HealthyPlan.City: A Web Tool to Support Urban Environmental Equity and Public Health in Canadian Communities.

Urban environmental factors such as air quality, heat islands, and access to greenspaces and community amenities impact public health. Some vulnerable populations such as low-income groups, children, older adults, new immigrants, and visible minorities live in areas with fewer beneficial conditions, and therefore, face greater health risks. Planning and advocating for equitable healthy urban environments requires systematic analysis of reliable spatial data to identify where vulnerable populations intersect with positive or negative urban/environmental characteristics. To facilitate this effort in Canada, we developed HealthyPlan.City ( https://healthyplan.city/ ), a freely available web mapping platform for users to visualize the spatial patterns of built environment indicators, vulnerable populations, and environmental inequity within over 125 Canadian cities. This tool helps users identify areas within Canadian cities where relatively higher proportions of vulnerable populations experience lower than average levels of beneficial environmental conditions, which we refer to as Equity priority areas. Using nationally standardized environmental data from satellite imagery and other large geospatial databases and demographic data from the Canadian Census, HealthyPlan.City provides a block-by-block snapshot of environmental inequities in Canadian cities. The tool aims to support urban planners, public health professionals, policy makers, and community organizers to identify neighborhoods where targeted investments and improvements to the local environment would simultaneously help communities address environmental inequities, promote public health, and adapt to climate change. In this paper, we report on the key considerations that informed our approach to developing this tool and describe the current web-based application.

Daily Summer Temperatures and Hospitalization for Acute Cardiovascular Events: Impact of Outdoor PM 2.5 Oxidative Potential on Observed Associations Across Canada.

BACKGROUND: Oxidative stress plays an important role in the health impacts of both outdoor fine particulate air pollution (PM 2.5 ) and thermal stress. However, it is not clear how the oxidative potential of PM 2.5 may influence the acute cardiovascular effects of temperature. METHODS: We conducted a case-crossover study of hospitalization for cardiovascular events in 35 cities across Canada during the summer months (July-September) between 2016 and 2018. We collected three different metrics of PM 2.5 oxidative potential each month in each location. We estimated associations between lag-0 daily temperature (per 5ºC) and hospitalization for all cardiovascular (n = 44,876) and ischemic heart disease (n = 14,034) events across strata of monthly PM 2.5 oxidative potential using conditional logistical models adjusting for potential time-varying confounders. RESULTS: Overall, associations between lag-0 temperature and acute cardiovascular events tended to be stronger when outdoor PM 2.5 oxidative potential was higher. For example, when glutathione-related oxidative potential (OP GSH ) was in the highest tertile, the odds ratio (OR) for all cardiovascular events was 1.040 (95% confidence intervals [CI] = 1.004, 1.074) compared with 0.980 (95% CI = 0.943, 1.018) when OP GSH was in the lowest tertile. We observed a greater difference for ischemic heart disease events, particularly for older subjects (age >70 years). CONCLUSIONS: The acute cardiovascular health impacts of summer temperature variations may be greater when outdoor PM 2.5 oxidative potential is elevated. This may be particularly important for ischemic heart disease events.

Short-term exposure to ambient air pollution and individual emergency department visits for COVID-19: a case-crossover study in Canada.

BACKGROUND: Ambient air pollution is thought to contribute to increased risk of COVID-19, but the evidence is controversial. OBJECTIVE: To evaluate the associations between short-term variations in outdoor concentrations of ambient air pollution and COVID-19 emergency department (ED) visits. METHODS: We conducted a case-crossover study of 78 255 COVID-19 ED visits in Alberta and Ontario, Canada between 1 March 2020 and 31 March 2021. Daily air pollution data (ie, fine particulate matter with diameter less than 2.5 µm (PM2.5), nitrogen dioxide (NO2) and ozone were assigned to individual case of COVID-19 in 10 km × 10 km grid resolution. Conditional logistic regression was used to estimate associations between air pollution and ED visits for COVID-19. RESULTS: Cumulative ambient exposure over 0-3 days to PM2.5 (OR 1.010; 95% CI 1.004 to 1.015, per 6.2 µg/m3) and NO2 (OR 1.021; 95% CI 1.015 to 1.028, per 7.7 ppb) concentrations were associated with ED visits for COVID-19. We found that the association between PM2.5 and COVID-19 ED visits was stronger among those hospitalised following an ED visit, as a measure of disease severity, (OR 1.023; 95% CI 1.015 to 1.031) compared with those not hospitalised (OR 0.992; 95% CI 0.980 to 1.004) (p value for effect modification=0.04). CONCLUSIONS: We found associations between short-term exposure to ambient air pollutants and COVID-19 ED visits. Exposure to air pollution may also lead to more severe COVID-19 disease.

