changes consistent with silicosis increased with: number of years worked at the foundry (6% for 20-29 years and 12% for 30 or more years); cigarette smoking (12.2% among smokers with high silica exposure vs. 4.4% among never smokers with high silica exposure); work area within the foundry (cleaning room, core room, mold area, core knockout); and quantitative silica exposure (0.3-2.7% of workers at the current Occupational Safety and Health Administration (OSHA) standard and 4.9-9.9% of workers above the OSHA standard). In addition, the odds of developing radiographic changes consistent with silicosis were increased for African Americans (odds ratio = 2.14, 95% confidence interval 0.85-5.60) in comparison with whites. (The risk was similar when silica exposure was equal, but African-American workers on average had greater exposure to silica, despite having a similar duration of work as white workers.) Another eight workers had radiographic evidence of asbestosis, and 24 had pleural plaques. These asbestos-related changes were not associated with increasing exposure to silica but rather were associated with being in the maintenance department and performing repair work. After controlling for cigarette smoking, race, and exposure to silica at another job besides the foundry, the authors found a 1.45 increased risk of developing a radiograph consistent with silicosis after 20 years of work at the current OSHA standard, and a 2.10 increased risk after 40 years of work at the current OSHA standard. On the basis of these findings, the authors recommend maintaining silica air levels no higher than the exposure level of 0.05 mg/m3 recommended by the National Institute for Occupational Safety and Health.
A meta-analysis of colorectal cancer and asbestos exposure. D.M. Homa, D.H. Garabrant, B.W. Gillespie. 1994;139(12):1210-22. Meta-analysis PubMed · Publisher

Abstract

A meta-analysis of the relation between asbestos exposure and colorectal cancer mortality was conducted, using published reports of 20 asbestos-exposed cohorts. Summary standardized mortality ratios (SMRs) for colorectal cancer were examined in relation to asbestos type and estimates of dust exposure (as direct estimators of asbestos exposure) and in relation to lung cancer SMR and the proportion of all deaths due to mesothelioma (as proxy estimators of asbestos exposure). An elevated summary SMR was observed in cohorts exposed to amphibole asbestos (summary SMR = 1.47; 95% confidence interval (CI) 1.09-2.00), but not in cohorts exposed to serpentine asbestos (summary SMR = 1.04; 95% CI 0.81-1.33) or in cohorts exposed to both serpentine and amphibole asbestos (summary SMR = 1.03; 95% CI 0.74-1.42). Cohorts having a lung cancer SMR greater than 2.00 had a summary SMR of 1.51 (95% CI 1.29-1.76), and cohorts in which more than 1% of all deaths were attributed to mesothelioma had a summary SMR of 1.24 (95% CI 0.94-1.64). After stratifying the cohorts based on mortality due to all cancers excluding those known or suspected to be associated with asbestos exposure, lung cancer mortality was not clearly associated with colorectal cancer mortality, suggesting that the crude association between these factors may be due to misdiagnosis of lung cancer as other types of cancer in the reported causes of death. These results suggest that exposure to amphibole asbestos may be associated with colorectal cancer, but these findings may reflect an artifact of miscertification of cause of death. The results also suggest that serpentine asbestos is not associated with colorectal cancer.
Attributable risk: advantages of a broad definition of exposure. S. Wacholder, J. Benichou, E.F. Heineman, et al. 1994;140(4):303-9. PubMed · Publisher

Abstract

Classification of exposure into two levels--one consisting exclusively of unexposed individuals and the other consisting of exposed and perhaps unexposed ones--yields an unbiased estimate of attributable risk when misclassification is nondifferential. The authors advocate, therefore, the use of a broad definition of exposure when estimating attributable risk. Based on this idea, they justify a simple and robust method for estimating the overall attributable risk from several exposures that is based on a division of subjects into two groups, a baseline consisting of those unexposed to all exposures and everyone else.
Incidence of cancer among lighthouse keepers exposed to asbestos in drinking water. A. Andersen, E. Glattre, B.V. Johansen. 1993;138(9):682-7. PubMed · Publisher

