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R. S. Koskela, J. A. Sorsa, A. Koski, P. Mutanen. Finnish Institute of Occupational Health
ObjectivesThe study investigated long‐term effects of exposure to polycyclic aromatic hydrocarbons (PAHs) on foundry workers' morbidity from lung cancer.
MethodsThis study comprised 931 men hired in 1950–1972 by 20 foundries. The men were still actively working in foundries in 1972, had been potentially exposed to PAHs for at least 4.2 years, and took part in a health examination in 1973. A questionnaire on working history and smoking habits was carried out in 1973 and in 1993. Cancer morbidity was followed from the Finnish Cancer Register. Workers were classified into PAH exposure categories based on the measurements of PAH in 1972. The statistical method was person‐year analysis. The observed numbers of lung cancer were tested against the national (sex‐, age‐, and period‐specific) expected numbers by the Poisson distribution model.
ResultsDuring the follow‐up (1953–2002) 60 lung cancer cases occurred (exp 44.9, SIR 134, 95% CI 102 to 172), 35 cases were from iron foundries (exp 27.2, SIR 129, 95% CI 90 to 179), 34 of them with at least 25 latency years (exp 23.3, SIR 146, 95% CI 101 to 204); 23 cases were from steel foundries (exp 15.9, SIR 144, 95% CI 92 to 217), 20 of them with at least 25 latency years (exp 12.8, SIR 157, 95% CI 96 to 242); and only two cases from non‐ferrous foundries. Of the 34 lung cancer patients with at least 25 years of latency, 17 had been heavily exposed to PAHs in iron foundries (exp 9.6, SIR 177, CI 95% 103 to 283), and of them 14 had at least 40 years of latency (exp 4.8, SIR 289, CI 158 to 485). Of the same 34 patients, 16 had some, miscellaneous, or low exposure to PAHs (exp 13.7, SIR 117, 95% CI 67 to 190), and of them six had at least 40 years of latency (exp 6.6, SIR 91, 95% CI 33 to 198). Of the 20 lung cancer patients from steel foundries with at least 25 latency years, only five had been heavily exposed to PAHs (exp 3.5, SIR 142, 95% CI 46 to 331); 15 patients had some, miscellaneous or low exposure (exp 9.2, SIR 163, 95% CI 91 to 269).
ConclusionHeavy exposure to PAHs in iron foundries in 1950–1972 further results in excess lung cancer morbidity.
Key wordslung cancer; foundry; follow‐up
G. W. Gibbs. Safety Health Environment International Consultants Corporation
ObjectivesTo monitor ongoing mortality and cancer incidence in Quebec aluminium reduction plant workers.
MethodsAll 9844 workers with seniority greater than 1 year and hired for the first time at three Quebec aluminium reduction plants between 1950 and 1999 were included in the program. Similarly, 610 workers at another plant were defined at plant start‐up for immediate follow‐up and workers at three other plants were identified for follow‐up beginning in 1999 only. It is planned that new workers will be added to the cohorts as they meet criteria for inclusion. Cohorts were divided into 10‐year sub‐cohorts by year of first hire. Exposure to benzo(a)pyrene and benzene soluble material used as indices of coal tar pitch exposure were compiled for each worker. Smoking information was obtained from various sources. Mortality data were obtained using the Canadian Mortality Data Base and cancer incidence ascertained through the “Fichiers des tumours” in Quebec. Mortality and cancer incidence was compared to Quebec rates using standardised mortality and incidence ratios. Trends were examined. Plans call for future follow‐up of these same cohorts at 5–10‐year intervals.
ResultsCompared to workers hired before 1950, risks of mortality and cancer incidence were reduced in most categories of mortality and cancer incidence. For example, results showed reductions over time in the risk of lung cancer and bladder cancer mortality, although bladder cancer incidence remains elevated at two plants compared to Quebec general population rates. There were indications that cancers not identified in the pre‐1950 cohorts using the same methodology may be emerging in the post‐1950 cohorts. These may or may not be occupationally related.
ConclusionThe study demonstrates the value of sequentially defined cohorts in evaluating the effects of controlling exposure and other risk factors at work. The rates of major causes of excess mortality and cancer in workers hired before 1950 are decreasing, most likely as the result of reductions in exposure to CTPVs, prevention programs and reduced tobacco consumption. Causes of death and cancers occurring at elevated rates in the various cohorts should be monitored in future follow‐ups and aetiological factors for elevated risks not related to CTPVs sought.
Key wordscancer; aluminium reduction industry; polycyclic aromatic hydrocarbons
I. T. S. Yu, L. A. Tse. Center for Occupational and Environmental Health Studies, School of Public Health, The Chinese University of Hong Kong
ObjectivesCigarette smoking could only explain about 58% of the risk of lung cancer among Hong Kong males. Although many studies showed that a number of occupational lung carcinogens could account for a substantial proportion of lung cancers, the relationships between occupational exposures and lung cancer have not been properly studied in Hong Kong. The objective of this study is to identify occupational exposures associated with increased risk of lung cancer among Hong Kong males.
