矽肺对肺癌及总死亡影响的回顾性队列研究

目的 利用香港矽肺患者队列的资料进行分析,探讨矽尘、矽肺与肺癌的关系.方法 选择1981年1月1日至1998年12月31日期间在香港尘肺诊所登记的2789例男性矽肺病例为研究对象,取用同时期一般男性人群作为对照.用人年的方法估计各死因的标化死亡比(SMR),用Axelson's法间接调整吸烟的混杂影响.矽尘与肺癌的剂量-效应关系采用多因素p-spline平滑法模型来拟合最佳风险模型.结果 该组研究队列人数为2789,共观察24 992.6人年,失访率仅为2.9%.该队列主要工种为建筑工人(5 1.09%)和地下沉箱操作工人(37.54%).队列总死亡人数为853人,平均死亡年龄为(63.8±10.27)岁,整个队列中86例死于肺癌.全死因及全癌的SMR均明显上升,首位死因是呼吸道疾病,肺癌的5MR明显增加(SMR:1.69,95%CI:1.35～2.09).去除年龄、时期和吸烟的混杂因素的影响,矽肺对肺癌的相对危险度下降到1.12(95%CI:0.89～1.38).间接调整吸烟的混杂影响后建筑工人及地下沉箱工人肺癌的相对危险度分别为1.09(95%CI:0.82～1.42)和1.56(0.98～2.36).多因素p-spline平滑法风险模型分析显示,肺癌与累积呼吸性矽尘总量或平均矽尘浓度的关系无剂量-效应关系.结论 队列研究未发现接触矽尘或矽肺能增加肺癌死亡的危险,平滑法模型拟合的风险模型并不支持矽尘与肺癌死亡之间存在剂量-效应关系.     

Mortality of a cohort of men in a silicosis register: further evidence of an association with lung cancer

Lung cancer mortality from 1980 to 1986 was studied in a cohort of 1,419 men in a silicosis register who had no previous exposure to asbestos and polyaromatic hydrocarbons. The 28 deaths from lung cancer were statistically in excess of expected (SMR 2.03; 95% CI 1.35-2.93). Excess risks of lung cancer were found in both underground workers (SMR 3.41; 95% CI 1.10-7.97; based on 5 deaths) and surface workers (SMR 1.87, 95% CI 1.18-2.81; based on 23 deaths). All lung cancer deaths were smokers. There was an increase in SMRs with longer latency periods and years of exposure, with the greatest risk found in those who had worked for 30 or more years after more than 30 years since first exposed (SMR 3.07, based on 16 deaths). The risk for lung cancer was higher in those with tuberculosis (SMR 2.52; 95% CI 1.52-3.94) and showed an increasing trend with severity of silicosis, from category 1 to 3 and from category A to C, with highest risk in those with tuberculosis and category 3 (SMR 4.44 based on 3 deaths) or tuberculosis and category C (SMR 7.63 based on 7 deaths). Most of the excess lung cancer risk in silicotics is due to smoking, but a synergistic effect between smoking and silica/silicosis on the risk of lung cancer is also likely. In particular, a possible role of silicosis and tuberculosis as the fibrotic seedbed for malignant growth in the lung is strongly supported.     

Mortality from lung cancer among Sardinian patients with silicosis

The mortality of 724 subjects with silicosis, first diagnosed in 1964-70 in the Sardinia region of Italy, was followed up through to 31 December 1987. Smoking, occupational history, chest x ray films, and data on lung function were available from clinical records for each member of the cohort. The overall cohort accounted for 10,956.5 person-years. The standardised mortality ratios (SMRs) for selected causes of death (International Classification of Diseases (ICD) eighth revision) were based on the age specific regional death rates for each calendar year. An excess of deaths for all causes (SMR = 1.40) was found, mainly due to chronic obstructive lung disease, silicosis, and tuberculosis with an upward trend of the SMR with increasing severity of the International Labour Office (ILO) radiological categories. Twenty two subjects died from lung cancer (SMR = 1.29, 95% confidence interval (95% CI) = 0.8-2.0). The risk increased after a 10 and 15 year latency but the SMR never reached statistical significance. No correlation was found between lung cancer and severity of the radiological category, the type of silica (coal or metalliferous mines, quarries etc), or the degree of exposure to silica dust. A significant excess of deaths from lung cancer was found among heavy smokers (SMR = 4.11) and subjects with airflow obstruction (SMR = 2.83). A nested case-control study was planned to investigate whether the association between lung cancer and airway obstruction was due to confounding by smoking. No association was found with the ILO categories of silicosis or the estimated cumulative exposure to silica. The risk estimate for lung cancer by airflow obstruction after adjusting by cigarette consumption was 2.86 for a mild impairment and 7.23 for a severe obstruction. The results do not show any clear association between exposure to silica, severity of silicosis, and mortality from lung cancer. Other environmental or individual factors may act as confounders in the association between silicosis and lung cancer. Among them, attention should be given to chronic airways obstruction as an independent risk factor for lung cancer in patients with silicosis.     