Abstract

The study population comprises 690 Norwegian male lighthouse keepers whose water supply came from cisterns that received rain water off asbestos-cement-tiled roofs. The asbestos-cement tiles were installed in the late 1950s, and two decades later the fiber content in the tap water was analyzed. The fiber content ranged from 1,760 to 71,350 million fibers per liter, which is significantly higher than measured in any other Norwegian public water supply. During the follow-up period, 1960-1991, no statistically significant excess risk was found for any type of cancer in the group with a latency period of 20 years or more, except for stomach cancer (11 observed cases vs. 4.57 expected, standardized incidence ratio = 241, 95% confidence interval 120-431). No cases of malignant mesothelioma were found. The study is limited by lack of knowledge as to when the tiles began to deteriorate and, thus, the magnitude of total exposure as well as by the inability to control for such potential confounding factors as diet.
Asbestos and colon cancer: lack of association in a large case-control study. D.H. Garabrant, R.K. Peters, D.M. Homa. 1992;135(8):843-53. PubMed · Publisher

Abstract

Previous studies linking exposure to asbestos with human colon cancer have used mortality rather than incidence as their endpoint and have neither assessed nor controlled for confounding by diet, genetic factors, or other risk factors for colon cancer. A case-control study of 746 histologically confirmed cases of colon cancer and 746 matched neighborhood controls was conducted in Los Angeles County, California. In univariate analyses of the 419 male pairs, a weak association was found between asbestos exposure and colon cancer (odds ratio (OR) = 1.16, 95% confidence interval (CI) 0.80-1.69). When confounding by family history of large bowel cancer, diet, body weight, and physical activity was controlled, there was no association between colon cancer and exposure to asbestos among males (OR = 0.99, 95% CI 0.66-1.50). When asbestos exposure was restricted to occurrences preceding diagnosis by more than 15 years, there was no clear association between such exposure and colon cancer, either before (OR = 1.14, 95% CI 0.76-1.70) or after confounding was controlled (OR = 0.93, 95% CI 0.60-1.44). Further analyses by frequency and duration of exposure failed to show any association between asbestos and risk of colon cancer, but did show a consistent pattern of confounding by nonoccupational factors that, when controlled, invariably produced a weak protective effect of asbestos exposure. Among the 327 female pairs, only 6 cases and 11 controls reported asbestos exposure (OR = 0.55, 95% CI 0.20-1.48), and there was no evidence of risk increasing as the frequency or duration of exposure increased. This study suggests not only that occupational exposure to asbestos is not a risk factor for colon cancer in the general population of Los Angeles, but also that observed associations between asbestos and colon cancer should not be interpreted as causal unless confounding by nonoccupational factors has been evaluated and controlled.
Diet and other risk factors for laryngeal cancer in Shanghai, China. W. Zheng, W.J. Blot, X.O. Shu, et al. 1992;136(2):178-91. PubMed · Publisher

Abstract

A population-based, case-control study of laryngeal cancer was conducted in Shanghai, China, during 1988-1990, in which 201 incident cases (177 males, 24 females) and 414 controls (269 males, 145 females) were interviewed. Cigarette smoking was the major risk factor, accounting for 86% of the male and 54% of the female cases. After adjusting for smoking, there was little increase in risk associated with drinking alcoholic beverages. Among men, cases more often reported occupational exposures to asbestos and coal dust. A protective effect was associated with the intake of fruits (particularly oranges and tangerines), certain dark green/yellow vegetables, and garlic, but there was an increased risk with the intake of salt-preserved meat and fish. The findings suggest that risk factors for laryngeal cancer in Shanghai resemble those in Western countries, and they provide further evidence that dietary factors play an important etiologic role.
Performance of two general job-exposure matrices in a study of lung cancer morbidity in the Zutphen cohort. H. Kromhout, D. Heederik, L.M. Dalderup, et al. 1992;136(6):698-711. PubMed · Publisher

