Background Climate change is broadly affecting human health, with grave concern that continued warming of the earth’s atmosphere will result is serious harm. Since the mid-20th century, skin cancer incidence rates have risen at an alarming rate worldwide. Objective This review examines the relationship between climate change and cutaneous carcinogenesis. Methods A literature review used the National Institutes of Health databases (PubMed and Medline), the Surveillance, Epidemiology, and End Results and International Agency for Research on Cancer registries, and published reports by federal and international agencies and consortia, including the Australian Institute of Health and Welfare, Climate and Clean Air Coalition, U.S. Environmental Protection Agency, Intergovernmental Panel on Climate Change, National Aeronautics and Space Administration, National Oceanic and Atmospheric Administration, United Nations Environment Programme, World Health Organization, and World Meteorological Organization. Results Skin cancer risk is determined by multiple factors, with exposure to ultraviolet radiation being the most important. Strong circumstantial evidence supports the hypothesis that factors related to climate change, including stratospheric ozone depletion, global warming, and ambient air pollution, have likely contributed to the increasing incidence of cutaneous malignancy globally and will continue to impose a negative on influence skin cancer incidence for many decades to come. Conclusion Because much of the data are based on animal studies and computer simulations, establishing a direct and definitive link remains challenging. More epidemiologic studies are needed to prove causality in skin cancer, but the evidence for overall harm to human health as a direct result of climate change is clear. Global action to mitigate these negative impacts to humans and the environment is imperative.

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Chronic ulcerative stomatitis protein (CUSP), the most abundant cutaneous isoform of p63, is a p53-related gene essential for epithelial development. CUSP lacks the N-terminal transactivation domain found on other p53 family members and has been shown to inhibit p53 function in vitro. In this study, biopsies of normal skin (21 of 21), benign neoplasms [seborrheic keratosis (3 of 3), acrochordon (2 of 3), and verruca plana (3 of 3)], and squamous cell carcinomas (SCC) (4 of 4) displayed strong nuclear CUSP immuno-reactivity in epidermal cells. In contrast few basal cell carcinomas (BCC) (7 of 27) and sebaceous nevi (1 of 2) displayed this pattern of CUSP immunoreactivity. Thus, biopsies of cutaneous conditions characterized by sonic hedgehog (SHH) pathway dysregulation were more than 86 times as likely to lack CUSP/p63 immunofluorescence as were other cutaneous samples. Adjacent normal-appearing skin from patients with basal cell nevus syndrome (BCNS) (2 of 3) also lacked CUSP immuno-staining. Lastly, a BCC arising in a patched heterozygous mouse also lacked CUSP immuno-staining. Because CUSP mRNA and protein were detected via Northern and Western analysis in BCC samples lacking CUSP immuno-staining, we sequenced the coding region of CUSP from two non-staining BCCs but found no mutations. Therefore, CUSP appears to be present, unmutated, and yet frequently undetectable by immunofluorescence in cutaneous lesions in both humans and mice that are associated with SHH pathway dysregulation (BCCs, BCNS, and nevus sebaceous).

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