Risk of childhood cancer and adult lung cancer after childhood exposure to passive smoke: A meta-analysis

We identified more than 30 studies on the association between exposure to maternal tobacco smoke during pregnancy and cancer in childhood. We combined their results in meta-analyses based on a random effects model. The results of the meta-analyses suggest a small increase in risk of all neoplasms [relative risk (RR) 1.10; 95% confidence interval (CI), 1.03-1.19; based on 12 studies], but not of specific neoplasms such as leukemia (RR 1.05; CI, 0.82-1.34; 8 studies) and central nervous system tumors (RR 1.04; CI, 0.92-1. 18; 12 studies). Results for other specific neoplasms were sparse, but the available data did not suggest a strong association for any type of tumor. No clear evidence of dose response was present in the studies that addressed this issue. The results on exposure to maternal tobacco smoke before or after pregnancy are too sparse to allow a conclusion. The results on exposure to paternal tobacco smoke suggest an association with brain tumors (RR 1.22; CI, 1.05-1. 40; based on 10 studies) and lymphomas (RR 2.08; CI, 1.08-3.98; 4 studies). The data are too sparse for the other neoplasms, although the results of a few recent large studies are compatible with a weak carcinogenic effect of paternal smoke. For exposure from either maternal or paternal smoke, bias and confounding cannot yet be ruled out. Further studies are needed to confirm the hypothesis that parental tobacco smoke, from the father in particular, is a risk factor of childhood cancer. Results on the risk of lung cancer in adulthood and childhood passive smoking exposure are available from 11 studies: they do not provide evidence of an increased risk (summary RR 0.91; CI, 0.80-1.05).     

Mesothelioma and lung cancer among motor vehicle mechanics: a meta-analysis

We conducted a systematic review and analysis of the epidemiological literature that examines the risk of lung cancer and mesothelioma among motor vehicle mechanics who may have been engaged in brake repair and, thus, were potentially exposed to asbestos. All relevant studies were classified into three tiers according to their quality. Tier III (lowest quality) studies were cited for completeness, but were not included in the meta-analysis. Meta relative risks (meta-RRs) were calculated for mesothelioma and lung cancer using both fixed and random effects models for Tiers I and II, separately, followed by stratified analyses based on study design or exposure characterization (garage workers versus brake workers) and, for lung cancer studies, based on adequate adjustment for smoking. The meta-analysis for Tier I (higher quality) and Tier II (lower quality) studies of mesothelioma yielded RR estimates of 0.92 (95% CI 0.55-1.56) and 0.81 (95% CI 0.52-1.28), respectively. Further stratification according to exposure characterization did not affect the results. The meta-analysis for lung cancer produced RR estimates of 1.07 (95% CI 0.88-1.31) for Tier I and 1.17 (95% CI 1.01-1.36) for Tier II. When the lung cancer analysis was limited to studies that used adequate control for smoking, the resulting RR estimate was 1.09 (95% CI 0.92-1.28). Based on these findings, we conclude that employment as a motor vehicle mechanic does not increase the risk of developing mesothelioma. Although some studies showed a small increase in risk of lung cancer among motor vehicle mechanics, the data on balance do not support a conclusion that lung cancer risk in this occupational group is related to asbestos exposure.     

Dairy products, dietary calcium and vitamin D intake as risk factors for prostate cancer: a meta-analysis of 26,769 cases from 45 observational studies

In this study, we examined the available evidence and sources of heterogeneity for studies of dairy products, calcium, and vitamin D intake and the risk of prostate cancer. We pooled data from 45 observational studies using a general variance-based, meta-analytic method employing CIs. Summary relative risks (RRs) were calculated for specific dairy products such as milk and dairy micronutrients. Sensitivity analyses were performed to test the robustness of these summary measures of effect. Cohort studies showed no evidence of an association between dairy [RR = 1.06; 95% confidence interval (CI) = 0.92-1.22] or milk intake (RR = 1.06; 95% CI = 0.91-1.23) and risk of prostate cancer. This was supported by pooled results of case-control analyses (RR = 1.14; 95% CI = 1.00-1.29), although studies using milk as the exposure of interest were heterogeneous and could not be combined. Calcium data from cohort studies were heterogeneous. Case-control analyses using calcium as the exposure of interest demonstrated no association with increased risk of prostate cancer (RR = 1.04; 95% CI = 0.90-1.15). Dietary intake of vitamin D also was not related to prostate cancer risk (RR = 1.16; 95% CI = 0.98-1.38). The data from observational studies do not support an association between dairy product use and an increased risk of prostate cancer.     

