Air and Climate Epidemiology Section, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency, 1515 Clay Street, 16th Floor, Oakland, CA, 94612, USA.
Department of Environmental Health Sciences, Yale School of Public Health, Yale University, New Haven, CT, USA.
Environ Health. 2020 Nov 5;19(1):111. doi: 10.1186/s12940-020-00663-1.
Exposure to particulate matter air pollution has been associated with cardiovascular disease (CVD) morbidity and mortality; however, most studies have focused on fine particulate matter (PM) exposure and CVD. Coarse particulate matter (PM) exposure has not been extensively studied, particularly for long-term exposure, and the biological mechanisms remain uncertain.
We examined the association between ambient concentrations of PM and inflammatory and hemostatic makers that have been linked to CVD. Annual questionnaire and clinical data were obtained from 1694 women (≥ 55 years old in 1999) enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) at six study sites from 1999 to 2004. Residential locations and the USEPA air monitoring network measurements were used to assign exposure to one-year PM, as well as co-pollutants. Linear mixed-effects regression models were used to describe the association between PM exposure and markers, including demographic, health and other covariates.
Each interquartile (4 μg/m) increase in one-year PM exposure was associated with a 5.5% (95% confidence interval [CI]: 1.8, 9.4%) increase in levels of plasminogen activator inhibitor-1 (PAI-1) and 4.1% (95% CI: - 0.1, 8.6%) increase in high-sensitivity C-creative Protein (hs-CRP). Stratified analyses suggested that the association with PAI-1 was particularly strong in some subgroups, including women who were peri-menopausal, were less educated, had a body mass index lower than 25, and reported low alcohol consumption. The association between PM and PAI-1 remained unchanged with adjustment for PM, ozone, nitrogen dioxide, and carbon monoxide.
Long-term PM exposure may be associated with changes in coagulation independently from PM, and thus, contribute to CVD risk in midlife women.
暴露于颗粒物空气污染与心血管疾病(CVD)发病率和死亡率有关;然而,大多数研究都集中在细颗粒物(PM)暴露与 CVD 上。粗颗粒物(PM)暴露尚未得到广泛研究,特别是对于长期暴露,其生物学机制仍不确定。
我们研究了环境 PM 浓度与已与 CVD 相关的炎症和止血标志物之间的关系。1999 年,1694 名(≥55 岁)女性参加了纵向妇女健康全国研究(SWAN),从 1999 年到 2004 年在六个研究地点进行了年度问卷调查和临床数据收集。使用居住地点和美国环保署空气质量监测网络测量结果来分配一年 PM 暴露以及共同污染物。线性混合效应回归模型用于描述 PM 暴露与标志物之间的关系,包括人口统计学、健康和其他协变量。
每年 PM 暴露每增加一个四分位数(4μg/m),纤溶酶原激活物抑制剂-1(PAI-1)水平增加 5.5%(95%置信区间[CI]:1.8,9.4%),高敏 C 反应蛋白(hs-CRP)增加 4.1%(95% CI:-0.1,8.6%)。分层分析表明,这种与 PAI-1 的关联在一些亚组中尤为强烈,包括围绝经期、受教育程度较低、BMI 低于 25、低酒精摄入量的女性。在调整 PM、臭氧、二氧化氮和一氧化碳后,PM 与 PAI-1 之间的关联仍然不变。
长期 PM 暴露可能与 PM 独立的凝血变化有关,从而增加中年女性的 CVD 风险。