Does early life exposure to exogenous sources of reactive oxygen species (ROS) increase the risk of respiratory and allergic diseases in children? A longitudinal cohort study.

BACKGROUND: Excess reactive oxygen species (ROS) can cause oxidative stress damaging cells and tissues, leading to adverse health effects in the respiratory tract. Yet, few human epidemiological studies have quantified the adverse effect of early life exposure to ROS on child health. Thus, this study aimed to examine the association of levels of ROS exposure at birth and the subsequent risk of developing common respiratory and allergic diseases in children. METHODS: 1,284 Toronto Child Health Evaluation Questionnaire (T-CHEQ) participants were followed from birth (born between 1996 and 2000) until outcome, March 31, 2016 or loss-to-follow-up. Using ROS data from air monitoring campaigns and land use data in Toronto, ROS concentrations generated in the human respiratory tract in response to inhaled pollutants were estimated using a kinetic multi-layer model. These ROS values were assigned to participants' postal codes at birth. Cox proportional hazards regression models, adjusted for confounders, were then used to estimate hazard ratios (HR) with 95% confidence intervals (CI) per unit increase in interquartile range (IQR). RESULTS: After adjusting for confounders, iron (Fe) and copper (Cu) were not significantly associated with the risk of asthma, allergic rhinitis, nor eczema. However, ROS, a measure of the combined impacts of Fe and Cu in PM2.5, was associated with an increased risk of asthma (HR = 1.11, 95% CI: 1.02-1.21, p < 0.02) per IQR. There were no statistically significant associations of ROS with allergic rhinitis (HR = 0.96, 95% CI: 0.88-1.04, p = 0.35) and eczema (HR = 1.03, 95% CI: 0.98-1.09, p = 0.24). CONCLUSION: These findings showed that ROS exposure in early life significantly increased the childhood risk of asthma, but not allergic rhinitis and eczema.

Long-term Exposure to Oxidant Gases and Mortality: Effect Modification by PM 2.5 Transition Metals and Oxidative Potential.

BACKGROUND: Populations are simultaneously exposed to outdoor concentrations of oxidant gases (i.e., O 3 and NO 2 ) and fine particulate air pollution (PM 2.5 ). Since oxidative stress is thought to be an important mechanism explaining air pollution health effects, the adverse health impacts of oxidant gases may be greater in locations where PM 2.5 is more capable of causing oxidative stress. METHODS: We conducted a cohort study of 2 million adults in Canada between 2001 and 2016 living within 10 km of ground-level monitoring sites for outdoor PM 2.5 components and oxidative potential. O x exposures (i.e., the redox-weighted average of O 3 and NO 2 ) were estimated using a combination of chemical transport models, land use regression models, and ground-level data. Cox proportional hazards models were used to estimate associations between 3-year moving average O x and mortality outcomes across strata of transition metals and sulfur in PM 2.5 and three measures of PM 2.5 oxidative potential adjusting for possible confounding factors. RESULTS: Associations between O x and mortality were consistently stronger in regions with elevated PM 2.5 transition metal/sulfur content and oxidative potential. For example, each interquartile increase (6.27 ppb) in O x was associated with a 14.9% (95% CI = 13.0, 16.9) increased risk of nonaccidental mortality in locations with glutathione-related oxidative potential (OP GSH ) above the median whereas a 2.50% (95% CI = 0.600, 4.40) increase was observed in regions with OP GSH levels below the median (interaction P value <0.001). CONCLUSION: Spatial variations in PM 2.5 composition and oxidative potential may contribute to heterogeneity in the observed health impacts of long-term exposures to oxidant gases.

Sex-difference in air pollution-related acute circulatory and respiratory mortality and hospitalization.

