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The prevalence of peanut allergy in British children at school entry age in 2003

Project Code: T07035

31/05/2006

Allergy and Inflammation Sciences, University of Southampton.
Hourihane, J

Background

It is scientifically uncertain whether total avoidance of an allergen prevents or promotes sensitisation. Experiments with animal models suggest that high dose exposure can lead to tolerance (no adverse reaction to the food) and low dose exposure may lead to sensitisation - a potentially harmful outcome (Strobel, 2002). Clinical experience suggests that total avoidance of peanut is very difficult to achieve(Hourihane, 1997, Sicherer, 2001), so mere avoidance of obvious peanut may simply change exposure from “high” to “moderate or low” exposure. The UK prevalence of sensitisation to peanut more than doubled from 1.3% to 3.3% in 2 single centre birth cohorts born in 1989-90 and 1994-1996 (Tariq, 1996, Grundy 2002). The 1998 COT report advised peanut avoidance by infants and pregnant or lactating mothers, aimed at atopic families. This precautionary advice was issued due to uncertainty about the link between maternal peanut consumption and peanut allergy and it was considered unwise to discount possible sensitisation of offspring resulting from maternal exposure to allergen. It is not known what effect this advice may have had on the dietary habits of atopic and non-atopic mothers, or if its intended effect on the prevalence of peanut sensitisation in their offspring has been realised.

Rationale and objectives

Between 2003-2005 we studied children born between March 1999 (9 months after the COT report) and March 2000. The two basic aspects of the study - did mothers pay any attention to the COT report and did their behaviour affect the prevalence of peanut allergy in children - are key questions for the FSA trying to assess, retrospectively, the impact of the COT report and of any future strategies for affecting the dietary habits of nursing mothers.

Approach

Mothers were approached via schools and they and their child were recruited with written informed personal and parental consent. The mothers were asked in personal interviews about their own and their family’s allergic conditions, their recall of the COT advice and their own peanut consumption during pregnancy and breastfeeding Children were evaluated for maternal recall of their peanut consumption in infancy, current or resolved allergic conditions and for sensitisation to common food and aeroallergens. All children with positive screening skin prick tests (SPTs) to peanut were offered a formal double-blind, placebo-controlled food challenge with peanut to confirm the diagnosis.

Outcome / Key results obtained

The study was completed in August 2005. 1072 mother-child pairs were studied. 653 mothers (61%) recalled hearing the COT advice about peanut avoidance. Parental (mother and father) atopy rates did not affect this figure or the action taken on the advice. 376 (58%) mothers who recalled the advice changed their peanut intake while pregnant, but only 38 stopped eating all forms of peanut, which was the advice given. This figure represents 10% of those who changed their diet, 6% of those who recalled the advice and only 3.5% of the whole group. 328 (42%) mothers reduced their peanut consumption but did not eliminate peanut from their diet. The prevalence of peanut allergy known to parents before the study, on the basis of clinical assessments, that may or may not have included formal challenges was 9/1072 = 0.8%. 29 children were found to have a positive SPT to peanut. 1 child was considered to be peanut allergic but his parent refused SPT; he had known peanut allergy and high peanut antibody levels. 30 children with positive SPT or high peanut -specific IgE gives a prevalence of peanut sensitisation of 30/1072 = 2.8% (95%CIs 1.8-3.7).The prevalence of known sesame allergy was 1/1072 = 0.1%. Four other children had positive SPT to sesame without a history of reactivity. All 5 sesame-sensitised children (0.5%) had positive SPT to peanut and 4 were considered peanut allergic. 4/30 subjects with positive SPT declined the offer of a food challenge. 6 challenges were negative. 20/1068 subjects were considered to have peanut allergy (15 by challenge and 5 by strong positive recent history and supportive skin and blood tests), giving a prevalence of peanut allergy of 1.8% (95%CIs 1.1-2.7) in this cohort of school entry children born in 1999-2000. These data represents a real increase compared to the Isle of Wight cohort of children born in 1989, before the COT report, where the prevalence of peanut allergy was 0.6%. We did not demonstrate a significant difference in the prevalence of peanut allergy in this group from the 1994-1996 cohort in the Isle of Wight. 5 children (0.5%) were found to be sensitised to sesame, by SPT but only one child (0.1%) reported sesame allergy. All 5 sesame allergic children were also sensitised to peanut.

What it means and why it is important

A majority of mothers recalled hearing the COT advice when they were pregnant. Only 3.5% recalled having adhered to the advice, for reasons that are not clear. Parental allergy status did not appear to have been an important factor in any decision taken about peanut consumption while pregnant or breast feeding.

The prevalence of peanut allergy seems to have increased despite the publication of the COT report. Sesame allergy is unusual in the UK population and all cases of sesame sensitisation were in children who were allergic to peanut and had other allergic conditions.

The prevalence of peanut allergy is continuing to increase in the 21st century. Government advice has not had a significant impact on this trend and may have been assimilated by the general population, rather than acted upon by the target group identified as at highest risk of having children who would develop allergies.

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