Maternal testosterone in pregnancy and atopic outcomes in

Evidence is accumulating to suggest that the prenatalenvironment plays an important role in the aetiology ofchildhood atopy and asthma. Maternal exposures inpregnancy, which have been implicated, include tobaccosmoke, antibiotics, paracetamol, infections and othercomplications, and nutrition (1–8). Cytokine productionby the fetoplacental unit is thought to provide a keymechanism by which the prenatal environment influencesmaturation of the fetal immune system and risk of atopyafter birth (9).The relation between maternal sex hormone levels inpregnancy and atopic outcomes in the offspring has beenlittle studied, although in vivo studies of adult mice haveshown that androgens can reduce allergy. In particular,castration promotes, and testosterone inhibits, produc-tion of antigen-specific immunoglobulin E (IgE) in males(10), and dehydroepiandrosterone (DHEA), the precur-sor of sex steroids and a weak androgen, lowers total IgElevels in males (11) and females (12). However, effects inadults may not be the same as those during criticalperiods of early development. Prenatal testosteroneexposure is known to have a powerful programminginfluence on physical, neural and behavioural sex differ-ences (13, 14), and could also influence sexual dimorph-ism in immune development (15, 16). In the case ofallergic immune responses, boys tend to have a higherprevalence of allergen sensitization and higher total IgElevels than girls (17, 18). We have explored whethermaternal blood testosterone level in pregnancy is negat-ively associated with allergy in the offspring.Methods