BACKGROUND: Numerous studies have estimated adverse effects of short-term exposure to ambient air pollution on public health. Few have focused on sex-differences, and results have been inconsistent. The purpose of this study was three-fold: to identify sex-differences in air pollution-related health outcomes; to examine sex-differences by cause and season; and to examine time trends in sex-differences. METHODS: Daily data were collected on circulatory- and respiratory-related mortality (for 29 years) and cause-specific hospitalization (for 17 years) with hourly concentrations of ozone (O3), nitrogen dioxide (NO2), and fine particulate matter (PM2.5). For hospitalization, more specific causes were examined: ischemic heart disease (IHD), other heart disease (OHD), cerebrovascular disease (CEV), chronic lower respiratory diseases (CLRD), and Influenza/Pneumonia (InfPn). Generalized Poisson models were applied to 24 Canadian cities, and the city-specific estimates were combined for nationwide estimates for each sex using Bayesian hierarchical models. Finally, sex-differences were tested statistically based on their interval estimates, considering the correlation between sex-specific national estimates. RESULTS: Sex-differences were more frequently observed for hospitalization than mortality, respiratory than circulatory health outcomes, and warm than cold season. For hospitalization, males were at higher risk (M > F) for warm season (OHD and InfPn from O3; IHD from NO2; and InfPn from PM2.5), but F > M for cold season (CEV from O3 and OHD from NO2). For mortality, we found F > M only for circulatory diseases from ozone during the warm season. Among the above-mentioned sex-differences, three cases showed consistent time trends over the years: while M > F for OHD from O3 and IHD from NO2, F > M for OHD from NO2. CONCLUSIONS: We found that sex-differences in effect of ambient air pollution varied over health outcome, cause, season and time. In particular, the consistent trends (either F > M or M > F) across 17 years provide stronger evidence of sex-differences in hospitalizations, and warrant investigation in other populations.

Association of Sulfur, Transition Metals, and the Oxidative Potential of Outdoor PM2.5 with Acute Cardiovascular Events: A Case-Crossover Study of Canadian Adults.

BACKGROUND: We do not currently understand how spatiotemporal variations in the composition of fine particulate air pollution [fine particulate matter with aerodynamic diameter ≤2.5µm (PM2.5)] affects population health risks. However, recent evidence suggests that joint concentrations of transition metals and sulfate may influence the oxidative potential (OP) of PM2.5 and associated health impacts. OBJECTIVES: The purpose of the study was to evaluate how combinations of transition metals/OP and sulfur content in outdoor PM2.5 influence associations with acute cardiovascular events. METHODS: We conducted a national case-crossover study of outdoor PM2.5 and acute cardiovascular events in Canada between 2016 and 2017 (93,344 adult cases). Monthly mean transition metal and sulfur (S) concentrations in PM2.5 were determined prospectively along with estimates of OP using acellular assays for glutathione (OPGSH), ascorbate (OPAA), and dithiothreitol depletion (OPDTT). Conditional logistic regression models were used to estimate odds ratios (OR) [95% confidence intervals (CI)] for PM2.5 across strata of transition metals/OP and sulfur. RESULTS: Among men, the magnitudes of observed associations were strongest when both transition metal and sulfur content were elevated. For example, an OR of 1.078 (95% CI: 1.049, 1.108) (per 10µg/m3) was observed for cardiovascular events in men when both copper and S were above the median, whereas a weaker association was observed when both elements were below median values (OR=1.019, 95% CI: 1.007, 1.031). A similar pattern was observed for OP metrics. PM2.5 was not associated with acute cardiovascular events in women. DISCUSSION: The combined transition metal and sulfur content of outdoor PM2.5 influences the strength of association with acute cardiovascular events in men. Regions with elevated concentrations of both sulfur and transition metals in PM2.5 should be examined as priority areas for regulatory interventions. https://doi.org/10.1289/EHP9449.

Does exposure to air pollution increase the risk of acute care in young children with asthma? An Ontario, Canada study.

