Jessie Loving Carr Shmool1, Ellen Kinnee2, Perry Elizabeth Sheffield3, Jane Ellen Clougherty4. 1. University of Pittsburgh Graduate School of Public Health, Department of Environmental and Occupational Health, 100 Technology Drive, Ste. 350, Pittsburgh, PA 15219, USA. Electronic address: jlcshmool@pitt.edu. 2. University of Pittsburgh Graduate School of Public Health, Department of Environmental and Occupational Health, 100 Technology Drive, Ste. 350, Pittsburgh, PA 15219, USA. Electronic address: ejk40@pitt.edu. 3. Icahn School of Medicine at Mount Sinai, DPM, 1 Gustave L. Levy Pl., Box 1057, New York, NY 10029, USA. Electronic address: perry.sheffield@mssm.edu. 4. University of Pittsburgh Graduate School of Public Health, Department of Environmental and Occupational Health, 100 Technology Drive, Ste. 350, Pittsburgh, PA 15219, USA. Electronic address: jcloughe@pitt.edu.
Abstract
BACKGROUND: Childhood asthma morbidity has been associated with short-term air pollution exposure. To date, most investigations have used time-series models, and it is not well understood how exposure misclassification arising from unmeasured spatial variation may impact epidemiological effect estimates. Here, we develop case-crossover models integrating temporal and spatial individual-level exposure information, toward reducing exposure misclassification in estimating associations between air pollution and child asthma exacerbations in New York City (NYC). METHODS: Air pollution data included: (a) highly spatially-resolved intra-urban concentration surfaces for ozone and co-pollutants (nitrogen dioxide and fine particulate matter) from the New York City Community Air Survey (NYCCAS), and (b) daily regulatory monitoring data. Case data included citywide hospital records for years 2005-2011 warm-season (June-August) asthma hospitalizations (n=2353) and Emergency Department (ED) visits (n=11,719) among children aged 5-17 years. Case residential locations were geocoded using a multi-step process to maximize positional accuracy and precision in near-residence exposure estimates. We used conditional logistic regression to model associations between ozone and child asthma exacerbations for lag days 0-6, adjusting for co-pollutant and temperature exposures. To evaluate the effect of increased exposure specificity through spatial air pollution information, we sequentially incorporated spatial variation into daily exposure estimates for ozone, temperature, and co-pollutants. RESULTS: Percent excess risk per 10ppb ozone exposure in spatio-temporal models were significant on lag days 1 through 5, ranging from 6.5 (95% CI: 0.2-13.1) to 13.0 (6.0-20.6) for inpatient hospitalizations, and from 2.9 (95% CI: 0.1-5.7) to 9.4 (6.3-12.7) for ED visits, with strongest associations consistently observed on lag day 2. Spatio-temporal excess risk estimates were consistently but not statistically significantly higher than temporal-only estimates on lag days 0-3. CONCLUSION: Incorporating case-level spatial exposure variation produced small, non-significant increases in excess risk estimates. Our modeling approach enables a refined understanding of potential measurement error in temporal-only versus spatio-temporal air pollution exposure assessments. As ozone generally varies over much larger spatial scales than that observed within NYC, further work is necessary to evaluate potential reductions in exposure misclassification for populations spanning wider geographic areas, and for other pollutants.
BACKGROUND: Childhood asthma morbidity has been associated with short-term air pollution exposure. To date, most investigations have used time-series models, and it is not well understood how exposure misclassification arising from unmeasured spatial variation may impact epidemiological effect estimates. Here, we develop case-crossover models integrating temporal and spatial individual-level exposure information, toward reducing exposure misclassification in estimating associations between air pollution and child asthma exacerbations in New York City (NYC). METHODS: Air pollution data included: (a) highly spatially-resolved intra-urban concentration surfaces for ozone and co-pollutants (nitrogen dioxide and fine particulate matter) from the New York City Community Air Survey (NYCCAS), and (b) daily regulatory monitoring data. Case data included citywide hospital records for years 2005-2011 warm-season (June-August) asthma hospitalizations (n=2353) and Emergency Department (ED) visits (n=11,719) among children aged 5-17 years. Case residential locations were geocoded using a multi-step process to maximize positional accuracy and precision in near-residence exposure estimates. We used conditional logistic regression to model associations between ozone and child asthma exacerbations for lag days 0-6, adjusting for co-pollutant and temperature exposures. To evaluate the effect of increased exposure specificity through spatial air pollution information, we sequentially incorporated spatial variation into daily exposure estimates for ozone, temperature, and co-pollutants. RESULTS: Percent excess risk per 10ppb ozone exposure in spatio-temporal models were significant on lag days 1 through 5, ranging from 6.5 (95% CI: 0.2-13.1) to 13.0 (6.0-20.6) for inpatient hospitalizations, and from 2.9 (95% CI: 0.1-5.7) to 9.4 (6.3-12.7) for ED visits, with strongest associations consistently observed on lag day 2. Spatio-temporal excess risk estimates were consistently but not statistically significantly higher than temporal-only estimates on lag days 0-3. CONCLUSION: Incorporating case-level spatial exposure variation produced small, non-significant increases in excess risk estimates. Our modeling approach enables a refined understanding of potential measurement error in temporal-only versus spatio-temporal air pollution exposure assessments. As ozone generally varies over much larger spatial scales than that observed within NYC, further work is necessary to evaluate potential reductions in exposure misclassification for populations spanning wider geographic areas, and for other pollutants.
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