Switchenko Jeffrey M, Bulka Catherine, Ward Kevin, Koff Jean L, Bayakly A Rana, Ryan P Barry, Waller Lance A, Flowers Christopher R
Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
Department of Hematology and Oncology, Winship Cancer Institute, Emory University, Atlanta, GA, USA.
Cancer Epidemiol. 2016 Apr;41:139-51. doi: 10.1016/j.canep.2016.01.008. Epub 2016 Mar 2.
Benzene is a known occupational carcinogen associated with increased risk of hematologic cancers, but the relationships between quantity of passive benzene exposure through residential proximity to toxic release sites, duration of exposure, lag time from exposure to cancer development, and lymphoma risk remain unclear.
We collected release data through the Environmental Protection Agency's Toxics Release Inventory (TRI) from 1989 to 2003, which included location of benzene release sites, years when release occurred, and amount of release. We also collected data on incident cases of non-Hodgkin lymphoma (NHL) from the Georgia Comprehensive Cancer Registry (GCCR) for the years 1999-2008. We constructed distance-decay surrogate exposure metrics and Poisson and negative binomial regression models of NHL incidence to quantify associations between passive exposure to benzene and NHL risk and examined the impact of amount, duration of exposure, and lag time on cancer development. Akaike's information criteria (AIC) were used to determine the scaling factors for benzene dispersion and exposure periods that best predicted NHL risk.
Using a range of scaling factors and exposure periods, we found that increased levels of passive benzene exposure were associated with higher risk of NHL. The best fitting model, with a scaling factor of 4 kilometers (km) and exposure period of 1989-1993, showed that higher exposure levels were associated with increased NHL risk (Level 4 (1.1-160kilograms (kg)) vs. Level 1: risk ratio 1.56 [1.44-1.68], Level 5 (>160kg) vs. Level 1: 1.60 [1.48-1.74]).
Higher levels of passive benzene exposure are associated with increased NHL risk across various lag periods. Additional epidemiological studies are needed to refine these models and better quantify the expected total passive benzene exposure in areas surrounding release sites.
苯是一种已知的职业致癌物，与血液系统癌症风险增加相关，但通过居住在靠近有毒物质释放场所而被动接触苯的量、接触持续时间、从接触到癌症发生的滞后时间与淋巴瘤风险之间的关系仍不清楚。
我们通过美国环境保护局的有毒物质排放清单（TRI）收集了1989年至2003年的排放数据，其中包括苯排放场所的位置、排放发生年份以及排放量。我们还从佐治亚州综合癌症登记处（GCCR）收集了1999年至2008年非霍奇金淋巴瘤（NHL）的发病病例数据。我们构建了距离衰减替代暴露指标以及NHL发病率的泊松和负二项回归模型，以量化被动接触苯与NHL风险之间的关联，并研究接触量、接触持续时间和滞后时间对癌症发生的影响。使用赤池信息准则（AIC）来确定最能预测NHL风险的苯扩散和暴露期的比例因子。
使用一系列比例因子和暴露期，我们发现被动苯暴露水平升高与NHL风险增加相关。拟合效果最佳的模型，比例因子为4公里（km），暴露期为1989 - 1993年，显示较高的暴露水平与NHL风险增加相关（第4级（1.1 - 160千克（kg））与第1级：风险比1.56 [1.44 - 1.68]，第5级（>160kg）与第1级：风险比1.60 [1.48 - 1.74]）。
在不同的滞后时期，较高水平的被动苯暴露与NHL风险增加相关。需要更多的流行病学研究来完善这些模型，并更好地量化释放场所周边地区预期的总被动苯暴露量。
