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The Guidelines indicate that by reducing particulate matter (PM10) pollution from 70 to 20 micrograms per cubic metre (μg/m), we can cut air pollution-related deaths by around 15%.
This is the first large national cohort studied with individual BP measurements and the use of advanced modeling methods to assess fine-scale intraurban gradients in major criteria air pollutants, PM2.5 and NO2. Prior studies have either used coarser-scale exposure assessment (e.g., nearest regulatory monitor) or administrative records (e.g., records of hypertension diagnoses) for outcome assessment. With exposures in the range currently experienced in the United States, these findings are interesting and important.
Our study demonstrates an association between increases in long-term residential exposure to PM2.5 and NO2 and higher measures of blood pressure (SBP, PP, and MAP for PM2.5 and PP for NO2). These relationships were robust to adjustment for multiple potential confounders, including SES and spatial characteristics, and apparently without threshold. The study also found an inverse relationship between NO2 and DBP in the fully adjusted model (model 5). We saw little evidence of effect modification by age, race/ethnicity, smoking, diabetes, anti-hypertensive medication use, or BMI (see Supplemental Material, Figure S3). Evidence of a long-term impact of air pollution on BP in our study population provides support to the hypothesis that air pollution induces autonomic dysfunction that may ultimately lead to vascular remodeling, increased BP, and atherosclerosis ().
The consistency of our findings with those of , our observed consistency of combined ORs and between-center heterogeneity (τ2 values) for meta-analyses of ORs adjusted for center-specific covariates, and our meta-analyses of unadjusted or SES-adjusted ORs give us confidence that synthesizing effect estimates for the air pollution–pregnancy outcomes associations reported by studies with different designs is informative. Further, experience from this study could be important for policy makers in incorporating research evidence into policy—for example, by including estimates of fetal growth in the future reviews of air quality standards.
Our study shows that personal PM2.5 exposure is positively associated with both SBP and DBP among adult women, particularly in those > 50 years of age. Although our findings should be confirmed in prospective cohort studies, they suggest that cardiovascular diseases may be an important component of the public health burden of indoor cooking and heating with biomass fuels. Issues of energy and indoor air pollution should therefore be considered in the formulation of policies and interventions aimed at reducing the cardiovascular disease burden in China and other countries where domestic use of biomass fuels is common.
Participants were assigned a metropolitan area of residence based on their enrollment address and three-digit ZIP code area. Complete data were available for 100 metropolitan statistical areas (MSAs) (). The mean concentrations of PM2.5 mass and trace constituents were compiled for 2000–2005 from the Health Effects Institute (HEI) Atmospheric and Environmental Research (AER) database (), derived from the U.S. EPA Air Quality System that archived Chemical Species Network (CSN) and gaseous criteria pollutant data. The present analysis focuses on further investigations of the PM2.5–IHD association, so gaseous air pollutants, evaluated in past analyses (), are not considered here, except in the derivation of the source factors (), as discussed below. These PM2.5 constituent data were analyzed to derive estimates of source apportioned PM2.5 mass exposure concentrations using the absolute principal component analysis (APCA) PM2.5 source apportionment method (). Because this process results in orthogonal source components, the source impacts developed have the advantage that they are derived to be as independent of one another as possible. This method involved a) a factor analysis of the trace constituents; b) identification of source-related factors (based on key tracers in each component); c) adjustment of factor scores into absolute scores; and d) a regression of the PM2.5 mass data on the source-related components, yielding apportionments of PM2.5 mass to each source-related factor ().
Deaths were ascertained through personal inquiries (e.g., direct contact with participants by volunteers) through September 1988, and subsequently via the National Death Index () through 31 December 2004. Mortality from IHD was studied because this was the category found most associated with PM2.5 exposure in past analyses of this cohort (e.g., ; ). More than 99% of known deaths were assigned a cause using the International Classification of Diseases, 9th and 10th Revision (ICD-9 codes 410–414; ICD-10 codes I20–I25). The analytic cohort included 445,860 participants having questionnaire, known vital status through 2004, and contextual census data, residing in 100 U.S. metropolitan areas within the contiguous United States where the required air pollution data were available, with 34,408 IHD deaths (of a total of 157,572 deaths from all causes) occurring during follow-up. Seventy-six of the metropolitan study areas were included in previously published ACS studies (e.g., , ).
Biomass (wood, crop residues, and animal dung) and coal are the primary fuels for almost half the world’s population, who live mostly in low-income regions (). These fuels are often burned inside poorly ventilated spaces with thermally inefficient stoves (; ) that emit a complex pollutant mixture of particulate matter (PM) and other toxic compounds at concentrations much higher than most urban ambient pollution levels (). The effects of indoor air pollution on chronic obstructive pulmonary disease and lung cancer (coal use only) in adults and pneumonia in children are well documented (; ; ; ; ; ). Limited evidence also suggests an association with tuberculosis (), cataracts (; ), and low birth weight ().
Exposures to ambient air pollution and tobacco smoke have been associated with increased risk of myocardial infarction, stroke, and cardiovascular mortality (; ; U.S. Department of Health and Human Services 2006). Several mechanisms have been proposed for these cardiovascular effects, including PM-induced increases in blood pressure (BP) (). Human experiments (; ; ) and observational studies (; ; ; ; ; ; ; ; ; ) suggest that ambient air pollution exposure could raise systolic BP (SBP) and diastolic BP (DBP), although other studies failed to replicate these findings (; ; ; ; ; ).