Inequality in the Distribution of Air Pollution Attributable Mortality Within Canadian Cities.

Recent studies have identified inequality in the distribution of air pollution attributable health impacts, but to our knowledge this has not been examined in Canadian cities. We evaluated the extent and sources of inequality in air pollution attributable mortality at the census tract (CT) level in seven of Canada's largest cities. We first regressed fine particulate matter (PM2.5) and nitrogen dioxide (NO2) attributable mortality against the neighborhood (CT) level prevalence of age 65 and older, low income, low educational attainment, and identification as an Indigenous (First Nations, Métis, Inuit) or Black person, accounting for spatial autocorrelation. We next examined the distribution of baseline mortality rates, PM2.5 and NO2 concentrations, and attributable mortality by neighborhood (CT) level prevalence of these characteristics, calculating the concentration index, Atkinson index, and Gini coefficient. Finally, we conducted a counterfactual analysis of the impact of reducing baseline mortality rates and air pollution concentrations on inequality in air pollution attributable mortality. Regression results indicated that CTs with a higher prevalence of low income and Indigenous identity had significantly higher air pollution attributable mortality. Concentration index, Atkinson index, and Gini coefficient values revealed different degrees of inequality among the cities. Counterfactual analysis indicated that inequality in air pollution attributable mortality tended to be driven more by baseline mortality inequalities than exposure inequalities. Reducing inequality in air pollution attributable mortality requires reducing disparities in both baseline mortality and air pollution exposure.

Circulatory health risks from additive multi-pollutant models: short-term exposure to three common air pollutants in Canada.

Numerous studies have reported adverse health effects of ambient air pollution on circulatory health outcomes mainly based on single-pollutant models. However, limited studies have focused on adjusted effect of multi-pollutant exposures on public health. This study aimed to examine short-term effects of three common air pollutants-ground-level ozone (ozone), nitrogen dioxide (NO2), and fine particulate matter (PM2.5)-through multi-pollutant models for mixed effect of adjustment. Daily data (circulatory hospitalization and mortality) and hourly data (air pollutants and temperature) were collected for 24 Canadian cities for 2001-2012. We applied generalized additive over-dispersion Poisson regression models with 1, 2, or 3 pollutants for city-specific risks, and Bayesian hierarchical models for national risks. This study found little mixed effect of adjustment through multi-pollutant models (ozone and/or NO2 and/or PM2.5) for circulatory hospitalization or mortality in Canada for 2001-2012, indicating that the 1-pollutant model did not result in considerable under- or over-estimates. It seemed weak-to-moderate correlations among air pollutants did not change the significant effect of one air pollutant after accounting for others. Inconsistent findings between other previous studies and this study indicate the need of comparable study design for multi-pollutant effect analysis.

Air Pollution and the Effectiveness of Positive Airway Pressure Therapy in Individuals With Sleep Apnea: A Retrospective Community-Based Repeated-Measures Longitudinal Study.

BACKGROUND: Ambient air pollution may affect the severity of untreated OSA, but it is unknown whether air pollution adversely impacts the effectiveness of positive airway pressure (PAP) therapy. RESEARCH QUESTION: Do short-term changes in outdoor air pollution adversely impact adults with OSA using PAP therapy? STUDY DESIGN AND METHODS: We conducted a retrospective community-based repeated-measures longitudinal study of adults with OSA who purchased a PAP device from a registered equipment provider between 2013 and 2017 (Ontario, Canada) and had data on the daily device-derived residual apnea-hypopnea index (AHIFlow). We linked daily PAP-derived data to air pollution databases using postal codes. The primary exposures were mean nocturnal (8 pm to 8 am) residential concentrations of ozone, fine particulate matter, nitrogen dioxide, carbon monoxide, sulfur dioxide, and the Air Quality Health Index (AQHI). Potential confounders considered were demographics, season and year of exposure, initial OSA severity, other PAP parameters, and climate-related variables. RESULTS: Eight thousand one hundred forty-eight adults were analyzed with a median of 89 days (interquartile range [IQR], 29-302 days) of observation during which PAP was used for ≥ 4 h. The median daily AHIFlow was 1.2/h (IQR, 0.5-2.5/h). In mixed multivariate regression analyses, an increase in air pollution was associated with a statistically significant increase in AHIFlow for most statistical models. The largest effect was for the AQHI: an increase in AHIFlow while comparing highest vs lowest quartiles was 0.07/h (95% CI, 0.05-0.10/h). INTERPRETATION: We demonstrated a modest but statistically significant increase in residual respiratory events during PAP therapy associated with an increase in air pollution concentrations.