Owing to their greater outdoor activity and ongoing lung development, children are particularly vulnerable to the harmful effects of exposure to fine particulate matter (PM2.5). However, the effects of PM2.5 components are poorly understood. This study aimed to use a longitudinal birth cohort of children with physician-diagnosed incident asthma to investigate the effect of PM2.5 components at birth on morbidity measured by health services utilization. Of 1277 Toronto Child Health Evaluation Questionnaire (T-CHEQ) participants, the study population included 362 children diagnosed with asthma who were followed for a mean of 13 years from birth until March 31, 2016, or loss-to-follow-up. Concentrations of PM2.5 and its components were assigned based on participants' postal codes at birth. Study outcomes included counts of asthma, asthma-related, and all-cause health services use. Poisson regression in single-, two-, and multi-pollutant models was used to estimate rate ratios (RR) per interquartile range (IQR) increase of exposures. Covariates were included in all models to further adjust for potential confounding. The adjusted RR for sulfate (SO4) and all-cause hospitalizations was statistically significant with RR = 2.23 (95% confidence interval [CI]: 1.25-3.96) in a multi-pollutant model with nitrogen dioxide (NO2) and ozone (O3). In multi-pollutant models with oxidants, the adjusted RRs for SO4 of all-cause hospitalizations and emergency department (ED) visits were also statistically significant with RR = 2.31 (95% CI: 1.32-4.03) and RR = 1.39 (95% CI: 1.02-1.90), respectively. While unadjusted single-pollutant RRs for asthma-specific and asthma-related health services use with the SO4 component of PM2.5 were above one, none were statistically significant. This study found significant associations with exposure to SO4 in PM2.5 and all-cause acute care, chiefly for hospitalizations, in children with asthma.

Temporal and spatial effect of air pollution on hospital admissions for myocardial infarction: a case-crossover study.

BACKGROUND: In studies showing associations between ambient air pollution and myocardial infarction (MI), data have been lacking on the inherent spatial variability of air pollution. The aim of this study was to determine whether the long-term spatial distribution of air pollution influences short-term temporal associations between air pollution and admission to hospital for MI. METHODS: We identified adults living in Calgary who were admitted to hospital for an MI between 2004 and 2012. We evaluated associations between short-term exposure to air pollution (ozone [O3], nitrogen dioxide [NO2], sulfur dioxide [SO2], carbon monoxide [CO], particulate matter < 10 µm in diameter [PM10] and particulate matter < 2.5 µm in diameter [PM2.5]), and hospital admissions for MI using a time-stratified, case-crossover study design. Air Quality Health Index (AQHI) scores were calculated from a composition of O3, NO2 and PM2.5. Conditional logistic regression models were stratified by low, medium and high levels of neighbourhood NO2 concentrations derived from land use regression models; results of these analyses are presented as odds ratios (ORs) with 95% confidence intervals (CIs). RESULTS: From 2004 to 2012, 6142 MIs were recorded in Calgary. Individuals living in neighbourhoods with higher long-term air pollution concentrations were more likely to be admitted to hospital for MI after short-term elevations in air pollution (e.g., 5-day average NO2: OR 1.20, 95% CI 1.03-1.40, per interquartile range [IQR]) as compared with regions with lower air pollution (e.g., 5-day average NO2: OR 0.90, 95% CI 0.78-1.04, per IQR). In high NO2 tertiles, the AQHI score was associated with MI (e.g., 5-day average OR 1.13, 95% CI 1.02-1.24, per IQR; 3-day average OR 1.13, 95% CI 1.04-1.23, per IQR). INTERPRETATION: Our results show that the effect of air pollution on hospital admissions for MI was stronger in areas with higher NO2 concentrations than that in areas with lower NO2 concentrations. Individuals living in neighbourhoods with higher traffic-related pollution should be advised of the health risks and be attentive to special air quality warnings.

Evaluating an Air Quality Health Index (AQHI) amendment for communities impacted by residential woodsmoke in British Columbia, Canada.

