Markey Johnson

Development of temporally refined land-use regression models predicting daily household-level air pollution in a panel study of lung function among asthmatic children

Regulatory monitoring data and land-use regression (LUR) models have been widely used for estimating individual exposure to ambient air pollution in epidemiologic studies. However, LUR models lack fine-scale temporal resolution for predicting acute exposure and regulatory monitoring provides daily concentrations, but fails to capture spatial variability within urban areas. This study coupled LUR models with continuous regulatory monitoring to predict daily ambient nitrogen dioxide (NO2) and particulate matter (PM2.5) at 50 homes in Windsor, Ontario. We compared predicted versus measured daily outdoor concentrations for 5 days in winter and 5 days in summer at each home. We also examined the implications of using modeled versus measured daily pollutant concentrations to predict daily lung function among asthmatic children living in those homes. Mixed effect analysis suggested that temporally refined LUR models explained a greater proportion of the spatial and temporal variance in daily household-level outdoor NO2 measurements compared with daily concentrations based on regulatory monitoring. Temporally refined LUR models captured 40% (summer) and 10% (winter) more of the spatial variance compared with regulatory monitoring data. Ambient PM2.5 showed little spatial variation; therefore, daily PM2.5 models were similar to regulatory monitoring data in the proportion of variance explained. Furthermore, effect estimates for forced expiratory volume in 1 s (FEV1) and peak expiratory flow (PEF) based on modeled pollutant concentrations were consistent with effects based on household-level measurements for NO2 and PM2.5. These results suggest that LUR modeling can be combined with continuous regulatory monitoring data to predict daily household-level exposure to ambient air pollution. Temporally refined LUR models provided a modest improvement in estimating daily household-level NO2 compared with regulatory monitoring data alone, suggesting that this approach could potentially improve exposure estimation for spatially heterogeneous pollutants. These findings have important implications for epidemiologic studies — in particular, for research focused on short-term exposure and health effects.

Ambient air pollution and adverse birth outcomes: Differences by maternal comorbidities

BACKGROUND Prenatal exposure to ambient air pollution has been associated with adverse birth outcomes, but the potential modifying effect of maternal comorbidities remains understudied. Our objective was to investigate whether associations between prenatal air pollution exposures and birth outcomes differ by maternal comorbidities. METHODS A total of 818,400 singleton live births were identified in the province of Ontario, Canada from 2005 to 2012. We assigned exposures to fine particulate matter (PM2.5), nitrogen dioxide (NO2) and ozone (O3) to maternal residences during pregnancy. We evaluated potential effect modification by maternal comorbidities (i.e. asthma, hypertension, pre-existing diabetes mellitus, heart disease, gestational diabetes and preeclampsia) on the associations between prenatal air pollution and preterm birth, term low birth weight and small for gestational age. RESULTS Interquartile range (IQR) increases in PM2.5 (2μg/m(3)), NO2 (9ppb) and O3 (5ppb) over the entire pregnancy were associated with a 4% (95% CI: 2.4-5.6%), 8.4% (95% CI: 5.5-10.3%) and 2% (95% CI: 0.5-4.1%) increase in the odds of preterm birth, respectively. Increases of 10.6% (95% CI: 0.2-2.1%) and 23.8% (95% CI: 5.5-44.8%) in the odds of preterm birth were observed among women with pre-existing diabetes while the increases were of 3.8% (95% CI: 2.2-5.4%) and 6.5% (95% CI: 3.7-8.4%) among women without this condition for pregnancy exposure to PM2.5 and NO2, respectively (Pint<0.01). The increase in the odds of preterm birth for exposure to PM2.5 during pregnancy was higher among women with preeclampsia (8.3%, 95% CI: 0.8-16.4%) than among women without (3.6%, 95% CI: 1.8-5.3%) (Pint=0.04). A stronger increase in the odds of preterm birth was found for exposure to O3 during pregnancy among asthmatic women (12.0%, 95% CI: 3.5-21.1%) compared to non-asthmatic women (2.0%, 95% CI: 0.1-3.5%) (Pint<0.01). We did not find statistically significant effect modification for the other outcomes investigated. CONCLUSIONS Findings of this study suggest that associations of ambient air pollution with preterm birth are stronger among women with pre-existing diabetes, asthma, and preeclampsia.