Fine particulate matter concentration and composition and the incidence of childhood asthma.

BACKGROUND: Several studies have found positive associations between outdoor fine particulate air pollution (≤2.5 µm, PM2.5) and childhood asthma incidence. However, the impact of PM2.5 composition on children's respiratory health remains uncertain. OBJECTIVE: We examined whether joint exposure to PM2.5 mass concentrations and its major chemical components was associated with childhood asthma development. METHODS: We conducted a population-based cohort study by identifying 1,130,855 singleton live births occurring between 2006 and 2014 in the province of Ontario, Canada. Concentrations of PM2.5 and its seven major chemical components were assigned to participants based on their postal codes using chemical transport models and remote sensing. The joint impact of outdoor PM2.5 concentrations and its major components and childhood asthma incidence (up to age 6) were estimated using Cox proportional hazards models, allowing for potential nonlinearity. RESULTS: We identified 167,080 children who developed asthma before age 6. In adjusted models, outdoor PM2.5 mass concentrations during childhood were associated with increased incidence of childhood asthma (Hazard Ratio (HR) for each 1 µg/m3 increase = 1.026, 95% CI: 1.021-1.031). We found that the joint effects of PM2.5 and its components on childhood asthma incidence may be 24% higher than the conventional approach. Specific components/source markers such as black carbon, ammonium, and nitrate appeared to play an important role. CONCLUSIONS: Early life exposure to PM2.5 and its chemical components is associated with an increased risk of asthma development in children. The heterogeneous nature of PM2.5 should be considered in future health risk assessments.

Air Pollution and Emergency Department Visits for Mental Disorders among Youth.

Although exposure to ambient air pollution has been linked to mental health problems, little is known about its potential effects on youth. This study investigates the association between short-term exposure to air pollutants and emergency department (ED) visits for mental health disorders. The National Ambulatory Care Reporting System database was used to retrieve ED visits for young individuals aged 8-24 years in Toronto, Canada. Daily average concentrations of nitrogen dioxide (NO2), fine particulate matter (PM2.5), and daily maximum 8 h ozone (O3) were calculated using measurement data from seven fixed stations. A case-crossover (CC) design was implemented to estimate the associations between ED visits and air pollution concentrations. Mental health ED visits were identified using International Classification of Diseases 10th Revision (ICD-10) codes, with seven categories considered. Models incorporating air pollutants and ambient temperature (with lags of 0-5 days) using a time-stratified CC technique were applied. Multivariable regression was performed by sex, three age groups, and seven types of mental health disorders to calculate relative risk (RR). The RRs were reported for one interquartile range (IQR) change in the air pollutant concentrations. Between April 2004 and December 2015 (4292 days), there were 83,985 ED visits for mental-health related problems in the target population. Several exposures to air pollutants were shown to have associations with ED visits for mental health including same day exposure to fine particulate matter (IQR = 6.03 µg/m3, RR = 1.01 (95% confidence interval: 1.00-1.02), RR = 1.02 (1.00-1.03)) for all and female-only patients, respectively. One-day lagged exposure was also associated with ED visits for PM2.5 (RR = 1.02 (1.01-1.03)), for nitrogen dioxide (IQR = 9.1 ppb, RR = 1.02 (1.00-1.04)), and ozone (IQR = 16.0 ppb, RR = 1.06 (1.01-1.10)) for males. In this study, urban air pollution concentration-mainly fine particulate matter and nitrogen dioxide-is associated with an increased risk for ED visits for adolescents and young adults with diagnosed mental health disorders.

