Tobacco smoke exposure and allergic sensitization in children: A propensity score analysis

Abstract

Background and objective There is conflicting evidence of the effect of environmental tobacco smoke (ETS) on the development of allergic diseases in children. Studies have shown that this relationship differs depending on maternal history of the disease. We sought to employ the rigor of propensity score methods to assess this relationship using data from a birth cohort. Methods Using n=662 children from the Wayne County Health, Environment, Allergy and Asthma Longitudinal Study (WHEALS) we assessed the relationship between early life ETS and subsequent allergic sensitization via a positive skin prick test (SPT+) or at least 1 specific IgE ≥ 0.35 (sIgE+) in children aged 2–3 years. Propensity score estimation followed by full and nearest neighbor matching was compared to standard multivariable regression models. Results Among children without a maternal history of allergic disease ETS was positively associated with allergic sensitization in children with an adjusted odds ratio (aOR) for SPT+ of 2.32 (95% confidence interval (CI): 1.28–4.22) and the aOR for sIgE+ was 2.53 (95% CI: 1.43–4.48). Contrarily, for children with a positive maternal history the aOR for SPT+ and sIgE+ was 0.56 (95% CI: 0.24–1.32) and 0.43 (95% CI: 0.20–0.91), respectively. Conclusion Using propensity score methods to rigorously control for confounding factors we found that early life ETS exposure reduces the risk of allergic sensitization in children aged 2–3 years, but only in children with a positive maternal history. There is a strong association between early life ETS and the development of allergic sensitization for children without maternal history.

Environmental tobacco smoke exposure and risk of allergic sensitisation in children: a systematic review and meta-analysis

“…Our results are consistent with earlier observations from several large prospective cohorts and cross-sectional studies demonstrating higher risks of atopic asthma, eczema and rhinitis in children exposed to ETS,1 6 19 33 42 46 as well as with the latest reports confirming its detrimental effect on the incidence of asthma in children. 2 40 42 47 However, in this report we included only studies assessing the influence of ETS exposure on objective markers of allergic sensitisation, and not the studies assessing particular allergic disease (asthma, atopic eczema, hay fever, wheezing) as an outcome.…”

“…The four studies eligible for meta-analysis involved 6629 participants (2161 ETS-exposed and 4468 non-exposed) with moderate heterogeneity calculated at I 2 =54% (p=0.09) 5 6 21 33. The FE estimate demonstrated that ETS exposure increased the risk of allergic sensitisation (OR=1.12; 95% CI 1.00 to 1.25), and the effect was on the border of statistical significance (p=0.06).…”

“…Eight studies (9033 participants) 4 5 19 22 27 29 33 36 were eligible for dichotomous meta-analysis. In two other reports (4080 children) analysis was based on OR only, we therefore applied generic inverse variance analysis in order to estimate an overall effect.…”

Prevalence of allergic sensitization in the United States: Results from the National Health and Nutrition Examination Survey (NHANES) 2005-2006

“…43 The inverse association may either reflect selective avoidance of smoking or immuno-suppressive effects of tobacco smoke. 42, 44 Some studies report that those with asthma and allergies in childhood are less likely to initiate smoking than their healthy peers.…”

Janus-faced Acrolein prevents allergy but accelerates tumor growth by promoting immunoregulatory Foxp3+ cells: Mouse model for passive respiratory exposure

“…The rationale behind the study is the knowledge that tobacco smoking is an established risk factor for a large number of major diseases including cancer, but seemed to be protective against allergic sensitization, when allergy is not yet established1415161718. The inverse correlation of smoking to allergic sensitization and cancer risk is striking and suggests that smoking may be causative in the aberrant immune regulation of both diseases.…”