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Clinical Investigations: AIRWAYS |

Polycyclic Aromatic Hydrocarbons, Environmental Tobacco Smoke, and Respiratory Symptoms in an Inner-city Birth Cohort*

Rachel L. Miller, MD; Robin Garfinkel, PhD; Megan Horton, MS; David Camann, MS; Frederica P. Perera, DrPH; Robin M. Whyatt, DrPH; Patrick L. Kinney, ScD
Author and Funding Information

*From the Division of Pulmonary, Allergy, Critical Care Medicine (Dr. Miller and Ms. Horton), Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY; Columbia Center for Children’s Environmental Health (Drs. Garfinkel, Perera, Whyatt, and Kinney), Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY; and Department of Analytical and Environmental Chemistry (Mr. Camann), Southwest Research Institute, San Antonio, TX.

Correspondence to: Rachel L. Miller, MD, PH8C, 630 168th St, New York, NY 10032; e-mail:rlm14@columbia.edu



Chest. 2004;126(4):1071-1078. doi:10.1378/chest.126.4.1071
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Study objectives: Several studies have found associations between diesel exposure, respiratory symptoms, and/or impaired pulmonary function. We hypothesized that prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAH), important components of diesel exhaust and other combustion sources, may be associated with respiratory symptoms in young children. We also hypothesized that exposure to environmental tobacco smoke (ETS) may worsen symptoms beyond that observed to be associated with PAH alone.

Design/participants: To test our hypotheses, we recruited 303 pregnant women from northern Manhattan believed to be at high risk for exposure to both PAH and ETS, collected 48-h personal PAH exposure measurements, and monitored their children prospectively.

Results: By 12 months of age, more cough and wheeze were reported in children exposed to prenatal PAH in concert with ETS postnatally (PAH × ETS interaction odds ratios [ORs], 1.41 [p < 0.01] and 1.29 [p < 0.05], respectively). By 24 months, difficulty breathing and probable asthma were reported more frequently among children exposed to prenatal PAH and ETS postnatally (PAH × ETS ORs, 1.54 and 1.64, respectively [p < 0.05]).

Conclusions: Our results suggest that early exposure to airborne PAH and ETS can lead to increased respiratory symptoms and probable asthma by age 12 to 24 months. Interventions to lower the risk of respiratory disease in young children living in the inner city may need to address the importance of multiple environmental exposures.

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