Influence of the environmental relative humidity on the inflammatory response of skin model after exposure to various environmental pollutants

November 2, 2020

Emeline Seurat a, Anthony Verdin b, Fabrice Cazier c, Dominique Courcot b, Richard Fitoussi d, Katell Vi´e d, Val´erie Desauziers e, Isabelle Momas a, Nathalie Seta a, Sophie Achard a
a Laboratoire de Sant´e Publique et Environnement, Hera “Health Environmental Risk Assessment”, Inserm UMR1153-CRESS (Centre de Recherche en Epid´emiologie et StatistiqueS), Universit´e de Paris, Facult´e de Pharmacie de Paris, 4, Avenue de L’Observatoire, 75006, Paris, France
b Unit´e de Chimie Environnementale et Interactions sur le Vivant UR4492, SFR Condorcet FR CNRS 3417, Maison de La Recherche en Environnement Industriel 2, Universit´e Du Littoral Cˆote D’Opale, 189A Avenue Maurice Schumann, 59140, Dunkerque, France
c Centre Commun de Mesures (CCM), Universit´e Du Littoral-Cˆote D’Opale, 145 Avenue Maurice Schumann, 5914, Dunkerque, France
d Laboratoires Clarins, 5 Rue Amp`ere, 95300, Pontoise, France
e IPREM, IMT Mines Ales, Universit´e de Pau et des Pays de L’Adour, E2S UPPA, CNRS, Pau, France


In the course of this study, they tested various pollutants with different chemical compositions, applying them to the apical side of Reconstructed Human Epidermis and being particularly interested in the effect relative humidity has on the reaction to pollutants. Investigating several cytokines and chemokines, they showed that IL-1α, IL-6, IL-8, and RANTES are the cytokines/chemokines almost systematically induced by most pollutants.


The skin is an essential barrier, protecting the body against the environment and its numerous pollutants. Several environmental pollutants are known to affect the skin, inducing premature aging through mechanisms including oxidative stress, inflammation, and impairment of skin functions. Even climate conditions can impact the skin. Therefore, using a Reconstructed Human Epidermis (RHE), we tested the effect of two samples of fine particulate matters (PM0.3-2.5 – one metals-rich sample and the other organic compounds-rich), two Volatile Organic Compounds mixtures (VOCs – from a solvent-based paint and a water-based paint) and Tobacco Smoke (TS). All pollutants affected cellular functionality, but to a lesser extent for the water-based paint VOC. This effect was enhanced when RHE were preconditioned for 2 h by a semi-dry airflow (45% relative humidity) before pollutants application, compared to preconditioning by a humid airflow (90% relative humidity). In the absence of preconditioning, IL-1α, IL-6, IL-8, and RANTES were almost systematically induced by pollutants. When RHE were preconditioned by a semi-dry or humid airflow before being subjected to pollutants, the increase of IL-1α, IL-8, and RANTES falls into two groups. Similarly to RHE not treated with pollutants, RHE treated with VOCs after preconditioning by a semi-dry airflow showed increased IL-1α, IL-8, and RANTES release. On the contrary, RHE treated with PM or TS after preconditioning by a semi-dry airflow show a lower increase in IL-1α, IL-8, and RANTES compared to preconditioning by a humid airflow. The effect of real environmental relative humidity conditions of the air, combined with acute exposure to various environmental pollutants, seemed to relate mainly to structural changes of the skin, determining the outcome of the inflammatory response depending on the physicochemical characteristics of pollutants.

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