Cancer and occupational exposure to inorganic lead compounds: a meta-analysis of published data.

OBJECTIVES--To review and summarise the epidemiological evidence on the carcinogenicity of occupational exposure to inorganic lead. METHODS--Case-control and cohort studies were reviewed and combined for meta-analysis. Fixed and random effect methods were used to estimate the summary effects. RESULTS--The combined results show a significant excess risk of overall cancer, stomach cancer, lung cancer, and bladder cancer, with relative risk ratios (RRs) and 95% confidence intervals (95% CIs) in the meta-analysis of 1.11 (1.05-1.17), 1.33 (1.18-1.49), 1.29 (1.10-1.50), and 1.41 (1.16-1.71) respectively. The RR (95% CI) for kidney cancer was also high, but did not reach significance (1.19 (0.96-1.48)). A separate analysis of studies of heavily exposed workers provided slightly increased RRs for cancers of the stomach (1.50) and lung (1.42). CONCLUSIONS--The findings from the workers with heavy exposure to lead provided some evidence to support the hypothesis of an association between stomach and lung cancer and exposure to lead. The main limitation of the present analysis is that the excess risks do not take account of potential confounders, because little information was available for other occupational exposures, smoking, and dietary habits. To some extent, the risk of lung cancer might be explained by confounders such as tobacco smoking and exposure to other occupational carcinogens. The excess risk of stomach cancer may also be explained, at least in part, by non-occupational factors. For bladder and kidney cancers, the excess risks are only suggestive of a true effect because of possible publication bias.     

Occupation and lung cancer risk in the province of Trieste: a case-control study]

To investigate the relationship between occupation and lung cancer, a case-control study was performed in the province of Trieste, Italy, where metallurgical and mechanical industries, dock activities and shipbuilding and ship repairing are predominant. Through the local Cancer Registry, pathology records of 938 men who died of primary lung cancer (ICD 162) in a five-year period were examined. Residential, smoking and occupational histories were obtained from interviews of next of kin of 756 cases and 756 age-matched male controls (+/- 2 years). Occupational exposures to lung carcinogens were assessed according to a job-title based approach, identifying industries/occupations with well-recognized lung carcinogen exposures (list A) and industries/occupations with suspected lung carcinogen exposures (list B). Exposure to asbestos was classified as absent, possible or definite. After adjustment for cigarette smoking (four levels) and residence (three levels), a significant association was found between lung cancer and occupations in list A (RR = 2.28, 95% CI = 1.70-3.07) and in list B (RR = 1.33, 95% CI = 1.04-1.71). A significant excess risk was found for workers with definite exposure to asbestos when compared to those with no exposure to lung carcinogens (RR = 1.99, 95% CI = 1.43-2.76). A very high relative risk was observed among heavy smokers with definite exposure to asbestos (RR = 42.8). A stratified analysis showed that the combined effect of asbestos and smoking was compatible with that expected under a multiplicative model. The overall attributable risk in the population (ARp) for cigarette smoking was found to be 87.6%. The ARp fraction for occupations with well-established exposures to lung carcinogens (list A) was 16.2%. The ARp fraction increased to 25.5% (85% CI = 1.4-34.6) when occupations with suspected exposure to lung carcinogens (list B) were included. The ARp fraction for possible or definite exposure to asbestos was 20.1% (95% CI = 11.6-28.6).     