Accounting for spatial effects in land use regression for urban air pollution modeling.

In order to accurately assess air pollution risks, health studies require spatially resolved pollution concentrations. Land-use regression (LUR) models estimate ambient concentrations at a fine spatial scale. However, spatial effects such as spatial non-stationarity and spatial autocorrelation can reduce the accuracy of LUR estimates by increasing regression errors and uncertainty; and statistical methods for resolving these effects--e.g., spatially autoregressive (SAR) and geographically weighted regression (GWR) models--may be difficult to apply simultaneously. We used an alternate approach to address spatial non-stationarity and spatial autocorrelation in LUR models for nitrogen dioxide. Traditional models were re-specified to include a variable capturing wind speed and direction, and re-fit as GWR models. Mean R(2) values for the resulting GWR-wind models (summer: 0.86, winter: 0.73) showed a 10-20% improvement over traditional LUR models. GWR-wind models effectively addressed both spatial effects and produced meaningful predictive models. These results suggest a useful method for improving spatially explicit models.

Within- and between-city contrasts in nitrogen dioxide and mortality in 10 Canadian cities; a subset of the Canadian Census Health and Environment Cohort (CanCHEC)

The independent and joint effects of within- and between-city contrasts in air pollution on mortality have been investigated rarely. To examine the differential effects of between- versus within-city contrasts in pollution exposure, we used both ambient measurements and land use regression models to assess associations with mortality and exposure to nitrogen dioxide (NO2) among ~735,600 adults in 10 of the largest Canadian cities. We estimated exposure contrasts partitioned into within- and between-city contrasts, and the sum of these as overall exposures, for every year from 1984 to 2006. Residential histories allowed us to follow subjects annually during the study period. We calculated hazard ratios (HRs) adjusted for many personal and contextual variables. In fully-adjusted, random-effects models, we found positive associations between overall NO2 exposures and mortality from non-accidental causes (HR per 5 p.p.b.: 1.05; 95% confidence interval (CI): 1.03–1.07), cardiovascular disease (HR per 5 p.p.b.: 1.04; 95% CI: 1.01–1.06), ischaemic heart disease (HR per 5 p.p.b.: 1.05; 95% CI: 1.02–1.08) and respiratory disease (HR per 5 p.p.b.: 1.04; 95% CI: 0.99–1.08), but not from cerebrovascular disease (HR per 5 p.p.b.: 1.01; 95% CI: 0.96–1.06). We found that most of these associations were determined by within-city contrasts, as opposed to by between-city contrasts in NO2. Our results suggest that variation in NO2 concentrations within a city may represent a more toxic mixture of pollution than variation between cities.

Ambient Ozone Concentrations and the Risk of Perforated and Nonperforated Appendicitis: A Multicity Case-Crossover Study

Background: Environmental determinants of appendicitis are poorly understood. Past work suggests that air pollution may increase the risk of appendicitis. Objectives: We investigated whether ambient ground-level ozone (O3) concentrations were associated with appendicitis and whether these associations varied between perforated and nonperforated appendicitis. Methods: We based this time-stratified case-crossover study on 35,811 patients hospitalized with appendicitis from 2004 to 2008 in 12 Canadian cities. Data from a national network of fixed-site monitors were used to calculate daily maximum O3 concentrations for each city. Conditional logistic regression was used to estimate city-specific odds ratios (ORs) relative to an interquartile range (IQR) increase in O3 adjusted for temperature and relative humidity. A random-effects meta-analysis was used to derive a pooled risk estimate. Stratified analyses were used to estimate associations separately for perforated and nonperforated appendicitis. Results: Overall, a 16-ppb increase in the 7-day cumulative average daily maximum O3 concentration was associated with all appendicitis cases across the 12 cities (pooled OR = 1.07; 95% CI: 1.02, 1.13). The association was stronger among patients presenting with perforated appendicitis for the 7-day average (pooled OR = 1.22; 95% CI: 1.09, 1.36) when compared with the corresponding estimate for nonperforated appendicitis [7-day average (pooled OR = 1.02, 95% CI: 0.95, 1.09)]. Heterogeneity was not statistically significant across cities for either perforated or nonperforated appendicitis (p > 0.20). Conclusions: Higher levels of ambient O3 exposure may increase the risk of perforated appendicitis.

