Effects of prolonged exposure to ambient particulate and gaseous pollutants on cardiovascular and reproductive health
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Abstract 1: Whereas Particulate matter (PM) air pollution is increasingly recognized as an important and modifiable risk factor for cardiovascular disease (CVD), the association between CVD and PM has been established predominantly in acute exposure studies. There are still gaps regarding large population risk estimation of long-term exposures. Results from the nationwide Behavioral Risk Factor Surveillance System (BRFSS) were used along with air quality monitoring measurements to implement a systematic evaluation of PM-related CVD risks at the national and regional scales. CVD status and individual-level risk factors were available from more than 500,000 BRFSS respondents across 2,231 contiguous U.S. counties for 2007 and 2009. Chronic exposures to PM pollutants were estimated with spatial modeling from measurement data. CVD outcomes attributable to PM pollutants were assessed by mixed-effects logistic regression and latent class regression (LCR), with adjustment for multicausality. There were positive associations between CVD and PM after accounting for competing risk factors: the multivariable-adjusted odds for the multiplicity of CVD outcomes increased by 1.32 (95% confidence interval: 1.23-1.43) and 1.15 (1.07-1.22) times per 10 μg/m3 increase in PM2.5 and PM10 respectively in the LCR analyses. After controlling for spatial confounding, there were moderate estimated effects of PM exposure on multiple cardiovascular manifestations. These results suggest that chronic exposures to ambient particulates are important environmental risk factors for cardiovascular morbidity.Abstract 2: Despite the increased awareness of the cardiovascular effects associated with both air pollutants and asthma, population-based studies on their potentially synergistic relationship in cardiovascular morbidity are lacking. Epidemiological studies that support the formulation of plausible causal pathways are thus needed in order to better understand the link between air pollution and asthma in their effects on cardiovascular health. Using a hierarchical modeling approach that combined individual-level risk factors and local-scale air quality data, this study evaluated the effects of particulate matter and ozone pollution on ischaemic heart disease (IHD), adjusting for effect modification by asthma status. IHD status and co-risk factors including asthma were assessed in more than 600,000 Behavioral Risk Factor Surveillance System respondents across 2,318 contiguous U.S. counties for 2005, 2007 and 2009. Chronic exposures to particulate matter (PM) and ozone pollutants were estimated with kriging from measurement data. Overall, the study found elevated odds for IHD from long-term exposure to PM or ozone in adults with prior or current asthma, with effect modification more pronounced in regard to PM exposure. Further research is needed to clarify what conditions produce observable interactions between air pollutants and asthma, and to evaluate the biological mechanisms by which air pollution may engender an excess cardiovascular risk in asthmatics.Abstract 3: There is expanding evidence that ambient air pollution is associated with adverse birth outcomes. In the absence of definite biological mechanisms for such an association, it is important to determine the consistency of the putative effects of specific pollutants by exploring the relation in different populations and sites. The objective of this study is to assess whether air pollution is associated with term low birth weight (LBW) among residents of Southern Nevada, and to provide empirical evidence that might help evaluate plausible biological explanations. The frequency of LBW was assessed from a retrospective cohort of singletons born alive in Clark County during the period 1995-2008. Stationary air sampling data were obtained from the U.S. EPA to estimate average trimester exposures to ambient air pollutants. The effects of pollutant exposure on LBW were estimated by logistic regression with adjustment for co-risk factors including gestational age, type of delivery, gender, period and season of birth, maternal age, education, race, marital status, parity, adequacy of prenatal care, and maternal tobacco and alcohol use. Birth weight was also analyzed as a continuous variable to estimate the reduction of birth weight associated with changes in mean exposure to air pollution during each trimester of pregnancy. Controlling for maternal and fetal covariates and average pollutant measurements in each trimester (trimester exposures assessed simultaneously), exposure to ambient CO during the third trimester was associated with a significantly increased risk for LBW (odds ratio per 1-ppm increment=1.25; 95% CI: 1.06-1.47). PM10 also exhibited an inverse pattern with birth weight, although mean birth weight reductions associated with PM10 were small and only significant for the last trimester exposure. These results suggest that fetuses in the late stages of development are particularly vulnerable to particulate and CO pollution. Further studies are necessary to validate fetal susceptibility to air pollutants in terms of critical exposure windows, magnitude of effects, and relevant toxic components.