Faculty Bibliography

Fine particulate matter air pollution (PM2.5) is a major contributor to cardiovascular morbidity and mortality, potentially via increased inflammation. PM2.5 exposure increases inflammatory biomarkers linked to cardiovascular disease, including CRP, IL-6 and TNFα. Portable air cleaners (PACs) reduce individual PM2.5 exposure but evidence is limited regarding whether PACs also reduce inflammatory biomarkers. We performed a systematic review and meta-analysis of trials evaluating the use of PACs to reduce PM2.5 exposure and inflammatory biomarker concentrations. We identified English-language articles of randomized sham-controlled trials evaluating high efficiency particulate air filters in non-smoking, residential settings measuring serum CRP, IL-6 and TNFα before and after active versus sham filtration, and performed meta-analysis on the extracted modeled percent change in biomarker concentration across studies. Of 487 articles identified, we analyzed 14 studies enrolling 778 participants that met inclusion criteria. These studies showed PACs reduced PM2.5 by 61.5 % on average. Of the 14 included studies, 10 reported CRP concentrations in 570 participants; these showed active PAC use was associated with 7 % lower CRP (95 % CI: −14 % to 0.0 %, p = 0.05). Nine studies of IL-6, with 379 participants, showed active PAC use was associated with 13 % lower IL-6 (95 % CI: [−23 %, −3 %], p = 0.009). Six studies, with 269 participants, reported TNF-α and demonstrated no statistical evidence of difference between active and sham PAC use. Portable air cleaners that reduce PM2.5 exposure can decrease concentrations of inflammatory biomarkers associated with cardiovascular disease. Additional studies are needed to evaluate clinical outcomes and other biomarkers.

BACKGROUND:Greenhouse gas emissions are changing the Earth's climate, most directly by modifying temperatures and temperature variability (TV). Residents of low- and middle-income countries (LMICs) are likely more adversely affected, due to lack of air conditioning to compensate. To date, there is no local epidemiological evidence documenting the cardio-respiratory health effects of TV in Dhaka, Bangladesh, one of the most climate change vulnerable cities in the world. OBJECTIVES/OBJECTIVE:We assessed short-term TV associations with daily cardiovascular disease (CVD) and respiratory emergency department (ED) visits, as well as effect modification by age and season. METHODS:TV was calculated from the standard deviations of the daily minimum and maximum temperatures over exposure days. Time-series regression modeling was applied to daily ED visits for respiratory and CVD from January 2014 through December 2017. TV effect sizes were estimated after controlling for long-term trends and seasonality, day-of-week, holidays, and daily mean relative humidity and ambient temperature. RESULTS:) was associated with a 7.45% (95 %CI: 2.33%, 12.57%) increase in respiratory ED visits among patients above 50 years of age. CONCLUSION/CONCLUSIONS:This study provided novel and important evidence that cardio-pulmonary health in Dhaka is adversely affected year-round by day-to-day increases in TV, especially among older adults. TV is a key factor that should be considered in evaluating the potential human health impacts of climate change induced temperature changes.

Although PM_2.5 mass varies in source and composition over time and space, most health effects assessment have made the inherent assumption that all PM_2.5 mass has the same health implications, irrespective of composition. Nationwide estimates of source-specific PM_2.5 mass and constituents at local-scale would allow for epidemiological studies and health effects assessments that consider the variability in PM_2.5 characteristics in their health impact assessments. In response, we developed US models of annual exposures at the census tract level for five major PM_2.5 sources (traffic, soil, coal, oil, and biomass combustion) and six trace elements (elemental carbon, sulfur, silicon, selenium, nickel, and non-soil potassium) for 2001 through 2014. We employed Absolute Factor Analysis (APCA) to derive the source-specific PM_2.5 impacts at monitoring stations. Random forest algorithms that incorporated predictors derived from satellite, chemical transport model, and census tract resolution land-use data on traffic, meteorology, and emissions, which were rigorously tested by 10-fold cross-validation (CV), were then employed to estimate elemental and source-specific PM_2.5 levels at non-monitoring site census-tracts over the study years. Model performances were moderate to good, with CV R² ranging from 0.41 to 0.95. For PM_2.5 sources, the highest CV R² was attained for traffic PM_2.5 (CV R²Â = 0.73), followed by coal (CV R²Â = 0.65), oil (CV R²Â = 0.62), soil (CV R²Â = 0.60), and biomass (CV R²Â = 0.41). Among constituents, the CV was highest for sulfur (CV R²Â = 0.95). Our analyses provided highly resolved spatial estimates of annual elemental and source-specific PM_2.5 concentrations at the census-tract level, for 2001 through 2014. This dataset offers exposure estimates in support of future nationwide long-term health effects studies of source-specific PM_2.5 mass and constituents, enabling epidemiological research that addresses the fact that not all particles are the same.

