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D. McElvenny1, B. G. Armstrong2. 1Epidemiology Group, Health & Safety Executive and Public & Environmental Research Unit, London School of Hygiene & Tropical Medicine; 2London School of Hygiene & Tropical Medicine
ObjectivesIn a previous meta‐analysis of formaldehyde exposure and respiratory cancer, Collins et al (J Occup Environ Med 1997;39(7):639–51) concluded that the available studies do not support a causal relationship between formaldehyde exposure and cancers of the nasopharynx, nose and nasal cavities, or lung. In 2006 the International Agency for Research on Cancer (IARC) working group concluded that the evidence for carcinogenicity in humans is adequate for nasopharyngeal cancer, is limited for sinonasal cancer and does not support a causal role for formaldehyde for lung cancer. The aim of this study was to carry out an updated meta‐analysis of occupational exposure to formaldehyde and cancers of the nasopharynx, nose and nasal cavities, and lung.
MethodsRelevant studies were identified using searches of electronic databases and from previous meta‐analyses. Meta‐analyses were carried out on the original scale for cohort studies (because of the problem of studies with zero exposed cases for nasopharyngeal cancer and sinonasal cancer) and were carried out on the log scale in the usual way for case‐control and other studies.
ResultsThe random effects meta‐RR for nasopharyngeal cancer for cohort studies was 2.10 (95% CI 0.36 to 4.55) based on nine studies containing 14 cases. The equivalent result for case‐control and other studies was 1.39 (1.10 to 1.76) (seven studies; 234 cases). For sinonasal cancer, the fixed effect meta‐RR was 0.58 (0.19 to 1.39) for cohort studies (11 studies; five cases) and 1.37 (1.10 to 1.70) for case‐control and other studies (six studies; 178 cases). The random effects meta‐RR for lung cancer was 0.77 (0.62 to 0.92) for cohort studies (17 studies; 1990 cases) and was 0.99 (0.91 to 1.08) for case‐control and other studies (five studies; 614 cases).
ConclusionThe results of the meta‐analysis support IARC's finding that there is an excess risk for nasopharyngeal cancer and that there is no evidence to support an association for lung cancer. The evidence for an excess risk for sinonasal cancer is limited to case‐control and other studies.
Key wordsmeta‐analysis; formaldehyde; cancer
T. L. Kirkham1, P. A. Demers1, C. McLeod2, L. Tamburic2, M. Koehoorn3. 1School of Occupational and Environmental Hygiene, UBC; 2Centre for Health Services and Policy Research, UBC, 3Health Care and Epidemiology, UBC
ObjectivesMesothelioma is well recognised as an occupational cancer. However, many jurisdictions compensate less than half of identified cases; this is thought to be largely due to cases not seeking compensation. We examine potential factors that may be associated with the lack of compensation for mesothelioma in British Columbia.
MethodsWe requested data on all compensated mesothelioma claims from WorkSafeBC (the provincial workers' compensation authority) and all mesothelioma cases from the British Columbia Cancer Agency (BCCA) registry from 1970 to 2005. Compensated and non‐compensated mesothelioma cases were compared by age‐at‐diagnosis, gender, cancer site, and geographical area. Compensation trends over time were also examined.
ResultsBetween 1970 and 2005, 1182 mesothelioma cases (mean age 67, 85% male) were identified from the BCCA registry and 485 from WorkSafeBC claims (mean age 63, 97% male). Eighty‐one percent (n=391) of WorkSafeBC claims were linked to BCCA cases resulting in an overall compensation rate of 33%. The registry reflects few cases prior to the 1980s, after which case numbers increased until a peak in 2001 (n=77). Currently the number of cases has plateaued. The proportion of compensated cases generally increased over time: 1970–1974 (4%), 1975–1979 (17%), 1980–1984 (22%), 1985–1989 (31%), 1990–1994 (30%), 1995–1999 (38%), 2000–2004 (42%), and 2005 (35%; decrease may be due to reporting or diagnosis lag). Mean age‐at‐diagnosis was similar for compensated (65, range 36–88 years) and uncompensated cases (68, range 14–104 years), however the very young and old (<35, 35–44 and 75+) were compensated less (0%, 25% and 23%, respectively) than those between 55 and 64 years of age (45%). Women were compensated much less than men (7% vs 38%, p<0.001). Compensation varied significantly by cancer site: pleura (37%), lung (18%), other/unspecified (14%), male reproductive organs (12%), peritoneum (9%), and female reproductive organs (0%) (p<0.001). In addition, compensation rates varied by geographical area: Kootenay Boundary (77%) and Northeast (64%) being highest compared to Richmond (26%), Okanagan (27%), Fraser East (29%) and Vancouver (30%).
