Infant exposure to fine particulate matter and traffic and risk of hospitalization for RSV bronchiolitis in a region with lower ambient air pollution

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Abstract

Few studies investigate the impact of air pollution on the leading cause of infant morbidity, acute bronchiolitis. We investigated the influence of PM2.5 and other metrics of traffic-derived air pollution exposure using a matched case–control dataset derived from 1997 to 2003 birth and infant hospitalization records from the Puget Sound Region, Washington State. Mean daily PM2.5 exposure for 7, 30, 60 and lifetime days before case bronchiolitis hospitalization date were derived from community monitors. A regional land use regression model of NO2 was applied to characterize subject's exposure in the month prior to case hospitalization and lifetime average before hospitalization. Subject's residential proximity within 150 m of highways, major roadways, and truck routes was also assigned. We evaluated 2604 (83%) cases and 23,354 (85%) controls with information allowing adjustment for mother's education, mother's smoking during pregnancy, and infant race/ethnicity. Effect estimates derived from conditional logistic regression revealed very modest increased risk and were not statistically significant for any of the exposure metrics in fully adjusted models. Overall, risk estimates were stronger when restricted to bronchiolitis cases attributed to respiratory syncytial virus (RSV) versus unspecified and for longer exposure windows. The adjusted odds ratio (ORadj) and 95% confidence interval per 10 mcg/m3 increase in lifetime PM2.5 was 1.14, 0.88–1.46 for RSV bronchiolitis hospitalization. This risk was also elevated for infants who resided within 150 m of a highway (ORadj 1.17, 0.95–1.44). This study supports a developing hypothesis that there may be a modest increased risk of bronchiolitis attributable to chronic traffic-derived particulate matter exposure particularly for infants born just before or during peak RSV season. Future studies are needed that can investigate threshold effects and capture larger variability in spatial contrasts among populations of infants.

Introduction

Bronchiolitis is the most common cause of hospitalization in the first year of life with respiratory syncytial virus (RSV) the most important etiologic agent (Panitch, 2001). Many studies have linked increased exposure to ambient air pollution with increased risk of pediatric respiratory conditions including respiratory infections; however, few epidemiologic data on the infant period and bronchiolitis are available (Karr et al., 2006, Karr et al., 2007). Nonetheless, there is consistent epidemiological evidence of increased infant post-neonatal mortality due to respiratory causes associated with increased exposure to ambient air pollution (Ritz et al., 2006; Woodruff et al., 1997; Bobak and Leon, 1999).

Toxicological studies demonstrate that exposure to air pollutants such as particulate matter increases the severity of pulmonary pathology associated with viral respiratory infection in animal and in vitro models (Harrod et al., 2003; Castranova et al., 2001). As such, we hypothesize that infants who reside in settings of elevated ambient air pollutants may develop subclinical pulmonary compromise that places them at risk of developing more severe bronchiolitis when these infants encounter the common etiologic respiratory viruses in their communities, such as RSV. This was previously examined in a region of relatively high ambient air pollution in the Los Angeles area of California (South Coast Air Basin) (Karr et al., 2007). In that setting, a case–control analysis of infant bronchiolitis hospitalization and ambient air pollutant exposure found modestly increased risk for subchronic (30 day) and chronic (lifetime) fine particulate matter (PM2.5) exposure but not with other criteria air pollutants investigated (nitrogen dioxide, ozone, carbon monoxide) and not with shorter, more acute exposure periods investigated. For a 10 mcg/m3 increase in chronic PM2.5 exposure, the risk of hospitalization increased approximately 9% (adjusted OR 1.09, 95% confidence interval: 1.04, 1.14).

Here we investigate the influence of PM2.5 and metrics of traffic-derived air pollution exposure in the Puget Sound region of Washington State, where ambient concentrations of pollutants are generally low and are on average approximately half those experienced in the Los Angeles area (Karr et al., 2007).

While traffic predominates as a source in ambient air pollution in both areas and most US cities, woodsmoke is also a prominent air pollutant in the Puget Sound, particularly in wintertime, coinciding with the annual winter epidemic of RSV bronchiolitis. Observational studies have linked woodsmoke exposure with increased respiratory health events including acute lower respiratory tract infections in children (Naeher et al., 2007). We used the approach of linking population-based data on infant hospitalization for bronchiolitis with available community-based regulatory network monitor data for PM2.5 to test the primary hypothesis that increased exposure to ambient PM2.5 in infants in the Puget Sound region is associated with increased hospitalization for bronchiolitis. This approach is commonly employed in air pollution epidemiological studies and the density of PM2.5 monitors in this region provides an opportunity to capture community-wide spatial contrasts in PM2.5 specifically. In addition, we applied a NO2 land use regression (LUR) model to improve spatial heterogeneity regarding exposure to traffic exhaust, recognizing the potential increased toxicity of traffic-derived particulate matter in the ultrafine size range (<0.1 μm) and the observation that exposure to traffic-derived particulate can vary considerably at the neighborhood scale (US EPA, 2008). Lastly, we evaluated proximity to major highways and roadways as an additional proxy for traffic-derived air pollution exposure.

Section snippets

Methods

The study procedures were approved by the University of Washington and Washington State Department of Health Institutional Review Boards.

Results

In total, 3124 infants met the case definition for bronchiolitis and we identified 27,340 matched controls (Table 1). We constructed exposure windows to represent mean daily average PM2.5 for the 7, 30, and 60 days prior to case date of hospitalization for 99.8%, 86.2%, and 64.7% of our matched case–control subjects, respectively (Table 2). Those missing these exposure windows represent those not at risk (age at case diagnosis less than the length of the total exposure time window). A lifetime

Discussion

Few air pollution epidemiologic investigations address the impact of specific endpoints of respiratory morbidity in the infant period. We focused on the prominent respiratory disease of concern in infancy, bronchiolitis, in a region of modest air pollution exposure. For lifetime exposure to PM2.5, quartile-based exposure assessment suggested an increased risk in RSV bronchiolitis hospitalization as exposure increased. In addition, longer exposure windows yielded higher risk estimates than

Acknowledgments

Bill O’Brien, the Universtiy of British Columbia Border Air Quality Study Team and its leaders Michael Brauer and Paul Demers, and Ray Copes are acknowledged.

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Funding sources: Health Canada Border Air Quality Study—Western Pilot Initiative. British Columbia Centres for Disease Control Agreement No. GEH0404. Human subjects: The study has been reviewed and approved by the Washington State Institutional Review Board. Application B-080604-H Incidence of Infant Bronchiolitis and Particulate Matter Air Pollution (PI Jane Q. Koenig).

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