Temporal trends in associations between ozone and circulatory mortality in age and sex in Canada during 1984-2012.

BACKGROUND: Considerable research has been conducted on the association between ground-level ozone (ozone) and various causes of mortality, but the relationships by age and sex (biological) have been inconsistent, and temporal trends remain unexplored. OBJECTIVES: The study goals are to investigate the adverse health effects of short-term exposure to ozone on circulatory mortality by age and sex, and to examine trends in annual health effects. METHODS: Daily ozone, temperature, and circulatory mortality counts (ICD I00-I99) were collected for 24 urban cities for 29 years (1984-2012). Associations between ozone and circulatory mortality were estimated using generalized additive Poisson models for season (warm vs. cold), age [base (≥1) vs. seniors (>65)], and sex, accounting for confounders (calendar-time, temperature, day of the week). City-specific estimates were pooled to represent national associations through Bayesian hierarchical models. RESULTS: While the cold season returned insignificant estimates, the warm season showed statistically significant associations: a 10 ppb increase in ozone was associated with 0.7% increase in circulatory mortality with a 95% posterior interval of 0.2%, 1.1%. One-day lagged ozone in the warm season showed little age differences [0.7% (0.23%, 1.12%) vs. 0.8% (0.22%, 1.27%)], but visible sex differences: females were at a higher circulatory mortality risk than males [1.1% (0.31%, 1.71%) vs. 0.3% (-0.46%, 0.98%)]. Annual estimates suggest overall up-down temporal changes; a slightly increasing trend until 2002-2004, and a generally decreasing trend thereafter. CONCLUSION: This study found noticeable sex-related differences in circulatory mortality attributable to short-term exposure to ozone. Further research is warranted to understand whether sex alone, or unknown interactions with other factors derived the differences, and to clarify the specific biological mechanisms underlying differences in risk estimates between females and males.

Air Pollution, Physical Activity, and Cardiovascular Function of Patients With Implanted Cardioverter Defibrillators: A Randomized Controlled Trial of Indoor Versus Outdoor Activity.

OBJECTIVE: To investigate whether implanted cardioverter defibrillator (ICD) patients exercising indoors on higher air pollution (AP) days had reduced adverse cardiovascular effects compared with those exercising outdoors. METHODS: Eighteen participants were randomly divided into control or intervention groups. Blood pressure (BP), pulse rate (PR), and oxygen saturation (O2SAT) were measured daily before and after participants walked outdoors for 30 minutes. On days with higher forecast AP the intervention group exercised indoors. RESULTS: AP was significantly associated with increased BP and PR, and reduced O2SAT. After adjustment for exercise levels, AP was associated with increased diastolic BP and PR in controls only. Significant improvements in cardiovascular measures over time were observed in both groups. CONCLUSION: In ICD patients, reducing AP exposure may reduce adverse cardiovascular effects, while daily mild exercise may benefit cardiovascular function.

Variability in ambient ozone and fine particle concentrations and population susceptibility among Canadian health regions.

OBJECTIVES: To estimate the proportion of the Canadian population that is more susceptible to adverse effects of ozone (O3) and fine particle (PM2.5) air pollution exposure and how this varies by health region alongside ambient concentrations of O3 and PM2.5. METHODS: Using data from the census, the Canadian Community Health Survey, vital statistics and published literature, we generated cross-sectional estimates for 2014 of the proportions of the Canadian population considered more susceptible due to age, chronic disease, pregnancy, outdoor work, socio-economic status, and diet. We also estimated 2010-2012 average concentrations of O3 and PM2.5. Analyses were conducted nationally and for 110 health regions. RESULTS: Restrictive criteria (age < 10 or ≥ 75; asthma, chronic obstructive pulmonary disease, heart disease, or diabetes; pregnancy) suggested that approximately one third of the Canadian population is more susceptible, while inclusive criteria (restrictive plus age 10-19 and 65-74, outdoor work, less than high school education, low vitamin C intake) increased this proportion to approximately two thirds. Across health regions, estimates ranged from 24.4% to 41.2% (restrictive) and 61.2% to 87.0% (inclusive). Ten health regions were in the highest quartile of both population susceptibility and O3 or PM2.5 concentrations, all of which were outside major urban centres. CONCLUSIONS: A substantial proportion of the Canadian population exhibits at least one risk factor that increases their susceptibility to adverse effects of O3 and PM2.5 exposure. Both risk communication and management interventions need to be increasingly targeted to regions outside large urban centres in the highest quartiles of both susceptibility and exposure.

