Overview of Pollutants

Mobile source air toxics include any pollutants that are emitted from motor vehicle and nonroad engines. Examples of mobile source air toxics include lead, benzene, 1,3-butadiene, formaldehyde, acetaldehyde, acrolein, polycyclic organic matters, naphthalene, and diesel PM. Exposure to traffic-related air pollutants can affect multiple organs including the skin (12–14).

The US Environmental Protection Agency (EPA) sets six principal pollutants as National Ambient Air Quality Standards, which are referred to as criteria pollutants and are routinely monitored in ambient air. They include the following (15):

• Ozone (ground-level ozone)

• PMs (including particles <2.5 μm found in smoke and particles between 2.5 and 10 μm found near road ways)

• Carbon monoxide

• Nitrogen oxide

• Sulfur dioxide

• Lead

Indoor pollution has many sources including combustion products such as coal, wood, gas, cigarette smoke, certain furniture or carpets, building materials, household cleaning products, central air conditions, insecticides, and outdoor sources such as radon and outdoor air pollution (5,15,16).

See Table 20.1.

Skin and Pollution

Air pollution can potentially affect skin via different mechanisms including oxidative stress and induction of inflammation and by changing normal skin microbiome.

Oxidative stress is involved in pathogenesis of multiple skin disorders including inflammatory and neoplastic skin disorders (17). A number of gaseous pollutants, UV radiation, and ground level ozone can create oxidative stress in skin (18).

There is substantial evidence on the role of oxidative stress in cutaneous carcinogenesis as well as its effects on inflammation and aging (8,17,19,20). Oxidative stress was the subject of investigation by Thiele in the late 1990s, who showed on a series of studies on hairless mice that exposure to ozone causes lipid peroxidation in SC and depletes skin’s natural antioxidants such as vitamins E and C and adversely affects the barrier function of the epidermis, making it potentially susceptible to inflammation. Other investigators have also shown oxidative stress and free radical formation due to ozone exposure (18,21–26).

McCarthy et al. (27) in a study exposing normal human epidermal keratinocytes (NHEK) to ozone (at levels comparable to levels of ambient ozone in cities), observed an increase in levels of hydrogen peroxide and IL-1 alpha indicating the presence of oxidative stress and induction of a proinflammatory response as well as evidence of increased DNA breaks.

He at al. (28) showed that exposure to ozone using exposure chambers on human skin led to more than a twofold increase in lipid hydroperoxides in the superficial SC and 70% decrease in vitamin E, but it did not increase some of the enzymes involved in epidermal desquamation (28). Subjects in this study were exposed to ozone at 0.8 ppm for 2 hours, which is higher than the 0.075 ppm limit by EPA (15). It is of note that the ozone level as high as 0.68 ppm was recorded in Los Angeles in 1955 (29). Authors suggested that ozone in realistic environmental levels can pose a moderate oxidative stress, but these effects may be much less than the toxic effects showed in in vitro studies.

Inflammatory reactions mediated via various inflammatory cytokines are associated with pollution. Increased inflammatory cytokines such as IL-1 beta was observed with in vitro exposure of human keratinocytes to diesel exhaust particles (30). The induction of nuclear factor kappa B, which is a transcription factor largely known to have proinflammatory effects via the expression of proinflammatory cytokines, chemokines, and adhesion molecules, has been associated with exposure to diesel exhaust dust in mouse epidermal cell lines (31). Another important pathway that pollution can potentially affect skin is through the aryl hydrocarbon receptor (AhR). AhR is a multifunctional ligand-dependent cytosolic transcription factor, initially discovered as a cytosolic receptor and transcription factor for polycyclic aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (9,32–34). AhR is a ligand with an affinity for a wide range of low-molecular weight chemicals including dioxins, coal tar, tryptophan photoproducts, and flavonoids. After ligation, cytoplasmic AhR translocates to the nucleus via heterodimerization with AhR nuclear translocator and mediates multiple physiological and pathological cascades in the cell. AhR-dependent signal transduction pathways produce diverse biological and toxicological effects following activation with endogenous or xenobiotic ligands (35). For example, dioxin-activated AhR ligand induces the activation of various transcription factors including cytochrome P4501A1 (CYP1A1). While it exhibits a physiological role in detoxification of these compounds, the activation of CYP1A1 enzyme actually leads to the generation of ROS and causes oxidative stress (9). Interestingly, the activation of AhR with another set of ligands such as coal tar, ketoconazole, and other chemicals mediates antioxidant signaling via nuclear factor-erythroid 2-related factor-2 (9,36,37). Increased expression of FLG has been observed with both oxidative and antioxidative ligand activation of AhR (9). While the role of AhR in skin hemostasis, cellular proliferation, epidermal barrier protein metabolism, melanogenesis, and inflammation has been the subject of extensive research; its physiological and toxicological effects still need to be better elucidated (9,35,38). Nonetheless, pollutants such as dioxins and ozone are shown to be among the oxidative ligand activators of AhR and can adversely affect the cutaneous biology (8).

Barrier function can also be affected with ambient air pollution. Pan et al. (39

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