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ABSTRACT
Because the incidence of cutaneous malignant melanoma (CMM) was reported to increase with increasing terrestrial UVR (290–400 nm) doses in the US back in 1975 and a recent publication showed no association exists with UVR exposure at all, we set out to fully elucidate the role of UVR in CMM. To achieve this goal, we analyzed the CMM incidences over latitude and estimated the average personal UVR dose in the US and numerous countries (> 50) on 5 continents around the world. Using data from the International Agency for Research on Cancer in 2005, we performed worldwide analysis of CMM over UVR dose by sex, age group (0–14, 15–29, 30–49, 50–69, 70–85+) and Fitzpatrick skin types I-VI. Surprisingly, increasing UVR doses, which represent erythemally-weighted doses comprised primarily of UVB (290–315 nm) radiation, did not significantly correlate with increasing CMM incidence for people with any skin type anywhere in the world. Paradoxically, we found significant correlations between increasing CMM and decreasing UVB dose in Europeans with skin types I-IV. Both Europeans and Americans in some age groups have significant increasing CMM incidences with decreasing UVB dose, which shows UVB is not the main driver in CMM and suggests a possible role for lower cutaneous vitamin D3 levels and UVA (315–400 nm) radiation. CMM may be initiated or promoted by UVA radiation because people are exposed to it indoors through windows and outdoors through some sunscreen formulations. Thus, our findings may explain why some broad-spectrum sunscreen formulations do not protect against getting CMM.
Abbreviations
| CMM | = | cutaneous malignant melanoma |
| HPV | = | Human Papilloma Virus |
| PUVA | = | 8-methoxypsoralen and UVA |
| ROS | = | reactive oxygen species |
| US | = | United States |
| UVR | = | Ultraviolet Radiation (290–400 nm) |
| UVA | = | Ultraviolet-A (316–400 nm) |
| UVAI | = | (341–400 nm) |
| UVA2 | = | (316–340 nm) |
| UVB | = | Ultraviolet-B (290–315 nm) |
Disclosure of Potential Conflicts of Interest
No potential conflicts of interest were disclosed.
Acknowledgments
The authors wish to dedicate this paper to the memory of Professor Jan C. van der Leun who passed away on July 6, 2016; his greatest accomplishments include: chairman of UNEP's effects section of the coordinating Committee on the Ozone Layer from 1982 to 1988, head of the Photodermatology Department of Utrecth University (where his group significantly contributed toward developing the SCUPh action spectrum for photocarcinogenesis in 1993), founding co-chair of the Environmental Effects Assessment Panel (EEAP), winner of the UNEP Global Ozone Award in 1995, Finsen Medal award in Photobiology in 1996, UNEP Global 500 Roll of Honor for Environmental Achievement in 1997, European Society for Photobiology Medal Award in 2003, and he was made a Knight in the Order of the Dutch Lion by Queen Beatrix for his “scientific work and for applying the results for the sake of the environment” in 2004. Besides being a great scientist, Professor Jan C. van der Leun was also a great human being that will be dearly missed by multitudes of people worldwide.