Mortality from lung cancer among Sardinian patients with silicosis.

The mortality of 724 subjects with silicosis, first diagnosed in 1964-70 in the Sardinia region of Italy, was followed up through to 31 December 1987. Smoking, occupational history, chest x ray films, and data on lung function were available from clinical records for each member of the cohort. The overall cohort accounted for 10,956.5 person-years. The standardised mortality ratios (SMRs) for selected causes of death (International Classification of Diseases (ICD) eighth revision) were based on the age specific regional death rates for each calendar year. An excess of deaths for all causes (SMR = 1.40) was found, mainly due to chronic obstructive lung disease, silicosis, and tuberculosis with an upward trend of the SMR with increasing severity of the International Labour Office (ILO) radiological categories. Twenty two subjects died from lung cancer (SMR = 1.29, 95% confidence interval (95% CI) = 0.8-2.0). The risk increased after a 10 and 15 year latency but the SMR never reached statistical significance. No correlation was found between lung cancer and severity of the radiological category, the type of silica (coal or metalliferous mines, quarries etc), or the degree of exposure to silica dust. A significant excess of deaths from lung cancer was found among heavy smokers (SMR = 4.11) and subjects with airflow obstruction (SMR = 2.83). A nested case-control study was planned to investigate whether the association between lung cancer and airway obstruction was due to confounding by smoking. No association was found with the ILO categories of silicosis or the estimated cumulative exposure to silica. The risk estimate for lung cancer by airflow obstruction after adjusting by cigarette consumption was 2.86 for a mild impairment and 7.23 for a severe obstruction. The results do not show any clear association between exposure to silica, severity of silicosis, and mortality from lung cancer. Other environmental or individual factors may act as confounders in the association between silicosis and lung cancer. Among them, attention should be given to chronic airways obstruction as an independent risk factor for lung cancer in patients with silicosis.     

Mortality from lung cancer among silicotic patients in Sardinia: an update study with 10 more years of follow up

OBJECTIVES—To evaluate the association between silica, silicosis and lung cancer, the mortality of 724 patients with silicosis, first diagnosed by standard chest x ray film between 1964 and 1970, has been analysed by a cohort study extended to 31 December 1997.METHODS—Smoking and detailed occupational histories were available for each member of the cohort as well as the estimated lifetime exposure to respirable silica dust and radon daughters. Two independent readers blindly classified standard radiographs according to the 12 point International Labour Organisation (ILO) scale. Lung function tests meeting the American Thoracic Society''s criteria were available for 665 patients. Standardised mortality ratios (SMRs) for selected causes of death were based on the age specific Sardinian regional death rates.RESULTS—The mortality for all causes was significantly higher than expected (SMR 1.35, 95% confidence interval (95% CI) 1.24 to 1.46) mainly due to tuberculosis (SMR 22.0) and to non-malignant chronic respiratory diseases (NMCRD) (SMR 6.03). All cancer deaths were within the expected numbers (SMR 0.93; 95% CI 0.76 to 1.14). The SMR for lung cancer was 1.37 (95% CI 0.98 to 1.91, 34 observed), increasing to 1.65 (95% CI 0.98 to 2.77) allowing for 20 years of latency since the first diagnosis of silicosis. Although mortality from NMCRD was strongly associated to the severity of radiological silicosis and to the extent of the cumulative exposure to silica, SMR for lung cancer was weakly related to the ILO categories and to the cumulative exposure to silica dust only after 20 years of lag interval. A significant excess of deaths from lung cancer (SMR 2.35) was found among silicotic patients previously employed in underground metal mines characterised by a relatively high airborne concentration of radon daughters and among ever smokers who showed an airflow obstruction at the time of the first diagnosis of silicosis (SMR 3.29). Mortality for lung cancer related to exposure was evaluated with both the Cox''s proportional hazards modelling within the entire cohort and a nested case-control study (34 cases of lung cancer and 136 matched controls). Both multivariate analyses did not show any significant association with cumulative exposure to silica or severity of silicosis, but confirmed the association between mortality for lung cancer and relatively high exposure to radon, smoking, and airflow obstruction as significant covariates.CONCLUSIONS—The findings indicate that the slightly increased mortality for lung cancer in this cohort of silicotic patients was significantly associated with other risk factors—such as cigarette smoking, airflow obstruction, and estimated exposure to radon daughters in underground mines—rather than to the severity of radiological silicosis or to the cumulative exposure to crystalline silica dust itself.     