ConclusionCompensation rates are increasing but are much lower than the 80% or more believed to be occupationally caused. Gender, age, geographical location, and site of cancer all influence the probability of being compensated for mesothelioma.
Key wordsmesothelioma; workers' compensation; occupational cancer
Y. S. Ahn1, S. Y. Jung2. 1Dongguk University International Hospital; 2Osan Hankook Hospital
ObjectivesMedical surveillance for exposure to asbestos has been conducted for Korean workers since 2000. The cancer mortality and morbidity associated with occupational asbestos exposure, mainly chrysotile, is described.
MethodsCancer mortality from 2000 to 2004 was analysed in a cohort containing 4829 asbestos exposed workers and 3039 asbestos non‐exposed workers belonging to the 207 company. Asbestos non‐exposed workers were selected among workers just exposed to noise from the same company. Standardised mortality ratios (SMR) and standardised rate ratios (SRR) were estimated by Poisson regression methods. Similar analyses for cancer morbidity were conducted, using cases identified from the admissions records of specialty hospitals.
Results22 all causes and seven cancer deaths (five cases of lung cancer, one stomach cancer and one liver cancer) were observed during 2000–2004. The all‐cancer, stomach cancer and liver cancer mortalities were non‐significantly low compared to the Korean general population. Only lung cancer in the asbestos exposed workers was significantly higher than in the Korean general population (SMR 3.47, 95% CI 1.12 to 8.10). There were 86 all‐cancer admissions in this cohort (the asbestos exposed and non‐exposed groups had the same number of cancer admissions) during 2000–2005. Compared to the noise exposed workers, asbestos exposed workers had significantly higher lung cancer morbidity (SRR 6.54, 95% CI 1.33 to 32.14). However all‐cancer (SRR 0.97, 95% CI 0.61 to 1.54), stomach (SRR 0.53, 95% CI 0.23 to 1.23), colon (and rectum) (SRR 0.64, 95% CI 0.22 to 1.83) and liver cancer (SRR 0.84, 95% CI 0.18 to 3.89) morbidity were non‐significantly low.
ConclusionThis asbestos worker cohort with short follow‐up periods exhibits a strong healthy worker effect (HWE). Only lung cancers appear to be significantly elevated compared to both the Korean general population and noise exposed workers. This suggested that chrysotile increased lung cancer as much as amphibole. However, more detailed investigation of confounding variables, especially smoking, and future follow‐up of this cohort will better define cancer risks in asbestos workers.
Key wordsasbestos; cancer mortality; lung cancer
F. Bochmann. BGIA ‐ Hauptverband der gewerblichen Berufsgenossenschaften
ObjectivesTo explore whether the observed association between silica exposure and lung cancer was confounded by exposure to other occupational carcinogens, we conducted a nested case‐control study among a cohort of male workers in 29 Chinese mines and potteries.
Methods511 lung cancer cases and 1879 matched controls were selected. Exposure to respirable silica as well as relevant occupational confounders were evaluated quantitatively based on historical industrial hygiene data. The relationship between silica exposure and lung cancer mortality was analysed by conditional logistic regression analysis adjusted for exposure to arsenic, polycyclic aromatic hydrocarbons (PAHs) and radon, and smoking habit.
ResultsIn a crude analysis adjusted for smoking only, a significant trend of increasing risk of lung cancer with exposure to silica was found for tin and copper/iron miners, and pottery workers. However, after the relevant occupational confounders were adjusted, no association can be observed between silica exposure and lung cancer mortality (per mg/m3‐year increase in silica exposure: OR 1.01, 95% CI 0.99 to 1.02).
ConclusionThe results of this study suggest that the observed excess risk of lung cancer among silica exposed Chinese workers is more likely due to exposure to other occupational carcinogens such as arsenic and PAHs rather than due to exposure to respirable silica.