Occupational exposure and lung cancer risk in a coastal area of Northeastern Italy

Summary A case-control study of lung cancer and occupational exposure was conducted in a coastal area of Northeastern Italy where metallurgical and mechanical industries, docks and shipyards are located. Cases comprised 756 men who died of primary lung cancer in a 5-year period. Controls comprised 756 male subjects dying from other causes during the same period. Occupational exposures to lung carcinogens were assessed according to a job title-based approach, using two separate lists of industries/occupations recognized as being causally associated (list A) or suspected of being causally associated (list B) with lung cancer in humans. Exposure to asbestos was classified as absent, possible, or definite. After adjustment for cigarette smoking and place of residence, a significant association was found between lung cancer and occupations in both list A [relative risk (RR) = 2.25, 95% confidence interval (CI) = 1.68–3.03] and list B (RR = 1.33, 95% CI = 1.03–1.71). A significant excess risk was found for workers with definite exposure to asbestos as compared to those with no exposure to lung carcinogens (RR = 1.98, 95% CI = 1.42–2.75). Among occupations with recognized exposure to lung carcinogens other than asbestos, a significant excess risk for lung cancer was observed in iron and metalware workers. In occupational groups with definite exposure to asbestos, elevated risk estimates were found for shipyard workers, dockworkers, carpenters, and electricians. The combined effect of smoking and asbestos was found to be compatible with that expected under a multiplicative model. The overall population-attributable risk (ARp) for cigarette smoking was found to be 87.5%. The ARp estimate for occupations in list A was 16.0%. The estimate increased to 25.3% (95% CI = 16.2–34.4) when occupations in list B were included. The ARp estimate for possible or definite exposure to asbestos was 20.0% (95% CI = 11.5–28.5). With regard to the histologic types of lung cancer, significant associations were found between definite exposure to asbestos and squamous cell carcinoma (RR = 2.00, 95% CI = 1.28-–3.11), small cell carcinoma (RR = 2.11, 95% CI = 1.31–3.39), and adenocarcinoma (RR = 2.16, 95% CI = 1.32–3.53).     

Operating room nursing and lung cancer risk in a cohort of female registered nurses

OBJECTIVES: Smoke generated during laser surgery and electrocautery contains respiratory irritants and human carcinogens. Although laboratory and animal studies have demonstrated that this smoke has inflammatory and mutagenic potential, no population-based studies of the health effects of exposure to surgical smoke have been published. We examined the association between duration of employment as an operating room nurse, a proxy measure for surgical smoke exposure, and subsequent lung cancer risk. METHODS: This study was conducted among 86 747 women in the Nurses' Health Study. Information on the duration of prior operating room employment was collected in 1984, and the women were followed for incident, confirmed lung cancer. Cox proportional hazards regression was used to model the incidence rate ratio of lung cancer for each exposure category using women with no prior operating room employment for comparison. All of the models were adjusted for age, smoking history, passive smoke exposure, fruit and vegetable consumption, and alpha carotene and lycopene intake. RESULTS: A history of operating room employment was not associated with an increased rate of lung cancer in multivariable analyses [rate ratio (RR) 0.99, 95% confidence interval (95% CI) 0.86-1.15]. In fact, nurses in the highest exposure category, > or =15 years of operating room employment, had a significantly lower rate of lung cancer than nurses with no prior operating room employment (RR 0.58, 95% CI 0.37-0.91), possibly due to confounding by overall health status or residual confounding by smoking history. CONCLUSIONS: Long-term exposure to surgical smoke, as measured by the duration of operating room employment, does not appear to increase the risk of lung cancer.     

Smoking and lung cancer in China: combined analysis of eight case-control studies.

