Potential role of reduced environmental UV exposure as a driver of the current epidemic of atopic dermatitis

TY - JOUR

T1 - Potential role of reduced environmental UV exposure as a driver of the current epidemic of atopic dermatitis

AU - Thyssen, Jacob P

AU - Zirwas, Matthew J

AU - Elias, Peter M

N1 - Copyright © 2015 American Academy of Allergy, Asthma & Immunology. All rights reserved.

PY - 2015/4/30

Y1 - 2015/4/30

N2 - The basis for the sudden and dramatic increase in atopic dermatitis (AD) and related atopic diseases in the second half of the 20th century is unclear. The hygiene hypothesis proposes that the transition from rural to urban living leads to reduced childhood exposure to pathogenic microorganisms. Hence instead of having the normal TH1 bias and immune tolerance because of repeated exposure to pathogens, urban dwellers have TH2 cell immune activity and atopic disease in a more sterile environment. Various other environmental exposures have been implicated in the explosion of AD (and atopic disorders in general), including breast-feeding, tobacco smoking, alcohol consumption, and exposure to domesticated furry pets. Notably, the key role of a compromised barrier of neonatal skin as a predisposing factor in the development of childhood AD has recently been demonstrated. In this article we review the salubrious effects of suberythemogenic doses of UVB irradiation for the skin barrier. We then discuss how the lack of sufficient UVB exposure could have contributed to the rapid increase in the incidence of AD in developed countries. This hypothesis offers a separate but not competing partial explanation, which should be viewed as not discounting the role of the etiopathogenic factors that also could influence the prevalence of atopic disorders.

AB - The basis for the sudden and dramatic increase in atopic dermatitis (AD) and related atopic diseases in the second half of the 20th century is unclear. The hygiene hypothesis proposes that the transition from rural to urban living leads to reduced childhood exposure to pathogenic microorganisms. Hence instead of having the normal TH1 bias and immune tolerance because of repeated exposure to pathogens, urban dwellers have TH2 cell immune activity and atopic disease in a more sterile environment. Various other environmental exposures have been implicated in the explosion of AD (and atopic disorders in general), including breast-feeding, tobacco smoking, alcohol consumption, and exposure to domesticated furry pets. Notably, the key role of a compromised barrier of neonatal skin as a predisposing factor in the development of childhood AD has recently been demonstrated. In this article we review the salubrious effects of suberythemogenic doses of UVB irradiation for the skin barrier. We then discuss how the lack of sufficient UVB exposure could have contributed to the rapid increase in the incidence of AD in developed countries. This hypothesis offers a separate but not competing partial explanation, which should be viewed as not discounting the role of the etiopathogenic factors that also could influence the prevalence of atopic disorders.

KW - Animals

KW - Dermatitis, Atopic

KW - Epidemics

KW - Humans

KW - Hygiene Hypothesis

KW - Immunity, Cellular

KW - Incidence

KW - Infant

KW - Infant, Newborn

KW - Radiation Exposure

KW - Th2 Cells

KW - Ultraviolet Rays

KW - Urban Population

U2 - 10.1016/j.jaci.2015.06.042

DO - 10.1016/j.jaci.2015.06.042

M3 - Review

C2 - 26298230

SN - 0091-6749

VL - 136

SP - 1163

EP - 1169

JO - Journal of Allergy and Clinical Immunology

JF - Journal of Allergy and Clinical Immunology

IS - 5

ER -