[Figure: see text].

RATIONALE/BACKGROUND:To date, there is no published local epidemiological evidence documenting the respiratory health effects of source specific air pollution in South Asia, where PM2.5 composition is different from past studies. Differences include more biomass and residue crop-burning emissions, which may have differing health implications. OBJECTIVES/OBJECTIVE:We assessed PM2.5 associations with respiratory emergency department (ED) visits in a biomass-burning dominated high pollution region, and evaluated their variability by pollution source and composition. METHODS:Time-series regression modeling was applied to daily ED visits from January 2014 through December 2017. Air pollutant effect sizes were estimated after addressing long-term trends and seasonality, day-of-week, holidays, relative humidity, ambient temperature, and the effect modification by season, age, and sex. RESULTS:PM2.5 yielded a significant association with increased respiratory ED visits [0.84% (95% CI: 0.33%, 1.35%)] per 10 μg/m3 increase. The PM2.5 health effect size varied with season, the highest being during monsoon season, when fossil-fuel combustion sources dominated exposures. Results from a source-specific health effect analysis was also consistent with fossil-fuel PM2.5 having a larger effect size per 10 μg/m3 than PM2.5 from other sources [fossil-fuel PM2.5: 2.79% (0.33% to 5.31%), biomass-burning PM2.5: 1.27% (0% to 2.54%), and other-PM2.5: 0.95% (0.06% to 1.85%)]. Age-specific associations varied, with children and older adults being disproportionately affected by the air pollution, especially by the combustion-related particles. CONCLUSIONS:This study provided novel and important evidence that respiratory health in Dhaka is significantly affected by particle air pollution, with a greater health impact by fossil-fuel combustion derived PM2.5.

BACKGROUND:Fine-particulate-matter (i.e. with an aerodynamic diameter of ≤2.5 µm, PM2.5) air pollution is commonly treated as if it had 'equivalent toxicity', irrespective of the source and composition. We investigate the respective roles of fossil-fuel- and biomass-combustion particles in the PM2.5 relationship with cardiovascular morbidity and mortality using tracers of sources in Dhaka, Bangladesh. Results provide insight into the often observed levelling of the PM2.5 exposure-response curve at high-pollution levels. METHODS:A time-series regression model, adjusted for potentially confounding influences, was applied to 340 758 cardiovascular disease (CVD) emergency-department visits (EDVs) during January 2014 to December 2017, 253 407 hospital admissions during September 2013 to December 2017 and 16 858 CVD deaths during January 2014 to October 2017. RESULTS:Significant associations were confirmed between PM2.5-mass exposures and increased risk of cardiovascular EDV [0.27%, (0.07% to 0.47%)] at lag-0, hospitalizations [0.32% (0.08% to 0.55%)] at lag-0 and deaths [0.87%, (0.27% to 1.47%)] at lag-1 per 10-μg/m3 increase in PM2.5. However, the relationship of PM2.5 with morbidity and mortality effect slopes was less steep and non-significant at higher PM2.5 concentrations (during crop-burning-dominated exposures) and varied with PM2.5 source. Fossil-fuel-combustion PM2.5 had roughly a four times greater effect on CVD mortality and double the effect on CVD hospital admissions on a per-µg/m3 basis than did biomass-combustion PM2.5. CONCLUSION/CONCLUSIONS:Biomass burning was responsible for most PM2.5 air pollution in Dhaka, but fossil-fuel-combustion PM2.5 dominated the CVD adverse health impacts. Such by-source variations in the health impacts of PM2.5 should be considered in conducting ambient particulate-matter risk assessments, as well as in prioritizing air-pollution-mitigation measures and clinical advice.

In this review, we elucidate the central role played by fossil fuel combustion in the health-related effects that have been associated with inhalation of ambient fine particulate matter (PM2.5). We especially focus on individual properties and concentrations of metals commonly found in PM air pollution, as well as their sources and their adverse health effects, based on both epidemiologic and toxicological evidence. It is known that transition metals, such as Ni, V, Fe, and Cu, are highly capable of participating in redox reactions that produce oxidative stress. Therefore, particles that are enriched, per unit mass, in these metals, such as those from fossil fuel combustion, can have greater potential to produce health effects than other ambient particulate matter. Moreover, fossil fuel combustion particles also contain varying amounts of sulfur, and the acidic nature of the resulting sulfur compounds in particulate matter (e.g., as ammonium sulfate, ammonium bisulfate, or sulfuric acid) makes transition metals in particles more bioavailable, greatly enhancing the potential of fossil fuel combustion PM2.5 to cause oxidative stress and systemic health effects in the human body. In general, there is a need to further recognize particulate matter air pollution mass as a com-plex source-driven mixture, in order to more effectively quantify and regulate particle air pollution exposure health risks.