Smoking is well established as a principal risk factor for lung cancer. The risk of lung cancer is about ten times higher in smokers in Western countries. In China, a number of epidemiological studies have investigated the association between lung cancer and smoking and in the present paper, a combined analysis of eight such case-control studies is described. The summary odds ratio (OR), calculated by the Mantel-Haenszel method, and attributable risk (AR) of lung cancer associated with smoking were calculated from the combined data which were obtained from a literature review. The eight case-control studies were conducted in Beijing, Shanghai, Shenyang, Nanjing, Harbin, Zhengzhou, Taiyuan, and Nanchang, yielding a total of 4081 lung cancer cases and 4338 controls. The summary OR of lung cancer associated with smoking was 2.17 (95% CI (confidence interval): 1.98-2.39). The OR were 3.09 (95% CI: 2.61-3.66) for males and 2.30 (95% CI: 1.96-2.69) for females. The AR were 38.2% for both sexes, 56.7% for males and 25.5% for females. Risks of 1.00, 1.03, 2.04, and 3.33 showed a dose-response relationship between lung cancer and number of cigarettes smoked per day. There were also significant dose-response relationships of lung cancer with duration of smoking (OR = 1.00, 1.02, 2.66), and age at start of smoking (OR = 1.00, 3.30, 2.36, 1.18). The OR and AR of lung cancer associated with smoking in China were much lower than those reported in Western countries and the possible reasons for this are discussed.     

Physical activity, diabetes, and risk of thyroid cancer: a systematic review and meta-analysis

Thyroid cancer incidence has been increasing more rapidly over time than the occurrence of cancers of other sites, and interest in potential adverse relations of diabetes and lack of physical activity to thyroid cancer risk is accumulating. We conducted a systematic review and meta-analysis of published epidemiologic studies on the relations of physical activity and diabetes to thyroid cancer according to the Meta-analysis of Observational Studies in Epidemiology guidelines. Published studies were identified through a search in MEDLINE and EMBASE. Random-effects models were used to summarize thyroid cancer risk estimates comparing high versus low levels of physical activity, and separately, comparing individuals with diabetes versus those without diabetes. Meta-regression analyses were performed to evaluate potential effect modification by study design and thyroid cancer risk factors. Information was extracted from seven studies of physical activity and thyroid cancer and from six studies of diabetes and thyroid cancer. The number of individuals from studies on physical activity was 939,305 (yielding 2,250 incident thyroid cancer cases) and from studies on diabetes it was 960,840 (yielding 1,230 cases). The summary relative risk (RR) estimate from cohort and case–control studies combined indicated no association between physical activity and thyroid cancer (summary RR 1.06, 95 % confidence interval (CI) 0.79–1.42). Subgroup-analyses revealed a significant positive association between physical activity and thyroid cancer in cohort studies (summary RR 1.28; 95 % CI 1.01–1.63), whereas the relation was suggestively inverse in case–control studies (summary RR 0.70; 95 % CI 0.48–1.03; p for heterogeneity = 0.005). Individuals with diabetes showed a borderline statistically significant increased risk of thyroid cancer compared with those without diabetes (summary RR 1.17; 95 % CI 0.99–1.39). The relations of physical activity and diabetes to thyroid cancer were not modified by sex, number of adjustment factors, and adjustments for adiposity, smoking, and study quality. In this comprehensive systematic review and meta-analysis, no significant association between physical activity and thyroid cancer was found. Diabetes showed a suggestive positive relation with risk of thyroid cancer.     

Exposure to nickel compounds and smoking in relation to incidence of lung and nasal cancer among nickel refinery workers.

OBJECTIVES: To investigate the relation between occupational hazards among nickel refinery workers and their exposure to different forms of nickel over time and the interaction between smoking and total exposure to nickel. METHODS: The cohort consisted of 379 workers with first employment 1916-40 and at least three years of employment and 4385 workers with at least one year of employment 1946-83. Data on smoking (ever or never) were available for almost 95% of the cohort. Two analyses were used, indirect standardisation from observed and expected numbers and Poisson regression. RESULTS: During the follow up 1953-93, 203 new cases of lung cancer were observed v 68 expected (standardised incidence ratio (SIR) 3.0, 95% confidence interval (95% CI) 2.6-3.4) and 32 cases of nasal cancer were observed v 1.8 expected (SIR 18.0, 95% CI 12-25). The Poisson regression analysis showed an excess risk of lung cancer in association with exposure to soluble forms of nickel, with a threefold increase in relative risk (RR) (P < 0.001) and a multiplicative effect of smoking and exposure to nickel. The RRs were 1.1 (95% CI 0.2-5.1) for exposed workers who had never smoked and 5.1 (95% CI 1.3-20.5) for exposed workers who smoked. CONCLUSION: It is not possible to state with certainty which specific nickel compounds are carcinogenic, but a significant excess risk was found for workers exposed to soluble nickel alone or in combination with other forms of nickel. The present study suggests a multiplicative effect of smoking and nickel exposure.     