吸烟校正因素间接调整法在职业流行病学队列研究中的应用

目的介绍一种新的吸烟校正因素间接调整法在职业流行病学队列研究中的应用。方法以1981—1999年香港男性矽肺回顾性队列研究人群纯石英暴露组作为研究实例,用吸烟组[1/((1-PAR%)×RR)]与非吸烟组(1/(1-PAR%))各自的吸烟校正因素校正原始的标准化死亡比(SMR),用暴露超相对危险度和增效指数作为指标来判断吸烟与暴露对肺癌死亡的危险有无偏离乘法和相加模型。结果非吸烟和吸烟组矽肺队列人群的吸烟校正因素分别为1/0.33和1/1.62,校正吸烟后矽肺队列肺癌的SMR由原来的1.61(95%CI:1.22～2.10)显著地下降到1.08(95%CI:0.81～1.41),结果与Axelson方法完全一致。矽肺超相对危险度和增效指数分别为0.63(95%CI:0.08～0.79)和0.90(95%CI:0.42～1.94),提示吸烟与矽肺对肺癌死亡的危险呈明显的负相乘交互作用。结论吸烟校正因素间接调整法的优势是能定量分析和评估吸烟的混杂和交互作用的影响,但也有局限性。     

A mortality study of workers at seven beryllium processing plants.

The International Agency for Research on Cancer (IARC) has found that the evidence for the carcinogenicity of beryllium is sufficient based on animal data but "limited" based on human data. This analysis reports on a retrospective cohort mortality study among 9,225 male workers employed at seven beryllium processing facilities for at least 2 days between January 1, 1940, and December 31, 1969. Vital status was ascertained through December 31, 1988. The standardized mortality ratio (SMR) for lung cancer in the total cohort was 1.26 (95% confidence interval [CI] = 1.12-1.42); significant SMRs for lung cancer were observed for two of the oldest plants located in Lorain, Ohio (SMR = 1.69; 95% CI = 1.28-2.19) and Reading, Pennsylvania (SMR = 1.24; 95% CI = 1.03-1.48). For the overall cohort, significantly elevated SMRs were found for "all deaths" (SMR = 1.05; 95% CI = 1.01-1.08), "ischemic heart disease" (SMR = 1.08; 95% CI = 1.01-1.14), "pneumoconiosis and other respiratory diseases" (SMR = 1.48; 95% CI = 1.21-1.80), and "chronic and unspecified nephritis, renal failure, and other renal sclerosis" (SMR = 1.49; 95% CI = 1.00-2.12). Lung cancer SMRs did not increase with longer duration of employment, but did increase with longer latency (time since first exposure). Lung cancer was particularly elevated (SMR = 3.33; 95% CI = 1.66-5.95) among workers at the Lorain plant with a history of (primarily) acute beryllium disease, which is associated with very high beryllium exposure. The lung cancer excess was not restricted to plants operating in the 1940s, when beryllium exposures were known to be extraordinarily high. Elevated lung cancer SMRs were also observed for four of the five plants operating in the 1950s for workers hired during that decade. Neither smoking nor geographic location fully explains the increased lung cancer risk. Occupational exposure to beryllium compounds is the most plausible explanation for the increased risk of lung cancer observed in this study. Continued mortality follow-up of this cohort will provide a more definitive assessment of lung cancer risk at the newer plants and among cohort members hired in the 1950s or later at the older plants. Further clarification of the potential for specific beryllium compounds to induce lung cancer in humans, and the possible contribution of other exposures in specific processes at these plants, would require a nested case-control study. We are currently assessing whether available industrial hygiene data would support such an analysis.     

