Epidemiology

Our medical research library holds 21 studies published in Epidemiology (1994–2020). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 17 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it. For 1 study PubMed has no abstract for, we give the abstract printed in the article or, where there is none, a summary we wrote from it, each labeled as such.

About the journal

• Publisher: Lippincott Williams & Wilkins
• Published: 1990 to the present, United States
• Language: English
• ISSN: 1044-3983 (print), 1531-5487 (electronic)
• Its record in the NLM Catalog

2020s

• Laryngeal Cancer Risks in Workers Exposed to Lung Carcinogens: Exposure-Effect Analyses Using a Quantitative Job Exposure Matrix. A.L. Hall, H. Kromhout, J. Schüz, et al. 2020;31(1):145-154. PubMed · Publisher

  Abstract

  Introduction: Various established occupational lung carcinogens are also suspected risk factors for laryngeal cancer. However, individual studies are often inadequate in size to investigate this relatively rare outcome. Other limitations include imprecise exposure assessment and inadequate adjustment for confounders.

  Methods: This study applied a quantitative job exposure matrix (SYN-JEM) for four established occupational lung carcinogens to five case-control studies within the International Head and Neck Cancer Epidemiology Consortium. We used occupational histories for 2256 laryngeal cancer cases and 7857 controls recruited from 1989 to 2007. We assigned quantitative exposure levels for asbestos, respirable crystalline silica, chromium-VI, and chromium-VI and nickel combined (to address highly correlated exposures) via SYN-JEM. We assessed effects of occupational exposure on cancer risk for males (asbestos, respirable crystalline silica, chromium-VI, and chromium-VI and nickel combined) and females (asbestos and respirable crystalline silica), adjusting for age, study, tobacco smoking, alcohol consumption, and asbestos exposure where relevant.

  Results: Among females, odds ratios (ORs) were increased for ever versus never exposed. Among males, P values for linear trend were <0.05 for estimated cumulative exposure (all agents) and <0.05 for exposure duration (respirable crystalline silica, chromium-VI, and chromium-VI and nickel combined); strongest associations were for asbestos at >90th percentile cumulative exposure (OR = 1.3, 95% confidence interval [CI] = 1.0, 1.6), respirable crystalline silica at 30+ years duration (OR = 1.4, 95% CI = 1.2, 1.7) and 75th-90th percentile cumulative exposure (OR = 1.4, 95% CI = 1.1, 1.8), chromium-VI at >75th percentile cumulative exposure (OR = 1.9, 95% CI = 1.2, 3.0), and chromium-VI and nickel combined at 20-29 years duration (OR = 1.5, 95% CI = 1.1, 2.2).

  Conclusions: These findings support hypotheses of causal links between four lung carcinogens (asbestos, respirable crystalline silica, chromium-VI, and nickel) and laryngeal cancer.

2010s

• Talc, Asbestos, and Epidemiology: Corporate Influence and Scientific Incognizance. T.H. Tran, J.E. Steffen, K.M. Clancy, et al. 2019;30(6):783-788. PubMed · Publisher · Free full text

  Summary

  In this commentary, the authors described how talc mining and manufacturing companies and their trade association, the Cosmetic, Toiletry, and Fragrance Association, influenced research and regulation on asbestos in cosmetic talc and on talc and ovarian cancer. They drew on company documents and testimony produced in litigation. They reported that the association's 1976 test method (J4-1) had a detection limit above 0.5% for tremolite asbestos and did not test for chrysotile or fibrous talc. They also reported that 686 of 1032 tests produced in litigation found asbestos in talcs used in cosmetics from 1948 to 2017. Of 32 epidemiologic studies of talc and ovarian cancer, they stated that 12 incorporated the claim that cosmetic talc had been asbestos-free since 1976, only one considered confounding by occupational or other asbestos exposure, and only 2 considered nonperineal exposure routes. They argued that the resulting misclassification likely drove risk estimates toward the null. Eighteen of the 32 studies reported an elevated risk. The authors described the association's "fatal flaw" argument and the withdrawal of talc from the National Toxicology Program's Report on Carcinogens after scientific panels voted to list it. They also described undisclosed conflicts of interest in IARC talc reviews. They urged epidemiologists to work with other professionals, verify industry information and use litigation documents, and concluded that talc should not be sold. The authors disclosed that one of them serves as an expert witness in talc and asbestos litigation and that the others work for him.

