The connection between sun exposure and skin cancers, such as melanoma, is well acknowledged. However, some people are at higher risk of melanoma than others, meaning they may require less sun exposure to cause the DNA damage which can lead to skin cancers.
The development of melanoma is multifactorial, it involves environmental, phenotypic (e.g., our hair/eye/skin colour), and genetic factors. The extensive interplay between biological risk factors, including genes, skin complexion, gender, age, and the number and type of naevi, in combination with environmental factors such as geographical location, culture and sun protective practices, can all contribute to melanoma risk. Although, the most significant environmental risk factor is indisputably ultraviolet (UV) exposure, most commonly from the sun, but also from using tanning beds.
The most significant and recognised risk factors for melanoma include: genetic mutations, a high number of naevi and/or atypical naevi, a strong personal or family history of melanoma, fair skin, hair and eye colour, age, sex (male), excessive UV exposure, intermittent sun exposure in childhood, history of sun burn, and immunosuppression.
The environmental link between UV exposure and melanoma is well established, likewise, it is recognised that lighter skin types are more vulnerable to UV damage. Consequently, the incidence of melanoma is greater in areas with high UV exposure and largely fair skinned populations, such as North America, Australia, and New Zealand. Different types of sun exposure and their relation to melanoma have been studied extensively. Meta-analyses (where the results of numerous studies are combined), have consistently reported that intermittent sun exposure is the most dangerous, especially when resulting in sunburn. Intermittent sun exposure can be described as short, intense sun exposure, the type you would get when sunbathing, or on holidays, as opposed to chronic sun exposure relating to an outdoor occupation.
Our genetic variations can also make a big difference in our melanoma risk. While the average global lifetime risk of developing a melanoma is around 3%, those with high-penetrance germline mutations can face a lifetime risk of up to 84%. These types of mutations are inherited from one generation to the next, and that is why we sometimes see multiple melanomas within a family. However, while approximately 10% of those diagnosed with melanoma will have some kind of family history, it’s predicted that only about 1% of newly diagnosed melanomas may be related to this type of genetic mutation.
More commonly, it is expected that some melanoma-prone families are attributed to the cumulation of multiple medium or low penetrance genetic variations (polygenic risk), and/or shared environment. The most commonly studied medium penetrance variants in relation to melanoma risk are in the MC1R gene, which is associated with pigmentation in skin, hair, and eye colour. Those holding risk variations in this gene are more likely to have red hair, fair skin, and lower tanning ability. This sun-sensitive phenotype results in increased susceptibility to UV damage, and subsequent melanoma risk.
While we can’t control our genetic and phenotypic risks to melanoma, we can certainly decrease our environmental risk. If the UV index is over 3, then make sure you are taking precautions when in the sun, including wearing suncream and protective clothing, and when possible, seeking shade and avoiding sun exposure in the hottest part of the day. Furthermore, when melanoma is detected early, it is generally curable by skin excision, unlike later stage melanoma which involves extensive treatment regimens and higher mortality rates. So along with good sun protective behaviour, make sure you attend regular skin examinations to have a health professional check for any early signs of skin cancer.