Background Secondhand smoke (SHS) exposures have been linked to asthma-related outcomes but quantitative dose–responses using biomarkers of exposure have not been widely reported.
Objectives Assess dose–response relationships between plasma cotinine-determined SHS exposure and asthma outcomes in minority children, a vulnerable population exposed to higher levels of SHS and under-represented in the literature.
Methods We performed analyses in 1172 Latino and African-American children with asthma from the mainland USA and Puerto Rico. We used logistic regression to assess relationships of cotinine levels ≥0.05 ng/mL with asthma exacerbations (defined as asthma-related hospitalisations, emergency room visits or oral steroid prescription) in the previous year and asthma control. The shape of dose–response relationships was assessed using a continuous exposure variable in generalised additive logistic models with penalised splines.
Results The OR for experiencing asthma exacerbations in the previous year for cotinine levels ≥0.05 ng/mL, compared with <0.05 ng/mL, was 1.40 (95% CI 1.03 to 1.89), while the OR for poor asthma control was 1.53 (95% CI 1.12 to 2.13). Analyses for dose–response relationships indicated increasing odds of asthma outcomes related with increasing exposure, even at cotinine levels associated with light SHS exposures.
Conclusions Exposure to SHS was associated with higher odds of asthma exacerbations and having poorly controlled asthma with an increasing dose–response even at low levels of exposure. Our results support the conclusion that there are no safe levels of SHS exposures.
- asthma epidemiology
- tobacco and the lung
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Contributors AMN was responsible for data analyses and manuscript preparation with input from SSO, MW, AM, NLB, JRB, EAE and EGB. DH and SH performed statistical analyses. CE, DS, LNB, EBB, HJF, KM, AD, PCA, SMT, WRC, JRRS, SS, MAL, LKW, RK and EGB participated in the design and coordination of the initial study. All coauthors contributed to interpretation of results, and provided revisions and approval of the final manuscript.
Funding This study was supported in part by the Sandler Family Foundation, the American Asthma Foundation, the RWJF Amos Medical Faculty Development Program, Harry Wm and Diana V Hind Distinguished Professor in Pharmaceutical Sciences II, the Tobacco-Related Disease Research Program under Award No 24RT-0025, a grant by the Flight Attendants Medical Research Institute (FAMRI), and the following institutes of the National Institutes of Health: National Heart Lung and Blood Institute (NHLBI) 1R01HL117004, R01Hl128439, R01HL135156, 1X01HL134589, R01HL118267; National Institute of Environmental Health Sciences (NIEHS) R01ES015794, R21ES24844, K99ES027511; the National Institute on Minority Health and Health Disparities (NIMHD) 1P60MD006902, U54MD009523, 1R01MD010443; and National Institute of Allergy and Infectious Diseases (NIAID) R01AI079139.
Competing interests None declared.
Patient consent Not required.
Ethics approval University of California, San Francisco.
Provenance and peer review Not commissioned; externally peer reviewed.
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