Nested case-control study of lung cancer among pulp and paper workers in relation to exposure to dusts

BACKGROUND: Numerous studies have indicated an increased risk of lung cancer in pulp and paper industry workers. In a 1990 survey, standardized mortality ratio (SMR) was found to be 122 (95% CI:96-153) for lung cancer in Polish male workers in the pulp and paper industry, and 166 (95% CI:95-270) among workers engaged in paper production. METHODS: A nested case-control design within a cohort of pulp and paper workers was applied. Seventy-nine lung cancer cases and 237 "healthy" controls were selected from the cohort of 10,460 workers employed during the years 1968-1990, and observed until the end of 1995. Based on personnel files, occupational exposure was reconstructed by experts. Using a questionnaire, data on smoking habits were collected. ORs unadjusted and adjusted for smoking were calculated applying the model of conditional logistic regression. RESULTS: Occupational exposure to inorganic dusts (kaolin, lime, cement, brick, grindstone) adjusted for smoking was a significant lung cancer risk factor, with a 4.0-fold risk (95% CI:1.3-12.6), and a dose-response by cumulative dose index. Among organic dusts only wood dust increased albeit insignificantly the risk for those exposed (adjusted for smoking OR = 2.1, 95% CI:0.9-4.9), but without dose-response relationship. CONCLUSIONS: Exposure to occupational dust with relatively low content of silica, but at high concentrations may be considered as a factor increasing lung cancer risk. However, the observation made in this study should be viewed with caution as it was based on a small number of cases, and further evidence is needed to confirm or refute the authors' hypothesis.     

Silicosis and smoking strongly increase lung cancer risk in silica-exposed workers

It remains controversial whether silica is a human lung carcinogen. In this study, we estimated the relative risks of lung cancer due to silica and silicosis by meta-analysis. We collected papers published from 1966-2001 which epidemiologically reported on the relationship between silica/silicosis and lung cancer. We removed papers which did not exclude the effects of asbestos and radioactive materials including radon. We selected the most recent one if some papers were based on the same cohort. Based on the selected papers, we summarized the lung cancer risks from silica, silicosis and non-silicosis with exposure to silica, by meta-analysis using a random effects model. The pooled relative risks were 1.32 (95% confidence interval (CI), 1.23-1.41) for silica, 2.37 (95% CI, 1.98-2.84) for silicosis and 0.96 (95% CI, 0.81-1.15) for non-silicosis with exposure to silica. Since some papers on silica did not exclude silicosis, the risk due to silica itself may be smaller than 1.32. It was less possible that silica exposure directly increases lung cancer risk. On the other hand, the relative risk, 2.37 for silicosis suggested that silicosis increases lung cancer risk. Meta-analysis also revealed that cigarette smoking strongly increased the lung cancer risk in silicotic patients (relative risk, 4.47; 95% CI, 3.17-6.30). Thus, the present study suggested the great importance of preventing silicosis and smoking cessation in reducing lung cancer incidence in silica-exposed workers.     

游离二氧化硅暴露与肺肿瘤关系的Meta分析

目的采用Meta-analysis方法,对游离二氧化硅暴露与肺癌之间的关系进行了系统综合评价,为制定防制措施提供科学依据,亦为今后开展＂循证职业医学＂提供借鉴.方法本研究对所收集游离二氧化硅暴露和肺癌关系研究方面的原始文献（已公开发表）按所制定的纳入标准进行分类整理,然后采用适用于职业流行病学调查资料分析的固定效应模型和随机效应模型,分析其间的关联强度.可概括为：（1）分别计算所收集资料的各自合并后的队列研究和病例对照研究SMR值及其相应95%可信区间;（2）分别按不同研究设计,进行分层,计算总SMR值及其95%可信限区间.并计算本研究的失效安全系数（Fail-safe Number）.结果分别合并所收集资料的所有队列研究和病例对照研究后,得出SMR值及其95%可信区间,分别为SMR队=1.93,95%可信区间为0.55～6.92;SMR值=1.73,95%可信区间为1.01～2.99;SMR合=2.19,95%可信区间为1.45～3.31;均P＜0.05,游离二氧化硅暴露和肺癌之间的联系有统计学意义.结论游离二氧化硅暴露和肺癌之间属中等强度关联,与国内外大多数研究结论一致.     