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.

A national study of the association between traffic-related air pollution and adverse pregnancy outcomes in Canada, 1999-2008.

Numerous studies have examined the association of air pollution with preterm birth and birth weight outcomes. Traffic-related air pollution has also increasingly been identified as an important contributor to adverse health effects of air pollution. We employed a national nitrogen dioxide (NO2) exposure model to examine the association between NO2 and pregnancy outcomes in Canada between 1999 and 2008. National models for NO2 (and particulate matter of median aerodynamic diameter <2.5µm (PM2.5) as a covariate) were developed using ground-based monitoring data, estimates from remote-sensing, land use variables and, for NO2, deterministic gradients relative to road traffic sources. Generalized estimating equations were used to examine associations with preterm birth, term low birth weight (LBW), small for gestational age (SGA) and term birth weight, adjusting for covariates including infant sex, gestational age, maternal age and marital status, parity, urban/rural place of residence, maternal place of birth, season, year of birth and neighbourhood socioeconomic status and per cent visible minority. Associations were reduced considerably after adjustment for individual covariates and neighbourhood per cent visible minority, but remained significant for SGA (odds ratio 1.04, 95%CI 1.02-1.06 per 20ppb NO2) and term birth weight (16.2g reduction, 95% CI 13.6-18.8g per 20ppb NO2). Associations with NO2 were of greater magnitude in a sensitivity analysis using monthly monitoring data, and among births to mothers born in Canada, and in neighbourhoods with higher incomes and a lower proportion of visible minorities. In two pollutant models, associations with NO2 were less sensitive to adjustment for PM2.5 than vice versa, and there was consistent evidence of a dose-response relationship for NO2 but not PM2.5. In this study of approximately 2.5 million Canadian births between 1999 and 2008, we found significant associations of NO2 with SGA and term birth weight which remained significant after adjustment for PM2.5, suggesting that traffic may be a particularly important source with respect to the role of air pollution as a risk factor for adverse pregnancy outcomes.

Estimated public health impacts of changes in concentrations of fine particle air pollution in Canada, 2000 to 2011.

OBJECTIVES: To estimate the public health impacts of changes in fine particle air pollution in Canada between 2000 and 2011, employing nationally comprehensive exposure estimates and quantifying the impacts on life expectancy, mortality and morbidity. METHODS: We employed spatially comprehensive exposure estimates derived from satellite remote sensing to estimate the effects of actual observed changes in concentrations of fine particulate matter (PM), of median aerodynamic diameter <2.5 µm (i.e., PM2.5), from 2000 to 2011. We estimated changes in life expectancy using standard life table methods and changes in frequency of health outcomes as the product of population, baseline rate of the health outcome and the proportional change in health outcome per specified change in PM2.5 concentration. RESULTS: A population weighted average decrease in PM2.5 of nearly 25% (2.0 µg/m³) was observed between 2000 and 2011. This was estimated to result in a national population weighted average increase in life expectancy of 0.10 years (95% confidence interval 0.03-0.23; up to 0.34 years in specific census divisions) and reductions in the frequency of mortality and morbidity of up to 3.6%. Increases in PM2.5 up to 3.5 µg/m³ were observed in some census divisions, particularly in the prairies. CONCLUSION: At the national level, changes in PM2.5 concentrations between 2000 and 2011 were associated with an estimated improvement in national population weighted average life expectancy and a net reduction in mortality and morbidity. Areas that failed to improve or that worsened during this period warrant additional scrutiny to identify options for reducing PM2.5 concentrations.

