Follow-up study of chrysotile textile workers: cohort mortality and exposure-response

Follow-up study of chrysotile textile workers: cohort mortality and exposure-response
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DOI:
10.1136/oem.2006.031005
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发表时间:
2007-09-01
影响因子:
4.9
通讯作者:
Dement, John M.
Dement, John M.
中科院分区:
医学2区
文献类型:
--
作者:
Hein, Misty J.;Stayner, Leslie T.;Dement, John M.

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目的:本报告提供了南卡罗来纳州石棉纺织工人队列死亡率经验的更新。方法:对3072名在南卡罗莱纳石棉纺织厂(1916年至1977年)接触温石棉的工人的死亡率进行随访,直至2001年。使用美国和南卡罗来纳的死亡率计算标准化死亡率(SMRs)。工作暴露矩阵提供了与日历时间有关的温石棉暴露浓度估计。泊松回归模型拟合肺癌和石棉肺。协变量包括性别、种族、年龄、日历时间、出生队列和首次接触后的时间。通过忽略最近5年和最近10年的暴露,分别考虑了5年和10年的累积暴露滞后。结果:大多数队列已死亡(64%),1961例死亡中有702例发生在上次更新之后。基于包括所有原因在内的先验原因的美国参考死亡率升高(SMR为1.33,95% CI为1.28至1.39);所有癌症(SMR为1.27,95% CI为1.16 - 1.39);食管癌(SMR 1.87, 95% CI 1.09 ~ 2.99);肺癌(SMR为1.95,95% CI为1.68 ~ 2.24);缺血性心脏病(SMR 1.20, 95% CI 1.10 ~ 1.32);尘肺病和其他呼吸系统疾病(SMR 4.81, 95% CI 3.84至5.94)。当使用南卡罗来纳参考比率时,这些原因的死亡率仍然升高。在队列成员中观察到3例间皮瘤。当累积暴露滞后10年时,使用线性相对风险模型的肺癌暴露-反应模型产生的斜率系数为0.0198(纤维年/ ml)(标准误差0.00496)。泊松回归模型证实了该队列先前更新中观察到的温石棉暴露与肺癌和石棉沉滞死亡率之间的显著正相关。结论:本研究证实了先前关于肺癌和石棉沉滞死亡率过高的调查结果,以及温石棉暴露与肺癌和石棉沉滞死亡率之间存在很强的暴露-反应关系。
Objectives: This report provides an update of the mortality experience of a cohort of South Carolina asbestos textile workers.Methods: A cohort of 3072 workers exposed to chrysotile in a South Carolina asbestos textile plant (1916 77) was followed up for mortality through 2001. Standardised mortality ratios (SMRs) were computed using US and South Carolina mortality rates. A job exposure matrix provided calendar time dependent estimates of chrysotile exposure concentrations. Poisson regression models were fitted for lung cancer and asbestosis. Covariates considered included sex, race, age, calendar time, birth cohort and time since first exposure. Cumulative exposure lags of 5 and 10 years were considered by disregarding exposure in the most recent 5 and 10 years, respectively.Results: A majority of the cohort was deceased (64%) and 702 of the 1961 deaths occurred since the previous update. Mortality was elevated based on US referent rates for a priori causes of interest including all causes combined (SMR 1.33, 95% CI 1.28 to 1.39); all cancers (SMR 1.27, 95% CI 1.16 to 1.39); oesophageal cancer (SMR 1.87, 95% CI 1.09 to 2.99); lung cancer (SMR 1.95, 95% CI 1.68 to 2.24); ischaemic heart disease (SMR 1.20, 95% CI 1.10 to 1.32); and pneumoconiosis and other respiratory diseases (SMR 4.81, 95% CI 3.84 to 5.94). Mortality remained elevated for these causes when South Carolina referent rates were used. Three cases of mesothelioma were observed among cohort members. Exposure-response modelling for lung cancer, using a linear relative risk model, produced a slope coefficient of 0.0198 (fibre-years/ ml) (standard error 0.00496), when cumulative exposure was lagged 10 years. Poisson regression modelling confirmed significant positive relations between estimated chrysotile exposure and lung cancer and asbestosis mortality observed in previous updates of this cohort.Conclusions: This study confirms the findings from previous investigations of excess mortality from lung cancer and asbestosis and a strong exposure-response relation between estimated exposure to chrysotile and mortality from lung cancer and asbestosis.