Cancer mortality study of employees at lead battery plants and lead smelters, 1947-1995

BACKGROUND: This study has examined cancer mortality of a cohort of male U.S. workers exposed to lead. METHODS: The cohort consisted of 4,518 workers at lead battery plants and 2,300 at lead smelters. Vital status was ascertained between 1947 and 1995. Site-specific cancer standardized mortality ratios (SMRs) and 95% confidence intervals (95% CIs), based on the mortality rates of the U.S. male population and adjusted for age and calendar time, were calculated for the total cohort as well as subcohorts stratified by various exposure parameters. In addition, a nested case-control study of stomach cancer (30 cases and 120 age-matched controls) was also conducted. RESULTS: Mortality from all cancers was as expected (897 observed deaths, SMR = 103.8, 95% CI: 97.1-110.8). Mortality was significantly raised for stomach cancer (SMR = 147.4, 95% CI: 112. 5-189.8), lung cancer (SMR = 116.4, 95% CI: 103.9-129.9), and cancer of the thyroid and other endocrine glands (SMR = 308.0, 95% CI: 133. 0-606.8). There was a nonsignificant mortality deficit from kidney cancer (SMR = 63.6, 95% CI: 33.9-108.7). For bladder cancer, mortality was significantly lower than expected (SMR = 55.5, 95% CI: 31.7-90.1). Nonsignificant mortality deficits were also reported for cancer of the central nervous system (SMR = 74.8, 95% CI: 41.9-123. 4) and lymphatic and hematopoietic cancer (SMR = 92.2, 95% CI: 72. 4-115.7). Additional analyses by type of facility (lead battery plants vs. lead smelters), length of employment, latency, and period of hire were also performed. In the nested case-control study of stomach cancer, odds ratios were calculated for various exposure indices, and none was found to be elevated. Furthermore, no exposure-response relationship between lead exposure and stomach cancer was found in the nested case-control study. CONCLUSIONS: A significant mortality increase from stomach cancer was found. However, based on the analyses in the cohort study and the nested case-control study, the increase did not appear to be related to lead exposure. A small, but statistically significant mortality increase from lung cancer was also observed. The small increase, in the absence of an exposure-response relationship, could be the result of confounding due to smoking, and was not likely causally related to lead exposure. Although the significant increase in cancer of the thyroid and other endocrine glands appeared to be consistent with an occupational interpretation, the small number of deaths (8), the lack of information on potential confounding factors, and the lack of reporting of a similar increase in other studies underscore the need to view this finding with caution. No increased mortality was found for kidney cancer, bladder cancer, cancer of the central nervous system, or lymphatic and hematopoietic cancer.     

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.     

Cancer mortality in German carbon black workers 1976-98

Background

Few studies have investigated cancer risks in carbon black workers and the findings were inconclusive.

Methods

The current study explores the mortality of a cohort of 1535 male German blue‐collar workers employed at a carbon black manufacturing plant for at least one year between 1960 and 1998. Vital status and causes of death were assessed for the period 1976–98. Occupational histories and information on smoking were abstracted from company records. Standardised mortality ratios (SMR) and Poisson regression models were calculated.

Results

The SMRs for all cause mortality (observed deaths (obs) 332, SMR 120, 95% CI 108 to 134), and mortality from lung cancer (obs 50, SMR 218, 95% CI 161 to 287) were increased using national rates as reference. Comparisons to regional rates from the federal state gave SMRs of 120 (95% CI 107 to 133) and 183 (95% CI 136 to 241), respectively. However, there was no apparent dose response relationship between lung cancer mortality and several indicators of occupational exposure, including years of employment and carbon black exposure.

Conclusions

The mortality from lung cancer among German carbon black workers was increased. The high lung cancer SMR can not fully be explained by selection, smoking, or other occupational risk factors, but the results also provide little evidence for an effect of carbon black exposure.     

