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Household peanut consumption as a risk factor for the development of peanut allergy
Adam T Fox1, Peter Sasieni, George du Toit
1King's College London, the Medical Research Council and Asthma UK Centre in Allergic Mechanisms of Asthma, Division of Asthma, Allergy and Lung Biology, Guy's and St Thomas' National Health Service Foundation Trust, London, United Kingdom.
Insights
Environmental exposure to peanut during infancy promotes sensitization, while low levels may be protective for atopic children. Maternal consumption during pregnancy or lactation showed no effect on peanut allergy development.
Area of Science:
- Allergy and immunology
- Pediatric allergy
- Environmental health
Background:
- Most children with peanut allergy (PA) react upon first oral exposure.
- Emerging data suggest cutaneous exposure as a potential route for sensitization.
Purpose of the Study:
- To determine the primary route of peanut exposure in the development of peanut allergy.
- To investigate the influence of environmental and maternal peanut consumption on allergy development.
Main Methods:
- Administered questionnaires to children with PA, high-risk controls (egg allergy), and non-allergic controls.
- Collected data on maternal peanut intake (pregnancy, breastfeeding, first year) and household environmental exposure.
- Quantified household peanut exposure to assess non-oral routes.
Main Results:
- Significantly higher median weekly household peanut exposure in PA cases compared to controls.
- No difference in infant peanut consumption between groups.
- A dose-response relationship between environmental peanut exposure and PA development, particularly with peanut butter; early oral exposure in highly exposed infants may be protective.
Conclusions:
- High environmental peanut exposure in infancy appears to promote sensitization.
- Low environmental exposure may offer protection in atopic children.
- Maternal peanut consumption during pregnancy/lactation had no observed effect, supporting environmental exposure as the primary sensitization route.
Background:
Most children with peanut allergy (PA) react on first known oral exposure to peanut. Recent data suggest cutaneous exposure as a route of sensitization.
Objectives:
This study aimed to establish the relevant route of peanut exposure in the development of allergy.
Methods:
Questionnaires were administered to children with PA and to high-risk controls (with egg allergy) and controls without allergy. Questionnaires were completed before subjects were aware of their PA status, avoiding recall bias. Questionnaires recorded maternal peanut consumption during pregnancy, breast-feeding, and the first year of life. Peanut consumption was determined among all household members, allowing quantification of environmental household exposure (household peanut).
Results:
Median weekly household peanut in the 133 PA cases was significantly elevated (18.8 g) compared with 150 controls without allergy (6.9 g) and 160 high-risk controls (1.9 g). There were no differences in infant peanut consumption between groups. Differences in maternal peanut consumption during pregnancy (and lactation) were significant but become nonsignificant after adjusting for household peanut. A dose-response relationship was observed between environmental (nonoral) peanut exposure and the development of PA, which was strongest for peanut butter. Early oral exposure to peanut in infants with high environmental peanut exposure may have had a protective effect against the development of PA.
Conclusions:
High levels of environmental exposure to peanut during infancy appear to promote sensitization, whereas low levels may be protective in atopic children. No effect of maternal peanut consumption during pregnancy or lactation is observed, supporting the hypothesis that peanut sensitization occurs as a result of environmental exposure.