Table 2.
Effects of polycyclic aromatic hydrocarbons (PAH), dioxin (TCDD) and Ozone (O3) in the skin.
| Skin effects | Pollutants | Type of study | Skin damage | Mechanism skin damage | References |
|---|---|---|---|---|---|
| Oxidative stress/inflammation | PAH B[a]P |
In vitro | ↑ROS ↑IL-8 |
↑AhR ↑CYP1A1 |
(Tsuji et al., 2011; Fuyuno et al., 2018) |
| TCDD |
In vivo
HRS/hr/hr mice |
↑Mast cells ↑Macrophages ↑Immune cells ↑ IL1β, IL6, IL22 ↑TNF-α ↑CCN1 |
↑AhR ↑Expression of proinflammatory genes |
(Rudyak et al., 2018) | |
| O3 | In vitro | ↑ROS | DNA breakage mitochondrial damage ↓ ATP ↓Sirtuin |
(McCarthy et al., 2013) | |
| In vitro | ↑ROS ↑IL-8 ↓keratinocytes proliferation |
↑4-HNE protein adduct ↑Nrf2 nuclear translocation ↑NF-kB |
(Valacchi et al., 2015) | ||
|
In vivo
SKH-1 mice |
↑ROS | ↑Lipid peroxidation ↑4-HNE |
(Valacchi et al., 2002) |
4-HNE, 4-hydroxy-2-nonenal; AhR, aryl hydrocarbon receptor; B[a]P, benzo (a) pyrene; CCN1, cysteine-rich protein 61; CYP1A1, cytochrome P450 (CYP1A1); IL, interleukin; NF-kB, nuclear factor kappa B; Nrf2, nuclear factor erythroid 2-like 2; ROS, reactive oxygen species; TCDD, dioxin/2,3,7,8-tetrachlorodibenzo; TNF-α, tumor necrosis factor.