Methods1207 histologically or cytologically confirmed male lung cancer cases and 1323 hospital patients without cancer matched for age and gender from the same hospital were recruited for this case‐control study. A full occupational history for each subject was recorded, including information on specific occupational exposures. Unconditional multiple logistic regression analyses were performed to examine the associations between specific occupational exposures and lung cancer after adjusting for smoking habits, alcohol drinking habits, dietary habits, indoor air pollutants, past history of lung diseases, cancer history in first‐degree relatives and educational level.
ResultsLung cancer risk was significantly associated with regular exposures to welding fumes (OR 1.43, 95% CI 1.02 to 2.19), man‐made fibres (OR 3.81, 95% CI 1.29 to 11.24), silica dust (OR 1.70, 95% CI 1.32 to 2.38), and emissions from plastic heating/melting (OR 4.09, 95% CI 1.34 to 12.51). Nevertheless, an exposure–response relationship was only observed with the duration of exposures to emissions from plastic heating/melting. Stratified analyses by histological subtype showed that man‐made fibres (OR 4.37, 95% CI 1.22 to 15.66) were only significantly associated with adenocarcinoma but emissions from plastic heating/melting (OR 6.88, 95% CI 1.59 to 29.71) were more strongly linked to squamous (and small) cell carcinoma of lung, while the effects of silica dust on the risk of adenocarcinoma and squamous (and small) cell carcinoma of lung were similar.
ConclusionThis study has identified welding fumes, man‐made fibres, silica dust, and emissions from plastic heating/melting to be the high risk occupational exposures related to lung cancer among Hong Kong males.
Key wordsoccupation; industry; lung carcinoma
F. de Vocht1, I. Burstyn2, G. Ferro3, A. Olsson3, M. Hashibe3, H. Kromhout4, P. Boffetta3. 1Occupational and Environmental Health Research Group, School of Translational Medicine, Faculty of Medical and Human Sciences, The University of Manchester; 2Community and Occupational Medicine Program, Department of Medicine, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, Canada; 3Gene‐Environment Epidemiology Group, International Agency for Research on Cancer (IARC), Lyon, France; 4Environmental Epidemiology Division, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands
ObjectivesA multi‐centre cohort study involving asphalt workers from the Netherlands, Sweden, Norway, Finland, Denmark, France, Germany and Israel provided evidence that lung cancer risk may be associated in a dose‐dependent manner with exposure to bitumen fumes. The strongest association was found with average exposure, and relative risks (RR) increased from 1.82 (0.97–1.24 mg/m3) to 2.54 in the highest exposed group (>1.39 mg/m3). Quantitative exposure assessment in this study was based on statistical models derived from measurements collected between the 1960s and 1997 by the industry, governments and research institutes. Several assumptions, based on discussions between researchers and industry experts, had to be made in constructing company‐ and time‐period‐specific exposure matrices where measurements were absent. We conducted analyses to assess whether the increased lung cancer risks were robust to the assumptions not supported by measurements of exposure.
MethodsAlgorithms were constructed to re‐calculate individual measures of bitumen fume exposure from the original company data files. Subsequently, new exposure estimates were generated by changing assumptions on historical levels, frequency of tasks that generated high exposure, applied exposure lags, and coal tar use (potential confounder). Logistic regression models with the same adjustments as in the original analyses calculated lung cancer RRs with new and original exposure variables. RRs and model fit were compared with models that used the original exposure estimates.
ResultsThe influence of the original assumptions in the exposure assessment was minimal, with deviations from the original log‐likelihood values between −5.0% and 4.7%. Although the differences between new RRs and original estimates were between −46% and +69%, patterns in dose‐dependent increases in lung cancer risk were similar to the original/published results. In the highest exposure categories, RRs were between 2.07 and 2.83 for average, and 1.22 to 2.23 for cumulative bitumen fume exposure. Assuming 10, 15 or 20‐year lags for average and cumulative exposures also did not alter the pattern of results.
ConclusionThese analyses suggest that a small increase in risk of lung cancer related to bitumen fume exposure depends only to a limited extent on the subjective judgments made by researchers and industry experts in the exposure assessment for this multi‐centre cohort.