Follow-up study of chrysotile asbestos textile workers: Cohort mortality and case-control analyses

Previous studies of mortality among white males employed in a Charleston, South Carolina asbestos textile plant using chrysotile demonstrated significant excess mortality due to asbestos-related disease and a steep exposure-response relationship for lung cancer. This cohort was further studied by adding 15 years of follow-up and including mortality among white female and black male workers. Nested case-control analyses were undertaken to further explore possible differences in lung cancer risk by textile operation as well as possible confounding by mineral oil exposures. Preliminary data for white males have been previously published. White males experienced statistically significant excess mortality due to lung cancer (standardized mortality ratio [SMR] = 2.30; confidence interval [CI] = 1.88–2.79), all causes (SMR = 1.48; CI = 1.38–1.58), all cancers (SMR = 1.50; CI = 1.29–1.72), diabetes mellitus (SMR = 2.05; CI = 1.18–3.33), heart disease (SMR = 1.41; CI = 1.26–1.58), cerebrovascular disease (SMR = 1.50; CI = 1.08–2.02), pneumoconiosis and other respiratory diseases (SMR = 4.10; CI = 3.10–5.31), and accidents (SMR = 1.49; CI = 1.15–1.91). Among white females, statistically significant excesses occurred for lung cancer (SMR = 2.75; CI = 2.06–3.61), all causes (SMR = 1.21; CI = 1.11–1.32), pneumoconiosis and other respiratory diseases (SMR = 2.40; CI = 1.53–3.60), and other respiratory cancers (SMR = 14.98; CI = 4.08–38.7). Among the total cohort of black males, the only statistically significant excess observed was for pneumoconiosis (SMR = 2.19; CI = 1.23–3.62). Based on historical exposure measurements at the plant, there was a positive exposure-response relationship for both lung cancer and pneumoconiosis. Data for the entire cohort demonstrate an increase in the lung cancer relative risk of 2–3% for each fiber/cc-year of cumulative chrysotile exposure. This relationship was more consistent for the white male workers. The excess risk for lung cancer among white males and females appeared to occur at cumulative exposures lower than those for black males. Possible reasons for the lesser lung cancer risk among black males include less smoking and differences in airborne fiber characteristics experienced by black males as a result of plant job placement patterns. The case-control analysis found employment in preparation and carding operations (where most of the black males worked) to be associated with a slightly reduced lung cancer risk, although not statistically significant, whereas spinning and twisting employment was associated with a statistically significant increased lung cancer risk compared to other plant operations. Airborne fiber size data, determined by transmission electron microscopy, demonstrated slightly longer fibers in spinning and twisting compared to other textile operations. Case-control analyses demonstrated little effect of mineral oil exposures on the lung cancer exposure-response estimates. Two deaths due to mesothelioma were observed among this cohort.     

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.     

Meta-analysis of studies of occupational exposure to vinyl chloride in relation to cancer mortality

OBJECTIVE: A meta-analysis was made of studies addressing occupational exposure to vinyl chloride in relation to cancer mortality. METHODS: Two recently updated multicenter cohort studies and six smaller studies were identified. For selected neoplasms, standardized mortality ratios (SMR) and 95% confidence intervals (95% CI) were abstracted (or calculated from raw data). In cases of lack of heterogeneity (P-value > or = 0.01), meta-analyses were conducted using a random-effects model. RESULTS: With SMR values ranging from 1.63 to 57.1, all six studies for which these ratios could be obtained suggested an increased risk of liver cancer. For four of these studies, excesses persisted when known cases of angiosarcoma of the liver (ASL) were excluded. The meta-SMR for liver cancers other than ASL (based on the 2 large cohorts) was 1.35 (95% CI 1.04-1.77). The meta-SMR for lung cancer was 0.90 (95% CI 0.77-1.00, based on 5 studies), although higher SMR values were reported in early studies. The meta-SMR for brain cancer, based on 5 studies, was 1.26 (95% CI 0.98-1.62). For soft tissue sarcomas, the meta-SMR based on 4 studies was 2.52 (95% CI 1.56-4.07). The meta-SMR for lymphatic and hematopoietic neoplasms in the 2 large studies was 0.90 (95% CI 0.75-1.01), although 3 of the smaller studies reported significant excesses. CONCLUSIONS: Apart from the known risk of ASL, workers exposed to vinyl chloride may experience an increased risk of hepatocellular carcinoma and soft-tissue sarcoma; however, these results may have been influenced by the underdiagnosis of true ASL. Increased mortality from lung and brain cancers and from lymphatic and hematopoietic neoplasms cannot be excluded; mortality from other neoplasms does not appear to be increased.     

