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Project at a Glance

Title: Risk of pediatric asthma morbidity from multipollutant exposures

Principal Investigator / Author(s): Delfino, Ralph and Michael Kleeman

Contractor: UC Irvine

Contract Number: 10-319

Research Program Area: Health & Exposure

Topic Areas: Health Effects of Air Pollution, Vulnerable Populations


Background: Little is known about the impact of primary and secondary organic aerosols (POA and SOA) on risk of acute asthma morbidity among children. We evaluated whether these important characteristics of particulate matter are associated with emergency department visits and hospital admissions for asthma. We hypothesized that traffic-related concentrations of ultrafine particles near subject homes and related estimates of exposure to POA will show associations with asthma morbidity that are additive with estimates of exposure to O3 and larger particles enriched in SOA. This addressed the multipollutant nature of human air pollution exposure. Finally, we evaluated air pollution susceptibility, including asthma recurrence, socioeconomic status, sex, age and race-ethnicity.

Methods: This is a case-crossover analysis in which subjects acted as their own control in a conditional logistic regression model adjusted for confounders. The period of exposure was the week leading up to the day each subject was seen at a hospital, and this was compared to a referent exposure period from the same days of the week and month. The hospital data included 11,390 hospital encounters (emergency department visits and hospital admissions) from 2000-2008 made by 7,954 children ages 0-18 years for a primary diagnosis of asthma 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 from 2000-2008 for the 7,954 subject residences. POA and SOA model output included size-resolved mass, speciation, and source apportionment. We obtained ambient air pollutant and weather data from US EPA Air Quality System (AQS). Traffic-related air pollution (TRAP) was assessed using CALINE4 dispersion models at subject residential locations for ultrafine particle number concentration, PM2.5, and NOx averaged seasonally (warm season: May-October; cool season: November-April) and weekly. Seasonal data was used to analyze the influence of spatial exposure variation on acute ambient exposure-response relations, and weekly data for acute effects analyses.

Results: Model prediction of the UCD/CIT model showed wood smoke was the single biggest source of total organic aerosol (TOA=POA+SOA) in winter in California, and meat cooking and other anthropogenic sources (including solvent use) and mobile emissions are the most important sources in summer. Predicted SOA concentrations were low, with biogenic emissions the largest source, followed by the other anthropogenic and mobile sources. In health regression analyses we found that hospital encounters (emergency department visits and admissions) for asthma were positively associated with ambient air pollution data, including PM2.5 and O3 in the warm season and PM2.5, CO, NO2, and NOx in the cool season. We observed that associations of daily ambient air pollution with asthma hospital morbidity are stronger among subjects living at residences with higher CALINE4-predicted air pollution from traffic, especially in the cool season. Weekly exposures to CALINE4 residential TRAP exposure were significantly associated with asthma hospital encounters in the cool season. We found no associations in the warm season with weekly exposures to UCD/CIT SOA and POA but positive associations of POA (including most specific sources) with asthma in the cool season. Results of the multipollutant models suggest that effects of warm-season ambient O3 and PM2.5 are largely independent of each other and not confounded by any other air pollutant. Cool-season PM2.5 was also not confounded by any other air pollutant. We found associations with ambient PM2.5, NO2, 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. Older subjects and female subjects were at nominally increased risk from several air pollutant exposures.

Conclusions: We found consistent results that acute asthma morbidity is increased in relation to short-term elevations in various indicators of air pollution from fossil fuel combustion sources (including traffic) during the cool season. This includes ambient gases (CO, NO2, and NOx), CALINE4 weekly TRAP indicators, and UCD/CIT POA (including on-road and off-road diesel plus gasoline emission sources). There were no associations with SOA in either season. We found that associations of warm-season ambient PM2.5 with asthma hospital morbidity were additive with estimates of exposure to O3. Associations of asthma with ambient CO, NO2, NOx, and PM2.5, were enhanced among subjects living in homes near high TRAP suggesting that this is a vulnerable/susceptible population.


For questions regarding research reports, contact: Heather Choi at (916) 322-3893

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