Key wordsasphalt; bitumen fume; sensitivity analyses
A. C. Olsson1, J. Fevotte2, A. ‘tMannetje3, T. Fletcher4, D. Zaridze5, N. Szeszenia‐Dabrowska6, P. Rudnai7, J. Lissowska8, E. Fabianova9, A. Cassidy10, D. Mates11, V. Bencko12, L. Foretova13, V. Janout14, P. Brennan15, P. Boffetta15. 1International Agency for Research on Cancer; 2Institut Universitaire de Médecine du Travail, Université Claude Bernard, Lyon; 3Centre for Public Health Research, Massey University, Wellington; 4Public and Environmental Health Research Unit, London School of Hygiene and Tropical Medicine, London; 5Institute of Carcinogenesis, Cancer Research Center, Moscow; 6Department of Epidemiology, Nofer Institute of Occupational Medicine, Lodz; 7National Institute of Environmental Health, Budapest; 8Cancer Center and Maria Sklodowska‐Curie Institute of Oncology, Warsaw; 9Department of Occupational Health, Specialized State Health Institute, Banska Bystrica; 10Roy Castle Lung Cancer Research Programme, University of Liverpool Cancer Research Centre, University of Liverpool; 11Institute of Hygiene, Public Health, Health Services and Management, Bucharest; 12Institute of Hygiene and Epidemiology, Charles University, First Faculty of Medicine, Prague; 13Department of Cancer Epidemiology and Genetics, Masaryk Memorial Cancer Institute, Brno; 14Department of Preventive Medicine, Palacky University Faculty of Medicine, Olomouc; 15International Agency for Research on Cancer, Lyon
ObjectivesInvestigate the role of occupational exposure to PAHs in the aetiology of lung cancer in Central and Eastern Europe, which has the highest lung cancer incidence in the world, while controlling for potential confounders.
MethodsA multi‐centre case‐control study was conducted in 16 centres in seven European countries between 1998 and 2002. Occupational and socio‐demographic information was collected through interviews from 2861 newly diagnosed lung cancer cases and 3118 frequency matched controls. Exposure to PAHs was automatically recorded in jobs involving exposures to engine emissions, lubricating oil mist, cutting fluid and other mineral oil mist, carbon black dust, soot and fumes from combustion of coal, coke, petroleum oil, or wood, plastics pyrolysis, and asphalt, coal tar and pitch, and creosote fumes. Odds ratios (OR) of lung cancer were calculated after adjusting for occupational exposures to silica, asbestos, MMVF, arsenic, cadmium, chromium and tobacco smoking. Only men were included in these analyses.
Results1022 cases and 949 controls were ever exposed to occupational PAHs. The overall OR for ever exposure to PAH was not elevated (OR 1.05, 95% CI 0.91 to 1.21). Regarding duration, 30 years and more of exposure gave OR 1.37 (95% CI 1.09 to 1.72). Similarly, 5250 h of exposure showed an increased OR 1.28 (95% CI 1.03 to 1.59) with a tendency for trend (p value 0.05), as well as the highest category of cumulative exposure (OR 1.29, 95% CI 1.04 to 1.60) with a significant trend (p value 0.04). Applying a 20‐year lag, in which all jobs held within 20 years before year of interview were considered not exposed, did not modify the results. In stratified analysis, the OR for lung cancer following ever exposure to occupational PAHs was elevated among men in the Czech Republic, (OR 1.96, 95% CI 1.28 to 2.98) and the UK (OR 2.00, 95% CI 1.12 to 3.56); in the other countries the ORs ranged between 0.61 and 1.18. Current analyses include applying a hierarchical regression model to enhance the precision, improve accuracy and account for correlation between multiple exposures.
ConclusionMen in the highest exposure categories of occupational PAHs experienced a moderately increased risk of lung cancer.
Key wordslung neoplasm; occupational exposure; polycyclic hydrocarbons, aromatic
M. K. Schubauer‐Berigan1, J. A. Deddens1, K. Steenland2, W. T. Sanderson3, M. R. Petersen1. 1National Institute for Occupational Safety and Health; 2Emory University; 3University of Iowa
ObjectivesEvidence for the carcinogenicity of beryllium has been recently challenged on the basis of presumed confounding. The purpose of this study was to evaluate potential confounding of the association between different beryllium exposure metrics and lung cancer in a re‐analysis of data from a published case‐control study of workers at a beryllium processing facility in Reading, PA (USA).
MethodsA dataset from a previously published study (Sanderson et al. Am J Ind Med 2001;39:133–144) was analysed using conditional logistic regression to evaluate the association between the log of cumulative, average, and maximum beryllium exposure and lung cancer mortality. The dataset consisted of 142 cases and five age‐match controls per case. Adjustment was made independently for the potential confounders hire age and birth year, which had not been considered in the published analysis. Alternative adjustments to avoid using the logarithm of zero were also explored.
ResultsAdjustment for either birth cohort or hire age (two highly correlated factors) attenuated lung cancer risk associated with cumulative exposure; however, risk remained significantly associated with both average and maximum exposure using a 10‐year lag. Stratification of analyses by birth cohort found greater lung cancer risk from cumulative and average exposure for workers born before 1900 than for workers born later. The magnitude of the association between lung cancer and average or maximum exposure was not reduced by modifying the method used to take the log of exposure.
ConclusionIn this reanalysis, average and maximum (but not cumulative) beryllium exposures were related to lung cancer risk after adjustment for birth cohort. Confounding by birth cohort is likely related to differences in smoking patterns for workers born before 1900 and the tendency for workers hired during the World War II era to have been older at hire. A forthcoming NIOSH cohort study of 5492 workers, which includes quantitative exposure estimation for two additional beryllium processing facilities, will be described.
DisclaimerThe findings and conclusions in this presentation have not been formally disseminated by the National Institute for Occupational Safety and Health and should not be construed to represent any agency determination or policy.
Key wordsconfounding; beryllium; methods