Smoke from burning biomass is an important source of fine particulate matter (PM2.5), but the health risks may not be fully captured by the Canadian Air Quality Health Index (AQHI). In May 2018, the province of British Columbia launched an evidence-based amendment (AQHI-Plus) to improve AQHI performance for wildfire smoke, but the AQHI-Plus was not developed or tested on data from the residential woodsmoke season. This study assesses how the AQHI and AQHI-Plus are associated with acute health outcomes during the cooler seasons of 2010-2017 in British Columbia, Canada. Monthly and daily patterns of temperature and PM2.5 concentrations were used to identify Local Health Areas (LHAs) that were impacted by residential woodsmoke. The effects of the AQHI and AQHI-Plus on five acute health outcomes (including non-accidental mortality, outpatient physician visits, and medical dispensations for cardiopulmonary conditions) were estimated using generalized linear mixed effect models with Poisson distributions adjusted for long- and short-term temperature trends. Values of the Akaike information criterion (AIC) were compared to evaluate whether the AQHI or AQHI-Plus was better fitted to each health outcome. Eleven LHAs were categorized as woodsmoke-impacted. In these LHAs, the AQHI and AQHI-Plus associations with acute health outcomes were sensitive to temperature adjustments. After temperature adjustments, the most consistent associations were observed for the two asthma-specific outcomes where the AQHI-Plus was better fitted than the AQHI. The improved performance of the AQHI-Plus for susceptible populations with asthma is consistent between communities impacted by residential woodsmoke and wildfire smoke. Implications: Canada's Air Quality Health Index (AQHI) is a three pollutant index used to communicate the short term health impact of degraded air quality. As fine particulate matter (PM2.5) is the lowest weighted pollutant in the AQHI, the index is poorly reflective of woodsmoke impacts. The present analysis found that an AQHI amendment developed for improved sensitivity to PM2.5 during wildfire seasons (AQHI-Plus) is also more predictive of acute asthma-related health outcomes in communities impacted by residential woodsmoke. The BC Ministry of Environment and Climate Change Strategy has piloted the AQHI-Plus year-round. Other jurisdictions should consider whether their air quality indices are reflective of the risks posed by woodsmoke.

Early life exposure to air pollution and incidence of childhood asthma, allergic rhinitis and eczema.

RATIONALE: There is growing evidence that air pollution may contribute to the development of childhood asthma and other allergic diseases. In this follow-up of the Toronto Child Health Evaluation Questionnaire (T-CHEQ) study, we examined associations between early life exposures to air pollution and incidence of asthma, allergic rhinitis and eczema from birth through adolescence. METHODS: 1286 T-CHEQ participants were followed from birth until outcome (March 31, 2016) or loss to follow-up, with a mean of 17 years of follow-up. Concentrations of nitrogen dioxide (NO2), ozone (O3) and particulate matter with a 50% cut-off aerodynamic diameter of 2.5 µm (PM2.5) from January 1, 1999 to December 31, 2012 were assigned to participants based on their postal codes at birth using ground observations, chemical/meteorological models, remote sensing and land-use regression models. Study outcomes included incidence of physician-diagnosed asthma, allergic rhinitis and eczema. Cox proportional hazard regression models were used to estimate hazard ratios per interquartile range of exposures and outcomes, adjusting for potential confounders. RESULTS: Hazard ratios of 1.17 (95% CI 1.05-1.31) for asthma and 1.07 (95% CI 0.99-1.15) for eczema were observed for total oxidants (O3 and NO2) at birth. No significant increase in risk was found for PM2.5. CONCLUSIONS: Exposures to oxidant air pollutants (O3 and NO2) but not PM2.5 were associated with an increased risk of incident asthma and eczema in children. This suggests that improving air quality may contribute to the prevention of asthma and other allergic disease in childhood and adolescence.

Assessment of the Air Quality Health Index (AQHI) and four alternate AQHI-Plus amendments for wildfire seasons in British Columbia.

