© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 23, 2046-2047,
December 1, 1999
© 1999 Oxford University Press
CORRESPONDENCE |
Re: Sunscreen Use and Duration of Sun Exposure: a Double-Blind, Randomized Trial
Affiliations of authors: K. Hemminki, V. J. Bykov, Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden; J. A. Marcusson, Department of Dermatology, Huddinge Hospital, Huddinge.
Correspondence to: Kari Hemminki, M.D., Ph.D., Department of Biosciences at Novum, Karolinska Institute, 141 57 Huddinge, Sweden.
Autier et al. (1) reported that sunscreen use seems to encourage longer recreational exposure to the sun. We wish to supplement their results with data on the effects of sunscreens and tanning on ultraviolet (UV)-induced DNA damage in human skin. Our data have become available through a recently developed method for measuring UV-induced DNA damage, i.e., cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone photoproducts, in human skin biopsy specimens (2-4). We used this method to test the effects of sunscreens on human skin in situ(2). Sunscreen was applied by one person, according to the manufacturer's instructions. While protection against the erythemal response varied fivefold among nine subjects, protection against DNA damage differed by a factor of 10 and was independent of the erythemal response. On average, sunscreen protected users against DNA damage in accordance with the sun protection factor (SPF), but the protection was highly individual. Since SPF is based on average erythemal response, it is no guarantee against individual DNA damage.
Tanning provides an endogenous "sunscreen" with an SPF of 3-5 (5). These measurements are based on protection against erythema, and, to our knowledge, fundamental data on how well tanning protects genetic material are lacking. In unpublished studies, simulating the use of sunbeds, we investigated the effects of tanning on DNA damage in situ. We measured the protective effects of tanning by quantifying the levels of UV-induced photoproducts in the skin of eight healthy, fair-skinned Caucasians. The study was approved by the South Stockholm Ethical Review Board, which serves both institutions involved in the work, and subjects gave written informed consent to participate. Each subject was irradiated on a 2 x 4-cm area of skin on the lower back with ultraviolet B (UVB) at a dose of 0.3 J/cm2 and on a second 2 x 4-cm area with a dose of 0.6 J/cm2. A punch biopsy was performed immediately after irradiation. An additional biopsy was performed on unirradiated skin to provide a background control specimen. Next, tanning was induced by 10-13 sessions of UVA irradiation for 3 weeks. Tanning was observed by a clear change in skin color toward brown and measured with a reflectometer adjusted to record melanin pigmentation. In the course of ultraviolet A (UVA) treatment, the instrumental readings indicated an increase in pigmentation of 38.8 ± 16.7 reflectometer units (mean ± standard deviation [SD], n = 8). After the last UVA dose, a challenge with UVB was made, and three biopsy specimens were taken, as described above, except that the control biopsy specimen was from tanned skin. The samples were coded for blinded analysis. Photoprotection was defined as the difference in photoproduct levels before and after the UVA treatment.
In subjects who received 0.6 J/cm2 of UVB, the levels of cyclobutane pyrimidine
dimers were slightly lower than those in untanned skin (Fig. 1)
. The
average tanning protection factor was 1.19 ± 0.17 (mean ± SD) (for four
outcomes [two UVB dosage levels x two types of DNA damage]). Since
tanning acts like a low-level suncreen to suppress the erythemal response without the benefit of
the unpredictable at best protection against DNA damage afforded by chemical sunscreen (2), people who have acquired a tan may prolong sun exposure, resulting
in DNA damage and an increased risk of skin cancer. Tanning may provide a false sense of
security that leads to inadvertently lengthened recreational sun exposure like that of the high-SPF
sunscreen users studied by Autier et al. (1).
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REFERENCES
1
Autier P, Dore JF, Negrier S, Lienard D, Panizzon R, Lejeune FJ,
et al. Sunscreen use and duration of sun exposure: a double-blind, randomized trial. J Natl
Cancer Inst 1999;91:1304-9.
2
Bykov VJ, Marcusson JA, Hemminki K. Ultraviolet B-induced
DNA damage in human skin and its modulation by a sunscreen. Cancer Res 1998;58:2961-4.
3 Bykov VJ, Janssen CT, Hemminki K. High levels of dipyrimidine dimers are induced in human skin by solar-simulating UV radiation. Cancer Epidemiol Biomarkers Prev 1998;7:199-202.[Abstract]cancerlit;98180729
4 Bykov VJ, Sheehan JM, Hemminki K, Young AR. In situ repair of cyclobutane pyrimidine dimers and 6-4 photoproducts in human skin exposed to solar simulating radiation. J Invest Dermatol 1999;112:326-31.[CrossRef][ISI][Medline]cancerlit;99181801
5
Gilchrest BA, Eller MS, Geller AC, Yaar M. The pathogenesis of
melanoma induced by ultraviolet radiation. N Engl J Med 1999;340:1341-8.
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