  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.

• Exposure-Response Analyses of Asbestos and Lung Cancer Subtypes in a Pooled Analysis of Case-Control Studies. A.C. Olsson, R. Vermeulen, J. Schüz, et al. 2017;28(2):288-299. PubMed · Publisher · Free full text

  Abstract

  Background: Evidence is limited regarding risk and the shape of the exposure-response curve at low asbestos exposure levels. We estimated the exposure-response for occupational asbestos exposure and assessed the joint effect of asbestos exposure and smoking by sex and lung cancer subtype in general population studies.

  Methods: We pooled 14 case-control studies conducted in 1985-2010 in Europe and Canada, including 17,705 lung cancer cases and 21,813 controls with detailed information on tobacco habits and lifetime occupations. We developed a quantitative job-exposure-matrix to estimate job-, time period-, and region-specific exposure levels. Fiber-years (ff/ml-years) were calculated for each subject by linking the matrix with individual occupational histories. We fit unconditional logistic regression models to estimate odds ratios (ORs), 95% confidence intervals (CIs), and trends.

  Results: The fully adjusted OR for ever-exposure to asbestos was 1.24 (95% CI, 1.18, 1.31) in men and 1.12 (95% CI, 0.95, 1.31) in women. In men, increasing lung cancer risk was observed with increasing exposure in all smoking categories and for all three major lung cancer subtypes. In women, lung cancer risk for all subtypes was increased in current smokers (ORs ~two-fold). The joint effect of asbestos exposure and smoking did not deviate from multiplicativity among men, and was more than additive among women.

  Conclusions: Our results in men showed an excess risk of lung cancer and its subtypes at low cumulative exposure levels, with a steeper exposure-response slope in this exposure range than at higher, previously studied levels. (See video abstract at, http://links.lww.com/EDE/B161.).

• Lung Cancer Risk Associated with Regulated and Unregulated Chrysotile Asbestos Fibers. G.B. Hamra, D.B. Richardson, J. Dement, et al. 2017;28(2):275-280. PubMed · Publisher

  Abstract

  Background: Regulation of asbestos fibers in the workplace is partly determined by which fibers can be visually counted. However, a majority of fibers are too short and thin to count this way and are, consequently, not subject to regulation.

  Methods: We estimate lung cancer risk associated with asbestos fibers of varying length and width. We apply an order-constrained prior both to leverage external information from toxicological studies of asbestos health effects. This prior assumes that risk from asbestos fibers increases with increasing length and decreases with increasing width.

  Results: When we apply a shared mean for the effect of all asbestos fiber exposure groups, the rate ratios for each fiber group per unit exposure appear mostly equal. Rate ratio estimates for fibers of diameter <0.25 μm and length <1.5 and 1.5-5.0 μm are the most precise. When applying an order-constrained prior, we find that estimates of lung cancer rate ratio per unit of exposure to unregulated fibers 20-40 and >40 μm in the thinnest fiber group are similar in magnitude to estimates of risk associated with long fibers in the regulated fraction of airborne asbestos fibers. Rate ratio estimates for longer fibers are larger than those for shorter fibers, but thicker and thinner fibers do not differ as the toxicologically derived prior had expected.

  Conclusion: Credible intervals for fiber size-specific risk estimates overlap; thus, we cannot conclude that there are substantial differences in effect by fiber size. Nonetheless, our results suggest that some unregulated asbestos fibers may be associated with increased incidence of lung cancer.

• Estimating the effect of cumulative occupational asbestos exposure on time to lung cancer mortality: using structural nested failure-time models to account for healthy-worker survivor bias. A.I. Naimi, S.R. Cole, M.G. Hudgens, et al. 2014;25(2):246-54. PubMed · Publisher · Free full text

  Abstract

  Background: Previous estimates of the effect of occupational asbestos on lung cancer mortality have been obtained by using methods that are subject to the healthy-worker survivor bias. G-estimation of a structural nested model provides consistent exposure effect estimates under this bias.