OBJECTIVE: Wildfire smoke is an important source of air pollution associated with a range of cardiopulmonary health conditions. The Air Quality Health Index (AQHI) is the most widely used tool in Canada to communicate with the public about air pollution, but it may not adequately reflect health risks from wildfire smoke. The objective of this study was to evaluate the ability of the AQHI and four alternate AQHI-Plus amendments to predict adverse population health effects from wildfire smoke. METHODS: The maximum 1-h values of the AQHI and the four amendments were calculated for each 48-h period of the wildfire seasons from 2010 to 2017 for 32 health units in British Columbia. Generalized Poisson models were used to estimate the association between these values and daily counts of five health outcomes: all-cause mortality; physician visits for all circulatory causes; visits for all respiratory causes, including asthma; asthma-specific visits; and dispensations of salbutamol sulfate (i.e., Ventolin®). Model fit was evaluated with the Akaike information criterion. RESULTS: The AQHI and the four amendments were all associated with all five health outcomes. The AQHI exhibited best fit to the all-cause mortality and circulatory physician visits during all wildfire seasons, while the 1-h PM2.5Only AQHI-Plus exhibited best fit to the asthma-related outcomes during all wildfire seasons. CONCLUSION: Individuals with common respiratory conditions such as asthma and chronic obstructive pulmonary disease are particularly susceptible to wildfire smoke. As such, the 1-h PM2.5Only AQHI-Plus amendment was recommended for communicating about potential health effects of air quality during wildfire seasons in BC.

Interdisciplinary-driven hypotheses on spatial associations of mixtures of industrial air pollutants with adverse birth outcomes.

BACKGROUND: Adverse birth outcomes (ABO) such as prematurity and small for gestational age confer a high risk of mortality and morbidity. ABO have been linked to air pollution; however, relationships with mixtures of industrial emissions are poorly understood. The exploration of relationships between ABO and mixtures is complex when hundreds of chemicals are analyzed simultaneously, requiring the use of novel approaches. OBJECTIVE: We aimed to generate robust hypotheses spatially linking mixtures and the occurrence of ABO using a spatial data mining algorithm and subsequent geographical and statistical analysis. The spatial data mining approach aimed to reduce data dimensionality and efficiently identify spatial associations between multiple chemicals and ABO. METHODS: We discovered co-location patterns of mixtures and ABO in Alberta, Canada (2006-2012). An ad-hoc spatial data mining algorithm allowed the extraction of primary co-location patterns of 136 chemicals released into the air by 6279 industrial facilities (National Pollutant Release Inventory), wind-patterns from 182 stations, and 333,247 singleton live births at the maternal postal code at delivery (Alberta Perinatal Health Program), from which we identified cases of preterm birth, small for gestational age, and low birth weight at term. We selected secondary patterns using a lift ratio metric from ABO and non-ABO impacted by the same mixture. The relevance of the secondary patterns was estimated using logistic models (adjusted by socioeconomic status and ABO-related maternal factors) and a geographic-based assignment of maternal exposure to the mixtures as calculated by kernel density. RESULTS: From 136 chemicals and three ABO, spatial data mining identified 1700 primary patterns from which five secondary patterns of three-chemical mixtures, including particulate matter, methyl-ethyl-ketone, xylene, carbon monoxide, 2-butoxyethanol, and n-butyl alcohol, were subsequently analyzed. The significance of the associations (odds ratio > 1) between the five mixtures and ABO provided statistical support for a new set of hypotheses. CONCLUSION: This study demonstrated that, in complex research settings, spatial data mining followed by pattern selection and geographic and statistical analyses can catalyze future research on associations between air pollutant mixtures and adverse birth outcomes.

The Oakville Oil Refinery Closure and Its Influence on Local Hospitalizations: A Natural Experiment on Sulfur Dioxide.

Background: An oil refinery in Oakville, Canada, closed over 2004⁻2005, providing an opportunity for a natural experiment to examine the effects on oil refinery-related air pollution and residents' health. Methods: Environmental and health data were collected for the 16 years around the refinery closure. Toronto (2.5 million persons) and the Greater Toronto Area (GTA, 6.3 million persons) were used as control and reference populations, respectively, for Oakville (160,000 persons). We compared sulfur dioxide and age- and season-standardized hospitalizations, considering potential factors such as changes in demographics, socio-economics, drug prescriptions, and environmental variables. Results: The closure of the refinery eliminated 6000 tons/year of SO2 emissions, with an observed reduction of 20% in wind direction-adjusted ambient concentrations in Oakville. After accounting for trends, a decrease in cold-season peak-centered respiratory hospitalizations was observed for Oakville (reduction of 2.2 cases/1000 persons per year, p = 0.0006 ) but not in Toronto (p = 0.856) and the GTA (p = 0.334). The reduction of respiratory hospitalizations in Oakville post closure appeared to have no observed link to known confounders or effect modifiers. Conclusion: The refinery closure allowed an assessment of the change in community health. This natural experiment provides evidence that a reduction in emissions was associated with improvements in population health. This study design addresses the impact of a removed source of air pollution.