Abstract

Data from a general population cohort of 878 men from the town of Zutphen, The Netherlands, were used to evaluate the performance of two general job-exposure matrices. Exposures generated by the job-exposure matrices on the basis of job histories were compared. The validity of those exposures was measured against exposures reported by the participants in 1977/1978. The performance of the different exposure measures was assessed in proportional hazards analyses of lung cancer morbidity incidence. The two general job-exposure matrices generally disagreed with regard to exposure classification because of differences in exposure assessment and level of detail of the job axis. When compared with self-reported exposures, the sensitivity of both job-exposure matrices was low (on average, below 0.51), while the specificity was generally high (on average, above 0.90). Self-reported exposures to asbestos, pesticides, and welding fumes showed elevated risk ratios for lung cancer which were absent for exposures generated by the two job-exposure matrices. Thus, a population-specific job-exposure matrix is proposed as an alternative to general job-exposure matrices developed elsewhere. Such a matrix can be constructed from the results of in-depth interviews of a job-stratified sample of cohort members. Sound validation and documentation of exposure assessment methods used in job-exposure matrices are recommended.
Proxy respondents and the validity of occupational and other exposure data. The Selected Cancers Cooperative Study Group. C.A. Boyle, E.A. Brann. 1992;136(6):712-21. PubMed · Publisher

Abstract

As part of a multicenter cancer case-control study conducted in 1984-1988, a proxy interview was attempted for all cases who were initially interviewed for the study but who died during the 4-year data collection period. To assess the validity of using wives, other relatives, or other informants to obtain information about a subject, the authors compared occupational and other exposure data obtained from 270 male cancer cases and their proxy respondents. The primary focus of the case-control study was on Vietnam military service and exposure to phenoxy herbicides, but cases and their proxy respondents were also asked about occupational and other exposures relevant to the cancers. The accuracy of reporting for specific occupational exposures (e.g., asbestos and formaldehyde) and specific occupations (e.g., dry cleaning and meat packing or processing) was poor, although the latter improved somewhat when only case-spouse pairs were examined. Similarly, there was poor sensitivity in the reporting of herbicide exposure information in farming and other related occupations. In contrast, the reporting of certain demographic characteristics, childhood history characteristics, and use of alcohol and cigarettes was relatively good, and was even better when only case-spouse pairs were examined. The poor quality of proxy information for detailed exposure information suggests the need for careful use and interpretation of proxy information in epidemiologic studies.
Lung cancer in mild steel welders. K. Steenland, J. Beaumont, L. Elliot. 1991;133(3):220-9. PubMed · Publisher

Abstract

To investigate lung cancer risk, the authors conducted a historical cohort mortality study of 4,459 mild steel welders who had been employed at three midwestern plants which manufactured heavy equipment. Follow-up began in the mid-1950s and extended through 1988. All welders had at least 2 years welding experience (average duration, 8.5 years). This cohort had no occupational exposure to asbestos or stainless steel fumes (containing nickel and chromium), two potential confounders in previous welders studies. A comparison population of 4,286 nonwelders, all with at least 2 years employment at the same plants, was also studied. Nonwelders had never been welders and were allowed to have no more than 90 days employment as a painter, foundryman, or machinist. Sampling data collected from 1974-1987 indicated that welders were exposed to 6-7 mg/m3 of total particulate and 3-4 mg/m3 of iron oxide, while nonwelders had negligible exposures to welding fumes. When compared with the United States population, both welders and nonwelders had elevated rates for lung cancer (standardized mortality ratios (SMRs): welders, SMR = 1.07; nonwelders, SMR = 1.17), but neither SMR was significantly elevated. Limited smoking data based on a 1985 survey indicated that both welders and nonwelders smoked more than the United States population, possibly accounting for part of their elevated lung cancer rates. There was no trend of increased risk for welders with increased duration of exposure. The only other cause of death significantly elevated was emphysema among welders. Nonmalignant respiratory disease was not elevated for welders (SMR = 0.96). When welders were compared with nonwelders directly for lung cancer, the rate ratio was 0.90.

