Division of Occupational and Environmental Health, Jockey Club School of Public Health and Primary Care, the Chinese University of Hong Kong, Hong Kong, China.
PLoS One. 2013 Aug 21;8(8):e71899. doi: 10.1371/journal.pone.0071899. eCollection 2013.
This study was conducted to assess the relationship of mortality from lung cancer and other selected causes to asbestos exposure levels.
A cohort of 1539 male workers from a chrysotile mine in China was followed for 26 years. Data on vital status, occupation and smoking were collected from the mine records and individual contacts. Causes and dates of death were further verified from the local death registry. Individual cumulative fibre exposures (f-yr/ml) were estimated based on converted dust measurements and working years at specific workshops. Standardized mortality ratios (SMRs) for lung cancer, gastrointestinal (GI) cancer, all cancers and nonmalignant respiratory diseases (NMRD) stratified by employment years, estimated cumulative fibre exposures, and smoking, were calculated. Poisson models were fitted to determine exposure-response relationships between estimated fibre exposures and cause-specific mortality, adjusting for age and smoking.
SMRs for lung cancer increased with employment years at entry to the study, by 3.5-fold in ≥ 10 years and 5.3-fold in ≥ 20 years compared with <10 years. A similar trend was seen for NMRD. Smokers had greater mortality from all causes than nonsmokers, but the latter also had slightly increased SMR for lung cancer. No excess lung cancer mortality was observed in cumulative exposures of <20 f-yrs/ml. However, significantly increased mortality was observed in smokers at the levels of ≥ 20 f-yrs/ml and above, and in nonsmokers at ≥ 100 f-yrs/ml and above. A similarly clear gradient was also displayed for NMRD. The exposure-response relationships with lung cancer and NMRD persisted in multivariate analysis. Moreover, a clear gradient was shown in GI cancer mortality when age and smoking were adjusted for.
There were clear exposure-response relationships in this cohort, which imply a causal link between chrysotile asbestos exposure and lung cancer and nonmalignant respiratory diseases, and possibly to gastrointestinal cancer, at least for smokers.
本研究旨在评估肺癌和其他选定死因的死亡率与石棉暴露水平之间的关系。
对中国某温石棉矿的 1539 名男性工人进行了一项队列研究,随访时间为 26 年。通过矿山记录和个人联系收集了生命状态、职业和吸烟的数据。死因和日期通过当地死亡登记处进一步核实。基于换算后的粉尘测量值和特定车间的工作年限,估算了个体累积纤维暴露量(f-yr/ml)。按就业年限、估计累积纤维暴露量和吸烟情况对肺癌、胃肠道(GI)癌、所有癌症和非恶性呼吸道疾病(NMRD)的标准化死亡率比(SMRs)进行分层,并进行计算。拟合泊松模型,以确定估计纤维暴露量与特定病因死亡率之间的暴露-反应关系,同时调整年龄和吸烟情况。
与 <10 年相比,进入研究时的就业年限≥ 10 年和≥ 20 年的肺癌 SMR 分别增加了 3.5 倍和 5.3 倍,NMRD 也出现了类似的趋势。吸烟者的全因死亡率高于非吸烟者,但后者的肺癌 SMR 略有增加。累积暴露量<20 f-yrs/ml 未观察到肺癌死亡过多。然而,在吸烟者中,在≥ 20 f-yrs/ml 及以上水平,以及在非吸烟者中,在≥ 100 f-yrs/ml 及以上水平,观察到明显的超额肺癌死亡率。NMRD 也显示出类似的清晰梯度。多变量分析中,肺癌和 NMRD 的暴露-反应关系仍然存在。此外,在调整年龄和吸烟情况后,胃肠道癌症死亡率也显示出明显的梯度。
在本队列中,存在明确的暴露-反应关系,这表明温石棉暴露与肺癌和非恶性呼吸道疾病之间存在因果关系,至少对吸烟者而言,与胃肠道癌症也可能存在因果关系。