Kate Johnson

March 22, 2012

March 22, 2012 (Orlando, Florida) — The risk for infant atopic eczema and dermatitis posed by maternal smoking is highest in the third trimester of pregnancy, according to a poster presented here at the American Academy of Allergy, Asthma and Immunology 2012 Annual Meeting.

"Our results indicate that maternal environmental tobacco smoke exposure impairs the immune response of the fetus, which facilitates the development of AEDS [atopic eczema/dermatitis syndrome]," note Miwa Shinohara, MD, PhD, a pediatric allergist from Kochi University in Japan, and colleagues.

"The mechanism is unclear, but we think it is antioxidant stress," Dr. Shinohara told Medscape Medical News. "Most previous studies have investigated the systemic immune effect, but we recently found a direct impact in the skin using a skin prick test," she said.

The study involved 1177 infant–mother pairs. Mean infant age was 12 months and mean maternal age was 31 years. Slightly more infants were female (n = 629) than male (n = 548).

A self-report questionnaire was used to determine family history of allergic diseases, number of older siblings, prenatal and postnatal maternal tobacco smoke exposure, and physician-diagnosed AEDS.

The study found an overall cumulative incidence of AEDS of 37.2% (385 of 1177 infants). However, when exposure to environmental tobacco smoke was examined, infants exposed at between 28 weeks of gestation and birth had a 6-fold increased likelihood of AEDS, compared with those exposed earlier in the pregnancy or after birth.

Specifically, the adjusted odds ratio (AOR) for AEDS for infants exposed before 28 of weeks gestation was 0.214; for infants exposed after 28 weeks, AOR was 6.146.

The odds of developing AEDS was similar for infants exposed during the first 6 months of birth and those exposed after that time (AOR, 1.013 vs 1.022).

Smoke exposure was believed to directly damage the airways in the lungs; however recently, researchers linked smoke exposure to higher rates of respiratory infections, suggesting an immune component, explained Dr. Shinohara.

The findings from this study linking prenatal smoke exposure to infant skin problems support this mechanism, she said.

When asked to comment on the study, Robert J. Boyle, MB ChB, PhD, clinical senior lecturer in pediatric allergy at Imperial College in London, United Kingdom, said that "this interesting study suggests that the developing fetus may have a specific vulnerability to the toxic effects of tobacco smoke during late pregnancy in relation to skin and/or immune development."

"It would be important to confirm the findings in a prospective cohort study, but they may have important implications for our understanding of eczema pathogenesis."

The study was funded in part by grants from the Foundation for Life Charitable Trust of the Kochi Shinbun and Kochi Broadcasting, and a grant from Child Health and Development and the Ministry of Health, Labor and Welfare of Japan. Dr. Shinohara has disclosed no relevant financial relationships. Dr. Boyle reports receiving research support from Danone, Lincoln Medical, Airsonett, and Allergy Therapeutics; and receiving speakers honoraria/travel grants from Meda Pharmaceuticals, Nutricia, SHS, Danone, and GlaxoSmithKline.

American Academy of Allergy, Asthma and Immunology (AAAAI) 2012 Annual Meeting: Abstract 153. Presented March 3, 2012.


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