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British Society for Investigative Dermatology Annual Meeting 2017, Hilton Deansgate Hotel, Manchester, 3–5 April 2017, British Journal of Dermatology, Volume 176, Issue 4, 1 April 2017, Pages e40–e81, https://doi.org/10.1111/bjd.15392
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Domestic hard water exposure in infancy and subsequent risk of childhood atopic eczema
Z. Jabbar‐Lopez,1 M.M.R. Perkin,2 K. Logan,3 T. Marrs,3 J. Craven,3 D.T. Greenblatt,1 D. Strachan,2 G. Lack,3 J.L. Peacock4 and C. Flohr1
1Unit for Population‐Based Dermatology Research, St John's Institute of Dermatology, King's College London, London, U.K.2Population Health Research Institute, St George's, University of London, London, U.K.3Children's Allergies Department, Division of Asthma, Allergy and Lung Biology, King's College London, London, U.K.4Division of Health and Social Care Research, King's College London, London, U.K.
Several ecological studies have identified an association between water hardness and atopic eczema. More recently, we conducted a cross‐sectional analysis as part of the Enquiring About Tolerance (EAT) study, which identified a 61–87% increased odds of atopic eczema at 3 months of age in infants exposed to hard (> 255 mg L−1 CaCO3) water compared with soft (≤ 255 mg L−1 CaCO3) water, depending on the level of chlorine coexposure (Perkin MR, Craven J, Logan K et al. Association between domestic water hardness, chlorine, and atopic dermatitis risk in early life: a population‐based cross‐sectional study. J Allergy Clin Immunol 2016; 138: 509–16.). We consequently performed a longitudinal analysis in the EAT cohort to examine whether water hardness was also associated with an increase in atopic eczema risk after 3 months of age. All children in the EAT study aged 3–36 months without visible eczema at 3 months were selected from a cohort of 1303 children participating in the EAT study. Water hardness exposure was defined as domestic water CaCO3 concentration supplied to the child's main residence. The primary outcome was the development of ‘any eczema’, a composite of visible eczema or parent‐reported eczema, between 3 and 36 months of age. A multiple logistic regression model was fitted with adjustment for key confounders including filaggrin (FLG) gene mutation status, ethnicity, home location (urban vs. rural) and the presence of a domestic water softener. Of the 947 of 1303 (73%) infants included in the analysis, 472 (50%) developed eczema by 36 months. There was no statistically significant association between exposure to harder vs. softer water, crude odds ratio (OR) 0.86 [95% confidence interval (CI) 0.67–1.11], and after adjustment for multiple confounders, OR 0.92 (95% CI 0.68–1.26). We also did not find any association between atopic eczema risk and domestic water chlorine exposure. FLG genotype did not appreciably alter these risk estimates. While living in a hard water area is associated with an increased risk of developing atopic eczema during the first 3 months of life, we did not find an association with atopic eczema development beyond this time point. This suggests that the first 3 months of life are critical in determining the risk of atopic eczema with hard water exposure in susceptible individuals. We are now conducting an intervention study with a water softening device installed around the time of birth to test further the effect of water hardness on skin barrier function and atopic eczema risk in early life.