  Methods: We estimated the effect of cumulative asbestos exposure on lung cancer mortality in a cohort comprising 2564 textile factory workers who were followed from January 1940 to December 2001.

  Results: At entry, median age was 23 years, with 42% of the cohort being women and 20% nonwhite. During the follow-up period, 15% of person-years were classified as occurring while employed and 13% as occupationally exposed to asbestos. For a 100 fiber-year/ml increase in cumulative asbestos, a Weibull model adjusting for sex, race, birth year, baseline exposure, and age at study entry yielded a survival time ratio of 0.88 (95% confidence interval = 0.83 to 0.93). Further adjustment for work status yielded no practical change. The corresponding survival time ratio obtained using g-estimation of a structural nested model was 0.57 (0.33 to 0.96).

  Conclusions: Accounting for the healthy-worker survivor bias resulted in a 35% stronger effect estimate. However, this estimate was considerably less precise. When healthy-worker survivor bias is suspected, methods that account for it should be used.

• Arsenic, tobacco smoke, and occupation: associations of multiple agents with lung and bladder cancer. C. Ferreccio, Y. Yuan, J. Calle, et al. 2013;24(6):898-905. PubMed · Publisher · Free full text

  Abstract

  Background: Millions of people worldwide are exposed to arsenic in drinking water, and many are likely coexposed to other agents that could substantially increase their risks of arsenic-related cancer.

  Methods: We performed a case-control study of multiple chemical exposures in 538 lung and bladder cancer cases and 640 controls in northern Chile, an area with formerly high drinking water arsenic concentrations. Detailed information was collected on lifetime arsenic exposure, smoking, secondhand smoke, and other known or suspected carcinogens, including asbestos, silica, and wood dust.

  Results: Very high lung and bladder cancer odds ratios (ORs), and evidence of greater than additive effects, were seen in people exposed to arsenic concentrations >335 µg/L and who were tobacco smokers (OR = 16, 95% confidence interval = 6.5-40 for lung cancer; and OR = 23 [8.2-66] for bladder cancer; Rothman Synergy Indices = 4.0 [1.7-9.4] and 2.0 [0.92-4.5], respectively). Evidence of greater than additive effects were also seen in people coexposed to arsenic and secondhand tobacco smoke and several other known or suspected carcinogens, including asbestos, silica, and wood dust.

  Conclusions: These findings suggest that people coexposed to arsenic and other known or suspected carcinogens have very high risks of lung or bladder cancer.

• Carcinoma of the pharynx and tonsils in an occupational cohort of asphalt workers. F. Zanardi, R. Salvarani, R.M. Cooke, et al. 2013;24(1):100-3. PubMed · Publisher

  Abstract

  Background: We investigated a possible association between pharyngeal/tonsillar carcinoma and mixed carcinogen exposures in an asphalt roll company in Italy that used asbestos until 1979, when a new factory was built using a different production process.

  Methods: We evaluated all workers involved in the entire production history of the company, divided into two subcohorts based on exposure status (workers in the original factory, 1964-1979, and those who worked only in the new factory, 1980-1997). We ascertained the vital status of the study population in February 2001.

  Results: Among the subset of workers in the earlier subcohort, there were five deaths from pharyngeal/tonsillar carcinoma for a standardized mortality ratio of 21 (95% confidence interval = 8.8-51). No cases were recorded among workers hired after 1979.

  Conclusion: The increased standardized mortality ratio for this relatively rare cancer among workers exposed before 1979 may have been due to carcinogenic exposures at the plant.

• Pulmonary fibrosis in workers exposed to non-asbestiform tremolite asbestos minerals. H.Y. Yang, R.H. Shie, P.C. Chen. 2013;24(1):143-9. PubMed · Publisher

  Abstract

  Background: Studies of the health effects of non-asbestiform asbestos minerals remain inconclusive. Nephrite is a type of non-asbestiform tremolite mineral. We assessed the risk for pulmonary fibrosis in workers who process nephrite.

