Jeffrey R. Brook

Particulate Matter Air Pollution and Cardiovascular Disease An Update to the Scientific Statement From the American Heart Association

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 &mgr;m in diameter (PM2.5) 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 PM2.5 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, PM2.5 exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality.

Effects of particulate and gaseous air pollution on cardiorespiratory hospitalizations.

We obtained data on daily numbers of admissions to hospital in Toronto, Canada, from 1980 to 1994 for respiratory, cardiac, cerebral vascular, and peripheral vascular diseases. We then linked the data to daily measures of particulate mass less than 10 microns in aerodynamic diameter (PM10), particulate mass less than 2.5 microns in aerodynamic diameter (PM2.5), and particulate mass between 2.5 and 10 microns in aerodynamic diameter (PM10-2.5), ozone, carbon monoxide, nitrogen dioxide, and sulfur dioxide. Air pollution was only associated weakly with hospitalization for cerebral vascular and peripheral vascular diseases. We controlled for temporal trends and climatic factors, and we found that increases of 10 microg/m3 in PM10, PM2.5, and PM10-2.5 were associated with 1.9%, 3.3%, and 2.9% respective increase in respiratory and cardiac hospital admissions. We further controlled for gaseous pollutants, and the percentages were reduced to 0.50%, 0.75%, and 0.77%, respectively. Of the 7.72 excess daily hospital admissions in Toronto attributable to the atmospheric pollution mix, 11.8% resulted from PM2.5, 8.2% to PM10-2.5, 17% to carbon monoxide, 40.4% to nitrogen dioxide, 2.8% to sulfur dioxide, and 19.8% to ozone.

Insights Into the Mechanisms and Mediators of the Effects of Air Pollution Exposure on Blood Pressure and Vascular Function in Healthy Humans

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, crossover studies. In Ann Arbor, 50 subjects were exposed to fine particles (150 &mgr;g/m3) plus ozone (120 parts per billion) for 2 hours on 3 occasions with pretreatments of an endothelin antagonist (Bosentan, 250 mg), antioxidant (Vitamin C, 2 g), or placebo. In Toronto, 31 subjects were exposed to 4 different conditions (particles plus 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 &agr;. In Ann Arbor, diastolic blood pressure significantly similarly increased during all of the exposures (2.5 to 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.

Acute blood pressure responses in healthy adults during controlled air pollution exposures

Exposure to air pollution has been shown to cause arterial vasoconstriction and alter autonomic balance. Because these biologic responses may influence systemic hemodynamics, we investigated the effect of air pollution on blood pressure (BP). Responses during 2-hr exposures to concentrated ambient fine particles (particulate matter < 2.5 μm in aerodynamic diameter; PM2.5) plus ozone (CAP+O3) were compared with those of particle-free air (PFA) in 23 normotensive, non-smoking healthy adults. Mean concentrations of PM2.5 were 147 ± 27 versus 2 ± 2 μg/m3, respectively, and those of O3 were 121 ± 3 versus 8 ± 5 ppb, respectively (p < 0.0001 for both). A significant increase in diastolic BP (DBP) was observed at 2 hr of CAP+O3 [median change, 6 mm Hg (9.3%); binomial 95% confidence interval (CI), 0 to 11; p = 0.013, Wilcoxon signed rank test] above the 0-hr value. This increase was significantly different (p = 0.017, unadjusted for basal BP) from the small 2-hr change during PFA (median change, 1 mm Hg; 95% CI, −2 to 4; p = 0.24). This prompted further investigation of the CAP+O3 response, which showed a strong association between the 2-hr change in DBP (and mean arterial pressure) and the concentration of the organic carbon fraction of PM2.5 (r = 0.53, p < 0.01; r = 0.56, p < 0.01, respectively) but not with total PM2.5 mass (r ≤ 0.25, p ≥ 0.27). These findings suggest that exposure to environmentally relevant concentrations of PM2.5 and O3 rapidly increases DBP. The magnitude of BP change is associated with the PM2.5 carbon content. Exposure to vehicular traffic may provide a common link between our observations and previous studies in which traffic exposure was identified as a potential risk factor for cardiovascular disease.

Risk of nonaccidental and cardiovascular mortality in relation to long-term exposure to low concentrations of fine particulate matter: a Canadian national-level cohort study.

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 (PM2.5)]. 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 PM2.5 and cardiovascular mortality in nonimmigrant Canadian adults. Methods: We assigned estimates of exposure to ambient PM2.5 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/m3 increase in concentrations of PM2.5. 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 PM2.5. Associations were observed with exposures to PM2.5 at concentrations that were predominantly lower (mean, 8.7 μg/m3; interquartile range, 6.2 μg/m3) than those reported previously.

A GIS - environmental justice analysis of particulate air pollution in Hamilton, Canada

The authors address two research questions: (1) Are populations with lower socioeconomic status, compared with people of higher socioeconomic status, more likely to be exposed to higher levels of particulate air pollution in Hamilton, Ontario, Canada? (2) How sensitive is the association between levels of particulate air pollution and socioeconomic status to specification of exposure estimates or statistical models? Total suspended particulate (TSP) data from the twenty-three monitoring stations in Hamilton (1985–94) were interpolated with a universal kriging procedure to develop an estimate of likely pollution values across the city based on annual geometric means and extreme events. Comparing the highest with the lowest exposure zones, the interpolated surfaces showed more than a twofold increase in TSP concentrations and more than a twentyfold difference in the probability of exposure to extreme events. Exposure estimates were related to socioeconomic and demographic data from census tract areas by using ordinary least squares and simultaneous autoregressive (SAR) models. Control for spatial autocorrelation in the SAR models allowed for tests of how robust specific socioeconomic variables were for predicting pollution exposure. Dwelling values were significantly and negatively associated with pollution exposure, a result robust to the method of statistical analysis. Low income and unemployment were also significant predictors of exposure, although results varied depending on the method of analysis. Relatively minor changes in the statistical models altered the significant variables. This result emphasizes the value of geographical information systems (GIS) and spatial statistical techniques in modelling exposure. The result also shows the importance of taking spatial autocorrelation into account in future justice – health studies.

