Lynch Shannon M, Mahajan Rajeev, Beane Freeman Laura E, Hoppin Jane A, Alavanja Michael C R
Epidemiology and Genetics Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, MD 20852, USA.
Environ Res. 2009 Oct;109(7):860-8. doi: 10.1016/j.envres.2009.06.006. Epub 2009 Jul 16.
Although limited, epidemiologic studies suggest possible associations between butylate use and cancer risk, specifically prostate cancer and non-Hodgkin lymphoma (NHL). We examined butylate use and cancer risk more broadly in the AHS, a cohort of licensed pesticide applicators in Iowa and North Carolina. Pesticide use information was collected using self-administered questionnaires. Poisson regression was used to calculate rate ratios (RR) and 95% confidence intervals (CI). Two exposure metrics were used: lifetime exposure days (LD) and intensity-weighted lifetime exposure days (IWLD). We used two referent groups: unexposed to butylate and the lowest butylate usage category. This analysis included 19,655 applicators with complete butylate use information; 5297 applicators were exposed to butylate, making this the largest study of butylate to date. The mean follow-up time since enrollment was 9 years. Prostate cancer risk was significantly elevated among applicators in the highest LD category in both referent groups (low-exposed referent: RR(LD)=2.09, 95% CI=1.27-3.44). We observed a significantly elevated joint effect of prostate cancer family history and high butylate usage across both exposure metrics and both referent groups (low-exposed referent: RR(LD)=2.00, 95% CI=1.07-3.74), and a non-significant, elevated interaction between butylate use and prostate cancer family history, similar to a previous AHS finding. Statistically significant increased risks and exposure-response trends were seen for all lymphohematopoietic cancers (AL) and NHL for both exposure metrics and referent groups (low-exposed referent: AL:RR(LD)=2.27, 95% CI=1.18-4.37; NHL: RR(LD)=3.44, 95% CI=1.29-9.21). Our analysis did not find meaningful associations for other cancers analyzed. Further study is warranted for AL, NHL and prostate cancers.
尽管相关研究有限,但流行病学研究表明,使用丁酯与癌症风险之间可能存在关联,特别是前列腺癌和非霍奇金淋巴瘤(NHL)。我们在AHS(爱荷华州和北卡罗来纳州有执照的农药施用者队列)中更广泛地研究了丁酯使用情况与癌症风险。通过自行填写问卷收集农药使用信息。采用泊松回归计算率比(RR)和95%置信区间(CI)。使用了两种暴露指标:终生暴露天数(LD)和强度加权终生暴露天数(IWLD)。我们使用了两个参照组:未接触丁酯组和丁酯使用量最低组。该分析纳入了19655名有完整丁酯使用信息的施用者;5297名施用者接触过丁酯,这使得该研究成为迄今为止关于丁酯的规模最大的研究。自入组以来的平均随访时间为9年。在两个参照组中,LD类别最高的施用者患前列腺癌的风险显著升高(低暴露参照组:RR(LD)=2.09,95%CI=1.27 - 3.44)。我们观察到,在两种暴露指标和两个参照组中,前列腺癌家族史与高丁酯使用量之间存在显著升高的联合效应(低暴露参照组:RR(LD)=2.00,95%CI=1.07 - 3.74),并且丁酯使用与前列腺癌家族史之间存在非显著的升高交互作用,这与AHS之前的一项发现类似。对于两种暴露指标和参照组,所有淋巴造血系统癌症(AL)和NHL均出现了具有统计学意义的风险增加和暴露 - 反应趋势(低暴露参照组:AL:RR(LD)=2.27,95%CI=1.18 - 4.37;NHL:RR(LD)=3.44,95%CI=1.29 - 9.21)。我们的分析未发现所分析的其他癌症存在有意义的关联。对于AL、NHL和前列腺癌,有必要进一步开展研究。