Lack G, Fox D, Northstone K, Golding J. N Engl J Med. 2003;348:977–985
Purpose of the Study.
Because peanut allergy has increased in prevalence and is an important cause of life-threatening reactions, the authors sought to investigate possible determinants of peanut allergy.
Data were obtained from the Avon Longitudinal Study of Parents and Children. This geographically defined cohort included 13 971 preschool-aged children. Forty-nine of those children had a history of peanut allergy. Thirty-six of those 49 underwent skin testing, and 29 demonstrated positive results. Peanut allergy was confirmed for 23 children with double-blind, placebo-controlled, food challenge.
Pregnant women were enrolled and questioned about their allergy history before delivery and were given serial questionnaires throughout their children’s infancy and childhood. The authors prospectively identified 49 children with a history of reactions to peanuts. Twenty-three children were then confirmed as being allergic to peanuts with skin testing and double-blind, placebo-controlled, food challenge. There were 2 control groups, including children with eczema in the first 6 months of life whose mothers also had eczema and 140 children without peanut allergy who were randomly selected from the cohort. Cord blood samples stored at birth were retrieved and analyzed for peanut-specific and total immunoglobulin E (IgE) for the children with peanut allergy. Retrospective data on maternal consumption of peanuts during pregnancy and lactation, family history of peanut allergy, and the use of specific lotions and creams (the interviewer was not aware of which products contained peanut oil) were then obtained.
Peanut allergy was found to be independently associated with eczematous dermatitis (rash over joints and creases or oozing crusted rash) in the first 6 months of life, intake of soy products, family history of peanut allergy, and the use of skin preparations containing peanut oil. Neither maternal peanut consumption during pregnancy and lactation nor duration of breastfeeding was found to be associated with the development of peanut allergy. Additional evidence not supporting previous concepts of in utero sensitization came from undetectable peanut-specific IgE and normal total IgE levels in cord blood.
Sensitization to peanut antigens appeared to be through inflamed atopic skin, rather than via the gastrointestinal tract, possibly from the use of skin preparations with even trace amounts of peanut oil. With respect to the independent association between intake of soy products and peanut allergy, soy protein fractions have shown homology to major peanut proteins and cross-sensitization could result from exposure to a common T cell epitope.
With the increase in peanut allergy and other food allergies, elucidation of risk factors for prevention of sensitization offers new strategies to combat this food allergy epidemic. Allergic sensitization through the skin has also been proposed for the development of asthma and has been demonstrated in mouse models of atopic dermatitis. Additional studies are needed to determine whether topical peanut oil treatment is definitely a risk factor for peanut allergy; however, it seems prudent to avoid the topical use of peanut oil-containing products among children with atopic dermatitis. The finding of soy consumption being associated with peanut allergy may be attributable to the increased likelihood of food-allergic children receiving soy products, rather than a specific association with peanut allergy. Confirmation of this association is needed.