Allergen exposure via the skin
- Allergen exposure and sensitisation through inflamed skin has been proven in a number of studies. There are several reports that demonstrate that primary sensitisation occurred through the skin, especially in food handlers (Saloga and Knop 2000).
- A 2003 study showed that exposure to peanut oil in creams used as emollients for the treatment of diaper rashes, eczema, dry skin, and inflammatory cutaneous conditions in infancy was the eliciting factor for a number of cases of peanut allergy in infants and young children (Lack et al 2003).
- There have been several similar reports of food allergy developing after exposure to a food allergen in topically applied creams and lotions. In 2016 researchers at Monash University in Melbourne, Australia reported a case of anaphylaxis to oat-containing food after cutaneous sensitization with skin products that contained oatmeal, used for the treatment of atopic dermatitis (Radhakrishna et al 2016). They confirmed this route of sensitisation by the immunological techniques of specific in vitro basophil activation, and inhibition serum IgE immunoblotting.
- Researchers at the same university used similar immunological tests to prove that exposure to goat’s milk through the skin in a moisturizer used to treat eczema caused subsequent anaphylaxis to goat’s cheese, even though the patient had eaten goat’s milk and cheese in the past with impunity (Voskamp et al 2014).
An excellent review of how allergic sensitisation occurs through the skin was published in the journal Children in September 2015 (Izadi et al 2015). The authors state that a damaged skin barrier may play a crucial role in the development of food sensitization and suggest that a better understanding of how patients initially become sensitised through routes other than the digestive tract may help lead to the development of better prevention strategies
New research confirms this route to sensitisation
A recent research study at Northwestern University in Chicago demonstrated that in genetically predisposed mice, exposure to food and environmental allergens through the skin led to the development of allergic markers such as inflammation, inflammatory mediators and anaphylactic reactions after the mice were fed the allergenic food (Walker et al 2018). Interestingly, mice of allergic mothers were more likely to develop reactions to lower sensitising doses of the allergenic food.
Following publication of this research, the idea that human babies could be similarly predisposed to be at risk of allergic sensitisation was suggested. An article in the popular press warned parents that using baby wipes could initiate food allergy by facilitating the passage of the food through the skin (Bodkin 2018).
Scratch and prick tests
It is ironic that the authors should suggest baby wipes as a means of facilitating the introduction of the allergenic food to the immune system, while ignoring the most obvious mechanism of intradermal exposure, namely scratch and prick tests commonly used in an effort to diagnose allergy to a specific food.
In such tests, allergen extracts are placed on the skin, which is scarified with a lancet or pricked with a needle, to ensure that the allergen encounters immune cells beneath the surface. In intradermal testing, the allergen is actually injected into the skin, thus ensuring an even greater exposure to the immune system.
All of these tests are incredibly efficient methods of delivering the allergen to the immune cells, which are more than ready to respond, with rapid development of food-specific IgE that, in predisposed children can, and will, lead to food allergy, and in severe cases, anaphylaxis – as demonstrated by the 2018 article mentioned above.
Many allergists will not skin test their atopic patients with highly allergenic foods, such as peanuts and nuts, because they are aware that antigen delivered via this route can trigger an anaphylactic reaction. It is only logical to assume that primary sensitisation can occur by this route. After all, vaccination using antigen delivered on skin patches is proving very effective (Partidos et al 2002).
Have allergies been caused by these diagnostic methods?
I often wonder how many innocent children and their unwitting families have been sentenced to a life-time of dealing with the miseries of allergies as a result of the tests so commonly used in diagnosis. I have actively discouraged my patients, especially atopic children, from having skin tests performed because of the risk of inducing IgE via this route. In good conscience I could never condone any action that might result, in an extreme case, in a life-threatening anaphylactic reaction. Even milder reactions can result in a life-time of misery. Until I see well-conducted scientific research that proves that there is no possibility of immunological sensitisation through this route, I shall continue to dissuade my patients from undergoing this method of allergy testing.
Alternative methods diagnostic procedures
There are alternative in vitro methods for detecting allergen-specific IgE; RAST, FAST and ELISA tests have the potential for providing information that in most cases is as useful as any skin test. The cost and need for laboratory facilities might limit their use for the present, but refinement of the technique should make them more economical and universally available in the near future. The newer techniques of component resolved diagnosis (CRD) which are currently being developed may prove to be a concise method for allergen identification in the future. Hopefully, awareness by clinicians of the potential for primary sensitisation to allergens through the skin will stimulate the speedy development of more specific in vitro tests, and discontinuance of the risky practice of skin testing in all its forms.
Blyth T, Lack G. Are we generating peanut allergy? Asthma J 2002;7:120-122
Bodkin, Henry. Baby wet wipes ’cause food allergy’, new study warns. Daily Telegraph April 7 2018
Izadi N, Luu M, Ong PY, Tam JS. The role of skin barrier in the pathogenesis of food allergy. Children 2015;2:382-402
Khakoo A, Lack G. Preventing food allergy. Current Allergy and Asthma Reports 2004 Jan;4(1):36-42
Lack G, Fox D, Northstone K, Golding J. Factors associated with the development of peanut allergy in childhood. New Eng J Med 2003;348:977-985
Matsuoko H, Maki N, Yoshida S, Arai M, Wang J, Oikawa Y, Ikeda T, Hirota
N, Nakagawa H, Ishii A. A mouse model of the atopic eczema/dermatitis syndrome by repeated application of a crude extract of house-dust mite Dermatophagoides farinae. Allergy 2003 Feb;58(2):139-145
Partidos CD, Beignon AS, Brown F, Kramer E, Briand JP, Muller S. Applying peptide antigens onto bare skin: induction of humoral and cellular immune responses and potential for vaccination. J Control Release 2002 Dec 13;85(1-3):27-34
Radhakrishna N, Prickett S, Phan T, Rolland JM, Puy R, O’Hehir RE. Anaphylaxis to oats after cutaneous sensitization by oatmeal in skin products used for the treatment of atopic dermatitis. J Allergy Clin Immunol Pract. 2016 Jan-Feb;4(1):152-3.
Saloga J, Knop J. Does sensitization through the skin occur? Allergy 2000;55:<905-909
Voskamp AL, Zubrinich CM, Abramovitch JB, Rolland JM, O’Hehir RE. Goat’s cheese anaphylaxis after cutaneous sensitization by moisturizer that contained goat’s milk. J Allergy Clin Immunol Pract 2014 Sep-Oct; 2(5):629-30
Walker M, Green J, Ferrie R, Queener A, Kaplan MH, Cook-Mills JM. Mechanism for initiation of food allergy: Dependence on skin barrier mutations and environmental allergen co-stimulation. J Allergy Clin Immunol 2018 Feb 15;[Epub ahead of print]
www.foodsmatter.com – April 2018