The increase in the incidence of allergic diseases began in the 1970s, first affecting respiratory allergies and then food allergies. The rapidity of this increase suggests that it cannot be explained solely by genetic background. This “epidemic” is contemporary with major environmental, industrial or agri-food changes and significant urbanization, which have also modified lifestyles.
Examples include the introduction of detergents into household cleaners or the consumption of increasingly processed foods with the addition of additives. Currently, there are on average more than 350,000 authorized chemicals in our environment.
The coincidence between the increase in the prevalence of allergies and these environmental changes has given rise to different hypotheses, which have also evolved over time, ranging from the hygienist hypothesis in 1989 to the “old friends theory”, then, around 2010, the biodiversity hypothesis. Finally, more recently the theory of epithelial barriers appeared, which suggests that exposure to environmental toxicants can alter epithelial barriers and the microbiota, which, in fineleads to inappropriate immune responses.
Epithelial barriers, places of dialogue
Epithelial barriers provide protection against physical, chemical or biological attacks while allowing a certain number of exchanges with the external environment, such as: absorption of nutrients in the intestine, gas exchanges in the lungs and evaporation and thermal regulation at the skin level.
Three epithelial barriers have been particularly studied: the skin, that of the gastrointestinal tract and that of the respiratory tract. What they all have in common is the presence of adjacent epithelial cells, linked together by complex junctions which control paracellular passages. Depending on the location and specific functions, different cell types make up the epithelial barrier:
- the structure of the skin barrier has a high level of stratification and a lipid matrix,
- at the level of the digestive tractthe epithelial barrier comprises a single layer of cells of different types (enterocytes, secretory cells, neuroendocrine cells, etc.) bathed in mucus, and having a large absorption surface,
- at the level respiratorythe structure of the epithelial barrier is of an intermediate type, also including different cell types.
Rather than a barrier, Karine Adel-Patient believes that we could speak of a “close dialogue” between a layer of epithelial cells, a microbiota and an immune system (1). This interaction makes it possible to establish and maintain homeostasis at the barrier level, guaranteeing an adapted immune response following stress.
Repeated environmental exposures cause chronic inflammation
The current hypothesis would be that these different homeostasis factors would be activated inappropriately by so-called harmful environmental exposures, which will alter epithelial barriers by destroying tight junctions. These release pro-inflammatory cytokines which activate the underlying immune systems. The alteration of the epithelium can also induce an imbalance in the microbiota and the immune system, and, again, produce inflammation which will be chronic if exposure continues. This is what is suspected in chronic “non-communicable”, degenerative or autoimmune diseases and allergies.
These harmful environmental exposures can be, for example, detergents and household products on the skin, or pesticides. At the pulmonary level, this concerns environmental and domestic pollution (aerosols, insecticides). In terms of the intestinal tract, this concerns the “modern” diet, rich in pro-inflammatory factors, ultra-processed products, nano-plastics, etc.
Accumulating evidence of transcutaneous allergen sensitization
At the skin level, different elements can alter the epithelial barrier, allowing allergens to cross the barrier. They are then taken up by cells of the immune system, which activate the immune response and the release of chemical mediators of inflammation.
The risk of sensitization to food allergens through the transcutaneous route is illustrated by a study carried out in 2003, which showed a link between the presence of allergens in dermatological preparations used for infants and peanut allergy. In this study, the risk of peanut allergy was almost 7 times higher in preschool children using skin creams containing peanut oil, compared to children who did not use them. (2).
A prospective study then shows that atopic dermatitis (AD) is a significant risk factor for IgE-mediated allergy: 50% of infants with AD before the age of 3 months will have a food allergy. at the age of 12 months, their risk of asthma increases by 3 at 18 years, and that of hay fever increases by 2.4 at 18 years (3). Then arises the hypothesis of dual exposure to allergens, according to which skin exposure favors allergy, while oral exposure favors the acquisition of tolerance.
A meta-analysis published in 2015 confirms a strong association between AD, food sensitization and food allergy, particularly in cases of severe form of AD. In the vast majority of cases, this precedes the development of food sensitization and allergy, confirming a probable causal relationship (4).
Thus, in recent years, evidence has been accumulating of sensitization by early exposure to the allergen through the skin and of a protective effect (tolerance) of oral exposure.
Frequent application of emollients would promote oral tolerance in populations at risk…
Several recent studies show that AD is the primary risk factor for food allergy. One of these studies shows that, in a cohort of infants aged 4 to 11 months, the main risk factors for peanut allergy are age and severity of AD, with family history having no influence. only very low risk (5).
Analysis of data from several large studies devoted to allergy prevention also shows that severe AD has an impact on the effectiveness of the acquisition of oral tolerance to peanut, by delaying this acquisition. This impact increases in parallel with the severity of eczema (6).
Over the course of studies, it appears that “delaying the onset of AD facilitates the early introduction of food allergens”. This data is confirmed by a meta-analysis which shows that the early prophylactic application of emollients can help prevent the occurrence of a food allergy, particularly in high-risk populations and provided that the emollient is applied daily.
The hypothesis is that these applications delay the onset of AD, facilitating the acquisition of tolerance through the digestive tract (7). The STOP-AD study confirms this point in high-risk populations and concludes that early application of a suitable emollient, up to the age of 2 months, reduces the incidence of AD by almost 50% during of the first year in high-risk children, without an increase in the risk of skin infections (8).
…but this does not seem true in the general population
However, the prevention of food allergy in all infants, through the application of emollients, is still the subject of contradictory results. Thus, in the EAT study, the application of emollients several times a day at the age of 3 months, in the presence or absence of AD, was associated with a higher risk of food allergy at 3 years of age. In this study, 70.7% of infants without eczema received emollients. The application was carried out for massage purposes, at least once a week.
Helen A. Brough puts forward some hypotheses to explain these contradictions. Applications of oily products can alter the skin barrier: increase in trans-epidermal water loss (TEWL), hindrance in the formation of lamellar structures of the skin barrier, alteration of this barrier by certain components (such as lauryl sulfate). sodium). Another hypothesis is that massages with oily products facilitate the transfer of allergens to the skin or that the massage mechanically opens the hair follicle allowing the allergen to enter.
What to remember in clinical practice?
Prevention of AD facilitates the early introduction of food allergens, which is key to the acquisition of tolerance. Emollients are the essential treatment for dry skin and eczema, and reducing the severity of this helps prevent food allergy.
For Helen A. Brough, the skin application of emollients should therefore not be definitively ruled out, but it must respect certain principles:
- It is necessary to check the absence of irritants or allergens in the composition of the emollient
- Never apply a food product to an infant’s skin.
- Do not apply oils to the skin or in the bath
- Hand washing is necessary before applying emollient to the infant’s skin
- In case of AD, a protective ointment can be applied before meals
- Never take the emollient from the jar directly with your fingers
- Dressing the child to feed him helps protect his skin from contact with allergens
- Finally, it is recommended not to introduce food allergen avoidance as a preventative measure.
This article was written in collaboration with the company Nutricia.
