Cancer Risk and Environmental Exposures to Nitrate, Pest

研究了周围环境中农用化学品致癌的危险因素，以估计这些环境暴露对农村人口癌症的贡献。农业地区的农村人口接触到饮用水中的杀虫剂和硝酸盐，介于职业接触群体和一般人口之间。对非霍奇金淋巴瘤和脑癌、膀胱癌、结肠癌、直肠癌、胃癌、食道癌、胰腺癌和肾癌进行了病例对照研究。在这些病例对照研究中，为常规监测目的收集的水污染物数据库正被用来估计过去通过公共供水对个人的暴露。爱荷华州公共供水中的硝酸盐水平与膀胱癌和胰腺癌的风险无关。然而，较高的饮食亚硝酸盐摄入量与胰腺癌风险增加相关。总体而言，饮用水硝酸盐水平与患结肠癌、直肠癌和肾癌的风险无关；然而，亚硝化能力增强的特定亚组患结肠癌和肾癌的风险增加。在那些水硝酸盐摄入量较高、红肉摄入量较高或维生素C摄入量较低的人中，结肠癌和肾癌的OR都增加了约两倍。内布拉斯加州公共供水中硝酸盐的升高与神经胶质瘤的风险无关。在内布拉斯加州，公共饮用水中硝酸盐水平的升高与非霍奇金淋巴瘤风险的增加有关。最近在爱荷华州、西雅图、洛杉矶和底特律地区四个中心完成的非霍奇金淋巴瘤病例对照研究中，对这一假说进行了研究。公共供应的硝酸盐监测数据与1960年以来的水源历史有关。采访家庭的私人水井被测量了硝酸盐。我们将大多数分析局限于那些自1960年以来(181例病例，142例对照)70%的人年的硝酸盐估计值。我们没有发现总体上与饮用水平均硝酸盐的最高四分位数(&gt；2.90 mg/L硝酸盐-N：OR=1.2，95%CI 0.6-2.2)或与&gt；5 mg/L(10多年：OR=1.4，95%CI 0.7-2.9)的关系。我们没有看到饮用水硝酸盐暴露与维生素C摄入量或红肉摄入量之间存在相互作用的证据，红肉摄入量分别是体内NOC形成的抑制物和前体。膳食硝酸盐与非霍奇金淋巴瘤发病风险呈负相关(最高四分位OR=0.54，95%CI 0.34~0.86)。膳食亚硝酸盐摄入量与增加风险相关(最高四分位OR=3.1，95%可信区间1.7-5.5)，主要是由于面包和谷类食物中亚硝酸盐的摄入。在一项针对内布拉斯加州和科罗拉多州普拉特河谷人口普查区组的生态研究中，硝酸盐作为癌症风险因素的问题正在进一步探讨，那里的硝酸盐水平是全国最高的之一。正在使用土地覆盖、牲畜饲养场位置、土壤类型和其他信息的数据来估计私人水井中的硝酸盐水平。我们还在开发新的方法，并改进现有的方法，在一般环境暴露研究中进行暴露评估，主要侧重于杀虫剂和硝酸盐。需要这些更好的方法来更好地估计风险，并检测在此类研究中经常遇到的相对较小的风险增加。正在利用地理信息系统开发估计间接接触杀虫剂和估计私人水井中硝酸盐暴露的新方法。遥感数据(卫星图像)和历史记录被用来估计内布拉斯加州和爱荷华州可能接触到农业杀虫剂的人口，因为他们的家园靠近经过杀虫剂处理的农田。

Risk factors for cancer from agricultural chemicals in the ambient environment are studied to estimate the contribution of these environmental exposures to cancer in the rural population. Rural populations in agricultural areas have exposures to pesticides and nitrates in drinking water that are intermediate between occupationally-exposed groups and the general population. Case-control studies have been conducted on non-Hodgkin's lymphoma and cancers of the brain, bladder, colon, rectum, stomach, esophagus, pancreas, and kidney. Databases of water contaminants, gathered for routine monitoring purposes, are being used to estimate past exposures via public water supplies to individuals in these case-control studies. Nitrate levels in public water supplies in Iowa were not associated with risk of bladder and pancreas cancer. However, higher intakes of dietary nitrite were associated with an increased risk of pancreas cancer. Overall, drinking water nitrate levels were not associated with risk of colon, rectal, and kidney cancer; however, specific subgroups with increased nitrosation ability were at increased risk of colon and kidney cancer. Among those with higher water nitrate intake and higher red meat intake or lower vitamin C intake, ORs were elevated about two-fold for both colon and kidney cancers. Elevated nitrate in public water supplies in Nebraska was not associated with risk of glioma. Elevated nitrate levels in public drinking water supplies were associated with an increased risk of non-Hodgkin's lymphoma in Nebraska. This hypothesis was investigated in a recently completed case-control investigation of non-Hodgkin's lymphoma in four centers: Iowa, Seattle, Los Angeles and the Detroit area. Nitrate monitoring data for public supplies was linked to water source histories from 1960 onwards. Private wells at interview homes were measured for nitrate. We limited most analyses to those with nitrate estimates for >70% of their person-years since 1960 (181 cases, 142 controls). We found no overall association with the highest quartile of average drinking water nitrate (>2.90 mg/L nitrate-N: OR=1.2, 95% CI 0.6-2.2) or with years >5mg/L (10+ years: OR=1.4, 95% CI 0.7-2.9). We saw no evidence of an interaction between drinking water nitrate exposure and either vitamin C intake or red meat intake, an inhibitor and precursor, respectively, of in vivo NOC formation. Dietary nitrate was inversely associated with risk of NHL (highest quartile OR=0.54, 95% CI 0.34-0.86). Dietary nitrite intake was associated with increasing risk (highest quartile OR=3.1, 95% CI 1.7-5.5), largely due to intakes of bread and cereal sources of nitrite. The issue of nitrate as a cancer risk factor is being pursued further in an ecologic study of census-block groups in the Platte River Valley of Nebraska and Colorado, where elevated nitrate levels are among the highest in the country. Nitrate levels in private wells are being estimated using data on land cover, livestock feedlot locations, soil type, and other information. We are also developing new approaches, and improving existing methods, of exposure assessment in studies of general environmental exposures, with a primary focus on pesticides and nitrate. These better methods are required to better estimate risk and to detect the relatively small increases in risk often encountered in such studies. Geographic information systems (GIS) are being utilized for developing new approaches to estimating indirect exposure to pesticides and for estimating exposure to nitrate in private wells. Remote sensing data (satellite imagery) and historical records were used to estimate the population in Nebraska and Iowa potentially exposed to agricultural pesticides through the proximity of their homes to agricultural land treated with pesticides.