In June 1998 the Department of Health (DH) published recommendations aimed at halting the rising incidence of peanut allergy. This guidance was based on the conclusion that peanut sensitization occurring as a result or exposure in utero or via lactation was mechanistically possible.
Most presentations of peanut allergy occur on the first known contact the child has had with peanut. The route by which sensitisation occurs is unclear. The possibilities are that sensitization is occurring in utero, via breast milk or via indirect low dose environmental exposure. Much work has focused on maternal consumption of allergen (during pregnancy or lactation) yet interventional studies have failed to demonstrate any benefit of dietary elimination. Recent data is supportive of the possibility of sensitization through low dose cutaneous exposure as a result of the application of arachis oil containing creams to inflamed skin.
This study aims to quantify the exposure to environmental allergen during the allergic child's infancy. Environmental peanut exposure can occur through a variety of ways as well as the application of peanut-containing creams. Other important environmental components include the peanut consumption of all household members and the cutaneous contact and vapour inhalation that can result from this.
If sensitisation is occurring through environmental exposure, this has important implications for current DH guidance on peanut avoidance and future allergy prevention studies.
This is a retrospective questionnaire based study. Information on environmental exposure in the first year of life will be gathered and used for comparisons in children with peanut allergy, normal children and high-risk children (egg allergic) who do not have peanut allergy. It is anticipated that information on 150 individuals will be obtained from the questionnaire.
In June 1998 the Department of Health (DH) published recommendations aimed at those infants considered to be at high risk of developing peanut allergy, advising that mothers of these infants may wish to avoid peanuts during pregnancy and whilst breastfeeding, and to delay introduction of peanuts into the infants diet until three years of age. This guidance was based on the conclusions of the Committee on Toxicity (COT) in 1998, after a review of all the available scientific evidence on peanut allergy, which found that allergic sensitisation to peanut, occurring as a result of exposure in the uterus during pregnancy or via breastfeeding, was mechanistically possible.
Most presentations of peanut allergy occur on the first known occasion of peanut consumption by the child. This has raised questions about the route by which sensitisation to peanut (the precursor to allergy), occurs. There are a number of possible routes of sensitisation, including via the placenta in the uterus, via breast milk during breastfeeding or via indirect exposure to low doses of peanut protein through environmental exposure (for example as a result of others in the household consuming peanuts and then transfer of low levels of allergen to the child through the skin or via inhalation of peanut dust). Much previous research has focussed on maternal consumption of allergen (during pregnancy or breastfeeding) as a route of exposure, yet interventional studies have failed to demonstrate any benefit of dietary elimination. Previous data (see Agency funded projects T07001 [create link to T07001 page] and T07022 [create link to T07022 page], have given rise to the hypothesis that low dose exposure to food allergens via the skin may result in sensitisation.
This study aimed to quantify the environmental exposure to peanut allergen during the allergic child’s infancy and to determine whether this might have an influence on the development of peanut sensitisation and peanut allergy in young children.
The researchers adopted a retrospective, case-controlled, observational cohort approach to investigate low dose environmental exposure to peanut as a possible route of allergic sensitisation and the development of peanut allergy in young children. A validated questionnaire was developed and used to retrospectively quantify the individual child’s dietary consumption of peanut during their first year of life, as well as the total household weekly consumption of peanut by all family members (environmental exposure). Other relevant information, such as maternal consumption of peanut during pregnancy, and whether peanut containing creams were used, was also collected. The questionnaire was applied to families before their child’s peanut allergy had been diagnosed to avoid recall bias.
Results were collected on 133 children with peanut allergy, 150 children with no food allergies (controls) and 160 children with egg allergy (but not sensitive to peanut). Egg allergic children were included in the study as they are considered at high risk (30-50%) of developing peanut allergy, therefore studying those egg allergic children who did not develop peanut allergy may provide clues as to what factors prevented them from becoming peanut allergic.
Median household peanut consumption during the first year of the child’s life was found to be significantly higher in peanut allergic children (77.2g/week) compared with the non-allergic controls (29.1g/week) and the egg-allergic (but not peanut allergic) children (8.1g/week). This relationship was found to be independent of the child’s own level of consumption of peanut. These results suggest that higher environmental exposure to peanuts during early life in the families of those children who went on to develop peanut allergy, may have promoted the development of peanut allergy. Further, the even greater differences seen between the level of household consumption in peanut allergics compared with egg-allergics, suggests that the very low levels of household peanut consumption in the egg-allergic families, protected these high-risk children from becoming allergic to peanut. The results have also suggested that the form that the peanut was consumed in by household members is important in terms of risk, with the consumption of peanut butter associated with a greater risk of peanut allergy than consumption of other types of peanut containing food.
The researchers hypothesise that environmental exposure to peanuts through the skin or via inhalation, might be a significant factor in the development of sensitisation, as distinct from maternal or infant consumption of peanut. Their findings also raise the question that early oral exposure may play an important role in the development of tolerance to peanut.
- Fox, A. T., Sasieni, P., du Toit, G., Syed, H. and Lack, G. (2009). Household peanut consumption as a risk factor for the development of peanut allergy. Journal of Allergy and Clinical Immunology. 123: 417-423.