Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2010 Nov 24;2(4):1980-9.
doi: 10.3390/cancers2041980.

Epidemiology of skin cancer: role of some environmental factors

Gabriella Fabbrocini  1 , Maria Triassi, Maria Chiara Mauriello, Guglielma Torre, Maria Carmela Annunziata, Valerio De Vita, Francesco Pastore, Vincenza D'Arco, Giuseppe Monfrecola
Affiliations

Epidemiology of skin cancer: role of some environmental factors

Gabriella Fabbrocini et al. Cancers (Basel). .

Abstract

The incidence rate of melanoma and non-melanoma skin cancer entities is dramatically increasing worldwide. Exposure to UVB radiation is known to induce basal and squamous cell skin cancer in a dose-dependent way and the depletion of stratospheric ozone has implications for increases in biologically damaging solar UVB radiation reaching the earth's surface. In humans, arsenic is known to cause cancer of the skin, as well as cancer of the lung, bladder, liver, and kidney. Exposure to high levels of arsenic in drinking water has been recognized in some regions of the world. SCC and BCC (squamous and basal cell carcinoma) have been reported to be associated with ingestion of arsenic alone or in combination with other risk factors. The impact of changes in ambient temperature will influence people's behavior and the time they spend outdoors. Higher temperatures accompanying climate change may lead, among many other effects, to increasing incidence of skin cancer.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Ozone Production. Ozone is created by oxygen molecules and energetic UV radiation [9].
Figure 2
Figure 2
UVB DNA damage. UVB radiation may lead to direct DNA damage, inducing the development of thymine dimers, whereby adjacent thymine bases bond with each other instead of across the DNA backbone ladder. This thymine dimer makes a bulge, and the distorted DNA molecule does not function properly [10].
Figure 3
Figure 3
Cellular targets of arsenic trioxide action, with multiple pathways in malignant cells resulting in apoptosis or in the promotion of differentiation. Potential molecular targets for arsenic trioxide and arsenite are shown in gray. Abbreviations: AP1, activator protein-1; Apaf, apoptotic protease-activating factor; CK2, casein kinase; Co-A, coenzyme A; DAXX, death-associated protein; ER, estrogen receptor; FADH, flavin adenine dinucleotide; PARP, poly-(ADP-ribose)-polymerase; PML, promyelocytic leukemia. Modified from Miller et al. (32) with permission from the American Association for Cancer Research.
See this image and copyright information in PMC

References

    1. Madronich S., de Gruijl F.R. Stratospheric ozone depletion between 1979 and 1992: Implications for biologically active ultraviolet-B radiation and non-melanoma skin cancer incidence. Photochem. Photobiol. 1994;59:541–546. doi: 10.1111/j.1751-1097.1994.tb02980.x. - DOI - PubMed
    1. De Fabo E.C. Artic stratospheric ozone depletion and increased UVB radiation: Potential impacts to human health. Int. J. Circumpolar. Health. 2005;64:509–522. - PubMed
    1. Schaart F.M., Garbe C., Orfanos C.E. Disappearance of the ozone layer and skin cancer: Attempt at risk assessment. Hautarzt. 1993;44:63–68. - PubMed
    1. McCarthy W.H. The Australian experience in sun protection and screening for melanoma. J. Surg. Oncol. 2004;86:236–245. doi: 10.1002/jso.20086. - DOI - PubMed
    1. de Gruijl F.R. Skin cancer and solar UV radiation. Eur. J. Cancer. 1999;35:2003–2009. doi: 10.1016/S0959-8049(99)00283-X. - DOI - PubMed