IUF - Leibniz Research Institute of Environmental Medicine, Düsseldorf, Germany.
Henkel Beauty Care, Düsseldorf, Germany.
Br J Dermatol. 2021 Nov;185(5):1026-1034. doi: 10.1111/bjd.20483. Epub 2021 Aug 20.
Melanism is more frequent in animals living in polluted areas on urban-industrial sites. Given that an increasing number of people are exposed to elevated air pollution levels, it is possible that environmental pollutants affect melanogenesis in human skin. Epidemiological studies have shown that exposure to traffic-related air pollutants such as diesel exhaust particles (DEP) is associated with more clinical signs of hyperpigmentation. However, mechanistic evidence linking DEP exposure to pigmentation has been elusive.
To develop an ex␣vivo skin model to allow for repetitive topical application of relevant ambient DEP, and to provide proof of concept in humans.
We measured skin pigmentation, melanin and pigmentation-associated gene expression, and evaluated oxidative stress.
Repetitive exposure of ex␣vivo skin to DEP at nontoxic concentrations increased skin pigmentation. This increase was visible to the naked eye, time dependent, and associated with an increase in melanin content and the transcription of genes involved in de novo melanin synthesis. Similarly, in healthy participants (n = 76), repetitive topical application of DEP at nontoxic concentrations increased skin pigmentation. DEP-induced pigmentation was mediated by an oxidative stress response. After the application of DEP, epidermal antioxidants were depleted, lipid peroxidation and oxidative DNA damage were enhanced, and in a vehicle-controlled, double-blind clinical study DEP-induced pigmentation was prevented by the topical application of an antioxidant mixture.
Similar to solar radiation, air pollutants cause skin tanning. As eumelanin is an antioxidant, it is proposed that this response serves to protect human skin against air pollution-induced oxidative stress.
在城市工业区受污染地区生活的动物中,黑变病更为常见。鉴于越来越多的人接触到更高水平的空气污染,环境污染物可能会影响人类皮肤的黑色素生成。流行病学研究表明,接触交通相关的空气污染物,如柴油尾气颗粒(DEP),与更多的皮肤色素沉着过度的临床迹象有关。然而,将 DEP 暴露与色素沉着联系起来的机制证据一直难以捉摸。
开发一种离体皮肤模型,以允许重复局部应用相关的环境 DEP,并为人类提供概念验证。
我们测量了皮肤色素沉着、黑色素和色素沉着相关基因表达,并评估了氧化应激。
在非毒性浓度下,重复暴露于 DEP 会增加离体皮肤的色素沉着。这种增加是肉眼可见的,是时间依赖性的,与黑色素含量的增加和新合成黑色素的基因转录增加有关。同样,在健康参与者(n=76)中,非毒性浓度的重复局部应用 DEP 也会增加皮肤色素沉着。DEP 诱导的色素沉着是通过氧化应激反应介导的。在应用 DEP 后,表皮抗氧化剂被消耗,脂质过氧化和氧化 DNA 损伤增强,并且在载体对照、双盲临床研究中,通过局部应用抗氧化混合物来预防 DEP 诱导的色素沉着。
与太阳辐射类似,空气污染物会导致皮肤晒黑。由于真黑素是一种抗氧化剂,因此有人提出这种反应是为了保护人类皮肤免受空气污染引起的氧化应激。