1980s

Ordinal regression models for epidemiologic data. B.G. Armstrong, M. Sloan. 1989;129(1):191-204. PubMed · Publisher

Abstract

Health status is often measured in epidemiologic studies on an ordinal scale, but data of this type are generally reduced for analysis to a single dichotomy. Several statistical models have been developed to make full use of information in ordinal response data, but have not been much used in analyzing epidemiologic studies. The authors discuss two of these statistical models--the cumulative odds model and the continuation ratio model. They may be interpreted in terms of odds ratios, can account for confounding variables, have clear and testable assumptions, and have parameters that may be estimated and hypotheses that may be tested using available statistical packages. However, calculations of asymptotic relative efficiency and results of simulations showed that simple logistic regression applied to dichotomized responses can in some realistic situations have more than 75% of the efficiency of ordinal regression models, but only if the ordinal scale is collapsed into a dichotomy close to the optimal point. The application of the proposed models to data from a study of chest x-rays of workers exposed to mineral fibers confirmed that they are easy to use and interpret, but gave results quite similar to those obtained using simple logistic regression after dichotomizing outcome in the conventional way.
Re: "US prevalence of occupational pleural thickening: a look at chest x-rays from the first National Health and Nutrition Examination Survey". W.C. Cooper. 1989;129(1):229-30. Letter PubMed · Publisher
A mortality study of a research, engineering, and metal fabrication facility in western New York State. M.J. Teta, M.G. Ott. 1988;127(3):540-51. PubMed · Publisher

Abstract

The mortality experience of 8,146 male employees of a research, engineering, and metal fabrication facility in Tonawanda, New York state was examined from 1946 to 1981. Potential workplace exposures included welding fumes, cutting oils, asbestos, organic solvents, and environmental ionizing radiation, as the result of disposal of wastes during the Manhattan Project of World War II. External comparisons with the US male population were supplemented by regional comparisons. For the total cohort, deficits were observed for all causes of death (standardized mortality ratio (SMR) = 87) and most non-cancer causes. The observed number of cancer deaths was close to expected (SMR = 99). There was an excess of connective and soft tissue cancer deaths, most notably in hourly employees hired prior to 1946. Among all hourly employees, there was an excess of respiratory cancer, which did not appear to be associated with length of employment. Mesothelioma was recorded as the cause of death for three decedents, two of whom were hourly employees who worked in production areas with high potential for asbestos exposure. The standardized mortality ratio for cirrhosis of the liver was elevated among long-term hourly employees hired prior to 1946. The roles of carbon tetrachloride exposure in the 1940s and alcohol consumption are discussed as possible contributory risk factors for the cirrhosis findings. The data do not provide evidence of radiation-induced cancers within this employee population.
Analysis of excess lung cancer risk in short-term employees. S.H. Lamm, M.S. Levine, J.A. Starr, et al. 1988;127(6):1202-9. PubMed · Publisher

Abstract

An excess of lung cancer found in a cohort of 741 New York State tremolitic talc workers observed from 1947 through 1978 has been shown paradoxically to be concentrated in short-term workers. Review of past work histories suggests that the excess of lung cancer in these short-term workers may be accounted for by prior exposures rather than by exposures at the employment under investigation. This finding has significant implications in view of the developing practice of including short-term workers in occupational cohort studies in contrast to the more traditional practice of excluding short-term workers. The traditional practice was based on the assumption that the inclusion of short-term workers with little exposure, and thus little risk, might dilute an otherwise apparent association between mortality and exposure. This study suggests that in certain instances the inclusion of short-term workers may magnify rather than dilute the estimation of risk, reflecting the presence of confounding variables.
Case-control study of lung cancer in civilian employees at the Portsmouth Naval Shipyard, Kittery, Maine. R.A. Rinsky, J.M. Melius, R.W. Hornung, et al. 1988;127(1):55-64. PubMed · Publisher

Abstract

Case-control analysis of deaths due to lung cancer (International Classification of Diseases, Eighth Revision, code 162) among persons who worked at the Portsmouth Naval Shipyard, Kittery, Maine, between 1952 and 1977 found elevated odds ratios for exposures to ionizing radiation, asbestos, and welding byproducts. The radiation-related excess was statistically significant in persons with cumulative lifetime exposures of 1.0-4.999 rem. When asbestos and welding histories were combined into a single risk factor, odds ratios for the combined exposure were significantly elevated for two of three duration-of-exposure categories examined. Further analysis of data on radiation exposure, controlling for exposures to asbestos and welding, found reductions in initial estimates of radiation risk at all levels of radiation exposure. This reduction suggests that radiation workers were more heavily exposed to asbestos and/or welding fumes than were other workers and that those exposures confounded the observed association between radiation and lung cancer. Analysis of mortality by time since first exposure to radiation revealed no pattern of progressive increase as latency increased. By contrast, odds ratios for asbestos/welding increased with latency. Data on cigarette smoking and socioeconomic status were not available. The results of this study do not preclude a possible association between radiation exposure at the Portsmouth Naval Shipyard and excess mortality from lung cancer. However, they provide no evidence in support of such a relation.
Mortality from lung cancer and respiratory disease among pottery workers exposed to silica and talc. T.L. Thomas, P.A. Stewart. 1987;125(1):35-43. PubMed · Publisher