  Methods: A cross-sectional study that included 344 stone workers and their families was undertaken in Taiwan in 2010. The diagnostic criteria for pulmonary fibrosis included (1) radiographic fibrosis profusion of 1/1 or greater and (2) audible lung crackles confirmed by physician. The nephrite samples were analyzed using polarized light and transmission electron microscopy combined with selected-area electron diffraction and energy-dispersive x-ray spectroscopy.

  Results: After excluding 16 subjects with histories of tuberculosis or previous employment in metal casting and welding, as well as 23 family members who had not worked in the stone industry, we analyzed 305 subjects. Processing nephrite increased the risk for pulmonary fibrosis (odds ratio = 2.8 [95% confidence interval = 1.0-9.9] and unchanged after adjustment for age and smoking). Bulk sample analyses showed that the nephrite is a tremolite mineral composed of both asbestiform and non-asbestiform components. The cat's-eye nephrite had the highest asbestiform fibrous content, and the average length and aspect ratio of elongated mineral particles were the highest of all the nephrite types. Compared with workers processing other types of nephrite, workers processing cat's-eye nephrite had the highest risk for pulmonary fibrosis.

  Conclusion: Processing non-asbestiform tremolite mineral may increase the risk for pulmonary fibrosis. Medical monitoring is warranted for workers with such exposure.

• Estimation with vanishing baseline risk. R.M. Park. 2012;23(6):937-8. Letter PubMed · Publisher · Free full text

• The ghost of public health journalism: past, present, and future. G.S. Cooper, R.C. Brown. 2010;21(2):263-6. Historical article PubMed · Publisher

  Abstract

  The news industry is undergoing shrinking newspaper circulations, cuts in science and health coverage, and expansion of Internet news sources. We examine the impact of these changes using a case study set in Libby, Montana. In 1999, a Seattle newspaper story focused attention on asbestos exposure and related diseases in this small town. In 2009, that newspaper became an online-only newspaper, just as coverage of a related criminal trial began. Later that year the U.S. Environmental Protection Agency issued a public health emergency. Online newspaper archives and a collaboration between the University of Montana's journalism and law schools contributed to coverage of these developments. Continued efforts to promote interest in and skills needed for high-quality public health and environmental reporting are needed.

2000s

• Occupational exposures, environmental tobacco smoke, and lung cancer. F. Veglia, P. Vineis, K. Overvad, et al. 2007;18(6):769-75. PubMed · Publisher

  Abstract

  Background: There is uncertainty regarding the association of occupational exposures with lung cancer. We have studied the association between 52 high-risk job titles and lung cancer incidence in a large prospective study, with more than 200,000 participants followed for more than 6 years and 809 incident cases of lung cancer.

  Methods: Hazard ratios and 95% confidence intervals were computed by the Cox proportional-hazard regression model, adjusting for country, age, sex, social class, diet, physical activity, and smoking habits. We used a CAREX-based job-exposure matrix to infer exposure to lung carcinogens. False-positive report probability was calculated as a measure of potentially false-positive results.

  Results: Eighteen occupations, mainly related with agriculture, constructions, and metal processing, were associated with increased risk. In addition, incidence tended to increase with the number of hazardous jobs reported. When the occupations were classified according to the presumed exposure to specific carcinogenic agents, the hazard ratios were 1.5 (95% confidence interval = 1.2-1.9) for asbestos, 1.4 (1.1-1.8) for heavy metals, 1.4 (1.1-1.8) for polycyclic aromatic hydrocarbons, and 1.6 (1.2-2.1) for work-related environmental tobacco smoke. The estimated population attributable risk for employment in at least 1 at-risk job was 16% in men and 12% in women.

  Conclusions: This large prospective study suggests that exposure to occupational lung carcinogens is still a problem, with such exposures producing moderate to large increases in risk.