Air Health Trend Indicator: Association between Short-Term Exposure to Ground Ozone and Circulatory Hospitalizations in Canada for 17 Years, 1996⁻2012.

The Air Health Trend Indicator is designed to estimate the public health risk related to short-term exposure to air pollution and to detect trends in the annual health risks. Daily ozone, circulatory hospitalizations and weather data for 24 cities (about 54% of Canadians) for 17 years (1996⁻2012) were used. This study examined three circulatory causes: ischemic heart disease (IHD, 40% of cases), other heart disease (OHD, 31%) and cerebrovascular disease (CEV, 14%). A Bayesian hierarchical model using a 7-year estimator was employed to find trends in the annual national associations by season, lag of effect, sex and age group (≤65 vs. >65). Warm season 1-day lagged ozone returned higher national risk per 10 ppb: 0.4% (95% credible interval, -0.3⁻1.1%) for IHD, 0.4% (-0.2⁻1.0%) for OHD, and 0.2% (-0.8⁻1.2%) for CEV. Overall mixed trends in annual associations were observed for IHD and CEV, but a decreasing trend for OHD. While little age effect was identified, some sex-specific difference was detected, with males seemingly more vulnerable to ozone for CEV, although this finding needs further investigation. The study findings could reduce a knowledge gap by identifying trends in risk over time as well as sub-populations susceptible to ozone by age and sex.

Biomass Burning as a Source of Ambient Fine Particulate Air Pollution and Acute Myocardial Infarction.

BACKGROUND: Biomass burning is an important source of ambient fine particulate air pollution (PM2.5) in many regions of the world. METHODS: We conducted a time-stratified case-crossover study of ambient PM2.5 and hospital admissions for myocardial infarction (MI) in three regions of British Columbia, Canada. Daily hospital admission data were collected between 2008 and 2015 and PM2.5 data were collected from fixed site monitors. We used conditional logistic regression models to estimate odds ratios (ORs) describing the association between PM2.5 and the risk of hospital admission for MI. We used stratified analyses to evaluate effect modification by biomass burning as a source of ambient PM2.5 using the ratio of levoglucosan/PM2.5 mass concentrations. RESULTS: Each 5 µg/m increase in 3-day mean PM2.5 was associated with an increased risk of MI among elderly subjects (≥65 years; OR = 1.06, 95% CI: 1.03, 1.08); risk was not increased among younger subjects. Among the elderly, the strongest association occurred during colder periods (<6.44°C); when we stratified analyses by tertiles of monthly mean biomass contributions to PM2.5 during cold periods, ORs of 1.19 (95% CI: 1.04, 1.36), 1.08 (95% CI: 1.06, 1.09), and 1.04 (95% CI: 1.03, 1.06) were observed in the upper, middle, and lower tertiles (Ptrend = 0.003), respectively. CONCLUSION: Short-term changes in ambient PM2.5 were associated with an increased risk of MI among elderly subjects. During cold periods, increased biomass burning contributions to PM2.5 may modify its association with MI.

The association between ambient air quality and cardiac rate and rhythm in ambulatory subjects.

BACKGROUND: Acute increases in ambient air pollution have been associated with increased hospitalization for cardiac diseases and stroke. Triggering of cardiac arrhythmia by changes in air quality could theoretically predispose individuals to cardiac arrest or heart failure, or stroke through precipitation of atrial fibrillation. We investigated the association between air quality and cardiac rate and rhythm characteristics measured by ambulatory cardiac monitoring. METHODS AND RESULTS: Daily ambient 3-h maximum concentrations of ozone, nitrogen dioxide and fine particulate matter, and an index summarizing these pollutants called the Air Quality Health Index (AQHI) were compared to the results of 24-h ambulatory cardiac monitoring performed for clinical purposes in 8662 patients and analyzed at the University of Ottawa Heart Institute, Canada, between 2004 and 2009. An interquartile increase in the daily 3 h- maximum AQHI was associated with a 0.9% (95% CI 0.3%, 1.5%) increase in the daily maximum heart rate and a 1.17% (95% CI 1.07%, 1.29%) increase in heart block frequency. An interquartile increase in NO2 was associated with an increase in the percentage of time in atrial fibrillation of 4.39% (-0.15, 9.15) among those ≤50 years old, and 7.1% (0.24, 14.5) among males. CONCLUSIONS: We found evidence that air pollution may affect cardiac rate and rhythm. This may be one mechanism partially explaining the increase in strokes and cardiac events observed on days of higher air pollution.