Abstract

A cohort mortality study of white men employed for at least one year between 1939 and 1966 at three plants of a single United States company was conducted to evaluate the risk of lung cancer and nonmalignant respiratory disease among workers exposed to silica dust and nonfibrous (nonasbestiform) talc in the manufacture of ceramic plumbing fixtures. Follow-up of 2,055 men through January 1, 1981, indicated a substantial excess of nonmalignant respiratory disease among those with high levels of exposure to silica dust (standardized mortality ratio = 2.26). The risk of nonmalignant respiratory disease rose with the number of years exposed, was not further enhanced by talc exposure, and appeared to be appreciably lower among those exposed in more recent time periods. For lung cancer, men exposed to high levels of silica dust with no talc exposure had a nonsignificant standardized mortality ratio of 1.37. However, those exposed to nonfibrous talc in addition to high levels of silica had a significant 2.5-fold excess risk of lung cancer. Among this group, the lung cancer standardized mortality ratio rose with increasing years of talc exposure to 3.64 among those exposed for 15 or more years. Although the role of silica as a cofactor cannot be ruled out, these data suggest that nonfibrous talc exposure is associated with excess lung cancer risk.
Re: "Excess mortality from stomach cancer, lung cancer, and asbestosis and/or mesothelioma in crocidolite mining districts in South Africa". H.P. Hart. 1987;125(3):542-3. Letter PubMed · Publisher
US prevalence of occupational pleural thickening. A look at chest X-rays from the first National Health and Nutrition Examination Survey. W.J. Rogan, B.C. Gladen, N.B. Ragan, et al. 1987;126(5):893-900. PubMed · Publisher

Abstract

The prevalence of occupational pleural thickening in the United States in the mid-1970s was estimated; since asbestos often produces pleural thickening, this estimate in turn was used to estimate the prevalence of asbestos exposure. Chest x-rays obtained by the 1971-1975 National Health and Nutrition Examination Survey were reread by three readers using the International Labour Office criteria for diagnosis of pleural thickening consistent with dust exposure. All 289 x-rays showing any pleural abnormalities plus a 3-to-1 age-, sex-, and race-matched control series were reread. Using two of three readings as "positive," and extrapolating to the US population from this defined sample, the authors showed that 2.3% of males and 0.2% of females had occupational pleural thickening on x-ray, with a strong increase with age in white males. This provides a US population estimate of 1.3 million people with occupational pleural thickening and approximately 8 million people with asbestos exposure in the mid-1970s. This cohort might make a substantial contribution to cancer mortality into the next century.
Excess mortality from stomach cancer, lung cancer, and asbestosis and/or mesothelioma in crocidolite mining districts in South Africa. J.L. Botha, L.M. Irwig, P.M. Strebel. 1986;123(1):30-40. PubMed · Publisher

Abstract

To determine whether exposure to crocidolite is associated with excess mortality, the authors calculated standardized mortality ratios based on deaths in South African crocidolite mining districts from 1968 to 1980 for selected causes of death. Contiguous districts were used as controls. To take account of background geographic variability, they divided the control districts into groups of population size similar to those of the crocidolite mining districts. Standardized mortality ratios in crocidolite mining districts were elevated for asbestosis and/or mesothelioma, and cancer of the lung and stomach. These findings could not be explained by background geographic variability in mortality and are likely to be due to exposure to South African crocidolite during mining and milling or to environmental contamination. The increased standardized mortality ratios for stomach cancer are of particular interest, since excess deaths have not previously been shown in individuals exposed to crocidolite alone.
Occupational risk factors for laryngeal carcinoma: Connecticut, 1975-1980. R.T. Zagraniski, J.L. Kelsey, S.D. Walter. 1986;124(1):67-76. PubMed · Publisher

