Prenatal Exposure to Butylbenzyl Phthalate and Early Eczema in an Urban Cohort (original) (raw)
Related papers
Environmental associations with eczema in early life
Background Although atopic eczema (AE) is a common disease, little is known about its causes. Objectives To investigate the role of dietary and environmental factors associated with the development of AE by the age of 2 years. Methods A cohort of children was recruited before birth from a consecutive series of newly pregnant mothers presenting for antenatal care at three general practices in Ashford, Kent, U.K. Data up to the age of 2 years were available for 624 (97%) of the original cohort. AE was defined using components of the U.K. diagnostic criteria for AE, maternal report of doctor-diagnosed eczema and maternally reported eczema. Exposures of interest were family history of allergic disease, dietary and breastfeeding patterns, family size and exposure to indoor domestic allergens. Results The cumulative prevalence of AE using the U.K. diagnostic criteria was 14% (95% confidence interval, CI 11±17%). The prevalence of maternally reported doctor-diagnosed eczema was much higher (31%, 95% CI 27±35%) and almost half (45%) the mothers reported that their child had ever had eczema (95% CI 41±49%). The relationship between parental atopy, parental history of allergic disease and the child's eczema was consistently stronger for the mothers than the fathers. There was a marked increase in the prevalence of eczema with increasing maternal education and in less crowded homes, associations that remained significant after controlling for other factors. Conclusions The associations with environmental factors are consistent with the hypothesis that more crowded houses, increased family size and birth order, which may possibly increase early exposure to infections, may offer protection from subsequent development of eczema.
The temporal sequence of allergic sensitization and onset of infantile eczema
Clinical & Experimental Allergy, 2007
Eczema is commonly associated with sensitization in infants, but the causative role of sensitization in the development of eczema has been questioned. To determine if allergic sensitization increases the risk of developing eczema, or alternatively, if eczema increases the risk of developing allergic sensitization. We used data from the Melbourne Atopy Cohort Study, a prospective birth cohort of 552 infants with a family history of atopic disease. The main outcomes were risk of developing eczema from 6 months to 7 years of age in asymptomatic infants; and risk of developing sensitization, as measured by skin prick tests to milk, egg white, peanut, house dust mite, rye grass pollen and cat extracts, in previously unsensitized infants. Sensitization to food extracts at 6 months was associated with an increased risk of developing eczema [hazard ratio (HR) 1.63, 95% confidence interval 1.13-2.35] up to 7 years of age, after excluding infants with eczema in the first 6 months. However, eczema in the first 6 months was also associated with increased risk of new sensitization at both 1 year (HR 2.34, 1.38-3.98) and 2 years (HR 3.47, 1.65-7.32). In some infants, sensitization precedes and predicts the development of eczema, while in others eczema precedes and predicts the development of sensitization. This indicates that there are multiple pathways to atopic eczema.