Original articleSystemic allergic disorderSeason of birth and food allergy in children
Introduction
Atopic diseases are a growing problem worldwide.1 Food allergy (FA), for example, currently affects 2% to 6% of children and 1% to 3% of adults,2, 3 and its prevalence seems to be rising based on epidemiologic studies in England, the United States, and Australia.4, 5, 6, 7 In general terms, atopic diseases are the consequence of maladaptive immune responses to environmental substances, such as pollens, fungal spores, dust mites, and foods. Some of the common pathologic features include an imbalance in the immune system with a TH2 bias and production of antigen specific IgE antibodies. Developmentally, the first signs of atopic disease are usually atopic dermatitis and FA, which present in early childhood and may persist for decades. There is growing evidence that programming of the atopic phenotype is affected in the antenatal, perinatal, and infant periods.8, 9 Nevertheless, and similar to other atopic conditions, a complete model of the risk factors and pathogenesis of FA remains elusive. Some risk factors for FA include genetic predisposition, atopic diathesis, and acidity of the gut.10, 11
In 2007, Camargo and colleagues12 proposed that vitamin D status might also affect risk of FA or anaphylaxis after observing a strong north-south gradient in EpiPen prescription rates in the United States. A similar finding has recently been confirmed in Australia,13 and a similar latitudinal gradient has been identified in hypoallergenic formula prescriptions in that country.14 Several lines of evidence link UV-B sunlight exposure or vitamin D status to atopic disorders.15, 16, 17, 18, 19 Because UV-B exposure and vitamin D status are strongly related to season at higher latitudes,20 with lowest levels of both observed during the late fall and winter seasons, we hypothesized that a higher percentage of Boston patients with FA would be born in the fall and winter seasons. To examine this novel hypothesis, we investigated whether (1) season of birth (SoB) might be associated with FA in a broad group of patients presenting to 3 Boston emergency departments (EDs) and (2) if such an association were identified, whether it would differ by age at presentation, suspected triggering food allergen, or the presence of comorbid allergic conditions.
Section snippets
Study Design
We created a cohort of patients by reviewing all cases of FA presenting to the EDs of Brigham and Women's Hospital (Boston) (adults), Children's Hospital Boston (children), and Massachusetts General Hospital (adults and children) between January 1, 2001, and December 31, 2006. Patients with FA were initially identified by screening hospital billing databases with International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM), codes indicative of food-related allergic
SoB Is Associated With FA in Children
We studied 1121 patient visits for documented food-related acute allergic reactions at the 3 Boston hospital EDs. Of these, 1002 were unique patients. The age range of the patients was 2 months to 94 years, with a median age of 15 years (interquartile range, 3-31 years). Half of the cohort was female, and 48% were white. Forty-seven percent of patients had a known allergy to the suspected offending allergen. Eighty-eight percent of patients arrived at the ED within 6 hours of exposure to a
Discussion
In an ED-based cohort of patients with FA in Boston, we found that birth in fall or winter was associated with FA in children younger than 5 years but not in older age groups. This rather simple but novel finding expands on the known risk factors associated with the development of FA. Previous studies have shown that a higher absolute latitude, in both the northern and southern hemispheres, is a risk factor for FA and anaphylaxis as measured by rates of epinephrine autoinjector prescriptions,12
Acknowledgments
Rose Xu (Knowledge Management Information Systems Department, Children's Hospital Boston), Stacey Duey and the Research Patient Data Registry group (Partners Health Care), and James K. West (Massachusetts Department of Public Health) for their help with the identification of cases and controls.
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Disclosures: Authors have nothing to disclose.
Funding Sources: Dr Vassallo was supported by T32 AI-60548 and Dr Rudders by T32 AI-007512 from the National Institutes of Health. Dr Camargo was supported, in part, by the Massachusetts General Hospital Center for D-receptor Activation Research.