Lutsey Pamela L, Misialek Jeffrey R, Young Michael T, Berman Jesse, Leiser Claire L, Pope Zachary C, Cushman Mary, Folsom Aaron R, Kaufman Joel D
Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN.
Department of Environmental and Occupational Health Sciences, Seattle, WA.
Blood. 2025 Mar 6;145(10):1089-1096. doi: 10.1182/blood.2024026399.
Air pollution exposure may induce procoagulant effects, and chronic exposure may be linked to greater risk of venous thromboembolism (VTE). We tested the hypothesis that air pollution is associated with increased VTE risk in the prospective Multi-Ethnic Study of Atherosclerosis, which has well-characterized air pollution measures and information on potential confounding factors. We included 6651 participants recruited in 2000 to 2002 (baseline age range, 45-84 years; 53% female). Air pollution was assessed with a validated spatiotemporal model that incorporates cohort-specific monitoring. Four indexes of air pollution updated each fortnight over follow-up were averaged to estimate participant-level chronic exposure: fine particulate matter ≤2.5 micrometers in aerodynamic diameter (PM2.5), oxides of nitrogen (NOx), nitrogen dioxide (NO2), and ozone (O3). Mean±SD PM2.5 was 13.5±3.0 μg/m3, NO2 17.9±8.2 parts per billion (ppb), NOx 36.1±19.6 ppb, and O3 22.2±3.7 ppb. Incident VTE was identified using hospitalization discharge codes through 2018. A total of 248 VTE events accrued over a median follow-up of 16.7 years. After adjustment for baseline demographics, health behaviors, and body mass index, the hazard ratio (95% confidence interval) for incident VTE associated per 3.6 μg/m3 higher PM2.5 was 1.39 (1.04-1.86); per 13.3 ppb higher NO2 concentration was 2.74 (1.57-4.77); and per 30 ppb higher NOx was 2.21 (1.42-3.44). O3 was not related. In this prospective community-based cohort with individual-level estimation of chronic air pollution exposure, higher average ambient concentrations of PM2.5, NO2, and NOX were associated with greater risk of developing VTE. Findings add to accumulating evidence of adverse health effects attributed to air pollution exposure.
暴露于空气污染中可能会引发促凝血效应，长期暴露可能与静脉血栓栓塞症（VTE）风险增加有关。我们在多民族动脉粥样硬化前瞻性研究中检验了空气污染与VTE风险增加相关这一假设，该研究具有完善的空气污染测量方法以及潜在混杂因素的信息。我们纳入了2000年至2002年招募的6651名参与者（基线年龄范围为45 - 84岁；女性占53%）。空气污染通过一个经过验证的时空模型进行评估，该模型纳入了特定队列的监测数据。在随访期间每两周更新一次的四个空气污染指标进行平均，以估计参与者层面的长期暴露情况：空气动力学直径≤2.5微米的细颗粒物（PM2.5）、氮氧化物（NOx）、二氧化氮（NO2）和臭氧（O3）。PM2.5的均值±标准差为13.5±3.0微克/立方米，NO2为17.9±8.2十亿分比（ppb），NOx为36.1±19.6 ppb，O3为22.2±3.7 ppb。通过2018年的住院出院编码识别新发VTE。在中位随访16.7年期间，共发生248例VTE事件。在对基线人口统计学、健康行为和体重指数进行调整后，PM2.5每升高3.6微克/立方米，新发VTE的风险比（95%置信区间）为1.39（1.04 - 1.86）；NO2浓度每升高13.3 ppb为2.74（1.57 - 4.77）；NOx每升高30 ppb为2.21（1.42 - 3.44）。O3无相关性。在这个基于社区的前瞻性队列中，对慢性空气污染暴露进行个体层面的估计，较高的平均环境浓度的PM2.5、NO2和NOx与发生VTE的风险增加相关。研究结果进一步证明了空气污染暴露对健康的不良影响。
