The Impact of Airborne Pollution on Atopic Dermatitis

A Literature Review

A.J. Hendricks; L.F. Eichenfield; V.Y. Shi


The British Journal of Dermatology. 2020;183(1):16-23. 

In This Article

Abstract and Introduction


The increasing prevalence of atopic dermatitis (AD ) parallels a global rise in industrialization and urban living over recent decades. This shift in lifestyle is accompanied by greater cutaneous exposure to environmental pollutants during the course of daily activities. The objectives of this review are to highlight the effects of airborne pollution on epidermal barrier function, examine evidence on the relationship between pollutants and AD, synthesize a proposed mechanism for pollution-induced exacerbation of AD, and identify potential methods for the reduction and prevention of pollutant-induced skin damage. The literature review was done by searching the PubMed, Embase and Google Scholar databases. Inclusion criteria were in vitro and animal studies, clinical trials and case series. Non-English-language publications, review articles and case reports were excluded. Pollutants induce cutaneous oxidative stress and have been shown to damage skin barrier integrity by altering transepidermal water loss, inflammatory signalling, stratum corneum pH and the skin microbiome. AD represents a state of inherent barrier dysfunction, and both long- and short-term pollutant exposure have been linked to exacerbation of AD symptoms and increased AD rates in population studies. Airborne pollutants have a detrimental effect on skin barrier integrity and AD symptoms, and appear to pose a multifaceted threat in AD through several parallel mechanisms, including oxidative damage, barrier dysfunction, immune stimulation and propagation of the itch–scratch cycle. Future research is needed to elucidate specific mechanisms of pollution-induced epidermal barrier dysfunction and to identify efficacious methods of skin barrier repair and protection against pollutant-driven damage.


While the number of children with atopic dermatitis (AD) continues to increase globally, developed countries such as New Zealand and the U.K., which previously reported high rates of AD, have experienced a plateau at around 10–15%.[1,2] However, the prevalence of AD is growing in developing nations, with rates higher than 15% and up to 24·6% reported in countries of Southeast Asia, Africa and Latin America.[1,2] For example, during its rapid industrial growth over the last two decades, China has experienced a dramatic rise in the prevalence of childhood AD, reported to be 2·8% in 1995 vs. 15·8% in 2012.[3,4] The rising prevalence of AD coincides with increased urbanization and industrialization worldwide, and investigation of the role of airborne pollution in the pathogenesis of AD and barrier dysfunction has become increasingly relevant. Environmental pollutants impart a significant and widespread disease burden, with 3 million deaths annually worldwide attributable to outdoor air pollution, according to the World Health Organization.[5] Developing nations in Asia, Africa and the Middle East experience elevated levels of airborne pollution compared with other parts of the world, further underscoring the global impact and urgency of this issue.[5]

AD represents a chronic cycle of intrinsic barrier disruption and entry of extrinsic pathogens and immunogens.[6] Staphylococcus aureus colonization is a prominent component of AD pathogenesis, as skin microbial dysbiosis and digestion of the epidermal barrier by S. aureus protease contribute to impaired barrier function. Skin barrier dysfunction manifests as increased transepidermal water loss (TEWL), decreased stratum corneum hydration and increased stratum corneum pH.[7] Barrier disruption facilitates the entry of environmental irritants, allergens and pathogens, inducing an inflammatory response.[7–9] Resulting pruritus and excoriation further damage the barrier to fuel a vicious itch–scratch cycle.[7,10] Airborne pollution is of significant concern in patients with AD, as existing deficits in skin barrier function and oxidative defence and repair result in increased permeability to pollutants and an exaggerated inflammatory response. The goal of this review was to explore the impact of airborne pollutants on skin barrier integrity, to examine the relationship between urbanization and AD, to analyse the mechanistic roles of pollutants in AD and to discuss potential strategies to combat pollution-induced exacerbation of barrier dysfunction.

Types of Pollution

Major constituents of airborne pollution include particulate matter (PM), volatile organic compounds (VOCs), traffic-related air pollution (TRAP) and cigarette smoke. PM describes liquid or solid particles in gas suspension and is classified by aerodynamic diameter.[11,12] Fine PM (PM2·5; ≤ 2·5μm in diameter) is generated from open fires, power plants and car exhaust. Coarse PM (PM10, 2·5–10μm) originates from soil, dust, pollen and industrial emissions.[11,12] VOCs are carbon-based substances that readily vaporize at ambient air pressure and contribute to indoor air pollution, and are primarily organic solvents such as benzene, toluene, xylene and formaldehyde.[13] TRAP includes PM, VOCs and gaseous components such as nitrogen oxides (NO, NO2, N2O), sulfur dioxide (SO2), carbon monoxide (CO) and ozone (O3) generated from gasoline and diesel-powered engines.[11] Cigarette smoke from burning tobacco contains antigenic and carcinogenic compounds such as nicotine, polycyclic aromatic hydrocarbons and metal residues.[14]