Environmental tobacco smoke and asthma exacerbations and severity: the difference between measured and reported exposure
- 1Department of Pediatrics, University of Illinois at Chicago, Chicago, Illinois, USA
- 2Institute for Healthcare Studies, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
- 3Center for Management of Complex Chronic Care, Edward Hines Jr. Veterans Affairs Hospital, Hines, Illinois, USA
- 4Accreditation Council for Graduate Medical Education, Chicago, Illinois, USA
- 5Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
- 6Department of Pediatrics, Ann and Robert H Lurie Children's Hospital, Chicago, Illinois, USA
- Correspondence to Dr Megan McCarville, Department of Pediatrics, University of Illinois at Chicago, 840 South Wood Street, Room 1410, Chicago, IL 60612, USA;
- Received 28 September 2012
- Revised 18 March 2013
- Accepted 24 March 2013
- Published Online First 20 April 2013
Objective To assess the impact of measured versus reported environmental tobacco smoke (ETS) exposure on asthma severity and exacerbations in an urban paediatric population.
Design We analysed cross-sectional data from the Chicago Initiative to Raise Asthma Health Equity study that followed a cohort of 561 children aged 8–14 with physician-diagnosed asthma between 2003 and 2005. Participant sociodemographic data and asthma symptoms were gathered by parental survey; exposures to ETS were determined by salivary cotinine levels and parent report. Multivariable negative binomial and ordered logistic regressions were used to assess associations between ETS and asthma outcomes.
Results Among 466 children included in our analysis, 58% had moderate or severe persistent asthma; 32% had >2 exacerbations requiring a hospitalisation or an emergency room visit or same day care in the previous year. Half of caregivers reported that at least one household member smoked. In multivariable analyses, salivary cotinine was significantly associated with frequently reported exacerbations in the previous year (adjusted incidence rate ratio=1.39, 95% CI 1.09 to 1.79), but not significantly associated with asthma severity. Reported household smoking was not significantly associated with either asthma severity or frequency of exacerbations.
Conclusions Salivary cotinine was more predictive of asthma exacerbation frequency but caregiver- reported household smoking was not. Use of a nicotine biomarker may be important in both the clinical and research settings to accurately identify an important risk factor for asthma exacerbations.