The External Exposome and Allergies: From the Perspective of the Epithelial Barrier Hypothesis

Abstract

IntroductionIn the last decades, we have seen a rapid increase in the prevalence of allergic diseases such as asthma, allergic rhinitis, atopic dermatitis, and food allergies. The environmental changes caused by industrialization, urbanization and modernization, including dramatic increases in air pollutants such as particulate matter (PM), diesel exhaust, nitrogen dioxide (NO2), ozone (O3), alarming effects of global warming, change and loss of biodiversity, affect both human health and the entire ecosystem.ObjectiveIn this review, we aimed to discuss the effects of the external exposome on epithelial barriers and its relationship with the development of allergic diseases by considering the changes in all stakeholders of the outer exposome together, in the light of the recently proposed epithelial barrier hypothesis.MethodTo reach current, prominent, and comprehensive studies on the subject, PubMed databases were searched. We included the more resounding articles with reliable and strong results.ResultsExposure to altered environmental factors such as increased pollution, microplastics, nanoparticles, tobacco smoke, food emulsifiers, detergents, and household cleaners, and climate change, loss and change in microbial biodiversity, modifications in the consumption of dietary fatty acids, the use of emulsifiers, preservatives and the decrease in the antioxidant content of the widely consumed western diet may disrupt the epithelial barriers of the skin, respiratory and gastrointestinal tracts, making us more vulnerable to exogeneous allergens and microbes. Epithelial cell activation, microbial dysbiosis and bacterial translocation disrupt the immune balance and a chronic Th2 inflammation ensues.ConclusionDramatic increases in air pollution, worrisome effects of global warming, dysbiosis, changing dietary habits and the complex interactions of all these factors affect the epithelial barriers and local and systemic inflammation. We want to draw attention to the emerging health effects of environmental changes and to motivate the public to influence government policies for the well-being of humans and the nature of the earth and the well-being of future generations.

Impact of the Family and Household Environment on Pediatric Atopic Dermatitis in Japan

“…The apparent increase in AD prevalence with second-hand smoke exposure and household pets in the current study is consistent with the concept of the exposome, whereby environmental exposure to various factors leads to disruption of the epithelial skin and mucosal barriers and subsequent development of atopic diseases such as AD, allergic rhinitis, food allergies, chronic rhinosinusitis, and asthma [5][6][7][8][9]. In this context, aryl hydrocarbon receptor (AhR) signaling pathways are thought to be involved in regulating skin homeostasis in response to environmental exposure, which may have therapeutic implications for the pharmacologic management of AD [37,38].…”

“…In particular, patients with atopic diathesis are genetically predisposed to develop one or more atopic diseases, including AD, hay fever, allergic rhinitis, and asthma [4]. In addition, the patient's exposome, a concept that encompasses all environmental exposure (e.g., chemical pollution, tobacco smoke, infectious agents, or lifestyle factors) encountered by an individual throughout their life, is thought to play an important role in AD development [5][6][7][8][9].…”

A short history from Karelia study to biodiversity and public health interventions

“…Thus, epigenetics serves as environmental biomarkers linking our genes with exposure and disease. The epigenetic reading of the exposome ( 58 ) modulates gene-environment interaction and have a central role in immune homeostasis.…”

The hen and the egg question in atopic dermatitis: allergy or eczema comes first

“…Several studies performed in mice describe immunological pathways involved in the progression from epicutaneous sensitization to food allergy [ 13 ]. Now it is clear that the mechanism of food allergy is through the epicutaneous sensitization, while the oral exposure leads to tolerance [ 13 , 14 ]. Clinical studies also support the concept of atopic march from early skin barrier dysfunction to the development of food sensitization and clinical food allergy.…”