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Exposure to ambient fine particulate matter (PM2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries-the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5-10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9-8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3-4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.

BackgroundStudies have reported associations between long-term air pollution exposures and cardiovascular mortality. The biological mechanisms connecting them remain uncertain.MethodsWe examined associations of fine particles (PM2.5) and ozone with serum markers of cardiovascular disease risk in a cohort of midlife women. We obtained information from women enrolled at six sites in the multi-ethnic, longitudinal Study of Women's Health Across the Nation, including repeated measurements of high-sensitivity C-reactive protein, fibrinogen, tissue-type plasminogen activator antigen, plasminogen activator inhibitor type 1, and factor VIIc (factor VII coagulant activity). We obtained residence-proximate PM2.5 and ozone monitoring data for a maximum five annual visits, calculating prior year, 6-month, 1-month, and 1-day exposures and their relations to serum markers using longitudinal mixed models.ResultsFor the 2,086 women studied from 1999 to 2004, PM2.5 exposures were associated with all blood markers except factor VIIc after adjusting for age, race/ethnicity, education, site, body mass index, smoking, and recent alcohol use. Adjusted associations were strongest for prior year exposures for high-sensitivity C-reactive protein (21% increase per 10 μg/m³ PM2.5, 95% confidence interval [CI]: 6.6, 37), tissue-type plasminogen activator antigen (8.6%, 95% CI: 1.8, 16), and plasminogen activator inhibitor (35%, 95% CI: 19, 53). An association was also observed between year prior ozone exposure and factor VIIc (5.7% increase per 10 ppb ozone, 95% CI: 2.9, 8.5).ConclusionsOur findings suggest that prior year exposures to PM2.5 and ozone are associated with adverse effects on inflammatory and hemostatic pathways for cardiovascular outcomes in midlife women.

BackgroundAlthough several cohort studies report associations between chronic exposure to fine particles (PM2.5) and mortality, few have studied the effects of chronic exposure to ultrafine (UF) particles. In addition, few studies have estimated the effects of the constituents of either PM2.5 or UF particles.MethodsWe used a statewide cohort of > 100,000 women from the California Teachers Study who were followed from 2001 through 2007. Exposure data at the residential level were provided by a chemical transport model that computed pollutant concentrations from > 900 sources in California. Besides particle mass, monthly concentrations of 11 species and 8 sources or primary particles were generated at 4-km grids. We used a Cox proportional hazards model to estimate the association between the pollutants and all-cause, cardiovascular, ischemic heart disease (IHD), and respiratory mortality.ResultsWe observed statistically significant (p < 0.05) associations of IHD with PM2.5 mass, nitrate, elemental carbon (EC), copper (Cu), and secondary organics and the sources gas- and diesel-fueled vehicles, meat cooking, and high-sulfur fuel combustion. The hazard ratio estimate of 1.19 (95% CI: 1.08, 1.31) for IHD in association with a 10-μg/m3 increase in PM2.5 is consistent with findings from the American Cancer Society cohort. We also observed significant positive associations between IHD and several UF components including EC, Cu, metals, and mobile sources.ConclusionsUsing an emissions-based model with a 4-km spatial scale, we observed significant positive associations between IHD mortality and both fine and ultrafine particle species and sources. Our results suggest that the exposure model effectively measured local exposures and facilitated the examination of the relative toxicity of particle species.

BackgroundSeveral cohort studies report associations between chronic exposure to ambient fine particles (PM2.5) and cardiovascular mortality. Uncertainty exists about biological mechanisms responsible for this observation, but systemic inflammation has been postulated. In addition, the subgroups susceptible to inflammation have not been fully elucidated.MethodsWe investigated whether certain subgroups are susceptible to the effects of long-term exposure to PM2.5 on C-reactive protein (CRP), a marker of inflammation directly linked to subsequent cardiovascular disease. We used data from the SWAN cohort of 1923 mid-life women with up to five annual repeated measures of CRP. Linear mixed and GEE models accounting for repeated measurements within an individual were used to estimate the effects of prior-year PM2.5 exposure on CRP. We examined CRP as a continuous and as binary outcome for CRP greater than 3mg/l, a level of clinical significance.ResultsWe found strong associations between PM2.5 and CRP among several subgroups. For example a 10 µg/m(3) increase in annual PM2.5 more than doubled the risk of CRP greater than 3mg/l in older diabetics, smokers and the unmarried. Larger effects were also observed among those with low income, high blood pressure, or who were using hormone therapy, with indications of a protective effects for those using statins or consuming moderate amounts of alcohol.ConclusionsIn this study, we observed significant associations between long-term exposure to PM2.5 and CRP in several susceptible subgroups. This suggests a plausible pathway by which exposure to particulate matter may be associated with increased risk of cardiovascular disease.