Diesel exhaust exposure and mortality among males in the American Cancer Society prospective study

In 1982, the American Cancer Society enrolled over 1.2 million American men and women in a prospective mortality study of cancer and other causes in relation to different risk factors. The 2-year mortality of 461,981 males aged 40-79 years with known smoking habit has been analyzed in relation to exposure to diesel exhaust (DE) and to employment in selected occupations related to DE exposure. The relative risk (RR) for all causes of death for those exposed was 1.05 (95% confidence interval [CI]: 0.97-1.13). For lung cancer, the RR was 1.18 (95% CI: 0.97-1.44). A dose-response effect was present. Railroad workers, heavy equipment operators, miners, and truck drivers had a higher mortality both for all causes and for lung cancer when compared with subjects with other occupations and no exposure to DE. Truck drivers exposed to DE were not at excess risk of lung cancer if compared with truck drivers unexposed to DE, but a trend of increasing risk with duration of exposure was suggested. DE exposure was also associated with increase in mortality for accidents, cerebrovascular disease, arteriosclerosis, and cirrhosis of the liver. An association based on small numbers was also present for Hodgkin's disease and lymphoid leukemia. No association with chronic non-neoplastic pulmonary diseases or with bladder cancer was found.     

Dairy Products,Dietary Calcium and Vitamin D Intake as Risk Factors for Prostate Cancer: A Meta-Analysis of 26,769 Cases From 45 Observational Studies

In this study, we examined the available evidence and sources of heterogeneity for studies of dairy products, calcium, and vitamin D intake and the risk of prostate cancer. We pooled data from 45 observational studies using a general variance-based, meta-analytic method employing CIs. Summary relative risks (RRs) were calculated for specific dairy products such as milk and dairy micronutrients. Sensitivity analyses were performed to test the robustness of these summary measures of effect. Cohort studies showed no evidence of an association between dairy [RR = 1.06; 95% confidence interval (CI) = 0.92–1.22] or milk intake (RR = 1.06; 95% CI = 0.91–1.23) and risk of prostate cancer. This was supported by pooled results of case-control analyses (RR = 1.14; 95% CI = 1.00–1.29), although studies using milk as the exposure of interest were heterogeneous and could not be combined. Calcium data from cohort studies were heterogeneous. Case-control analyses using calcium as the exposure of interest demonstrated no association with increased risk of prostate cancer (RR = 1.04; 95% CI = 0.90–1.15). Dietary intake of vitamin D also was not related to prostate cancer risk (RR = 1.16; 95% CI = 0.98–1.38). The data from observational studies do not support an association between dairy product use and an increased risk of prostate cancer.     

Smoking imputation and lung cancer in railroad workers exposed to diesel exhaust

BACKGROUND: An association between diesel exhaust exposure and lung cancer mortality in a large retrospective cohort study of US railroad workers has previously been reported. However, specific information regarding cigarette smoking was unavailable. METHODS: Birth cohort, age, job, and cause of death specific smoking histories from a companion case-control study were used to impute smoking behavior for 39,388 railroad workers who died 1959-1996. Mortality analyses incorporated the effect of smoking on lung cancer risk. RESULTS: The smoking adjusted relative risk of lung cancer in railroad workers exposed to diesel exhaust compared to unexposed workers was 1.22 (95% CI = 1.12-1.32), and unadjusted for smoking the relative risk was 1.35 (95% CI = 1.24-1.46). CONCLUSIONS: These analyses illustrate the use of imputation in record-based occupational health studies to assess potential confounding due to smoking. In this cohort, small differences in smoking behavior between diesel exposed and unexposed workers did not explain the elevated lung cancer risk.     

