Ostro Bart, Hu Jianlin, Goldberg Debbie, Reynolds Peggy, Hertz Andrew, Bernstein Leslie, Kleeman Michael J
Air Pollution Epidemiology Section, California Office of Environmental Health Hazard Assessment, Oakland, California, USA.
Environ Health Perspect. 2015 Jun;123(6):549-56. doi: 10.1289/ehp.1408565. Epub 2015 Jan 23.
Although several cohort studies report associations between chronic exposure to fine particles (PM2.5) and mortality, few have studied the effects of chronic exposure to ultrafine (UF) particles. In addition, few studies have estimated the effects of the constituents of either PM2.5 or UF particles.
We used a statewide cohort of > 100,000 women from the California Teachers Study who were followed from 2001 through 2007. Exposure data at the residential level were provided by a chemical transport model that computed pollutant concentrations from > 900 sources in California. Besides particle mass, monthly concentrations of 11 species and 8 sources or primary particles were generated at 4-km grids. We used a Cox proportional hazards model to estimate the association between the pollutants and all-cause, cardiovascular, ischemic heart disease (IHD), and respiratory mortality.
We observed statistically significant (p < 0.05) associations of IHD with PM2.5 mass, nitrate, elemental carbon (EC), copper (Cu), and secondary organics and the sources gas- and diesel-fueled vehicles, meat cooking, and high-sulfur fuel combustion. The hazard ratio estimate of 1.19 (95% CI: 1.08, 1.31) for IHD in association with a 10-μg/m3 increase in PM2.5 is consistent with findings from the American Cancer Society cohort. We also observed significant positive associations between IHD and several UF components including EC, Cu, metals, and mobile sources.
Using an emissions-based model with a 4-km spatial scale, we observed significant positive associations between IHD mortality and both fine and ultrafine particle species and sources. Our results suggest that the exposure model effectively measured local exposures and facilitated the examination of the relative toxicity of particle species.
尽管多项队列研究报告了长期暴露于细颗粒物(PM2.5)与死亡率之间的关联,但很少有研究探讨长期暴露于超细(UF)颗粒物的影响。此外,很少有研究估计PM2.5或UF颗粒物成分的影响。
我们使用了加利福尼亚教师研究中超过10万名女性的全州队列,这些女性在2001年至2007年期间接受随访。住宅层面的暴露数据由一个化学传输模型提供,该模型根据加利福尼亚州900多个污染源计算污染物浓度。除了颗粒物质量外,还在4公里网格上生成了11种物质和8种源或一次颗粒物的月浓度。我们使用Cox比例风险模型来估计污染物与全因、心血管、缺血性心脏病(IHD)和呼吸死亡率之间的关联。
我们观察到IHD与PM2.5质量、硝酸盐、元素碳(EC)、铜(Cu)、二次有机物以及汽油和柴油车辆、肉类烹饪和高硫燃料燃烧源之间存在统计学显著(p < 0.05)的关联。IHD与PM2.5每增加10μg/m³相关的风险比估计值为1.19(95%CI:1.08,1.31),这与美国癌症协会队列的研究结果一致。我们还观察到IHD与几种UF成分之间存在显著的正相关,包括EC、Cu、金属和移动源。
使用基于排放的4公里空间尺度模型,我们观察到IHD死亡率与细颗粒物和超细颗粒物种类及来源之间存在显著的正相关。我们的结果表明,该暴露模型有效地测量了局部暴露,并有助于检查颗粒物种类的相对毒性。