Cancer, heart disease, and diabetes in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin

Cancer, heart disease, and diabetes in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin
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DOI:
10.1093/jnci/91.9.779
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发表时间:
1999-05-05
期刊:
JOURNAL OF THE NATIONAL CANCER INSTITUTE
影响因子:
--
通讯作者:
Chang, LI
Chang, LI
中科院分区:
其他
文献类型:
--
作者:
Steenland, K;Piacitelli, L;Chang, LI

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背景资料:1997年,国际癌症研究机构将2,3,7,8-四氯二苯并对二恶英(TCDD)归类为第1类人类致癌物,主要基于四个高度暴露的工业队列,这些队列显示所有癌症的总和超过。在这项研究中,我们将这些队列中最大的一组的随访期延长了6年,并开发了一个工作暴露矩阵。研究方法:我们使用寿命表技术(美国人口参照)和考克斯回归(内部参照)对美国12家工厂的5132名化学工人进行了队列死亡率分析。我们对69%的队列进行了确认-响应分析,这些队列具有足够的工作历史数据和足够的TCDD污染工厂数据,所有P值均为双侧。结果:所有癌症合并的标准化死亡比(SMR)为1.13(95%置信区间= 1.02-1.25)。我们发现,所有癌症合并和肺癌的SMR随暴露量增加呈统计学显著的正线性趋势。最高暴露组所有癌症合并的SMR为1.60(95%置信区间= 1.15-1.82)。心脏病的SMR随暴露量增加呈微弱上升趋势(P = 0.14)。糖尿病(死亡证明上的任何提及)显示出负的确认反应趋势。采用考克斯回归的内部分析发现,癌症(15年滞后时间)和心脏病(无滞后)的趋势具有统计学意义。结论:我们的分析表明,高TCDD暴露导致所有癌症的过度组合,没有任何明显的特异性,然而,过度的癌症仅限于暴露最高的工人,暴露可能比普通人群高100-1000倍,与动物研究中使用的TCDD水平相似。
Background: In 1997, the International Agency for Research on Cancer classified 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as a group 1 human carcinogen, based largely on four highly exposed industrial cohorts that showed an excess of all cancers combined. In this study, we extended the follow-up period for the largest of these cohorts By 6 years and developed a job-exposure matrix. Methods: We did cohort mortality analyses involving 5132 chemical workers at 12 U.S. plants by use of life table techniques (U.S. population referent) and Cox regression (internal referent). We conducted exposure-response analyses for 69% of the cohort with adequate work history data and adequate plant data on TCDD contamination, All P values are two-sided. Results: The standardized mortality ratio (SMR) for all cancers combined was 1.13 (95% confidence interval = 1.02-1.25). We found statistically significant positive linear trends in SMRs with increasing exposure for all cancers combined and for lung cancer. The SMR for all cancers combined for the highest exposure group was 1.60 (95% confidence interval = 1.15-1.82). SMRs for heart disease showed a weak increasing trend with higher exposure (P = .14). Diabetes (any mention on the death certificate) showed a negative exposure-response trend. Internal analyses with Cox regression found statistically significant trends for cancer (15-year lag time) and heart disease (no lag). Conclusions: Our analyses suggest that high TCDD exposure results in an excess of all cancers combined, without any marked specificity, However, excess cancer was limited to the highest exposed workers, with exposures that were likely to have been 100-1000 times higher than those experienced by the general population and similar to the TCDD levels used in animal studies.