Biochemical and biological effects of air pollution on the function of human skin.
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Presented by: Wil Reynolds
According to the World Health Organisation, 99% of the world’s population live in areas where the air quality exceeds air quality guideline limits, and of even greater concern, over 4.2 million people die annually as a result of exposure to ambient air pollution. Alongside the already established inhalation route, dermal exposure to pollutants has now been implicated in the advancement of skin ageing, as well as a range of skin conditions including psoriasis and atopic dermatitis. This highlights a pressing need for an investigation into the mechanisms underlying pollutant-induced skin damage, so appropriate protective strategies can be developed. In this present study we aim to investigate the biological effects in human skin equivalents after exposure to two known air pollutants; particulate matter (PM) and ozone, and whether a combination of pollutants exhibit synergistic effects.
Human skin equivalents were exposed to 0.01µg/µl PM, 0.05µg/µl PM, 0.3ppm ozone, or a combination of 0.00µ1g/µl and 0.3ppm ozone daily for seven days, before harvesting equivalents and culture medium. Structural, gene and protein analyses were performed using histological staining, qPCR, Western blotting and ELISA assays. PM induced aberrant epidermal differentiation characterised by a concentration-dependent decrease in viable epidermal thickness, whereas ozone exposure induced an increase in keratinocyte proliferation showing a marked increase in viable epidermal thickness. Whilst PM showed no effect on any downstream marker, ozone was shown to upregulate the gene/protein expression of wrinkling-associated MMP-1 and MMP-3, and also induce the release of inflammatory marker PGE2. There were also some significant synergistic effects when comparing single pollutant exposure to combination pollutant exposure, which resulted in the acceleration of the ageing phenotype in skin equivalents. This study presents the differential effects of various pollutants, and shows how exposure to multiple pollutants simultaneously may augment the initial changes associated with ageing.
The pollutant concentrations in this study were based on recorded global values, and represents one of the first studies that not only uses real-world concentrations, but also investigates the synergistic effects of pollutant combinations. The results presented are indicative of oxidative damage which if sustained has the potential to cause accelerate cellular senescence and subsequently the skin aging process. However, further investigation into the precise mechanisms involved is necessary before preventative strategies can be implemented.
Human skin equivalents were exposed to 0.01µg/µl PM, 0.05µg/µl PM, 0.3ppm ozone, or a combination of 0.00µ1g/µl and 0.3ppm ozone daily for seven days, before harvesting equivalents and culture medium. Structural, gene and protein analyses were performed using histological staining, qPCR, Western blotting and ELISA assays. PM induced aberrant epidermal differentiation characterised by a concentration-dependent decrease in viable epidermal thickness, whereas ozone exposure induced an increase in keratinocyte proliferation showing a marked increase in viable epidermal thickness. Whilst PM showed no effect on any downstream marker, ozone was shown to upregulate the gene/protein expression of wrinkling-associated MMP-1 and MMP-3, and also induce the release of inflammatory marker PGE2. There were also some significant synergistic effects when comparing single pollutant exposure to combination pollutant exposure, which resulted in the acceleration of the ageing phenotype in skin equivalents. This study presents the differential effects of various pollutants, and shows how exposure to multiple pollutants simultaneously may augment the initial changes associated with ageing.
The pollutant concentrations in this study were based on recorded global values, and represents one of the first studies that not only uses real-world concentrations, but also investigates the synergistic effects of pollutant combinations. The results presented are indicative of oxidative damage which if sustained has the potential to cause accelerate cellular senescence and subsequently the skin aging process. However, further investigation into the precise mechanisms involved is necessary before preventative strategies can be implemented.