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The influence of dose and route of exposure on the early life origins of peanut allergy

Project Code: T07028

31/03/2004

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

1. Background

In June 1998, The Committee on Toxicity of Chemicals and Foods, Consumer Products and the Environment (COT) published a report on peanut allergy. This recommended that pregnant and lactating women who were atopic or had a first degree relative with atopy should avoid eating peanut and peanut products. Further, it was recommended that the infants themselves should not be exposed to these products until three years of age. However, there was no controlled intervention study to provide the evidence to support the advice. In fact, at the time, other forms of allergen avoidance had variable outcomes. However, the expert view was that it was reasonable to recommend early life avoidance based on the state of knowledge of the relationship between allergen exposure and sensitization, at that time.

2. Aims, Objectives and Approach

The aim of project T07028 was to investigate the effects of avoiding and/ or eating peanuts during pregnancy and lactation on the subsequent development of peanut allergy in children. More specifically, the objectives of the project were to:

1. Establish retrospectively, whether avoidance of peanut and peanut products during pregnancy and lactation did or did not effect the subsequent development of peanut allergy in children.

2. Establish the doses and routes of exposure to peanut proteins.

3. Establish whether any characteristic of the mother’s and newborn’s immune response to peanut proteins was associated with the development of peanut allergy.

During the course of a previous FSA funded project (T07005) investigating the effects of egg avoidance during pregnancy and lactation on the development of atopy, detailed dietary records were kept by women recruited either with atopy themselves or a first degree relative with atopy. Using the diet diaries from 227 of these women (completed at 17, 23 and 31 weeks of pregnancy) the frequency and dose of peanut exposure during pregnancy and lactation was estimated. Peanut avoidance advice had been given prior to recruitment by midwives and/or health visitors and by the study dietician at recruitment, in line with the COT advice. A questionnaire detailing peanut consumption over pregnancy was administered retrospectively to 165 of these women. Blood samples were taken from the mothers at recruitment and throughout pregnancy until birth and from the children at birth, 6, 12 and 18 months of age. Levels of peanutspecific IgG and IgE were measured in these blood samples and in any breast milk samples available. Levels of peanut allergen in the breast milk samples were also measured. Finally, at 3, 6, 12 and 18 months of age the children were medically assessed for symptoms of peanut allergy and atopy in general.

3. Key Findings

From the diet diary analysis (n=227), 32.3% of women ate peanut during pregnancy. 41 women ate peanut before recruitment, 33 of these (80.5%) did not eat it again after receiving dietetic advice. However, 33 women who had not eaten peanut prior to recruitment ate it at some point before delivery. From questionnaire analysis, 73% of women reported actively avoiding peanut during pregnancy but 28% of these were found to have eaten peanuts/peanut-containing foods upon diary analysis. No consistent relationship was found between estimated peanut intake over pregnancy and the development of peanut allergy in children at 6, 12 and 18 months.

Peanut was detected in 36% of the 72 breast milk samples collected at 3 months after delivery, but the concentration was not related to the development of peanut allergy in the children during the first 18 months of life.

The levels of peanut-specific IgG and IgE in the mothers blood and breast milk, measured over pregnancy and during breast feeding was not related to the development of peanut allergy in children at 6, 12 and 18 months. The same lack of association was apparent from the levels of peanut-specific IgG in the blood taken from the umbilical cord. In addition, levels of these antibodies did not correlate with the estimated levels of peanut intake over pregnancy or levels of peanut antigen detected in the breast milk samples.

Seven children were skin prick test positive (wheal 3mm or greater) for peanut at 6 months (total number skin prick tested at 6 months = 193), nine at 12 months (total number skin prick tested at 12 months = 179) and ten at 18 months (total number skin prick tested at 18 months = 181). Three children were positive at all time points, one was positive at both 6 and 12 months, but had resolved at 18 months and one was positive at both 12 and 18 months. One child had measurable peanut-specific IgE at 6, 12 and 18 months. In addition, another child had measurable peanut-specific IgE at 6 months, a further 5 children had measurable peanut-specific IgE at 12 months and another 2 children at 18 months. It was notable that the child with measurable peanut-specific IgE at all three time points, was also skin prick test positive to peanut at each time and had the highest measurable levels of peanut-specific IgG. A positive association was found between the levels of peanut-specific IgG in the children and a positive skin prick test to peanut at 6, 12 and 18 months (a higher peanut-specific IgG concentration was associated with a positive skin prick test).

4. Interpretation

The dietary analysis has shown that despite being given advice on avoiding peanut by a committed dietician, many pregnant women found this impossible to do. As the COT advice is not reinforced by input from a dietitian, it is highly probable that the advice will have had even less impact than was apparent from our very detailed investigation. Thus it is unlikely that the recommendations will have had any impact on the prevalence of peanut sensitisation or allergy.

The fact that we found no relationship between maternal peanut intake and subsequent sensitisation to peanut or allergy over the first 18 months of life, also suggests that advice to reduce intake will not have any impact on outcomes. However, there is a need for longer term follow-up and the statistical power of the study will not be particularly high as it is anticipated that only 5-7% of infants born to atopic families, as in this study, will develop peanut allergy. Furthermore, the quantities of peanut being ingested by mothers during pregnancy and lactation were relatively low. Thus we could not exclude the possibility that very high exposure could be protective.

The lack of association between levels of peanut specific IgG and IgE in the mother's blood over pregnancy and the breast milk during breast feeding, and the subsequent outcomes in the child or indeed the peanut intake of the mother over pregnancy, also suggest that modifying intakes will not have any impact on outcomes. We believe that this lack of association is because of the relatively low intakes of peanut, thus not giving a wide enough range of results to see an effect. It is possible that an exceedingly low exposure to peanut allergen will be enough to induce sensitisation. The test we employed to detect peanut allergen was more sensitive than any previously employed in published studies but was still not sensitive enough to investigate all potential routes of exposure such as that swallowed by the fetus in amniotic fluid.

A study designed ab initio, to focus on peanut intake during pregnancy and lactation and exposure of the infant during early life using sensitive and specific tests and followed at least to mid-childhood, may be the only way to finally establish whether avoidance recommendations during pregnancy and lactation are appropriate.

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