Atopic dermatitis increases the effect of exposure to peanut antigen in dust on peanut sensitization and likely peanut allergy

Helen A Brough, Andrew H Liu, Scott Sicherer, Kerry Makinson, Abdel Douiri, Sara J Brown, Alick C Stephens, W H Irwin McLean, Victor Turcanu, Robert A Wood, Stacie M Jones, Wesley Burks, Peter Dawson, Donald Stablein, Hugh Sampson, Gideon Lack, Helen A Brough, Andrew H Liu, Scott Sicherer, Kerry Makinson, Abdel Douiri, Sara J Brown, Alick C Stephens, W H Irwin McLean, Victor Turcanu, Robert A Wood, Stacie M Jones, Wesley Burks, Peter Dawson, Donald Stablein, Hugh Sampson, Gideon Lack

Abstract

Background: History and severity of atopic dermatitis (AD) are risk factors for peanut allergy. Recent evidence suggests that children can become sensitized to food allergens through an impaired skin barrier. Household peanut consumption, which correlates strongly with peanut protein levels in household dust, is a risk factor for peanut allergy.

Objective: We sought to assess whether environmental peanut exposure (EPE) is a risk for peanut sensitization and allergy and whether markers of an impaired skin barrier modify this risk.

Methods: Peanut protein in household dust (in micrograms per gram) was assessed in highly atopic children (age, 3-15 months) recruited to the Consortium of Food Allergy Research Observational Study. History and severity of AD, peanut sensitization, and likely allergy (peanut-specific IgE, ≥5 kUA/mL) were assessed at recruitment into the Consortium of Food Allergy Research study.

Results: There was an exposure-response relationship between peanut protein levels in household dust and peanut skin prick test (SPT) sensitization and likely allergy. In the final multivariate model an increase in 4 log2 EPE units increased the odds of peanut SPT sensitization (1.71-fold; 95% CI, 1.13- to 2.59-fold; P = .01) and likely peanut allergy (PA; 2.10-fold; 95% CI, 1.20- to 3.67-fold; P < .01). The effect of EPE on peanut SPT sensitization was augmented in children with a history of AD (OR, 1.97; 95% CI, 1.26-3.09; P < .01) and augmented even further in children with a history of severe AD (OR, 2.41; 95% CI, 1.30-4.47; P < .01); the effect of EPE on PA was also augmented in children with a history of AD (OR, 2.34; 95% CI, 1.31-4.18; P < .01).

Conclusion: Exposure to peanut antigen in dust through an impaired skin barrier in atopically inflamed skin is a plausible route for peanut SPT sensitization and PA.

Keywords: Atopic dermatitis; dust; environmental peanut exposure; peanut allergy; peanut sensitization.

Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.

Figures

Fig E1
Fig E1
A, Multivariate stratified predictive probability for the effect of EPE (displayed in log2 [microgram per gram] units and untransformed [microgram per gram] units) for peanut SPT sensitization in all children, children with a history of AD, and children with a history of severe AD. Results are adjusted for egg SPT wheal diameter, hay fever, maternal peanut consumption during pregnancy, and breast-feeding. B, Multivariate stratified predictive probability for the effect of EPE (displayed in log2 [microgram per gram] units and untransformed [microgram per gram] units) for peanut SPT sensitization in all children, children with a history of AD, and children with a history of severe AD. Results are adjusted for egg and milk wheal diameter and ethnicity.
Fig E2
Fig E2
Scatter plot of peanut protein concentration in bed versus living room dust. The Spearman tank correlation coefficient (rs) was 0.521 (P < .001).
Fig 1
Fig 1
A, Univariate stratified predictive probability for the effect of EPE (displayed in log2 [microgram per gram] units and untransformed [microgram per gram] units) for peanut SPT sensitization in all children, children with a history of AD, and children with a history of severe AD. B, Univariate stratified predictive probability for the effect of EPE (displayed in log2 [microgram per gram] units and untransformed [microgram per gram] units) for likely PA in all children, children with a history of AD, and children with a history of severe AD.

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