Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.
J Natl Cancer Inst. 2024 Jan 10;116(1):53-60. doi: 10.1093/jnci/djad170.
Fine particulate matter (PM2.5) has been inconsistently associated with breast cancer incidence, however, few studies have considered historic exposure when levels were higher.
Outdoor residential PM2.5 concentrations were estimated using a nationwide spatiotemporal model for women in the National Institutes of Health-AARP Diet and Health Study, a prospective cohort located in 6 states (California, Florida, Louisiana, New Jersey, North Carolina, and Pennsylvania) and 2 metropolitan areas (Atlanta, GA, and Detroit, MI) and enrolled in 1995-1996 (n = 196 905). Annual average PM2.5 concentrations were estimated for a 5-year historical period 10 years prior to enrollment (1980-1984). We used Cox regression to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between a 10 µg/m3 increase in PM2.5 and breast cancer incidence overall and by estrogen receptor status and catchment area.
With follow-up of participants through 2017, a total of 15 870 breast cancer cases were identified. A 10 ug/m3 increase in PM2.5 was statistically significantly associated with overall breast cancer incidence (HR = 1.08, 95% CI = 1.02 to 1.13). The association was evident for estrogen receptor-positive (HR = 1.10, 95% CI = 1.04 to 1.17) but not estrogen receptor-negative tumors (HR = 0.97, 95% CI = 0.84 to 1.13; Pheterogeneity = .3). Overall breast cancer hazard ratios were more than 1 across the catchment areas, ranging from a hazard ratio of 1.26 (95% CI = 0.96 to 1.64) for North Carolina to a hazard ratio of 1.04 (95% CI = 0.68 to 1.57) for Louisiana (Pheterogeneity = .9).
In this large US cohort with historical air pollutant exposure estimates, PM2.5 was associated with risk of estrogen receptor-positive breast cancer. State-specific estimates were imprecise but suggest that future work should consider region-specific associations and the potential contribution of PM2.5 chemical constituency in modifying the observed association.
细颗粒物（PM2.5）与乳腺癌发病率的关系不一致，但是，很少有研究考虑到在水平较高时的历史暴露。
使用全国范围内的时空模型估算美国国立卫生研究院-美国退休人员协会饮食与健康研究中妇女的室外住宅 PM2.5 浓度，该前瞻性队列研究位于 6 个州（加利福尼亚州，佛罗里达州，路易斯安那州，新泽西州，北卡罗来纳州和宾夕法尼亚州）和 2 个大都市地区（佐治亚州亚特兰大和密歇根州底特律），并于 1995-1996 年进行了登记（n = 196905）。在登记前的 10 年（1980-1984 年），估计了 5 年历史时期的年平均 PM2.5 浓度。我们使用 Cox 回归来估计 PM2.5 每增加 10μg/m3 与总体乳腺癌发病率以及雌激素受体状态和集水区之间的关联的调整后的危险比（HR）和 95％置信区间（CI）。
通过对参与者的随访直至 2017 年，共发现 15870 例乳腺癌病例。PM2.5 每增加 10μg/m3 与总体乳腺癌发病率呈统计学显著相关（HR = 1.08，95％CI = 1.02 至 1.13）。该关联对于雌激素受体阳性（HR = 1.10，95％CI = 1.04 至 1.17）但对于雌激素受体阴性肿瘤（HR = 0.97，95％CI = 0.84 至 1.13；P异质性=.3）是明显的。整个集水区的总体乳腺癌危险比均超过 1，范围从北卡罗来纳州的危险比 1.26（95％CI = 0.96 至 1.64）到路易斯安那州的危险比 1.04（95％CI = 0.68 至 1.57）（P异质性=.9）。
在这项具有历史空气污染物暴露估计值的大型美国队列研究中，PM2.5 与雌激素受体阳性乳腺癌的风险相关。各州的具体估计值并不准确，但表明未来的工作应考虑区域特定的关联以及 PM2.5 化学组成在改变观察到的关联中的潜在作用。