Fine particulate air pollution, nitrogen dioxide, and systemic autoimmune rheumatic disease in Calgary, Alberta

OBJECTIVE To estimate the association between fine particulate (PM2.5) and nitrogen dioxide (NO2) pollution and systemic autoimmune rheumatic diseases (SARDs). METHODS Associations between ambient air pollution (PM2.5 and NO2) and SARDs were assessed using land-use regression models for Calgary, Alberta and administrative health data (1993-2007). SARD case definitions were based on ≥2 physician claims, or ≥1 rheumatology billing code; or ≥1 hospitalization code (for systemic lupus, Sjogrens Syndrome, scleroderma, polymyositis, dermatomyositis, or undifferentiated connective tissue disease). Bayesian hierarchical latent class regression models estimated the probability that each resident was a SARD case, based on these case definitions. The sum of individual level probabilities provided the estimated number of cases in each area. The latent class model included terms for age, sex, and an interaction term between age and sex. Bayesian logistic regression models were used to generate adjusted odds ratios (OR) for NO2 and PM2.5. pollutant models, adjusting for neighbourhood income, age, sex, and an interaction between age and sex. We also examined models stratified for First-Nations (FN) and non-FN subgroups. RESULTS Residents that were female and/or aged >45 had a greater probability of being a SARD case, with the highest OR estimates for older females. Independently, the odds of being a SARDs case increased with PM2.5 levels, but the results were inconclusive for NO2. The results stratified by FN and non-FN groups were not distinctly different. CONCLUSION In this urban Canadian sample, adjusting for demographics, exposure to PM2.5 was associated with an increased risk of SARDs. The results for NO2 were inconclusive.

Air Pollution Exposure During Pregnancy and Fetal Markers of Metabolic Function The MIREC Study

Previous evidence suggests that exposure to outdoor air pollution during pregnancy could alter fetal metabolic function, which could increase the risk of obesity in childhood. However, to our knowledge, no epidemiologic study has investigated the association between prenatal exposure to air pollution and indicators of fetal metabolic function. We investigated the association between maternal exposure to nitrogen dioxide and fine particulate matter (aerodynamic diameter ≤2.5 µm) and umbilical cord blood leptin and adiponectin levels with mixed-effects linear regression models among 1,257 mother-infant pairs from the Maternal-Infant Research on Environmental Chemicals (MIREC) Study, conducted in Canada (2008-2011). We observed that an interquartile-range increase in average exposure to fine particulate matter (3.2 µg/m(3)) during pregnancy was associated with an 11% (95% confidence interval: 4, 17) increase in adiponectin levels. We also observed 13% (95% confidence interval: 6, 20) higher adiponectin levels per interquartile-range increase in average exposure to nitrogen dioxide (13.6 parts per billion) during pregnancy. Significant associations were seen between air pollution markers and cord blood leptin levels in models that adjusted for birth weight z score but not in models that did not adjust for birth weight z score. The roles of prenatal exposure to air pollution and fetal metabolic function in the potential development of childhood obesity should be further explored.

Assessing traffic and industrial contributions to ambient nitrogen dioxide and volatile organic compounds in a low pollution urban environment.

