Jeffrey R. Brook

In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM <2.5 microm in diameter (PM(2.5)) over a few hours to weeks can trigger cardiovascular disease-related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM(2.5) exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM(2.5) exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality.

BACKGROUND: Fine particulate air pollution and ozone are associated with increased cardiovascular events. To help explain the mechanism behind these observations, we investigated the effect of air pollution exposure on vascular function. METHODS AND RESULTS: Twenty-five healthy adults underwent a randomized, double-blind, crossover study comparing the vascular response to the 2-hour inhalation of approximately 150 microg/m(3) of concentrated ambient fine particles (CAP) plus ozone (120 ppb) versus the response to the inhalation of filtered air. High-resolution vascular ultrasonography was used to measure alterations in brachial artery diameter, endothelial-dependent flow-mediated dilatation (FMD) and endothelial-independent nitroglycerin-mediated dilatation (NMD). Exposure to CAP plus ozone caused a significant brachial artery vasoconstriction compared with filtered air inhalation (-0.09+/-0.15 mm versus +0.01+/-0.18 mm, P=0.03). There were no significant differences in FMD (+0.29+/-4.11% versus -0.03+/-6.63%, P=0.88), NMD (+3.87+/-5.43% versus +3.46+/-7.92%, P=0.83), or blood pressure responses between exposures. CONCLUSIONS: Short-term inhalation of fine particulate air pollution and ozone at concentrations that occur in the urban environment causes acute conduit artery vasoconstriction.

Abstract. A parameterization scheme for calculating gaseous dry deposition velocities in air-quality models is revised based on recent study results on non-stomatal uptake of O3 and SO2 over 5 different vegetation types. Non-stomatal resistance, which includes in-canopy aerodynamic, soil and cuticle resistances, for SO2 and O3 is parameterized as a function of friction velocity, relative humidity, leaf area index, and canopy wetness. Non-stomatal resistance for other chemical species is scaled to those of SO2 and O3 based on their chemical and physical characteristics. Stomatal resistance is calculated using a two-big-leaf stomatal resistance sub-model for all gaseous species of interest. The improvements in the present model compared to its earlier version include a newly developed non-stomatal resistance formulation, a realistic treatment of cuticle and ground resistance in winter, and the handling of seasonally-dependent input parameters. Model evaluation shows that the revised parameterization can provide more realistic deposition velocities for both O3 and SO2, especially for wet canopies. Example model output shows that the parameterization provides reasonable estimates of dry deposition velocities for different gaseous species, land types and diurnal and seasonal variations. Maximum deposition velocities from model output are close to reported measurement values for different land types. The current parameterization can be easily adopted into different air-quality models that require inclusion of dry deposition processes.

BACKGROUND: Few cohort studies have evaluated the risk of mortality associated with long-term exposure to fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM(2.5))]. This is the first national-level cohort study to investigate these risks in Canada. OBJECTIVE: We investigated the association between long-term exposure to ambient PM(2.5) and cardiovascular mortality in nonimmigrant Canadian adults. METHODS: We assigned estimates of exposure to ambient PM(2.5) derived from satellite observations to a cohort of 2.1 million Canadian adults who in 1991 were among the 20% of the population mandated to provide detailed census data. We identified deaths occurring between 1991 and 2001 through record linkage. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for available individual-level and contextual covariates using both standard Cox proportional survival models and nested, spatial random-effects survival models. RESULTS: Using standard Cox models, we calculated HRs of 1.15 (95% CI: 1.13, 1.16) from nonaccidental causes and 1.31 (95% CI: 1.27, 1.35) from ischemic heart disease for each 10-μg/m(3) increase in concentrations of PM(2.5). Using spatial random-effects models controlling for the same variables, we calculated HRs of 1.10 (95% CI: 1.05, 1.15) and 1.30 (95% CI: 1.18, 1.43), respectively. We found similar associations between nonaccidental mortality and PM2.5 based on satellite-derived estimates and ground-based measurements in a subanalysis of subjects in 11 cities. CONCLUSIONS: In this large national cohort of nonimmigrant Canadians, mortality was associated with long-term exposure to PM(2.5). Associations were observed with exposures to PM(2.5) at concentrations that were predominantly lower (mean, 8.7 μg/m(3); interquartile range, 6.2 μg/m(3)) than those reported previously.

BACKGROUND: Few studies examining the associations between long-term exposure to ambient air pollution and mortality have considered multiple pollutants when assessing changes in exposure due to residential mobility during follow-up. OBJECTIVE: We investigated associations between cause-specific mortality and ambient concentrations of fine particulate matter (≤ 2.5 μm; PM2.5), ozone (O3), and nitrogen dioxide (NO2) in a national cohort of about 2.5 million Canadians. METHODS: We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during 16 years of follow-up. Historical tax data allowed us to track subjects' residential postal code annually. We estimated hazard ratios (HRs) for each pollutant separately and adjusted for the other pollutants. We also estimated the product of the three HRs as a measure of the cumulative association with mortality for several causes of death for an increment of the mean minus the 5th percentile of each pollutant: 5.0 μg/m3 for PM2.5, 9.5 ppb for O3, and 8.1 ppb for NO2. RESULTS: PM2.5, O3, and NO2 were associated with nonaccidental and cause-specific mortality in single-pollutant models. Exposure to PM2.5 alone was not sufficient to fully characterize the toxicity of the atmospheric mix or to fully explain the risk of mortality associated with exposure to ambient pollution. Assuming additive associations, the estimated HR for nonaccidental mortality corresponding to a change in exposure from the mean to the 5th percentile for all three pollutants together was 1.075 (95% CI: 1.067, 1.084). Accounting for residential mobility had only a limited impact on the association between mortality and PM2.5 and O3, but increased associations with NO2. CONCLUSIONS: In this large, national-level cohort, we found positive associations between several common causes of death and exposure to PM2.5, O3, and NO2. CITATION: Crouse DL, Peters PA, Hystad P, Brook JR, van Donkelaar A, Martin RV, Villeneuve PJ, Jerrett M, Goldberg MS, Pope CA III, Brauer M, Brook RD, Robichaud A, Menard R, Burnett RT. 2015. Ambient PM2.5, O3, and NO2 exposures and associations with mortality over 16 years of follow-up in the Canadian Census Health and Environment Cohort (CanCHEC). Environ Health Perspect 123:1180-1186; http://dx.doi.org/10.1289/ehp.1409276.