Key wordsrespirable silica; lung cancer; risk assessment
D. Taeger1, U. Krahn2, T. Wiethege1, K. Ickstadt2, G. Johnen1, A. Eisenmenger3, H. Wesch3, T. Bruening1, B. Pesch1. 1Berufsgenossenschaftliches Forschungsinstitut fuer Arbeitsmedizin (BGFA), Institute of Ruhr‐University Bochum; 2Department of Statistics, University of Dortmund; 3German Cancer Research Center (DKFZ)
ObjectivesIn East Germany, uranium mining was undertaken on a large scale from 1946 to 1990 at the WISMUT company. This analysis evaluates the lung cancer risk attributed to occupational exposures to radon, quartz and arsenic by analysing pathological information from the WISMUT tissue repository in association with a comprehensive job‐exposure matrix.
MethodsThe study population comprised all male miners with data collected in the WISMUT repository who died from lung cancer (ICD‐9 162) and from diseases of the circulatory system (ICD‐9 390–459) with complete information on occupational exposure to radon, quartz and arsenic. To estimate the risk of dying from lung cancer in relation to the risk of dying from diseases of the circulatory system, we calculated standardised proportional mortality ratios (SPMR) comparing that ratio in miners with the general population of East Germany. In an additional multivariate logistic regression, the lung cancer cases were compared to the cases with diseases of the circulatory system regarding their cumulative exposure (reference <1st quartile; medium 1st–3rd quartile; high >3rd quartile) for radon, quartz and arsenic. We also considered age at time of death and year of death. A sensitivity analysis was performed to account for temporal effects by using re‐sampling procedures.
ResultsBased on 1593 lung cancer cases, a SPMR of 2.9 (95% CI 2.7 to 3.0) was estimated. Statistically significant effects of radon were found for medium (odds ratio (OR) 1.2; 95% CI 1.1 to 1.5) and high radon exposure (OR 1.4; 95% CI 1.1 to 1.7). For arsenic, medium exposure was associated with an elevated OR of 1.4 (95% CI 1.3 to 1.6). No increased lung cancer risk was found for quartz exposure. The results of the sensitivity analysis confirmed these results but with lower precision.
ConclusionAmong German uranium miners, relatively more deaths from lung cancer were observed than expected from the general population. Radon and arsenic turned out to be risk factors for lung cancer. Quartz could not be identified as a risk factor in the comparison of lung cancer with diseases of the circulatory system. That might because quartz dust is also a risk factor for diseases of the circulatory system.
Key wordslung cancer; occupational exposure; uranium miners
L. A. Tse, I. T. S. Yu. Center for Occupational and Environmental Health Studies, School of Public Health, The Chinese University of Hong Kong
ObjectivesAlthough cigarette smoking has been shown to be a stronger risk factor for squamous cell carcinoma than for adenocarcinoma, there is limited evidence to suggest that this is also the case for environmental tobacco smoke (ETS). Difficulties encountered in most previous male lung cancer studies in exploring the association with workplace ETS exposure included few non‐smoking lung cancer cases available, limited information on exposure assessment of ETS, and not controlling for the confounding effect from ETS exposure at home. The objective of this study is to demonstrate associations between various indicators of workplace ETS exposures and different histological subtypes of lung cancer among non‐smoking males after taking these limitations into consideration.
MethodsAs part of a large case‐control study in Hong Kong, we collected lifetime histories of ETS exposures at home and/or the workplace in 132 incident cases of biopsy confirmed primary lung cancer and 419 non‐cancer controls from the same hospital during 2004–06, all of whom were males and reported being lifetime non‐smokers. Lifetime ETS exposures were characterised using various indicators including ever ETS exposure, ETS exposure years, number of cohabitants and/or coworkers who smoked, and cumulative ETS exposure (sum of smoking coworkers*ETS hours per day*years). Unconditional multiple logistic regression analyses were performed.
ResultsNon‐smoking males ever exposed to ETS at the workplace had a 26% increase in lung cancer risk (odds ratio (OR) 1.26, 95% CI 0.83 to 1.90) after adjusting for the potential confounding effects of parental cancer history, lifetime cooking years, occupational carcinogens exposures, and ETS exposures at home. This borderline excess risk was mainly a result of an increased risk of adenocarcinoma. A significantly increased risk of adenocarcinoma was observed for workers classified as ever (OR 1.70, 95% CI 1.04 to 2.77) and in the highest level of cumulative workplace ETS exposures (OR 1.72, 95% CI 1.02 to 2.90), whereas the associations with years of workplace ETS exposure and number of smoking coworkers were not consistent. Nevertheless, strong dose–response relationships were observed between adenocarcinoma and all indicators of ETS exposure after combining lifetime ETS exposures from both home and the workplace.
