Objectives: Our skin is constantly exposed to light from solar radiation and electronic devices, which impact skin physiology and aging. The biological altering properties of ultraviolet (UV) solar radiation on skin have been well established. There is significant scientific and public interest on the effects of electronic device generated light (EDGL) on skin. Currently, the effects of EDGL on skin are largely unknown. EDGL includes UV, visible, and infrared light from consumer electronics such as smartphones, computers, and televisions. In this study, we measured the wavelength specific irradiance from electronic devices, and irradiated fibroblasts with white EDGL to determine changes in reactive oxygen species generation, apoptosis, and necrosis.
Methods: To determine the EDGL output of commonly used consumer electronic devices, we measured the irradiance from electronic devices at the manufacturers' recommended reading distances and at 1 cm. To determine the effect of EDGL on human skin cells, we irradiated AG13145 fibroblasts with EDGL for 1 hour at a distance of 1 cm and measured changes in reactive oxygen species generation, apoptosis, and necrosis.
Results: ROS increased significantly by 81.71%, 85.79%, and 92.98% relative to control following 1 hour of white EDGL from iPhone 8+, iPhone 6, and iPad (first generation), respectively. There was a non-significant change in apoptosis following irradiation with an iPhone 8+, iPhone 6, and iPad. Total necrosis was less than 2% for all treatment and control groups.
Conclusions: Our results suggest that short exposures of EDGL increase ROS generation, but the long-term effects associated with repeated exposures of EDGL are unknown. As electronic devices become more widely used and integrated into society globally, we anticipate greater scientific research and general public interest on the effects of visible EDGL on skin. Lasers Surg. Med. © 2018 Wiley Periodicals, Inc.
Keywords: apoptosis; electronic devices; fibroblast; reactive oxygen species; visible light.
© 2018 Wiley Periodicals, Inc.