Welding and lung cancer in Central and Eastern Europe and the United Kingdom

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.     

Passive smoking and lung cancer: a cumulative meta-analysis

OBJECTIVE: To review the epidemiological evidence for the association between passive smoking and lung cancer. METHOD: Primary studies and meta-analyses examining the relationship between passive smoking and lung cancer were identified through a computerised literature search of Medline and Embase, secondary references, and experts in the field of passive smoking. Primary studies meeting the inclusion criteria were meta-analysed. RESULTS: From 1981 to the end of 1999 there have been 76 primary epidemiological studies of passive smoking and lung cancer, and 20 meta-analyses. There were 43 primary studies that met the inclusion criteria for this meta-analysis; more studies than previous assessments. The pooled relative risk (RR) for never-smoking women exposed to environmental tobacco smoke (ETS) from spouses, compared with unexposed never-smoking women was 1.29 (95% CI 1.17-1.43). Sequential cumulative meta-analysed results for each year from 1981 were calculated: since 1992 the RR has been greater than 1.25. For Western industrialised countries the RR for never-smoking women exposed to ETS compared with unexposed never-smoking women, was 1.21 (95% CI 1.10-1.33). Previously published international spousal meta-analyses have all produced statistically significant RRs greater than 1.17. CONCLUSIONS: The abundance of evidence in this paper, and the consistency of findings across domestic and workplace primary studies, dosimetric extrapolations and meta-analyses, clearly indicates that non-smokers exposed to ETS are at increased risk of lung cancer. IMPLICATIONS: The recommended public health policy is for a total ban on smoking in enclosed public places and work sites.     

Smoking and the sudden infant death syndrome

The aims of this review are (a) to critically examine the epidemiologic evidence for a possible association between smoking and the sudden infant death syndrome (SIDS), (b) to review the pathology and postulated physiological mechanism(s) by which smoking might be causally related to SIDS, and (c) to provide recommendations for SIDS prevention in relation to tobacco smoking. Over 60 studies have examined the relation between maternal smoking during pregnancy and risk of SIDS. With regard to prone-sleep-position intervention programs, the pooled relative risk associated with maternal smoking was RR = 2.86 (95% CI = 2.77, 2.95) before and RR = 3.93 (95% CI = 3.78, 4.08) after. Epidemiologically, to distinguish the effect of active maternal smoking during pregnancy from involuntary tobacco smoking by the infants of smoking mothers is difficult. Clear evidence for environmental tobacco smoke exposure can be obtained by examining the risk of SIDS from paternal smoking when the mother is a non-smoker. Seven such studies have been carried out. The pooled unadjusted RR was 1.49 (95% CI = 1.25, 1.77). Consideration of the pathological and physiological effects of tobacco suggests that the predominant effect from maternal smoking comes from the in utero exposure of the fetus to tobacco smoke. Assuming a causal association between smoking and SIDS, about one-third of SIDS deaths might have been prevented if all fetuses had not been exposed to maternal smoking in utero.     

Meta-analysis of studies of passive smoking and lung cancer: effects of study type and continent

BACKGROUND: To calculate a pooled estimate of relative risk (RR) of lung cancer associated with exposure to passive smoking in never smoking women exposed to smoking spouses. This study is an updated meta-analysis that also assesses the differences between estimated risks according to continent and study type using meta-regression. METHODS: From a total of 101 primary studies, 55 studies are included in this meta-analysis, of which, 7 are cohort studies, 25 population-based case-control and 23 non-population-based case-control studies. Twenty previously published meta-analyses are also reviewed. Fixed and random effect models and meta-regression are used to obtain pooled estimates of RR and P-value functions are used to demonstrate consistency of results. RESULTS: The pooled RR for never-smoking women exposed to passive smoking from spouses is 1.27 (95% CI 1.17-1.37). The RR for North America is 1.15 (95% CI 1.03-1.28), Asia, 1.31 (95% CI 1.16-1.48) and Europe, 1.31 (1.24-1.52). Sequential cumulative meta-analysis shows no trend. There is no strong evidence of publication bias. CONCLUSIONS: The abundance of evidence, consistency of finding across continent and study type, dose-response relationship and biological plausibility, overwhelmingly support the existence of a causal relationship between passive smoking and lung cancer.     