Abstract

A case-control study of possible occupational risk factors for laryngeal carcinoma in white males in the New Haven, Connecticut, area included 92 cases diagnosed between 1975 and 1980 and 181 hospital controls individually matched to the cases on age, year and hospital of admission, county of residence, smoking status (current vs. ex-smoker), and type of tobacco used at the time of admission. Only cases and controls who were alive at the time of the study were included. With the effects of tobacco and alcohol controlled in a conditional linear logistic model, elevated odds ratios were found for men who had ever worked in rubber products manufacturing or transportation equipment manufacturing other than shipbuilding, and for men who had ever been machinists, bartenders, farmers, masons, or metal grinders. However, only one occupation, machinists, had a statistically significant odds ratio (2.5, 95% confidence interval = 1.2-5.2) in these multivariate analyses. Asbestos and nickel were not found to be risk factors for laryngeal carcinoma. Amount of tobacco smoked and alcohol consumed were positively associated with risk for laryngeal cancer.
A case-control study of asbestos in drinking water and cancer risk. L. Polissar, R.K. Severson, E.S. Boatman. 1984;119(3):456-71. PubMed · Publisher

Abstract

The authors conducted a case-control, interview-based study of the risk of developing cancer from asbestos in drinking water. The Everett, Washington area was selected for the study because of the unusually high concentration of chrysotile asbestos in the drinking water it draws from the Sultan River (200 X 10(6) fibers/liter). Through a population-based tumor registry, the authors identified 382 individuals with cancer of the buccal cavity, pharynx, respiratory system, digestive system, bladder, or kidney, diagnosed between 1977 and 1980, and then interviewed them or their next-of-kin. The authors conducted similar interviews of a control group of 462 individuals. Finally, interviews were validated in several ways, including comparing the collected data with that from secondary sources. Estimates of exposure to asbestos in drinking water were based on residence and workplace history, and on individual water consumption. Four different measures of exposure were used. Cancer risk was estimated by logistic regression and other methods. The authors found no convincing evidence for cancer risk from imbibed asbestos. Exposure was similar between cases and controls. Confidence intervals for relative odds for almost all sites included unity. Out of 84 dependent estimates of risk by sex, site, and exposure measure, 63 indicated a protective effect and 21 indicated an increased risk. In instances where relative odds differed appreciably from unity for both males and females, the effect was protective. The relative odds of cancer for 20 years of exposure to Sultan River drinking water varied from 0.92 to 0.99 for females and 0.82 to 1.01 for males for all study sites grouped. For cancer of the digestive system, the corresponding range was 1.03 and 1.08 for females and 0.85 to 1.00 for males. There were six statistically significant associations (p less than 0.05). All involved male stomach (eight cases) and male pharynx (four cases), and indicate elevated risk. This number of significant associations is close to that expected (for the number of comparisons made). The female risks for these two sites indicate a protective effect, and it is concluded that the male results are probably due to chance.
"Asbestos in drinking water and cancer incidence in the San Francisco Bay area". K. Browne. 1982;115(1):142-4. Letter PubMed · Publisher
Cancer incidence in relation to asbestos in drinking water in the Puget Sound region. L. Polissar, R.K. Severson, E.S. Boatman, et al. 1982;116(2):314-28. PubMed · Publisher

Abstract

Population-based and proportional odds ratios for various cancers, based on incidence data from 1974-1977 and mortality data from 1965-1975 for western Washington State, were calculated in relation to three measures of exposure to asbestos in community water supplies. Six odds ratios were calculated for each neoplasm that occurred in sufficient numbers in each sex. About half of the 332 odds ratios calculated were above unity and half were below unity, and no more of them differed significantly from unity at the 5% level than would be expected by chance. Odds ratios for tumors of the small intestine were consistently elevated in both sexes, as were those for neoplasms of the thyroid, eye, testis, and prostate in males; however, odds ratios for brain tumors and leukemia were consistently less than one in both sexes. Chance is the most likely explanation for these findings. Results of this study and prior studies of cancer in relation to waterborne asbestos are inconsistent, and provide little evidence that asbestos in community water supplies has altered the risk of any cancer. However, all investigations conducted to date are correlational studies which have an inherently higher probability of failing to detect actual increased risks associated with imbibed asbestos, and additional studies of individual exposures are warranted. Neoplasms of the pancreas and small intestine should be included in such studies.
Changing patterns of lung cancer in the United States. W.J. Blot, J.F. Fraumeni. 1982;115(5):664-73. PubMed · Publisher

