The incidence of human skin cancers has alarmingly increased over the past twenty years.  Recently, more attention has been placed on the hazards of sunlight with a subsequent rise in the use of sunscreens.  These sunscreens block ultraviolet (UV) B but they do not adequately protect against UVA radiation.  Although UVA is less erythrogenic and carcinogenic than UVB, increasing evidence has shown that UVA per se or in combination with certain chemicals significantly increases the risk of skin cancers in animals as well as humans.  Many chemicals, including polycyclic aromatic hydrocarbons (PAHs), can be sensitized by UVA and become highly toxic or tumorigenic.  Benzo[a]pyrene (BaP) is often used as an index of environmental PAH levels.  PAHs are ubiquitously present in the atmosphere from environmental pollutants and cigarette smoke, but their levels are usually below the carcinogenic threshold.  Thus, the combined impact of these two environmental factors at subcarcinogenic doses remains hotly debated.  It is justifiable to hypothesize that increased exposure to UVA, due to the deteriorating ozone layer and overuse of UVB sun blockers, combined with PAHs from cigarette smoke and other environmental pollutants may be contributory to the increased incidence of skin cancer in humans.

 

This paper reviews the epidemiological, animal, and cellular/molecular studies on the synergistic interactions of BaP and UVA light.  With the most updated studies and unpublished work from this laboratory, it was found that BaP serves as a photosensitizer to generate massive reactive oxygen species (ROS) upon UVA irradiation which in turn causes oxidative damage and BaP-DNA binding (genetic effect), and potentiates the activation of signal transduction cascades (epigenetic effect), thereby leading to carcinogenesis.