Lung cancer: is there an association with socioeconomic status in The Netherlands?

STUDY OBJECTIVE--To evaluate if there are differences in lung cancer incidence between socioeconomic groups in the Netherlands and if so, if smoking habits and other lifestyle characteristics could explain these differences. DESIGN--Prospective cohort study. Baseline measurement included information on socioeconomic status, smoking habits, and other covariates by means of a self-administered questionnaire. Follow up was established by computerised record linkage to cancer registries and a pathology register. SETTING--Population originating from 204 municipalities in The Netherlands. PARTICIPANTS--58,279 men aged 55-69 years in September 1986. After 3.3 years of follow up 490 microscopically confirmed incident lung cancer cases were detected. MAIN RESULTS--An inverse association between lung cancer risk and highest level of education was found, which persisted after adjustment for age, smoking, dietary intake of vitamin C, beta-carotene and retinol (rate ratio (RR) highest/lowest level of education = 0.52, 95% CI 0.33, 0.82, trend p < 0.001). Men with a lower white collar profession had a significantly lower relative rate of lung cancer compared with blue collar workers (RR = 0.66, 95% CI 0.47, 0.96), but after adjustment for smoking habits this difference was reduced (RR = 0.73, 95% CI 0.51, 1.08). CONCLUSIONS--There is an inverse association between highest level of education and lung cancer, which is still apparent after adjustment for age, smoking, dietary intake of vitamin C, beta-carotene and retinol. The significantly lower lung cancer risk of lower white collar workers compared with the risk of blue collar workers could be partially explained by smoking habits.     

Case-control study on occupational exposure to diesel exhaust and lung cancer risk.

The association between lung cancer and occupations with probable exposure to diesel exhaust (DE) was studied among 2,584 cases and 5,099 hospital controls. The crude odds ratio (OR) for probable exposure was 1.31 (95% confidence interval [CI] 1.09-1.57), but adjustment for smoking and other confounders reduced the estimate to 0.95 (95% CI = 0.78-1.16). Similar results were observed for truck drivers, the only occupational category large enough for separate analysis. Data on self-reported exposure for 477 cases and 946 controls revealed a crude OR of 1.45 (95% CI = 0.93-2.27), which was reduced to 1.21 (95% CI = 0.78-2.02) after controlling for smoking and other confounders. The present results and a review of the literature do not definitively support an etiologic association between DE exposure and elevated lung cancer risk.     

Lung cancer risk in painters: a meta-analysis

We conducted a meta-analysis to quantitatively compare the association between occupation as a painter and the incidence or mortality from lung cancer. PubMed and the reference lists of pertinent publications were searched and reviewed. For the meta-analysis, we used data from 47 independent cohort, record linkage, and case-control studies (from a total of 74 reports), including > 11,000 incident cases or deaths from lung cancer among painters. Three authors independently abstracted data and assessed study quality. The summary relative risk (meta-RR, random effects) for lung cancer in painters was 1.35 [95% confidence interval (CI), 1.29-1.41; 47 studies] and 1.35 (95% CI, 1.21-1.51; 27 studies) after controlling for smoking. The relative risk was higher in never-smokers (meta-RR = 2.00; 95% CI, 1.09-3.67; 3 studies) and persisted when restricted to studies that adjusted for other occupational exposures (meta-RR = 1.57; 95% CI, 1.21-2.04; 5 studies). These results support the conclusion that occupational exposures in painters are causally associated with the risk of lung cancer.