Ambient nitrogen dioxide and distance from a major highway

The primary objective of this pilot study was to measure the variation of ambient nitrogen dioxide (NO(2)) concentration with increasing distance from a major highway in Montréal, Canada, in order to assess the validity of distance from the roadways as a surrogate for exposure to traffic-related air pollution in epidemiologic studies. A total of 31 two-sided Ogawa passive samplers (using triethanolamine-impregnated filters as an absorbent) were installed for 7 days in groups of two or three along an axis perpendicular to a major highway where traffic density exceeds 100000 vehicles/day. Distances ranged from 0 to 1310 m from the highway. Concentrations of NO(2) ranged from 11.9 to 29.3 ppb, and decreased significantly with increasing logarithmic distance from the highway (P<0.0001). Concentrations of NO(2) were also significantly lower upwind than downwind relative to the highway (P=0.0012). These findings indicate that distance from highways may be a valid surrogate for traffic-related air pollution.

The Relationship Among TSP, PM10, PM2.5, and Inorganic Constituents of Atmospheric Participate Matter at Multiple Canadian Locations

Abstract The Canadian NAPS (National Air Pollution Surveillance) network has produced one of the largest and more geographically diverse databases of high quality atmospheric particle measurements in the world. A maximum of ten and a minimum of two years of data are available for 19 Canadian locations. These data were used to investigate relationships between collocated measurements of TSP, PM10, PM2.5, SO4 2-, and other inorganic ions and elements at a variety of urban and rural locations. Amongst all locations and all 24-hour measurements, the 10th and 90th percentile TSP concentrations were 22 and 98 μg m-3, respectively. A majority of the PM10 concentrations were below 47 μg m-3 and most of the PM2 5 concentrations across Canada were below 26 μg m-3 (90th percentiles). On average across all sites, PM25 accounted for 49% of the PM10, and PM10 accounted for 44% of the TSP. However, there was considerable variability among sites, with the mean PM2.5 to PM10 ratio ranging from 0.36 to 0.65. This ratio als...

The relationship between diabetes mellitus and traffic-related air pollution.

Objective: Air pollution is associated with an increased risk for cardiovascular events. Many of the biological pathways involved could also promote diabetes mellitus (DM). We therefore investigated the association between DM prevalence and exposure to traffic-related air pollution (nitrogen dioxide [NO 2]). Methods: Study participants were patients who attended two respiratory clinics in Hamilton (n = 5228) and Toronto (n = 2406). The diagnosis of DM was ascertained by linkage to administrative databases of the Ontario universal Health Insurance Plan for patients aged 40 years and above. Geographic Information systems methodology was used to assign individual estimates of NO2 based on a network of samplers in each city. Logistic regression was used to estimate the relations between NO2 exposures and the odds of DM diagnosis. Results: After adjusting for age, body mass index, and neighborhood income there were positive effects in women on the odds ratio for DM for each 1 ppb NO2 exposure in Toronto (OR 1.055, 95% CI: 0.99 to 1.11) and Hamilton (OR 1.029, 95% CI: 0.98 to 1.08). In a meta-analytic model including both cities, there was a significant effect in women (OR = 1.04; 95% CI: 1.00 to 1.08). Across the inter-quartile range (∼4 ppb NO2) there was nearly a 17% increase in the odds of DM for women. There were no positive associations among men. Conclusions: Exposure to NO2, a marker of traffic-related air pollutants, was associated with DM prevalence among women. Exposure estimate errors in men may explain the apparent gender difference. These results suggest that common air pollutants are associated with DM and warrant more investigation to determine if this is a cause-and-effect relationship.

Association between ambient carbon monoxide levels and hospitalizations for congestive heart failure in the elderly in 10 Canadian cities

We examined the role that ambient air pollution plays in exacerbating cardiac disease by relating daily fluctuations in admissions to 134 hospitals for congestive heart failure in the elderly to daily variations in ambient concentrations of carbon monoxide, nitrogen dioxide, sulfur dioxide, ozone, and the coefficient of haze in Canadas 10 largest cities for the 11‐year period 1981–1991 inclusive. We adjusted the hospitalization time series for seasonal, subseasonal, and weekly cycles and for hospital usage patterns. The logarithm of the daily high‐hour ambient carbon monoxide concentration recorded on the day of admission displayed the strongest and most consistent association with hospitalization rates among the pollutants, after stratifying the time series by month of year and adjusting simultaneously for temperature, dew point, and the other ambient air pollutants. The relative risk for a change from 1 ppm to 3 ppm, the 25th and 75th percentiles of the exposure distribution, was 1.065 (95% confidence interval = 1.028–1.104). The regression coefficients of the other air pollutants were much more sensitive to simultaneous adjustment for either multiple pollutant or weather model specifications.