Chronic Particulate Exposure, Mortality, and Coronary Heart Disease in the Nurses’ Health Study

Department of Environmental Health Sciences, University of South Carolina, 2221 Devine Street, Columbia, SC 29208, USA.
American journal of epidemiology (Impact Factor: 5.23). 10/2008; 168(10):1161-8. DOI: 10.1093/aje/kwn232
Source: PubMed


Adverse health effects of exposures to acute air pollution have been well studied. Fewer studies have examined effects of chronic exposure. Previous studies used exposure estimates for narrow time periods and were limited by the geographic distribution of pollution monitors. This study examined the association of chronic particulate exposures with all-cause mortality, incident nonfatal myocardial infarction, and fatal coronary heart disease (CHD) in a prospective cohort of 66,250 women from the Nurses' Health Study in northeastern US metropolitan areas. Nonfatal outcomes were assessed through self-report and medical record review and fatalities through death certificates and medical record review. During follow-up (1992-2002), 3,785 deaths and 1,348 incident fatal CHD and nonfatal myocardial infarctions occurred. In age- and calendar-time-adjusted models, 10-microg/m(3) increases in 12-month average exposures to particulate matter <10 microm in diameter were associated with increased all-cause mortality (16%, 95% confidence interval: 5, 28) and fatal CHD (43%, 95% confidence interval: 10, 86). Adjustment for body mass index and physical activity weakened these associations. Body mass index and smoking modified the association between exposure to particulate matter <10 microm in diameter and fatal CHD. In this population, increases in such exposures were associated with increases in all-cause and CHD mortality. Never smokers with higher body mass indexes were at greatest risk of fatal CHD.

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    • "Further, this approach has the added benefit of straightforward interpretation of covariate effects on predicted PM levels, albeit where not obscured by collinearity or concurvity. Since model predictions can be made at a subject’s residence or other relevant point location, rather than interpolated from a pre-defined grid, our models offer high spatial resolution which may reduce exposure error when estimating chronic exposures in epidemiologic studies, as has been shown in previous analyses [11,25,26]. The models have been used to provide PM2.5, PM10, and PM2.5–10 monthly exposure estimates at subject residences in recent epidemiologic analyses [47,48]. "
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    ABSTRACT: Background Exposure to atmospheric particulate matter (PM) remains an important public health concern, although it remains difficult to quantify accurately across large geographic areas with sufficiently high spatial resolution. Recent epidemiologic analyses have demonstrated the importance of spatially- and temporally-resolved exposure estimates, which show larger PM-mediated health effects as compared to nearest monitor or county-specific ambient concentrations. Methods We developed generalized additive mixed models that describe regional and small-scale spatial and temporal gradients (and corresponding uncertainties) in monthly mass concentrations of fine (PM2.5), inhalable (PM10), and coarse mode particle mass (PM2.5–10) for the conterminous United States (U.S.). These models expand our previously developed models for the Northeastern and Midwestern U.S. by virtue of their larger spatial domain, their inclusion of an additional 5 years of PM data to develop predictions through 2007, and their use of refined geographic covariates for population density and point-source PM emissions. Covariate selection and model validation were performed using 10-fold cross-validation (CV). Results The PM2.5 models had high predictive accuracy (CV R2=0.77 for both 1988–1998 and 1999–2007). While model performance remained strong, the predictive ability of models for PM10 (CV R2=0.58 for both 1988–1998 and 1999–2007) and PM2.5–10 (CV R2=0.46 and 0.52 for 1988–1998 and 1999–2007, respectively) was somewhat lower. Regional variation was found in the effects of geographic and meteorological covariates. Models generally performed well in both urban and rural areas and across seasons, though predictive performance varied somewhat by region (CV R2=0.81, 0.81, 0.83, 0.72, 0.69, 0.50, and 0.60 for the Northeast, Midwest, Southeast, Southcentral, Southwest, Northwest, and Central Plains regions, respectively, for PM2.5 from 1999–2007). Conclusions Our models provide estimates of monthly-average outdoor concentrations of PM2.5, PM10, and PM2.5–10 with high spatial resolution and low bias. Thus, these models are suitable for estimating chronic exposures of populations living in the conterminous U.S. from 1988 to 2007.
    Full-text · Article · Aug 2014 · Environmental Health
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    • "However, epidemiological evidence suggests that there is more to increased cardiovascular death than enhanced risk of MI. In the Women’s Health Initiative [7] and the Nurses’ Health Study [8], the impact of PM exposure on cardiovascular mortality was much larger than for incidence of MI events. The evidence suggests a biological mechanism for PM that also involves effects on the myocardium itself. "
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    ABSTRACT: Clinical studies have now confirmed the link between short-term exposure to elevated levels of air pollution and increased cardiovascular mortality, but the mechanisms are complex and not completely elucidated. The present study was designed to investigate the hypothesis that activation of pulmonary sensory receptors and the sympathetic nervous system underlies the influence of pulmonary exposure to diesel exhaust particulate on blood pressure, and on the myocardial response to ischemia and reperfusion.Methods & Results: 6 h after intratracheal instillation of diesel exhaust particulate (0.5 mg), myocardial ischemia and reperfusion was performed in anesthetised rats. Blood pressure, duration of ventricular arrhythmia, arrhythmia-associated death, tissue edema and reperfusion injury were all increased by diesel exhaust particulate exposure. Reperfusion injury was also increased in buffer perfused hearts isolated from rats instilled in vivo, excluding an effect dependent on continuous neurohumoral activation or systemic inflammatory mediators. Myocardial oxidant radical production, tissue apoptosis and necrosis were increased prior to ischemia, in the absence of recruited inflammatory cells. Intratracheal application of an antagonist of the vanilloid receptor TRPV1 (AMG 9810, 30 mg/kg) prevented enhancement of systolic blood pressure and arrhythmia in vivo, as well as basal and reperfusion-induced myocardial injury ex vivo. Systemic beta1 adrenoreceptor antagonism with metoprolol (10 mg/kg) also blocked enhancement of myocardial oxidative stress and reperfusion injury. Pulmonary diesel exhaust particulate increases blood pressure and has a profound adverse effect on the myocardium, resulting in tissue damage, but also increases vulnerability to ischemia-associated arrhythmia and reperfusion injury. These effects are mediated through activation of pulmonary TRPV1, the sympathetic nervous system and locally generated oxidative stress.
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    • "In two studies, PM2.5 effect estimates were substantially higher among subjects with high body mass index [22,24]. "
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    ABSTRACT: Current day concentrations of ambient air pollution have been associated with a range of adverse health effects, particularly mortality and morbidity due to cardiovascular and respiratory diseases. In this review, we summarize the evidence from epidemiological studies on long-term exposure to fine and coarse particles, nitrogen dioxide (NO2) and elemental carbon on mortality from all-causes, cardiovascular disease and respiratory disease. We also summarize the findings on potentially susceptible subgroups across studies. We identified studies through a search in the databases Medline and Scopus and previous reviews until January 2013 and performed a meta-analysis if more than five studies were available for the same exposure metric.
    Full-text · Article · May 2013 · Environmental Health
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