Land use regression (LUR) modeling is an effective method for estimating fine-scale distributions of ambient air pollutants. The objectives of this study are to advance the methodology for use in urban environments with relatively low levels of industrial activity and provide exposure assessments for research on health effects of air pollution. Intraurban distributions of nitrogen dioxide (NO2) and the volatile organic compounds (VOCs) benzene, toluene and m- and p-xylene were characterized based on spatial monitoring and LUR modeling in Ottawa, Ontario, Canada. Passive samplers were deployed at 50 locations throughout Ottawa for two consecutive weeks in October 2008 and May 2009. Land use variables representing point, area and line sources were tested as predictors of pooled pollutant distributions. LUR models explained 96% of the spatial variability in NO2 and 75-79% of the variability in the VOC species. Proximity to highways, green space, industrial and residential land uses were significant in the final models. More notably, proximity to industrial point sources and road network intersections were significant predictors for all pollutants. The strong contribution of industrial point sources to VOC distributions in Ottawa suggests that facility emission data should be considered whenever possible. The study also suggests that proximity to road network intersections may be an effective proxy in areas where reliable traffic data are not available.

Maternal exposure to ambient air pollution and risk of early childhood cancers: A population-based study in Ontario, Canada

BACKGROUND There are increasing concerns regarding the role of exposure to ambient air pollution during pregnancy in the development of early childhood cancers. OBJECTIVE This population based study examined whether prenatal and early life (<1year of age) exposures to ambient air pollutants, including nitrogen dioxide (NO2) and particulate matter with aerodynamic diameters ≤2.5μm (PM2.5), were associated with selected common early childhood cancers in Canada. METHODS 2,350,898 singleton live births occurring between 1988 and 2012 were identified in the province of Ontario, Canada. We assigned temporally varying satellite-derived estimates of PM2.5 and land-use regression model estimates of NO2 to maternal residences during pregnancy. Incident cases of 13 subtypes of pediatric cancers among children up to age 6 until 2013 were ascertained through administrative health data linkages. Associations of trimester-specific, overall pregnancy and first year of life exposures were evaluated using Cox proportional hazards models, adjusting for potential confounders. RESULTS A total of 2044 childhood cancers were identified. Exposure to PM2.5, per interquartile range increase, over the entire pregnancy, and during the first trimester was associated with an increased risk of astrocytoma (hazard ratio (HR) per 3.9μg/m3=1.38 (95% CI: 1.01, 1.88) and, HR per 4.0μg/m3=1.40 (95% CI: 1.05-1.86), respectively). We also found a positive association between first trimester NO2 and acute lymphoblastic leukemia (ALL) (HR=1.20 (95% CI: 1.02-1.41) per IQR (13.3ppb)). CONCLUSIONS In this population-based study in the largest province of Canada, results suggest an association between exposure to ambient air pollution during pregnancy, especially in the first trimester and an increased risk of astrocytoma and ALL. Further studies are required to replicate the findings of this study with adjustment for important individual-level confounders.

Upper gastrointestinal bleeding due to peptic ulcer disease is not associated with air pollution: a case-crossover study.

BackgroundRecent studies have demonstrated an association between short-term elevations in air pollution and an increased risk of exacerbating gastrointestinal disease. The objective of the study was to evaluate if day-to-day increases in air pollution concentrations were positively associated with upper gastrointestinal bleeding (UGIB) secondary to peptic ulcer disease (PUD).MethodsA time-stratified case-crossover study design was used. Adults presenting to hospitals with their first UGIB secondary to PUD from 2004–2010 were identified using administrative databases from Calgary (n = 1374; discovery cohort) and Edmonton (n = 1159; replication cohort). Daily concentrations of ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide, and particulate matter (PM10 and PM2.5) were estimated in these two cities. Conditional logistic regression models were employed, adjusting for temperature and humidity. Odds ratios (OR) with 95 % confidence intervals (CI) were expressed relative to an interquartile range increase in the concentration of each pollutant.ResultsNo statistically significant associations were observed for any of the individual pollutants based on same-day, or 1-day lag effects within the Calgary discovery cohort. When the air pollution exposures were assessed as 3-, 5-, and 7-day averages, some pollutants were inversely associated with UGIB in the discovery cohort; for example, 5-day averages of nitrogen dioxide (OR = 0.68; 95 % CI: 0.53–0.88), and particulate matter <2.5 μm (OR = 0.75; 95 % CI: 0.61–0.90). However, these findings could not be reproduced in the replication cohort.ConclusionOur findings suggest that short-term elevations in the level of ambient air pollutants does not increase the incidence of UGIB secondary to PUD.