Abstract

Although mortality from lung cancer increased throughout the United States during 1950-1975, the rate of change varied according to sex, race, and geographic sector. A pronounced shift in the geographic pattern of lung cancer was seen in white males. The elevation in rates in urban counties of the north in the 1950s faded over time and was not observed in the 1970s. The highest rates during 1970-1975 were in the south, both in rural and urban areas, particularly at younger ages. The sharpest rise in US mortality rates was reported among nonwhite males. Cohort analysis revealed that for males born before 1885 age-specific rates among whites exceeded those among nonwhites by nearly 50%, but for those born after 1915 a 50% excess was seen among nonwhites. Among nonwhite males the highest mortality in the 1970s occurred in urban areas of the south. Among females the rate of increase in lung cancer mortality was higher in the 1970s, but racial and geographic differences tended to be minor. Cigarette smoking accounts for a substantial part of the shifting patterns of lung cancer, but it is likely that other factors are involved, including industrial exposure (e.g., exposure to asbestos in shipyards during World War II) and possibly nutritional deficiencies and other determinants yet to be identified.
"Asbestos in drinking water and cancer incidence in the San Francisco Bay area". I.T. Higgins. 1981;114(1):161-4. Letter PubMed · Publisher
Asbestos in drinking water and cancer incidence in the San Francisco Bay area. M.S. Kanarek, P.M. Conforti, L.A. Jackson, et al. 1980;112(1):54-72. PubMed · Publisher

Abstract

Age-adjusted, sex- and race-specific 1969-1971 cancer incidence ratios for the 722 census tracts of the San Francisco-Oakland Standard Metropolitan Statistical Area were compared with measured chysotile asbestos counts in tract drinking waters. The water supplies serving the area have varying contact with naturally occurring serpentine. The t test for multiple regression coefficients and the t test for correlation coefficients showed significant (p less than 0.01) relationships between chrysotile asbestos content of tract drinking water and white male lung, white female gall bladder and pancreas, and peritoneal cancers in both sexes. Of weaker significance (0.01 less than or equal to 0.05) were female esophagus, pleura and kidney, as well as stomach cancers in both sexes. These associations appeared to be independent of income, education, asbestos occupation, marital status, country of origin and mobility.

1970s

An investigation of the use of asbestos cement pipe for public water supply and the incidence of gastrointestinal cancer in Connecticut, 1935-1973. J.M. Harrington, G.F. Craun, J.W. Meigs, et al. 1978;107(2):96-103. PubMed · Publisher

Abstract

The age adjusted sex specific incidence data for stomach, colon, and rectal cancer for Connecticut townships for the period 1935 to 1973 were used to investigate whether asbestos cement pipe usage for domestic drinking water is associated with gastrointestinal cancer. The townships were grouped according to the Assessment of Exposure (AOE) and Risk Factor (RF) for asbestos. These are composite indices of asbestos exposure including factors relating to the age of the pipe, the ability of water to leach asbestos from the pipe, and the length of pipes used by the population. No association was noted between these asbestos risk scores and gastrointestinal tumor incidence.
Occam's razor pares the choice among statistical models. K.J. Rothman. 1978;108(5):347-9. PubMed · Publisher

