Fine particulate matter air pollution plus ozone impairs vascular function and raises diastolic blood pressure. We aimed to determine the mechanism and air pollutant responsible. The effects of pollution on heart rate variability, blood pressure, biomarkers, and brachial flow-mediated dilatation were determined in 2 randomized, double-blind, cross-over studies. In Ann Arbor, 50 subjects were exposed to fine particles (150 μg/m3) + ozone (120 ppb) for 2 hours on 3 occasions with pretreatments of an endothelin antagonist (Bosentan 250 mg), anti-oxidant (Vitamin C 2 g), or placebo. In Toronto, 31 subjects were exposed to 4 different conditions (particles + ozone, particles, ozone, and filtered air). In Toronto, diastolic blood pressure significantly increased (2.9 and 3.6 mm Hg) only during particle-containing exposures in association with particulate matter concentration and reductions in heart rate variability. Flow-mediated dilatation significantly decreased (2.0 and 2.9%) only 24 hours after particle-containing exposures in association with particulate matter concentration and increases in blood tumor necrosis factor-alpha. In Ann Arbor, diastolic blood pressure significantly similarly increased during all exposures (2.5 - 4.0 mm Hg), a response not mitigated by pretreatments. Flow-mediated dilatation remained unaltered. Particulate matter, not ozone, was responsible for increasing diastolic blood pressure during air pollution inhalation most plausibly by instigating acute autonomic imbalance. Only particles from urban Toronto additionally impaired endothelial function likely via slower proinflammatory pathways. Our findings demonstrate credible mechanisms whereby fine particulate matter could trigger acute cardiovascular events and that aspects of exposure location may be an important determinant of the health consequences.

The Near-Road Exposures and Effects of Urban Air Pollutants Study (NEXUS) was designed to examine the relationship between near-roadway exposures to air pollutants and respiratory outcomes in a cohort of asthmatic children who live close to major roadways in Detroit, Michigan USA. From September 2010 to December 2012 a total of 139 children with asthma, ages 6–14, were enrolled in the study on the basis of the proximity of their home to major roadways that carried different amounts of diesel traffic. The goal of the study was to investigate the effects of traffic-associated exposures on adverse respiratory outcomes, biomolecular markers of inflammatory and oxidative stress, and how these exposures affect the frequency and severity of respiratory viral infections in a cohort of children with asthma. An integrated measurement and modeling approach was used to quantitatively estimate the contribution of traffic sources to near-roadway air pollution and evaluate predictive models for assessing the impact of near-roadway pollution on children’s exposures. Two intensive field campaigns were conducted in Fall 2010 and Spring 2011 to measure a suite of air pollutants including PM2.5 mass and composition, oxides of nitrogen (NO and NO2), carbon monoxide, and black carbon indoors and outdoors of 25 participants’ homes, at two area schools, and along a spatial transect adjacent to I-96, a major highway in Detroit. These data were used to evaluate and refine models to estimate air quality and exposures for each child on a daily basis for the health analyses. The study design and methods are described, and selected measurement results from the Fall 2010 field intensive are presented to illustrate the design and successful implementation of the study. These data provide evidence of roadway impacts and exposure variability between study participants that will be further explored for associations with the health measures.

Wildland fires are diminishing air quality on a seasonal and regional basis, raising concerns about respiratory health risks to the public and occupational groups. This American Thoracic Society (ATS) workshop was convened in 2019 to meet the growing health threat of wildland fire smoke. The workshop brought together a multidisciplinary group of 19 experts, including wildland fire managers, public health officials, epidemiologists, toxicologists, and pediatric and adult pulmonologists. The workshop examined the following four major topics: 1) the science of wildland fire incidence and fire management, 2) the respiratory and cardiovascular health effects of wildland fire smoke exposure, 3) communication strategies to address these health risks, and 4) actions to address wildland fire health impacts. Through formal presentations followed by group discussion, workshop participants identified top priorities for fire management, research, communication, and public policy to address health risks of wildland fires. The workshop concluded that short-term exposure to wildland smoke causes acute respiratory health effects, especially among those with asthma and chronic obstructive pulmonary disease. Research is needed to understand long-term health effects of repeated smoke exposures across fire seasons for children, adults, and highly exposed occupational groups (especially firefighters). Other research priorities include fire data collection and modeling, toxicology of different fire fuel sources, and the efficacy of health protective measures to prevent respiratory effects of smoke exposure. The workshop committee recommends a unified federal response to the growing problem of wildland fires, including investment in fire behavior and smoke air quality modeling, research on the health impacts of smoke, and development of robust clinical and public health communication tools.

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