Mortality and hospital admission rates for unintentional nonfire-related carbon monoxide poisoning across Canada: a trend analysis.

BACKGROUND: The epidemiology of mortality and morbidity from carbon monoxide poisoning in Canada has received little attention. Our objective was to evaluate trends in mortality and hospital admission rates for unintentional nonfire-related carbon monoxide poisoning across Canada. METHODS: Age- and sex-standardized mortality (1981-2009) and hospital admission (1995-2010) rates by age group, sex and site of carbon monoxide exposure were calculated for each province and for all of Canada. We quantified the long-term trends by calculating the average annual percent change. Multivariable Poisson regression was used to estimate incidence rate ratios (IRRs) of carbon monoxide poisoning across age groups, sex and month of occurrence. RESULTS: In Canada, there were 1808 unintentional nonfire-related carbon monoxide poisoning deaths between 1981 and 2009 and 1984 admissions to hospital between 1995 and 2010. Average annual decreases of 3.46% (95% confidence interval [CI] -4.59% to -2.31%) and 5.83% (95% CI -7.79% to -3.83%) were observed for mortality and hospital admission rates, respectively. Mortality (IRR 5.31, 95% CI 4.57 to 6.17) and hospital admission (IRR 2.77, 95% CI 2.51 to 3.03) rates were elevated in males compared with females. Decreased trends in the rates were observed for all sites of carbon monoxide exposure, but the magnitude of this decrease was lowest in residential environments. Deaths and admissions to hospital were most frequent from September to April, with peaks in December and January. INTERPRETATION: Mortality and hospital admission rates for unintentional nonfire-related carbon monoxide poisoning in Canada have declined steadily. Continued efforts should focus on reducing carbon monoxide poisoning during the cooler months and in residential environments.

Assessment of long-term exposure to air pollution in a longitudinal national health survey.

Self-reported data on the municipality of residence were used to assess long-term exposure to outdoor air pollution from 1980 to 2002 in the longitudinal Canadian National Population Health Survey. Exposure to carbon monoxide, nitrogen dioxide, ozone, sulfur dioxide, and particulate matter was determined using data obtained from fixed-site air pollution monitors operated principally in urban areas. Four different methods of attributing pollution exposure were used based on residence in (1) 1980, (2) 1994, (3) 1980 and 1994, and (4) at all locations between 1980 and 2002. Between 1,693 and 4,274 of 10,515 members of the cohort could be assigned exposures to individual pollutants using these methods. On average, subjects spent 71.4% of the 1980-2002 period in the census subdivision where they lived in 1980. A single exposure measure in 1980 or 1994 or a mean of the two measures was highly correlated (r>0.7, P<0.0001) with a measure which accounted for all moves between 1980 and 2002. Although our ability to characterize long-term exposure was constrained by a lack of data from fixed-site monitors, the low frequency of moves meant that measures based on a single year generally provided a good approximation of long-term exposure at the census subdivision level.

The influence of living near roadways on spirometry and exhaled nitric oxide in elementary schoolchildren.

BACKGROUND: Living near major roadways has been associated with an increase in respiratory symptoms, but little is known about how this relates to airway inflammation. OBJECTIVE: We assessed the effects of living near local residential roadways based on objective indicators of ventilatory function and airway inflammation. METHODS: We estimated ambient air pollution, resolved to the level of the child's neighborhood, using a land-use regression model for children 9-11 years of age. We also summed the length of roadways found within a 200-m radius of each child's neighborhood. We had measurements of both air pollution exposure and spirometry for 2,328 children, and also had measurements of exhaled nitric oxide (eNO) for 1,613 of these children. RESULTS: Each kilometer of local roadway within a 200-m radius of the home was associated with a 6.8% increase in eNO (p = 0.045). Each kilometer of any type of roadway (local, major, highway) was also associated with an increase in eNO of 10.1% (p = 0.002). Each microgram per cubic meter increase in PM2.5 was associated with a 3.9% increase in eNO (p = 0.058) and 0.70% decrease in forced vital capacity (FVC) expressed as a percentage of predicted (p = 0.39). Associations between roadway density and both forced expired volume in 1 sec and FVC were negative but not statistically significant at p < 0.05. CONCLUSION: Traffic from local neighborhood roadways may cause airway inflammation as indicated by eNO. This may be a more sensitive indicator of adverse air pollution effects than traditional measures of ventilatory function.