• Can lung cancer risk among nickel refinery workers be explained by occupational exposures other than nickel?. T.K. Grimsrud, S.R. Berge, T. Haldorsen, et al. 2005;16(2):146-54. PubMed · Publisher

  Abstract

  Background: Exposures in nickel refineries represent complex chemical mixtures, but only the effect of nickel has been evaluated quantitatively in epidemiologic studies of nickel workers.

  Methods: For a Norwegian refinery, time- and department-specific exposure estimates were developed for arsenic, sulfuric acid mists, and cobalt in air on the basis of personal measurements and chemical data on raw materials and process intermediates. Exposure to asbestos, as well as employment in high-risk occupations outside the refinery, were assessed. We conducted a case-control study nested in a cohort of refinery workers, with 213 cases (diagnosed 1952-1995) and 525 age-matched controls. We analyzed lung cancer risk, adjusted for smoking, by cumulative exposure and duration of work.

  Results: There was a substantial association between cumulative exposure to water-soluble nickel and lung cancer risk. Weaker effects were suggested for exposure to arsenic at the refinery and for occupational exposures outside the refinery for 15 years or more. No detectable excess risk was found for refinery exposure to asbestos or sulfuric acid mists, and no dose-related increase in risk was seen from cobalt.

  Conclusions: Exposure to water-soluble nickel remained the most likely explanation for the excess lung cancer risk in the cohort. Other occupational exposures did not confound the strong dose-related effect of nickel to any appreciable degree.

  In plain English

  This study asked whether workplace exposures other than nickel explained high lung cancer rates at a Norwegian nickel refinery. Researchers compared 213 refinery workers with lung cancer diagnosed 1952 to 1995 with 525 workers matched by sex and birth year. All had worked there at least one year. They estimated each worker's exposure to water-soluble nickel, arsenic, sulfuric acid mists and cobalt. They also counted years in departments with likely asbestos exposure (fiber type not stated) and years in cancer-risk outside jobs, and adjusted for smoking. Refinery asbestos exposure had no detectable effect on lung cancer risk. The longest asbestos-exposed group (9.1 to 47 years) had an odds ratio of 0.8 (95% CI 0.3 to 1.7). Arsenic suggested a modest 20 to 30% higher risk with no dose pattern. Fifteen or more years in outside high-risk jobs suggested a 50% excess. Sulfuric acid mists suggested some effect with only smoking adjustment but none after full adjustment; a separate cobalt effect could not be sorted out. The authors concluded water-soluble nickel remained the most likely explanation for the excess lung cancer.

  We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

• Residential radon and risk of lung cancer in Eastern Germany. M. Kreuzer, J. Heinrich, G. Wölke, et al. 2003;14(5):559-68. PubMed · Publisher

  Abstract

  Background: There is suggestive evidence that residential radon increases lung cancer risk. To elucidate this association further, we conducted a case-control study in Thuringia and Saxony in Eastern Germany during 1990-1997.

  Methods: Histologically confirmed lung cancer patients from hospitals and a random sample of population controls matched on age, sex and geographical area were personally interviewed with respect to residential history, smoking, and other risk factors. One-year radon measurements were performed in houses occupied during the 5-35 years prior to the interview. The final analysis included a total of 1,192 cases and 1,640 controls. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by logistic regression.

  Results: Measurements covered on average 72% of the exposure time window, with mean radon concentrations of 76 Bq/m3 among the cases and 74 Bq/m3 among the controls. The smoking- and asbestos-adjusted ORs for categories of radon (50-80, 80-140 and >140 Bq/m*3, compared with 0-50 Bq/m3) were 0.95 (CI = 0.77 to 1.18), 1.13 (CI = 0.86 to1.50) and 1.30 (CI = 0.88 to 1.93). The excess relative risk per 100 Bq/mł was 0.08 (CI = -0.03 to 0.20) for all subjects and 0.09 (CI = -0.06 to 0.27) for subjects with complete measurements for all 30 years.

  Conclusions: Our data indicate a small increase in lung cancer risk as a result of residential radon that is consistent with the findings of previous indoor radon and miner studies.

