ARB Research Seminar

This page updated March 11, 2015

Risk of Pediatric Asthma Morbidity from Multipollutant Exposures

Photo of Ralph Delfino

Ralph Delfino

Photo of Michael Kleeman

Michael Kleeman

Ralph J. Delfino, M.D., Ph.D., Department of Epidemiology, University of California, Irvine and Michael J. Kleeman, Ph.D., Department of Civil and Environmental Engineering, University of California, Davis

April 07, 2015
Cal EPA Headquarters, 1001 "I" Street, Sacramento, CA


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Overview

Little is known about the impact of primary and secondary organic aerosols (POA and SOA) on risk of acute asthma morbidity. We evaluated whether these important characteristics of particulate matter are associated with hospital encounters (emergency department visits and hospital admissions) for pediatric asthma. We hypothesized that traffic-related concentrations of ultrafine particles near subject homes and related estimates of exposure to POA are associated with asthma morbidity, and that these associations are additive with O₃ and SOA. Finally, we evaluated air pollution susceptibility, including recurrent asthma, socioeconomic status, and race-ethnicity.

This is a case-crossover analysis in which subjects acted as their own control in a conditional logistic regression model adjusted for confounders. Hospital data included 11,390 asthma hospital encounters from 2000-2008 made by 7,954 children ages 0-18 years in Orange County. The UC Davis/California Institute of Technology (UCD/CIT) Source Oriented Chemical Transport Model was used to output daily POA and SOA at a 4x4 km resolution. Model output included size-resolved mass, speciation, and source apportionment. Traffic-related air pollution (TRAP) was assessed using CALINE4 dispersion models at subject residential locations averaged seasonally and weekly.

Interestingly, the UCD/CIT model showed wood smoke was the single biggest source of total organic aerosol (OA=POA+SOA) in winter, with other anthropogenic sources dominating OA in summer. Case-crossover models showed that asthma hospital encounters were positively associated with ambient PM₂.₅ and O₃ in the warm seasons and PM₂.₅, CO, NO₂, and NOₓ in the cool seasons. Overall, there were consistent results that acute asthma morbidity is increased in relation to short-term elevations in various indicators of primary air pollution from fossil fuel combustion sources (including traffic), but not estimated SOA. We observed that associations of asthma hospital morbidity with daily ambient primary air pollutants and PM2.5 are stronger among subjects living at residences with higher seasonal CALINE4-predicted TRAP. Multipollutant models revealed independent effects of ambient PM₂.₅ from O₃. The PM₂.₅ association was also largely independent from other primary gas- and particle-phase pollutants, suggesting these exposure markers incompletely represent important particle components in PM₂.₅. We found associations with ambient PM₂.₅, NOₓ, and CO in the cool season were nominally stronger among Hispanics compared with non-Hispanic whites. Subjects living in neighborhoods with lower socioeconomic status were at increased risk from elevations in ambient PM₂.₅. Associations of asthma with ambient air pollutants were enhanced among subjects living in homes near high TRAP suggesting that this is a vulnerable/susceptible population. Demographic data shows that this population was more likely to be Hispanic and living in lower socioeconomic status communities.

Speaker Biographies

Ralph J. Delfino, M.D., Ph. D. is Professor and Vice Chair for Research and Graduate Studies, Department of Epidemiology and Associate Director of the Genetic Epidemiology Research Institute, University of California, Irvine. Dr. Delfino's research and teaching focus over the past 30 years has been in environmental epidemiology. Professor Delfino's studies have been designed to evaluate the relation of health outcomes to well-characterized air pollution exposures in potentially susceptible populations. His research group has evaluated multiple clinical, biological and genetic factors to understand the effects of air pollutants on respiratory and cardiovascular health. Major ongoing research efforts are to better characterize the pollutant chemicals and particle oxidative potential that are responsible for exposure-response relations, and to evaluate the health effects of combustion-generated nanoparticles from traffic sources as compared with larger particles that dominate US EPA-regulated ambient particle mass. Ongoing research aims to explore the effects of air pollutant exposures on leukocyte gene expression in several key biological pathways. Dr. Delfino is also evaluating whether polymorphisms in candidate genes involved in oxidative stress and other responses modify associations between air pollutants and health outcomes. Overall, Dr. Delfino's findings are generating new data on susceptibility to the adverse effects of air pollutants and the role that toxic pollutants in urban air play in respiratory and cardiovascular health. Dr. Delfino received his MD degree from the University of Chicago in 1987, and his PhD in epidemiology from McGill University, Montreal in 1993.

Michael J. Kleeman, Ph. D. is Professor at the Department of Civil and Environmental Engineering, University of California, Davis since 1999. Professor Kleeman's research is focused on the study of urban and regional air quality problems with an emphasis on the size and composition of atmospheric particles and gas-to-particle conversion processes. Professor Kleeman has measured particle size and composition directly at sources and in the environment to provide data for statistical source receptor models. Dr. Kleeman has also constructed mechanistic air quality models to identify the most important atmospheric processes, and to better track source contributions to size-resolved ambient particulate matter. Professor Kleeman's current goals are to better understand climate-energy-air quality interactions and to determine the health effects of ultrafine particles. Professor Michael Kleeman has a B.A.Sc. in Mechanical Engineering and M.S./Ph.D. in Environmental Engineering Science.


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