Several investigators have documented the effect of temperature on mortality, although fewer have studied its impact on morbidity. In addition, little is known about the effectiveness of mitigation strategies such as use of air conditioners (AC). We investigated the association between temperatures and hospital admissions in California from 1999 to 2005. We also determined whether AC ownership and usage, assessed at the zip code level, mitigates this association. Because of the unique spatial pattern of income and climate in the state, confounding of AC effects by other local factors is less likely. We only included individuals who had a temperature monitor within 25 kilometers of their residential zip codes. Using a time-stratified case-crossover approach, we observed a significantly increased risk for hospitalization for multiple diseases including cardiovascular, ischemic heart disease, ischemic stroke, respiratory disease, pneumonia, dehydration, heat stroke, diabetes and acute renal failure with same-day apparent temperature. We also found that ownership and usage of air conditioning significantly reduced the effects of temperature on these health outcomes, after controlling for the potential confounding effects of family income and other socioeconomic factors. Our results demonstrate important effects of temperature on public health and the potential for mitigation.Several investigators have documented the acute effect of temperature on mortality in the U.S. and Europe, and in developing nations(1-3). There are far fewer studies, however, on the effects of temperature on morbidity outcomes, such as hospitalizations (4-6). According to the recent IPCC report (7), temperatures are expected to increase in the future with more frequent and severe heat waves. Therefore, it is important to obtain a better understanding of these heat-associated health risks and susceptible populations for future surveillance and targeted interventions. In addition, relatively little is known about the effectiveness of proposed mitigation strategies, such as cooling shelters, and personal use of air conditioners (AC). Studies on the effects of actual AC use on temperature-related health outcomes, however, are limited, since data are typically available for AC prevalence, rather than AC use, and only for broad geographic regions. Thus, effects of AC may be confounded by other regional characteristics (8) such as demographic and economic factors. As a result, there is need for more localized estimates of the effects of temperature on morbidity and on the effectiveness of AC use in mitigating these effects.For several reasons, California serves as an ideal study area for examining the effects of AC use on temperature-related adverse health. First, it includes a large and diverse population, residing within a wide array of climatic regions. Second, individual-level data at small levels of spatial scale over a majority of the state are available from surveys conducted by the California Public Utilities Commission (9). Finally, income is less likely to confound the estimates of the effects of AC. In general, incomes are higher in the coastal regions, but lower in the inland areas, such as the Central Valley. However, AC use is greater in the Central Valley where the summers are much hotter, and many homes in the coastal areas of California lack AC (9). In this study, we used temperature data during the warm season in California to estimate the impact on several disease-specific categories of hospitalizations. To limit exposure misclassification, we limited our study to buffer areas with individuals living in zip codes within 25 kilometers (km) of a temperature monitor. Next, we quantified the likely reduction in health impacts based on both ownership and use of ACs using individual-level data for each buffer. Finally, we examined the potential confounding effect that local measures of family income may have on our effect estimates.

Exposure to fine particulate matter (PM2.5) is associated with adverse health effects, including mortality, even at low concentrations. Rail conveyance of coal, accounting for one-third of American rail freight tonnage, is a source of PM2.5. However, there are limited studies of its contribution to PM2.5, especially in urban settings where residents experience higher exposure and vulnerability to air pollution. We developed a novel artificial intelligence-driven monitoring system to quantify average and maximum PM2.5 concentrations of full and empty (unloaded) coal trains compared to freight and passenger trains. The monitor was close to the train tracks in Richmond, California, a city with a racially diverse population of 115,000 and high rates of asthma and heart disease. We used multiple linear regression models controlling for diurnal patterns and meteorology. The results indicate coal trains add on average 8.32 µg/m3 (95% CI = 6.37, 10.28; p < 0.01) to ambient PM2.5, while sensitivity analysis produced midpoints ranging from 5 to 12 µg/m3. Coal trains contributed 2 to 3 µg/m3 more of PM2.5 than freight trains, and 7 µg/m3 more under calm wind conditions, suggesting our study underestimates emissions and subsequent concentrations of coal train dust. Empty coal cars tended to add 2 µg/m3. Regarding peak concentrations of PM2.5, our models suggest an increase of 17.4 µg/m3 (95% CI = 6.2, 28.5; p < 0.01) from coal trains, about 3 µg/m3 more than freight trains. Given rail shipment of coal occurs globally, including in populous areas, it is likely to have adverse effects on health and environmental justice. [ABSTRACT FROM AUTHOR]

ABSTRACT Californians are exposed daily to concentrations of ozone ([O.sub.3]) that are among the highest in the United States. Recently, the state adopted a new 8-hr ambient standard of 0.070 [...]