Dietary Carbohydrate and Prostate Cancer Risk: A Meta-Analysis

Carbohydrate intake has been inconsistently associated with risk of prostate cancer. We review and quantitatively summarize the evidence from observational studies in a meta-analysis. We searched the PubMed database for observational studies related to the association of carbohydrate intake and prostate cancer risk up to December 25, 2013. Summary relative risks (RRs) were estimated by the use of a random effects model. We included 13 case-control studies with 4,367 cases and 6,205 controls, and 5 cohort studies with 3,679 cases and 74,115 participants in this meta-analysis. The summary RR of prostate cancer for the highest vs. the lowest carbohydrate intake was 1.06 [95% confidence interval (CI): 0.93–1.20, I² = 46.8%] for all included studies. In the subgroup analyses stratified by study design, the summary RRs for the highest vs. the lowest carbohydrate intake were 1.04 (95% CI: 0.87–1.23) for case-control studies and 1.06 (95% CI: 0.88–1.28) for cohort studies. For the 5 studies that reported results for advanced prostate cancer, the summary RR was 0.92 (95% CI: 0.71–1.20). This meta-analysis of observational studies indicates that there is no association between carbohydrate intake and prostate cancer risk. Further studies are needed to confirm our findings.     

Fish Consumption and Lung Cancer Risk: Systematic Review and Meta-Analysis

There is evidence pointing to a possible role of diet on cancer etiology. Prior studies evaluating the relationship between fish consumption and lung cancer risk reported inconclusive results. The aim of this study was to achieve a comprehensive assessment of the relationship between fish consumption and lung cancer risk through systematic review and meta-analysis. Case control and cohort studies up to September 1, 2012 about fish consumption and lung cancer risk were confirmed by an online search. Separate relative risk (RR) or odds ratio (OR) estimates with 95% confidence interval (CI) of the relationship between lung cancer risk and fish consumption level from the included articles were combined by Stata11.0 software. Publication bias was evaluated by Egger's linear regression test and funnel plot. Twenty articles (17 case-control and 3 cohort studies) comprising 8799 cases of lung cancer and 17,072 noncases were included in the final analysis. The pooled results from all studies indicated that high fish consumption was significantly associated with a decreased risk of lung cancer (pooled RR: 0.79; 95% CI: 0.69–0.92). There was heterogeneity among the studies (I² = 73%, P < 0.05). Pooled RR in case control and cohort studies were 0.76 (95% CI: 0.63–0.91) and 0.95 (95% CI: 0.73–1.24), respectively. Omission of any single study had little effect on the combined risk estimates. This article had no publication bias. This study identifies a significant association between fish consumption and lung cancer, confirming a protective role of fish in lung cancer. More well-designed prospective studies are required to further verify the effect of fish consumption on lung cancer.     

Dose-specific meta-analysis and sensitivity analysis of the relation between alcohol consumption and lung cancer risk

Alcohol drinking increases the risk of several types of cancer, but studies of the relation between alcohol and lung cancer risk are complicated by smoking. The authors carried out meta-analyses for four study designs and conducted sensitivity analyses to assess the results. Pooled smoking-unadjusted relative risks (RRs) for brewery workers and alcoholics were 1.17 (95% confidence interval (CI): 0.99, 1.39) and 1.99 (95% CI: 1.66, 2.39), respectively, relative to population rates. For cohort and case-control studies, the authors conducted dose-specific meta-analyses for ethanol consumption of 1-499, 500-999, 1,000-1,999, and > or = 2,000 g/month, relative to nondrinking. Smoking-adjusted RRs for ascending dose groups in cohort studies were 0.98 (95% CI: 0.79, 1.21), 0.92 (95% CI: 0.81, 1.04), 1.04 (95% CI: 0.88, 1.22), and 1.53 (95% CI: 1.04, 2.25), respectively. Smoking-adjusted odds ratios for ascending groups in case-control studies were 0.63 (95% CI: 0.51, 0.78), 1.30 (95% CI: 0.98, 1.70), 1.13 (95% CI: 0.46, 2.75), and 1.86 (95% CI: 1.39, 2.49), respectively. Elevated odds ratios were seen for hospital-based case-control studies but not for population-based case-control studies. Sensitivity analyses indicated that smoking explained the elevated RRs in studies of alcoholics and that strong misclassification of smoking status could produce an elevated smoking-adjusted RR in cohort and case-control studies. Overall, evidence for a smoking-adjusted association between alcohol and lung cancer risk is limited to very high consumption groups in cohort and hospital-based case-control studies. At lower levels, any associations observed appear to be explained by confounding.