ConclusionOur study provides positive evidence of an association between adenocarcinoma and workplace ETS exposure.
Key wordsadenocarcinoma; environmental tobacco smoke; workplace
A. Sapkota1, M. Hashibe2, V. Gajalakshmi3, D. Jetly4, S. Roychowdhury5, R. Dikshit6, P. Brennan2, P. Boffetta2. 1Maryland Institute of Applied Environmental Health; 2International Agency for Research on Cancer, Lyon, France; 3Epidemiological Research Center, Chennai, India; 4Gujarat Cancer and Research Institute, Ahmedabad, India; 5Chittaranjan National Cancer Institute, Kolkata, India; 6Tata Memorial Hospital, Mumbai, India
ObjectivesThe Indian subcontinent represents one of the high risk areas for hypopharyngeal/laryngeal cancer. Very few studies have evaluated the occupational risk factors of this cancer as well as lung cancer in India.
MethodsUsing a hospital based case‐control study conducted in four urban centres in India (Ahmedabad, Bhopal, Kolkata and Chennai), we investigated various occupations as risk factors for hypopharyngeal/laryngeal and lung cancer among Indian men who were either ex‐ or never smokers. We used unconditional logistic regression to compute odds ratios (ORs) and 95% CIs after adjusting for centre, age, socioeconomic status and tobacco person years.
ResultsAn increased risk of hypopharyngeal/laryngeal cancer was observed among bricklayers and transportation workers (OR 4.88, 95% CI 1.26 to 18.82 and OR 4.42, 95% CI 1.50 to 13.02, respectively). Transportation workers also had an increased risk of lung cancer (OR 5.02, 95% CI 1.53 to 16.50), with a significant dose–response relationship (p trend=0.04). Similar results were also observed when the analysis was restricted to drivers only, with a significant dose–response relationship for lung cancer (p trend=0.02).
ConclusionOur findings suggest that male transportation workers in India may have an increased risk of hypopharyngeal/laryngeal and lung cancer, while bricklayers and carpenters may have an increased risk of hypopharyngeal/laryngeal cancer.
Key wordslaryngeal cancer; lung cancer; occupation
C. F. Robinson, P. A. Sullivan, J. T. Walker. The National Institute for Occupational Safety and Health (NIOSH), USA
ObjectivesLung cancer is the leading cause of cancer death in US women, accounting for 454 deaths per 1 million women in 2000. Although tobacco use continues to be the single most important risk factor for lung cancer mortality, further reduction of the burden of lung cancer can be made through prevention of occupational exposure to lung carcinogens.
MethodsTrends in lung cancer mortality were evaluated for women employed in all sectors of US industry. Analyses of 3974622 deaths from 28 US states for 1984–1998 revealed elevated proportionate mortality ratios (PMRs) for lung cancer among 194382 US white, 18225 black and 1515 Hispanic women by usual industry sector.
ResultsThe highest significantly elevated proportionate mortality was experienced by women in four manufacturing sub‐sectors: sawmills and planning mills (PMR=142), household appliance manufacturing (PMR=135), ordnance manufacturing (PMR=132) and motor vehicle and motor vehicle equipment manufacturing (PMR=130). Elevated proportionate mortality was also observed in the sector selling wholesale machinery and equipment (PMR=145). When trends were evaluated, proportionate mortality increased over the 15 year interval for only the trucking service sector and the household appliance manufacturing sector. For black women, proportionate mortality was highest among workers usually employed in three transportation sectors (trucking PMR=244, bus services and urban transit PMR=182, and the US Postal Service PMR=139), utilities (electric light and power PMR=199) and in a communications sub‐sector (telephone, wire and radio PMR=149). Among black women, the public administration sector experienced a 47% excess proportionate mortality. While based on a small number of deaths, the highest excess lung cancer proportionate mortality among Hispanic women occurred in the banking industry (PMR=333) and three manufacturing sub‐sectors (industrial chemicals PMR=590, rubber and plastics PMR=278, and printing and publishing PMR=330). Lung cancer mortality in the nursing and health care industry and government agencies appeared to be increasing.
ConclusionSmoking prevalence by sector was reviewed in the context of these results. Further follow‐up is recommended to investigate mortality in industrial settings where lung cancer mortality appears to be increasing or has remained consistently elevated.
Key wordslung cancer in women; occupational lung cancer; occupational epidemiology