Faculty Bibliography

Exposure to ambient fine particulate matter (PM_2.5) 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 PM_2.5 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 PM_2.5-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 PM_2.5 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 PM_2.5 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.

OBJECTIVE:Recent mechanistic and epidemiological evidence implicates air pollution as a potential risk factor for diabetes; however, mortality risks have not been evaluated in a large US cohort assessing exposures to multiple pollutants with detailed consideration of personal risk factors for diabetes. RESEARCH DESIGN AND METHODS/METHODS:. Associations between the air pollutants and the risk of diabetes mortality (N = 3598) were evaluated using multivariate Cox proportional hazards models adjusted for both individual-level and census-level contextual covariates. RESULTS:(HR = 1.09; 95% CI: 1.01-1.18 per 10 ppb). The strength of the relationship was robust to alternate exposure assessments and model specifications. We also observed significant effect modification, with elevated mortality risks observed among those with higher BMI and lower levels of fruit consumption. CONCLUSIONS:, is related to increased risk of diabetes mortality in the U.S, with attenuation of adverse effects by lower BMI and higher fruit consumption, suggesting that air pollution is involved in the etiology and/or control of diabetes.

This study provides the first comprehensive analysis of the seasonal variations and weekday/weekend differences in fine (PM2.5) and coarse (PM2.5-10) particulate matter mass concentrations, elemental constituents, and potential source origins in Jeddah, Saudi Arabia. Air quality samples were collected over one year, from June 2011 to May 2012 at a frequency of three times per week, and analyzed. The average mass concentrations of PM2.5 (21.9 mug/m3) and PM10 (107.8 mug/m3) during the sampling period exceeded the recommended annual average levels by the World Health Organization (WHO) for PM2.5 (10 mug/m3) and PM10 (20 mug/m3), respectively. Similar to other Middle Eastern locales, PM2.5-10 is the prevailing mass component of atmospheric particulate matter at Jeddah, accounting for approximately 80% of the PM10 mass. Considerations of enrichment factors, absolute principal component analysis (APCA), concentration roses, and backward trajectories identified the following source categories for both PM2.5 and PM2.5-10: 1) soil/road dust; 2) incineration; and 3) traffic; and for PM2.5 only, 4) residual oil burning. Soil/road dust accounted for a major portion of both the PM2.5 (27%) and PM2.5-10 (77%) mass, and the largest source contributor for PM2.5 was from residual oil burning (63%). Temporal variations of PM2.5-10 and PM2.5 were observed, with the elevated concentration levels observed for mass during the spring (due to increased dust storm frequency), and on weekdays (due to increased traffic). The predominant role of windblown soil and road dust in both the PM2.5 and PM2.5-10 masses in this city may have implications regarding the toxicity of these particles versus those in the western world where most PM health assessments have been made in the past. These results support the need for region-specific epidemiological investigations to be conducted and considered in future PM standard setting. Implications Temporal variation of fine and coarse PM mass, elemental constituents, and sources were examined in Jeddah, Saudi Arabia for the first time. The main source of PM2.5-10 is natural windblown soil and road dust, while the predominant source of PM2.5 is residual oil burning, generated from the port and oil refinery located west of the air sampler, suggesting that targeted emission controls could significantly improve the air quality in the city. The compositional differences point to a need for health effects studies to be conducted in this region, as to directly assess the applicability of the existing guidelines to the Middle East air pollution.

In this study, factor analysis and mass regression were used to identify four fine particulate matter sources and estimate their contributions to the ambient air pollution in Beijing. The identified sources were traffic re-suspended soil, mixed industrial sources, oil combustion, and secondary sulfate. The estimated source contributions were then introduced into two models as exposure variables to explore the relationships between cardiovascular responses in mice and PM exposures. We observed that PM2.5 has a small negative acute effect on heart rate, but the individual source factors showed much more significant effects. Traffic re-suspended soil had the most significant effect on heart rate, with a positive contribution on the day of exposure and a negative one on day lag 1. Acute heart rate variability outcomes were better explained by the total PM2.5 than by the source components. Chronic effects were observed as a decreased heart rate but an increased number of heart rate variability outcomes