Association of maternal diabetes and child asthma

Pediatr Pulmonol. 2013 Jun;48(6):545-52. doi: 10.1002/ppul.22668. Epub 2012 Sep 4.

Abstract

Background: Perinatal programming is an emerging theory for the fetal origins of chronic disease. Maternal asthma and environmental tobacco smoke (ETS) are two of the best-known triggers for the perinatal programming of asthma, while the potential role of maternal diabetes has not been widely studied.

Objective: To determine if maternal diabetes is associated with child asthma, and if so, whether it modifies the effects of ETS exposure and maternal asthma.

Methods: We studied 3,574 Canadian children, aged 7-8 years, enrolled in a population-based birth cohort. Standardized questionnaires were completed by the children's parents, and data were analyzed by multivariable logistic regression.

Results: Asthma was reported in 442 children (12.4%). Compared to those without asthma, asthmatic children were more likely to have mothers (P = 0.003), but not fathers (P = 0.89), with diabetes. Among children without maternal history of diabetes, the likelihood of child asthma was 1.4-fold higher in those exposed to ETS (adjusted odds ratio, 1.40; 95% confidence interval, 1.13-1.73), and 3.6-fold higher in those with maternal asthma (3.59; 2.71-4.76). Among children born to diabetic mothers, these risks were amplified to 5.7-fold (5.68; 1.18-27.37) and 11.3-fold (11.30; 2.26-56.38), respectively. In the absence of maternal asthma or ETS, maternal diabetes was not associated with child asthma (0.65, 0.16-2.56).

Conclusion: Our findings suggest that maternal diabetes may contribute to the perinatal programming of child asthma by amplifying the detrimental effects of ETS exposure and maternal asthma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Asthma / etiology*
  • Child
  • Cross-Sectional Studies
  • Diabetes Mellitus
  • Female
  • Health Surveys
  • Humans
  • Logistic Models
  • Male
  • Multivariate Analysis
  • Pregnancy
  • Pregnancy in Diabetics*
  • Prenatal Exposure Delayed Effects / etiology*
  • Risk Factors
  • Self Report
  • Tobacco Smoke Pollution / adverse effects*

Substances

  • Tobacco Smoke Pollution