Most children with peanut allergy react the first time they eat peanut. This raises the possibility that sensitization may already have taken take place via some other route, such as through peanut contact with the skin or through inhalation of peanut proteins.
Various UK studies have supported this possibility and are summarized here.
The possible role of skin preparations
In 2003, researchers noted that peanut allergy commonly occurs in children who have suffered eczema and rashes in early infancy. They explored the hypothesis that applying preparations containing arachis oil (peanut oil) to the skin of infants with rashes was associated with an increased risk of developing peanut allergy. In eczema the skin barrier breaks down and there is an abundance of immune cells in the skin that could be exposed to substances that cause allergies.
Although the peanut oil present in skin preparations will have been refined, even refined oils are likely to contain minute amounts of protein. These may be hydrophobic proteins which stay bound to fat and which may be difficult to detect. The important point is that very low concentrations of protein may be more likely to sensitise than high levels.
Professor Gideon Lack, a leading doctor involved in the study, said at the time: “My own view is that infants with inflammatory conditions should not be prescribed creams or ointments containing peanut or nut oils. However, patients must not stop any medications for eczema without first consulting with their GP or specialist.”
The authors of the paper acknowledged there would be other factors, such as a family history of allergy, that contribute to the development of peanut allergy. They also suggested that exposure through the skin need not necessarily occur through skin preparations, but could occur through direct contact with peanut butter and other foods that contain peanut. Infants may be exposed to large amounts of peanut on their skin either directly when eating the food themselves, or indirectly when touched by their siblings or other children in nursery schools.
Reference: Lack G, Fox D, Northstone K, Golding J (2003). Factors Associated with the Development of Peanut Allergy in Childhood. New England Journal of Medicine 13 March 2003; 348(11): 977-985.
Exposure to peanut through the skin may prevent tolerance
The lining of the stomach and intestines is the usual site where the body first encounters food proteins and the normal result is a suppression of immune responses to the protein (known as tolerance), rather than allergy.
In 2005, UK research showed that in mice, if you apply oil containing peanut protein on the skin, you can interfere with the process whereby tolerance is induced when peanut is eaten. If this is true for humans, too, it would mean that actually eating peanuts at a young age might not be the problem in terms of inducing peanut allergy. The additional factor of skin exposure might be a crucial factor in the process of sensitisation, at least in some children.
Reference: Strid J, Hourihane J, Kimber I, Callard R, Strobel S (2005). Epicutaneous exposure to peanut protein prevents oral tolerance and enhances allergic sensitisation. Clin Exp Allergy 2005; 35:757-766.
The LEAP study (Learning Early About Peanut Allergy)
In December 2006 the LEAP study was launched in order to determine how to prevent peanut allergy in high-risk children (those with eczema and/or egg allergy). Children taking part in the study were randomly assigned by computer to follow one of two approaches.
- Children in one group follow a non-peanut diet.
- Children in the other group eat a peanut snack three times a week.
The London-based team is testing the hypothesis that peanut allergy will be prevented from occurring in children in the consumption group (those eating peanut), whilst allergy will be more likely to occur in the avoidance group. When the children are five they will be tested for peanut allergy. The study is due to end in 2014.
Results of the LEAP study were published early in 2015 in the New England Journal of Medicine and an “interim” guidance document was published to assist the clinical decision-making of healthcare providers, highlighting emerging evidence to existing guidelines regarding potential benefits of supporting early, rather than delayed, peanut introduction during the period of complementary food introduction in infants.
“Consensus Communication on Early Peanut Introduction and the Prevention of Peanut Allergy in High-Risk Infants” was published on behalf of American Academy of Asthma Allergy and Immunology, American Academy of Pediatrics, American College of Allergy, Asthma & Immunology, Australasian Society of Clinical Immunology and Allergy, Canadian Society of Allergy & Clinical Immunology, European Academy of Allergy and Clinical Immunology, the Israel Association of Allergy and Clinical Immunology, the Japanese Society for Allergology, Society for Pediatric Dermatology, and the World Allergy Organization.
A follow-up paper – “Effect of Avoidance on Peanut Allergy after Early Peanut Consumption” was published on 4th May 2016.
The “Persistence of Oral Tolerance to Peanut (LEAP-On)” study was a 12-month extension of the LEAP trial. Researchers investigated whether participants who had consumed peanut in the primary trial would remain protected against peanut allergy after cessation of peanut consumption for 12 months. The study design represented an opportunity to investigate the mechanisms of loss of protection from allergic responses, with potential implications for other food allergies and immune-mediated diseases.
The sudy concluded: “Among children at high risk for allergy in whom peanuts had been introduced in the first year of life and continued until 5 years of age, a 12-month period of peanut avoidance was not associated with an increase in the prevalence of peanut allergy. Longer-term effects are not known.”
Read the full study here.
Household peanut consumption
In 2009 it was shown that childhood peanut allergy appears to be more prevalent in homes of children with eczema where weekly peanut consumption is high among other family members.
Reference: Household peanut consumption as a risk factor for the development of peanut allergy. Adam T. Fox, Peter Sasieni, George du Toit, Huma Syed, Gideon Lack. J Allergy Clin Immunol 2009;123:417-23.
A further study published in 2010 added to the mounting evidence. Researchers set out to measure the amount of peanut protein that could be found in the home environment – including the infant’s bed and play-area – in households where there is high peanut consumption. They found that you can find measurable peanut protein in the environment where consumption is high.
Twenty families with infants were assessed. The main carer completed a retrospective food frequency questionnaire for household members over the previous six months. Dust samples were collected from bed-sheets of household members and infant play areas. Peanut level was quantified by an ELISA against whole peanut protein. The results showed that peanut levels in dust measured in the infant’s bed correlated moderately with the peanut consumption of the mother and the father.
The researchers involved in the above projects believe that children with eczema are those at risk. There is no suggestion that children without eczema, living in homes where peanut consumption is high, are at risk of developing peanut allergy.
Reference: Brough H, Penagos M, Stephens A, Turcanu V, Grieve A, Lack G (2010). Household peanut consumption over six months is positively correlated with measurable peanut protein in an infant’s home environment. Abstract from the EAACI 2010 meeting.
The filaggrin gene and risk factors for peanut allergy
In 2011, researchers showed that specific mutations in filaggrin (a protein involved in the skin barrier) increases the risk of sensitisation to peanut.
Reference: Brown SJ, Asai Y, Cordell HJ, Campbell LE, Zhao Y, Liao H, Northstone K, Henderson J, Alizadehfar R, Ben-Shoshan M, Morgan K, Roberts G, Masthoff LJ, Pasmans SG, van den Akker PC, Wijmenga C, Hourihane JO, Palmer CN, Lack G, Clarke A, Hull PR, Irvine AD, McLean WH (2011). Loss-of-function variants in the filaggrin gene are a significant risk factor for peanut allergy. J. Allergy Clin Immunol. 2011 Mar;127(3):661-7.