Summary

This commentary was the author's reply to a preceding paper by Walter and Holford, who had argued against his position that independent effects in epidemiology are additive, meaning that the joint effect of two or more factors equals the sum of their separate effects. The author argued that Walter and Holford confused statistical interaction, which depends on the choice of scale, with biologic interaction. He also argued that models leading to divergent conclusions about the same data could not be equally acceptable when the goal was scientific inference rather than description or prediction. He used the example of smoking and asbestos exposure in causing lung cancer. Whatever scale was used, smoking had a greater effect on lung cancer incidence among asbestos workers than among people not exposed to asbestos. He argued that a worker asking about this should not be told the answer was arbitrary. He stated that Walter and Holford's "one-hit" model corresponded to causation and their "no-hit" multiplicative model to prevention, and noted that he had derived the same multiplicative relationship in a 1976 paper. He said he did not regard his approach as the only appropriate method and pointed to a technique developed by Walker. He also corrected what he described as inaccuracies about the assessment of causality, the meaning of necessary and sufficient causes, and the meaning of Occam's razor.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.
Cancer mortality and asbestos deposits. T.R. Fears. 1976;104(5):523-6. PubMed · Publisher

Abstract

Asbestos deposits are found in many parts of the United States. In this paper the question is asked: Is there an increase in risk from cancer associated with naturally-occurring asbestos? In an attempt to control for the urban effect, geographic gradient and socioeconomic class, each county in the United States with asbestos deposits was matched for percent of area that was urban and for median years in school with two nearby counties that did not have known asbestos deposits. The study of cancer mortality rates in these matched counties provides no evidence that naturally-occurring asbestos is a great hazard to the general population of counties with asbestos depostis.
Investigating possible effects of abestos in city water: surveillance of gastrointestinal cancer incidence in Duluth, Minnesota. B.S. Levy, E. Sigurdson, J. Mandel, et al. 1976;103(4):362-8. PubMed · Publisher

Abstract

The recent discovery of over one million asbestos-like fibers per liter of Duluth tap water and the suggestive evidence of a link between certain gastrointestinal (GI) cancers and work exposure to asbestos fibers in the air prompted this study. GI cancer incidence data were gathered for Duluth in the same manner as data previously gathered for comparison cities, Minneapolis and St. Paul. Although some differences in GI cancer incidence occurred among the three cities in 1969-1971, there was no consistent pattern of statistically significant differences observed. The number of GI cancers diagnosed in Duluth residents in 1972 was similar to that in each of the previous three years. This study represents the start of ongoing cancer surveillance in Duluth.
Latency periods in neoplastic diseases. A.P. Polednak. 1974;100(5):354-6. PubMed · Publisher

Summary

In this short commentary, the author discussed what the latency period between exposure to a presumed causal agent and the detection of, or death from, a cancer means. It followed a review of latency distributions by Armenian and Lilienfeld. The author argued that the meaning of latency depends on the causal model that applies to a particular cancer. The first was a "cumulative exposure" model, illustrated by cigarette smoking and lung cancer, in which accumulated insults produce cell changes that are reversible up to a critical point. Citing Burbank, the author noted an estimated population latency period of about 30 years. The second was a "one insult, co-carcinogenic" model, illustrated by pulmonary scars and lung cancer, in which an initiator interacts with a promoting factor during a critical period. The author said that pulmonary infection and scarring in adults, and apical scarring possibly caused by air pollution, needed study in relation to lung cancer. Cervical cancer, for which a one-insult model had been suggested, was also discussed, along with what each model implies for explanations based on DNA modification. Finally, the author noted that other causal mechanisms could bring cases with unusual latency periods into the data, affecting averages and dispersions more than medians. As an example, a latency of over 70 years had been suggested for one case of mesothelioma after asbestos exposure, but only if asbestos caused the disease.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.
The Philadelphia pulmonary neoplasm research project: basic risk factors of lung cancer in older men. K.R. Boucot, W. Weiss, H. Seidman, et al. 1972;95(1):4-16. PubMed · Publisher

Abstract

One hundred twenty-one new lung cancers developed among 6136 men aged 45 and over who volunteered to report semiannually for chest x-rays and questionnaires about symptoms, smoking habits, etc., over a 10-year period beginning in 1951. The risk of developing lung cancer increased with increasing age, was higher in nonwhites than in whites, and bore a dose-response relationship to cigarette smoking. As crudely measured by dust-fall and sulfur dioxide levels post facto in 1969, there was no evidence that the risk increased with increasing levels of these air pollutants. Exposure to asbestos was the greatest occupational hazard.

PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

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