Faculty Bibliography

Air pollution, especially exposure to particulate matter 2.5 (PM_2.5), has been associated with an increase in morbidity and mortality around the world. Specifically, it seems that PM_2.5 promotes the development of cardiovascular risk factors such as hypertension and atherosclerosis, while being associated with an increased risk of cardiovascular diseases, including myocardial infarction (MI), stroke, heart failure, and arrhythmias. In this review, we seek to elucidate the pathophysiological mechanisms by which exposure to PM_2.5 can result in adverse cardiovascular outcomes, in addition to understanding the link between exposure to PM_2.5 and cardiovascular events. It is hypothesized that PM_2.5 functions via 3 mechanisms: increased oxidative stress, activation of the inflammatory pathway of the immune system, and stimulation of the autonomic nervous system which ultimately promote endothelial dysfunction, atherosclerosis, and systemic inflammation that can thus lead to cardiovascular events. It is important to note that the various cardiovascular associations of PM_2.5 differ regarding the duration of exposure (short vs long) to PM_2.5, the source of PM_2.5, and regulations regarding air pollution in the area where PM_2.5 is prominent. Current strategies to reduce PM_2.5 exposure include personal strategies such as avoiding high PM_2.5 areas such as highways or wearing masks outdoors, to governmental policies restricting the amount of PM_2.5 produced by organizations. This review, by highlighting the significant impact between PM_2.5 exposure and cardiovascular health will hopefully bring awareness and produce significant change regarding dealing with PM_2.5 levels worldwide.

It is unclear whether cancers of the upper aerodigestive tract (UADT) and gastric cancer are related to air pollution, due to few studies with inconsistent results. The effects of particulate matter (PM) may vary across locations due to different source contributions and related PM compositions, and it is not clear which PM constituents/sources are most relevant from a consideration of overall mass concentration alone. We therefore investigated the association of UADT and gastric cancers with PM_2.5 elemental constituents and sources components indicative of different sources within a large multicentre population based epidemiological study. Cohorts with at least 10 cases per cohort led to ten and eight cohorts from five countries contributing to UADT- and gastric cancer analysis, respectively. Outcome ascertainment was based on cancer registry data or data of comparable quality. We assigned home address exposure to eight elemental constituents (Cu, Fe, K, Ni, S, Si, V and Zn) estimated from Europe-wide exposure models, and five source components identified by absolute principal component analysis (APCA). Cox regression models were run with age as time scale, stratified for sex and cohort and adjusted for relevant individual and neighbourhood level confounders. We observed 1139 UADT and 872 gastric cancer cases during a mean follow-up of 18.3 and 18.5 years, respectively. UADT cancer incidence was associated with all constituents except K in single element analyses. After adjustment for NO₂, only Ni and V remained associated with UADT. Residual oil combustion and traffic source components were associated with UADT cancer persisting in the multiple source model. No associations were found for any of the elements or source components and gastric cancer incidence. Our results indicate an association of several PM constituents indicative of different sources with UADT but not gastric cancer incidence with the most robust evidence for traffic and residual oil combustion.

Despite progress in many countries, air pollution, and especially fine particulate matter air pollution (PM_2.5) remains a global health threat: over 6 million premature cardiovascular and respiratory deaths/yr. have been attributed to household and outdoor air pollution. In this viewpoint, we identify present gaps in air pollution monitoring and regulation, and how they could be strengthened in future mitigation policies to more optimally reduce health impacts. We conclude that there is a need to move beyond simply regulating PM_2.5 particulate matter mass concentrations at central site stations. A greater emphasis is needed on: new portable and affordable technologies to measure personal exposures to particle mass; the consideration of a submicron (PM₁) mass air quality standard; and further evaluations of effects by particle composition and source. We emphasize the need to enable further studies on exposure-health relationships in underserved populations that are disproportionately impacted by air pollution, but not sufficiently represented in current studies.

In this study we investigated the concentration and composition of particulate matter (PM2.5) in the New York City subway system. Realtime measurements, at a 1-s cadence, and gravimetric measurements were performed inside train cars along 300 km of nine subway lines, as well as on 333 platforms on 287 subway stations. The mean (±SD) PM2.5 concentration on the underground platforms was 142 ± 69 μg/m³ versus 29 ± 20 μg/m³ for aboveground stations. The average concentrations inside train cars were 88 ± 14 μg/m³ when traveling through underground tunnels and platforms and 29 ± 31 μg/m³ while on aboveground tracks. The particle composition analysis of filtered samples was done using X-ray fluorescence (XRF), revealing that iron made up approximately 43% of the total PM2.5 mass on station platforms, approximately 126 times higher than the outdoor ambient iron concentration. Other trace elements include silicon, sulfur, copper, nickel, aluminum, calcium, barium, and manganese. Considering the very high iron content, the comparative analysis of the measured concentration versus the standards set by the Environmental Protection Agency (US EPA) is not appropriate since those limits are largely based on particulate matter from fossil fuel combustion. Health impact analysis of inhalation of iron-based particles is needed to contextualize the results presented here.

INTRODUCTION:The purpose of this study is to examine the associations between built environments and life expectancy across a gradient of urbanicity in the U.S. METHODS:Census tract‒level estimates of life expectancy between 2010 and 2015, except for Maine and Wisconsin, from the U.S. Small-Area Life Expectancy Estimates Project were analyzed in 2022. Tract-level measures of the built environment included: food, alcohol, and tobacco outlets; walkability; park and green space; housing characteristics; and air pollution. Multilevel linear models for each of the 4 urbanicity types were fitted to evaluate the associations, adjusting for population and social characteristics. RESULTS:Old housing (built before 1979) and air pollution were important built environment predictors of life expectancy disparities across all gradients of urbanicity. Convenience stores were negatively associated with life expectancy in all urbanicity types. Healthy food options were a positive predictor of life expectancy only in high-density urban areas. Park accessibility was associated with increased life expectancy in all areas, except rural areas. Green space in neighborhoods was positively associated with life expectancy in urban areas but showed an opposite association in rural areas. CONCLUSIONS:After adjusting for key social characteristics, several built environment characteristics were salient risk factors for decreased life expectancy in the U.S., with some measures showing differential effects by urbanicity. Planning and policy efforts should be tailored to local contexts.