• Urban air pollution and lung cancer in Stockholm. F. Nyberg, P. Gustavsson, L. Järup, et al. 2000;11(5):487-95. PubMed · Publisher

  Abstract

  We conducted a population-based case-control study among men 40-75 years of age encompassing all cases of lung cancer 1985-1990 among stable residents of Stockholm County 1950-1990. Questionnaires to subjects or next-of-kin (primarily wives or children) elicited information regarding smoking and other risk factors, including occupational and residential histories. A high response rate (>85%) resulted in 1,042 cases and 2,364 controls. We created retrospective emission databases for NOx/NO2 and SO2 as indicators of air pollution from road traffic and heating, respectively. We estimated local annual source-specific air pollution levels using validated dispersion models and we linked these levels to residential addresses using Geographical Information System (GIS) techniques. Average traffic-related NO2 exposure over 30 years was associated with a relative risk (RR) of 1.2 (95% confidence interval 0.8-1.6) for the top decile of exposure, adjusted for tobacco smoking, socioeconomic status, residential radon, and occupational exposures. The data suggested a considerable latency period; the RR for the top decile of average traffic-related NO2 exposure 20 years previously was 1.4 (1.0-2.0). Little association was observed for SO2. Occupational exposure to asbestos, diesel exhaust, and other combustion products also increased the risk of lung cancer. Our results indicate that urban air pollution increases lung cancer risk and that vehicle emissions may be particularly important.

1990s

• Synergy between asbestos and smoking on lung cancer risks. T.C. Erren, M. Jacobsen, C. Piekarski. 1999;10(4):405-11. Meta-analysis PubMed · Publisher

  Abstract

  We have examined data from 12 epidemiologic studies for quantitative evidence of biologic synergy between asbestos and smoking on lung cancer risks. Estimates of the effect associated with joint exposure to the two agents exceeded the sum of their separate effects in each study. We explored the variations in the strength of the synergistic effect across the studies using three indices: the ratio of the combined effects to the sum of the separate effects of smoking and asbestos (S), the relative excess risk due to interaction (RERI), and the attributable proportion of risk due to interaction (AP). The weighted average of S across all studies was 1.64 (95% confidence interval = 1.33-2.03). The attributable proportion associated with this average S was estimated as 33%, that suggests that one-third of cancer cases among smokers who were exposed to asbestos can be attributed to the synergistic behavior of the two carcinogens, as distinct from their separate effects and those attributable to other ("background") factors.

• Cancer mortality among man-made vitreous fiber production workers. C.E. Rossiter, H.G. Grimm. 1998;9(2):218-9; author reply 219-20. Comment · Letter PubMed · Publisher

• Cancer mortality among man-made vitreous fiber production workers. P. Boffetta, R. Saracci, A. Andersen, et al. 1997;8(3):259-68. PubMed · Publisher

  Abstract

  We have updated the follow-up of cancer mortality for a cohort study of man-made vitreous fiber production workers from Denmark, Finland, Norway, Sweden, United Kingdom, Germany, and Italy, from 1982 to 1990. In the mortality analysis, 22,002 production workers contributed 489,551 person-years, during which there were 4,521 deaths. Workers with less than 1 year of employment had an increased mortality [standardized mortality ratio (SMR) = 1.45; 95% confidence interval (CI) = 1.37-1.53]. Workers with 1 year or more of employment, contributing 65% of person-years, had an SMR of 1.05 (95% CI = 1.02-1.09). The SMR for lung cancer was 1.34 (95% CI = 1.08-1.63, 97 deaths) among rock/slag wool workers and 1.27 (95% CI = 1.07-1.50, 140 deaths) among glass wool workers. In the latter group, no increase was present when local mortality rates were used. Among rock/slag wool workers, the risk of lung cancer increased with time-since-first-employment and duration of employment. The trend in lung cancer mortality according to technologic phase at first employment was less marked than in the previous follow-up. We obtained similar results from a Poisson regression analysis limited to rock/slag wool workers. Five deaths from pleural mesothelioma were reported, which may not represent an excess. There was no apparent excess for other categories of neoplasm. Tobacco smoking and other factors linked to social class, as well as exposures in other industries, appear unlikely to explain the whole increase in lung cancer mortality among rock/slag wool workers. Limited data on other agents do not indicate an important role of asbestos, slag, or bitumen. These results are not sufficient to conclude that the increased lung cancer risk is the result of exposure to rock/slag wool; however, insofar as respirable fibers were an important component of the ambient pollution of the working environment, they may have contributed to the increased risk.