Tracking national and regional spatial-temporal mortality risk associated with NO2 concentrations in Canada: a Bayesian hierarchical two-level model.

The association between daily variations in urban air quality and mortality has been well documented using time series statistical methods. This approach assumes a constant association over time. We develop a space-time dynamic model that relaxes this assumption, thus more directly examining the hypothesis that improvements in air quality translate into improvements in public health. We postulate a Bayesian hierarchical two-level model to estimate annual mortality risks at regional and national levels and to track both risk and heterogeneity of risk within and between regions over time. We illustrate our methods using daily nitrogen dioxide concentrations (NO2) and nonaccidental mortality data collected for 1984-2004 in 24 Canadian cities. Estimates of risk and heterogeneity are compared by cause of mortality (cardio-pulmonary [CP] versus non-CP) and season, respectively. Over the entire period, the NO2 risk for CP mortality was slightly lower but with a narrower credible interval than that for non-CP mortality, mainly due to an unusually low risk for a single year (1998). Warm season NO2 risk was higher than cold season risk for both CP and non-CP mortality. For 21 years overall there were no significant differences detected among the four regional NO2 risks. We found overall that there was no strong evidence for time trends in NO2 risk at national or regional levels. However, an increasing linear time trend in the annual between-region heterogeneities was detected, which suggests the differences in risk among the four regions are getting larger, and further studies are necessary to understand the increasing heterogeneity.

Health effects of outdoor air pollution: approach to counseling patients using the Air Quality Health Index.

OBJECTIVE: To inform family physicians about the health effects of air pollution and to provide an approach to counseling vulnerable patients in order to reduce exposure. SOURCES OF INFORMATION: MEDLINE was searched using terms relevant to air pollution and its adverse effects. We reviewed English-language articles published from January 2008 to December 2009. Most studies provided level II evidence. MAIN MESSAGE: Outdoor air pollution causes substantial morbidity and mortality in Canada. It can affect both the respiratory system (exacerbating asthma and chronic obstructive pulmonary disease) and the cardiovascular system (triggering arrhythmias, cardiac failure, and stroke). The Air Quality Health Index (AQHI) is a new communication tool developed by Health Canada and Environment Canada that indicates the level of health risk from air pollution on a scale of 1 to 10. The AQHI is widely reported in the media, and the tool might be of use to family physicians in counseling high-risk patients (such as those with asthma, chronic obstructive pulmonary disease, or cardiac failure) to reduce exposure to outdoor air pollution. CONCLUSION: Family physicians can use the AQHI and its health messages to teach patients with asthma and other high-risk patients how to reduce health risks from air pollution.

From good intentions to proven interventions: effectiveness of actions to reduce the health impacts of air pollution.

BACKGROUND: Associations between air pollution and a multitude of health effects are now well established. Given ubiquitous exposure to some level of air pollution, the attributable health burden can be high, particularly for susceptible populations. OBJECTIVES: An international multidisciplinary workshop was convened to discuss evidence of the effectiveness of actions to reduce health impacts of air pollution at both the community and individual level. The overall aim was to summarize current knowledge regarding air pollution exposure and health impacts leading to public health recommendations. DISCUSSION: During the workshop, experts reviewed the biological mechanisms of action of air pollution in the initiation and progression of disease, as well as the state of the science regarding community and individual-level interventions. The workshop highlighted strategies to reduce individual baseline risk of conditions associated with increased susceptibility to the effects of air pollution and the need to better understand the role of exposure duration in disease progression, reversal, and adaptation. CONCLUSION: We have identified two promising and largely unexplored strategies to address and mitigate air pollution-related health impacts: reducing individual baseline risk of cardiovascular disease and incorporating air pollution-related health impacts into land-use decisions.