A new multipollutant, no-threshold air quality health index based on short-term associations observed in daily time-series analyses.

Air quality indices currently in use have been criticized because they do not capture additive effects of multiple pollutants, or reflect the apparent no-threshold concentration-response relationship between air pollution and health. We propose a new air quality health index (AQHI), constructed as the sum of excess mortality risk associated with individual pollutants from a time-series analysis of air pollution and mortality in Canadian cities, adjusted to a 0-10 scale, and calculated hourly on the basis of trailing 3-hr average pollutant concentrations. Extensive sensitivity analyses were conducted using alternative combinations of pollutants from single and multipollutant models. All formulations considered produced frequency distributions of the daily maximum AQHI that were right-skewed, with modal values of 3 or 4, and less than 10% of values at 7 or above on the 10-point scale. In the absence of a gold standard and given the uncertainty in how to best reflect the mix of pollutants, we recommend a formulation based on associations of nitrogen dioxide, ozone, and particulate matter of median aerodynamic diameter less than 2.5 microm with mortality from single-pollutant models. Further sensitivity analyses revealed good agreement of this formulation with others based on alternative sources of coefficients drawn from published studies of mortality and morbidity. These analyses provide evidence that the AQHI represents a valid approach to formulating an index with the objective of allowing people to judge the relative probability of experiencing adverse health effects from day to day. Together with health messages and a graphic display, the AQHI scale appears promising as an air quality risk communication tool.

Intra-urban variability of air pollution in Windsor, Ontario--measurement and modeling for human exposure assessment.

There are acknowledged difficulties in epidemiological studies to accurately assign exposure to air pollution for large populations, and large, long-term cohort studies have typically relied upon data from central monitoring stations. This approach has generally been adequate when populations span large areas or diverse cities. However, when the effects of intra-urban differences in exposure are being studied, the use of these existing central sites are likely to be inadequate for representing spatial variability that exists within an urban area. As part of the Border Air Quality Strategy (BAQS), an international agreement between the governments of Canada and the United States, a number of air health effects studies are being undertaken by Health Canada and the US EPA. Health Canada's research largely focuses on the chronic exposure of elementary school children to air pollution. The exposure characterization for this population to a variety of air pollutants has been assessed using land-use regression (LUR) models. This approach has been applied in several cities to nitrogen dioxide (NO2), as an assumed traffic exposure marker. However, the models have largely been developed from limited periods of saturation monitoring data and often only represent one or two seasons. Two key questions from these previous efforts, which are examined in this paper, are: If NO2 is a traffic marker, what other pollutants, potentially traffic related, might it actually represent? How well is the within city spatial variability of NO2, and other traffic-related pollutants, characterized by a single saturation monitoring campaign. Input data for the models developed in this paper were obtained across a network of 54 monitoring sites situated across Windsor, Ontario. The pollutants studied were NO2, sulfur dioxide (SO2) and volatile organic compounds, which were measured in all four seasons by deploying passive samplers for 2-week periods. Correlations among these pollutants were calculated to assess what other pollutants NO2 might represent, and correlations across seasons for a given pollutant were determined to assess how much the within-city spatial pattern varies with time. LUR models were then developed for NO2, SO2, benzene, and toluene. A multiple regression model including proximity to the Ambassador Bridge (the main Canada-US border crossing point), and proximity to highways and major roads, predicted NO2 concentrations with an R2=0.77. The SO2 model predictors included distance to the Ambassador Bridge, dwelling density within 1500m, and Detroit-based SO2 emitters within 3000m resulting in a model with an R2=0.69. Benzene and toluene LUR models included traffic predictors as well as point source emitters resulting in R2=0.73 and 0.46, respectively. Between season pollutant correlations were all significant although actual concentrations for each site varied by season. This suggests that if one season were to be selected to represent the annual concentrations for a specific site this may lead to a potential under or overestimation in exposure, which could be significant for health research. All pollutants had strong inter-pollutant correlations suggesting that NO2 could represent SO2, benzene, and toluene.