• Asbestos-related mortality among Italian migrants to Western Australia. E. Merler, D. Balzi, E. Buiatti, et al. 1996;7(5):556-7. Letter PubMed · Publisher

• Intraocular melanoma linked to occupations and chemical exposures. E.A. Holly, D.A. Aston, D.K. Ahn, et al. 1996;7(1):55-61. PubMed · Publisher

  Abstract

  We conducted a case-control study in the western United States to determine the relation between occupations or chemical exposures and increased risk of uveal melanoma. Among men (221 patients, 447 controls), we found increased risks for occupational groups who had intense exposure to ultraviolet light [odds ratio (OR) = 3.0; 95% confidence interval (CI) = 1.2-7.8], welding exposure (OR = 2.2; 95% CI = 1.3-3.5), and asbestos exposure (OR = 2.4; 95% CI = 1.5-3.9 for most likely exposed). The highest odds ratio was for the small number of men (nine cases, three controls) who were chemists, chemical engineers, and chemical technicians (OR = 5.9; 95% CI = 1.6-22.7). Odds ratios also were elevated for exposures to antifreeze, formaldehyde, pesticides, and carbon tetrachloride, but these findings, based on recall of specific chemical exposures, are more subject to recall bias than the findings based on occupational groups.

• Pancreatic cancer and occupational exposures. T. Kauppinen, T. Partanen, R. Degerth, et al. 1995;6(5):498-502. PubMed · Publisher

  Abstract

  We conducted a nationwide case-control study in Finland to identify occupational risk factors for pancreatic cancer. We constructed the occupational exposure histories for 595 incident cases of primary exocrinic cancer of the pancreas and of 1,622 cancer controls, using three different methods. We found elevated odds ratios (OR) for ionizing radiation [OR = 4.3; 95% confidence interval (CI) = 1.6-11.4], nonchlorinated solvents (OR = 1.6-1.8), and pesticides (OR = 1.7; 95% CI = 0.8-3.4). Asbestos, chromates, cleaning agents, waxes, polishes, and most other exposures were not meaningfully associated with pancreatic cancer. Inorganic dust containing crystalline silica (OR = 2.0; 95% CI = 1.2-3.5), heat stress (OR = 2.2; 95% CI = 0.8-6.6), and rubber chemicals including acrylonitrile (OR = 2.1; 95% CI = 0.9-4.7) emerged as previously unsuspected risk factors. Occupational exposure probably has a small role in the etiology of pancreatic cancer in the present-day industrialized or postindustrial work environment.

• A case-control study of mesothelioma and employment in the Hawaii sugarcane industry. T. Sinks, M.T. Goodman, L.N. Kolonel, et al. 1994;5(4):466-8. PubMed · Publisher

  Abstract

  We conducted a case-control study of 93 mesothelioma cases and 281 cancer controls to determine whether sugarcane workers exposed to biogenic silica fibers were at increased risk of mesothelioma. We found no important excess risk of mesothelioma in sugarcane workers [odds ratio (OR) = 1.3; 95% confidence interval (CI) = 0.4-3.8] when we excluded all control subjects with cancer of sites suspected of being associated with asbestos exposure. We could not identify any sugarcane workers who developed mesothelioma and worked in jobs where high exposure levels of biogenic silica fibers have been measured. We did confirm that mesothelioma risk in Hawaii is associated with probable occupational asbestos exposure. Work at the Pearl Harbor Naval Shipyard was associated with a 10-fold increase in mesothelioma when we excluded controls with cancer of sites related to asbestos exposure (OR = 10.1; 95% CI = 2.6-56.6). Work in the medical industry was also associated with an unexpected increased risk for mesothelioma (OR = 4.2; 95% CI = 1.2-15.5).

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