News

Sunscreens With Retinyl Palmitate Do Not Cause Skin Cancer


 

Published in the Journal of the American Academy of Dermatology

In spite of an alarming report earlier this year by the Environmental Working Group, an analysis of human and animal studies found little support for the assertion that sunscreens containing retinyl palmitate cause skin cancer.

In a commentary published online in the Journal of the American Academy of Dermatology, Dr. Steven Q. Wang of Memorial Sloan-Kettering Cancer Center, New York, and his colleagues evaluated the compound from several points of view, and concluded that “there is no convincing evidence” that retinyl palmitate, a form of vitamin A, is carcinogenic in sunscreens (J. Amer. Acad. Dermatol. 2010 [doi:10.1016/j.jaad.2010.07.015]).

“In fact, clinical observations spanning over decades suggest that retinoids are helpful in skin cancer chemoprevention,” the authors wrote. “Correcting this false impression is an important and necessary step to ensure that the public continues to use sunscreen as a component of photoprotective strategy.”

The suggestion by the Environmental Working Group, a nonprofit public health research and advocacy organization, that retinyl palmitate in sunscreens may cause skin cancer garnered widespread media attention, because 41% of sunscreens on the market contain this compound. Retinyl palmitate, an antioxidant, does not directly provide sun protection, but instead is added as a cosmetic ingredient.

Dr. Wang and his colleagues noted that retinyl palmitate and other closely related compounds are natural components of human skin. In 2000, the compound was referred to the National Institutes of Health’s National Toxicology Program (NTP) for phototoxicity and photocarcinogenicity testing, along with many other common ingredients such as alpha- and beta-hydroxy acids, aloe vera, and nanoscale titanium dioxide and zinc oxide.

Between 2002 and 2009, the Food and Drug Administration published eight in vitro studies and three animal studies of retinyl palmitate. Several of these studies showed that the combination of retinyl palmitate and UV light induced reactive oxygen species. In addition, an NTP study involving 430 SKH-1 hairless mice examined two concentrations of retinyl palmitate and placebo at three levels of solar radiation.

This study has not been subject to peer review, but some of the data are available online, and Dr. Wang and his colleagues analyzed them. The only statistically significant results were an apparent increase in neoplasms in animals given the higher concentrations (0.5%) of retinyl palmitate at an intermediate level of simulated solar radiation (6.75 mJ/cm2). Higher levels of solar radiation resulted in no significant increase in neoplasms, so the authors concluded that the study failed to provide conclusive evidence indicating that the combination of retinyl palmitate and UV radiation is carcinogenic.

In addition, that study had several limitations, including the fact that the SKH-1 strain of hairless mice is highly susceptible to the development of skin cancer after UV exposure. In fact, at the higher level of solar radiation, 82% of the mice developed malignant skin lesions when given the placebo.

Although no similar studies in humans have been published, Dr. Wang and his colleagues noted that dermatologists have been prescribing various forms of topical retinoids to manage a variety of skin conditions for more than 40 years. While millions of patients have received these compounds, dermatologists have published no evidence suggesting that topical retinoids increase cancer risk.

The authors declared that they had no financial conflicts of interest.

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