As the skin acts as a barrier organ, it is an ideal model to study environmentally-induced (extrinsic) aging. Extrinsic aging is restricted to environmentally exposed skin sites like the face, the dorsal side of the hands or the neck. 

Extrinsic skin aging phenotypes develop from exposure to exposomal factors (like air pollution, solar radiation, climate characteristics, nutrition, etc.), their interaction with each other, and their modification by genetic factors.

Exposure to these exposomal factors causes extrinsic skin aging by the accumulation of macromolecular damage and the succeeding evolution of functionally altered and/or senescent fibroblasts in the dermal compartment of the skin.

Deeply understanding the skin aging exposome and its interaction with genetic factors will help in developing efficient and customized strategies to significantly slow down extrinsic skin aging. 

Furthermore, a more detailed examination of the mechanisms causing the dermal accumulation of macromolecular damage by exposomal factors beyond ultraviolet radiation is warranted. Targeting the resulting functional consequences, like, deleting injured and/or senescent fibroblasts using senolytics, enhancing their ability to adapt or overriding their malfunctions through cell-based interventions might help partially to revert extrinsic skin aging.