Liu Rui, Young Michael T, Chen Jiu-Chiuan, Kaufman Joel D, Chen Honglei
Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
Environ Health Perspect. 2016 Nov;124(11):1759-1765. doi: 10.1289/EHP135. Epub 2016 Jun 10.
Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).
We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 μm in diameter (PM10) and < 2.5 μm in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.
Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders.
We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORQ5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations.
Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. Citation: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765; http://dx.doi.org/10.1289/EHP135.
很少有流行病学研究评估空气污染对帕金森病(PD)风险的影响。
我们调查了长期居住环境中直径小于10μm的颗粒物(PM10)、直径小于2.5μm的颗粒物(PM2.5)和二氧化氮(NO2)的浓度与PD风险之间的关联。
我们的巢式病例对照分析纳入了1995年至2006年间自我报告经医生诊断的1556例PD病例以及3313例按年龄、性别和种族进行频率匹配的对照。我们对1995 - 1996年报告的家庭住址进行地理编码,并使用纳入道路信息和其他地理协变量的国家精细尺度地理统计模型估算PM10、PM2.5和NO2的平均环境浓度。将空气污染物暴露分析为五分位数和连续变量,并对匹配变量和潜在混杂因素进行了调整。
我们观察到PM或NO2暴露与PD风险之间总体上无统计学显著关联。然而,在预先计划的亚组分析中,女性中较高的PM10暴露与较高的PD风险相关(第五分位数与第一分位数相比的比值比=1.65;95%置信区间:1.11, 2.45;p趋势=0.02),从不吸烟者中较高的PM2.5暴露与较高的PD风险相关(第五分位数与第一分位数相比的比值比=1.29;95%置信区间:0.94, 1.76;p趋势=0.04)。在女性从不吸烟者的事后分析中,PM2.5(第五分位数与第一分位数相比的比值比=1.79;95%置信区间:1.01, 3.17;p趋势=0.05)和PM10(第五分位数与第一分位数相比的比值比=2.34;95%置信区间:1.29, 4.26;p趋势=0.01)均与PD风险呈正相关。基于连续暴露变量的分析总体上显示出类似但无显著意义的关联。
总体而言,可以证明环境PM10、PM2.5或NO2暴露与PD风险之间关联的证据有限。PM2.5和PM10暴露可能增加女性从不吸烟者的PD风险这一提示性证据值得进一步研究。引文:Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759 - 1765; http://dx.doi.org/10.1289/EHP135.