Anti-Pollution and Sunscreens

Anti-Pollution Matrix > Interdisciplinary Topics > Sun protection > Anti-Pollution and Sunscreens

Introduction

Traffic-related pollution manifests in increased levels of particulate matter, soot, nitrogen dioxide, tropospheric ozone and polycyclic aromatic hydrocarbons (PAHs) in the air. Mechanistic studies [1] and also epidemiological evidence [2] suggest that such air pollution may accelerate skin damage causing premature occurrence of wrinkles and dark spots on the face [3 - 8]. There is increasing evidence that UVA alone and especially in combination with common environmental pollutants significantly increases visible photodamage and risk of skin cancer [9].

 

Particulate Matter and Polycyclic Aromatic Hydrocarbons (PAHs)

Particulate matter from fuel combustion contains polycyclic aromatic hydrocarbons (PAHs), some of which are highly photoreactive and induce oxidative stress under solar UV exposure [10]. Several PAHs absorb photons in the UVA-range or, in case of five or more aromatic rings, even in the visible range. The excited PAHs can act as photosensitizers, transferring their energy to oxygen, leading to singlet oxygen or the superoxide anion. UVA-I appears to be a major contributor in the phototoxic process. Some severe phototoxic reactions were observed under sunlight exposure and triggered by UVA-visible domain [11].

Penetration of particulate matter (PM) and nano-particles in general is very unlikely with healthy skin. There is no penetration found for particle sizes > 20 nm [12]. For this reason, topical contamination of the deep epidermis by PAHs is probably very weak. However, PAHs might reach the hypodermis, dermis and deep epidermis via blood circulation that means indirectly via inhalation. This is consistent with the observation, that when excessive sun exposure and heavy smoking occurred together, the risk of developing wrinkles was more than 10 times higher compared to non-smokers or people with less sun exposure [13].

Benzo(a)pyrane (BaP) serves as an indicator and a model substance for PAHs. A few nanomoles of BaP together with UVA produced high levels of reactive oxygen species (ROS) inside human keratinocytes [14]. UVA radiation probably acts as a photo-catalyst of PAH traces and may then induce strong local oxidative stress. Reactive oxygen species (ROS) may cause oxidation of 2’-deoxyguanosine nucleotide to form 8-oxo-2’-deoxyguanosine (8-oxodG). The amount of 8-oxodG is proportionally correlated with BaP concentration and UV dose [15]. Low doses of either UVA or BaP alone are not carcinogetic but both together at subcarcinogetic levels resulted in skin tumors [16].

 

Effects of NO₂ and Tropospheric Ozone

Exposure of patients with healthy skin or atopic eczema to NO₂ (0.1 ppm) resulted in a significant trans-epidermal water loss and skin roughness [17]. Ozone can indirectly damage the stratum corneum (SC) by depleting antioxidants such as vitamin C and vitamin E. It also oxidizes squalene. UV-induced squalene peroxidation products trigger a global pro-inflammatory response when delivered to keratinocyte cultures [10].

 

Measures for Protection

Barrier function is the first line of defence against environmental skin aggression. Provision of exogenous vitamin C and E or carotinoids as efficient singlet oxygen scavengers is an effective approach to protection [18, 19]. Due to synergistic impact of UV and pollutants the use of sunscreens is recommended.

 

References

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