The association between low level exposures to ambient air pollution and term low birth weight: a retrospective cohort study.

BACKGROUND: Studies in areas with relatively high levels of air pollution have found some positive associations between exposures to ambient levels of air pollution and several birth outcomes including low birth weight (LBW). The purpose of this study was to examine the association between LBW among term infants and ambient air pollution, by trimester of exposure, in a region of lower level exposures. METHODS: The relationship between LBW and ambient levels of particulate matter up to 10 um in diameter (PM10), sulfur dioxide (SO2) and ground-level ozone (O3) was evaluated using the Nova Scotia Atlee Perinatal Database and ambient air monitoring data from the Environment Canada National Air Pollution Surveillance Network and the Nova Scotia Department of Environment. The cohort consisted of live singleton births (> or =37 weeks of gestation) between January 1, 1988 and December 31, 2000. Maternal exposures to air pollution were assigned to women living within 25 km of a monitoring station at the time of birth. Air pollution was evaluated as a continuous and categorical variable (using quartile exposures) for each trimester and relative risks were estimated from logistic regression, adjusted for confounding variables. RESULTS: There were 74,284 women with a term, singleton birth during the study period and with exposure data. In the analyses unadjusted for year of birth, first trimester exposures in the highest quartile for SO2 and PM10 suggested an increased risk of delivering a LBW infant (relative risk = 1.36, 95% confidence interval = 1.04 to 1.78 for SO2 exposure and relative risk = 1.33, 95% confidence interval = 1.02 to 1.74 for PM10). After adjustment for birth year, the relative risks were attenuated somewhat and not statistically significant. A dose-response relationship for SO2 was noted with increasing levels of exposure. No statistically significant effects were noted for ozone. CONCLUSION: Our results suggest that exposure during the first trimester to relatively low levels of some air pollutants may be associated with a reduction in birth weight in term-born infants. These findings have implications for the development of effective risk management strategies to minimize the public health impacts for pregnant women.

Exposure time and place: do COPD patients differ from the general population?

Time-activity patterns in a panel of 70 patients with COPD (35 males) are compared to an age-matched subgroup from the randomly sampled Canadian Human Activity Pattern Survey. Total time indoors and outdoors were similar in both groups but significantly more indoor time in COPD subjects was spent at home than the indoor time of controls, who were more often indoors elsewhere. As part of improving their indoor air at home, COPD subjects were significantly more likely to have air conditioning at home. These results suggest that while outdoor air exposure strategies need not differ in COPD subjects from normals, indoor mitigation strategies should emphasize source pollutant control in the patient's home.

Air pollution and sudden infant death syndrome.

BACKGROUND: Sudden infant death syndrome (SIDS) affects approximately 1 in 1000 live births and is the most common cause of infant death after the perinatal period. OBJECTIVE: To determine the influence of air pollution on the incidence of SIDS. METHODS: Time-series analyses were performed to compare the daily mortality rates for SIDS and the daily air pollution concentrations in each of 12 Canadian cities during the period of 1984-1999. Serial autocorrelation was controlled for by city, and then the city-specific estimates were pooled. Increased daily rates of SIDS were associated with increases, on the previous day, in the levels of sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide but not ozone or fine particles measured every sixth day. Effects persisted despite adjustments for season alone or the combination of daily mean temperature, relative humidity, and changes in barometric pressure for NO2 and SO2 but not carbon monoxide. RESULTS: Increases in both SO2 and NO2, equivalent to their interquartile ranges, were associated with a 17.72% increase in SIDS incidence. CONCLUSION: Ambient SO2 and NO2 may be important risk factors for SIDS.