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| Factor | Description | Incidence | LIT |
|
| BCC | | | |
| Ultraviolet light | Increased incidence of BCC has been noticed in individuals with fair skin, weaker tanning ability, fair hair, blue eyes, older individuals, men, and those with frequent sun exposure. | The incidence changes nearer to the Equator, where the ultraviolet B waves (UVB) are most frequent. Ultraviolet A waves (UVA) also have carcinogenic effects. | [18, 19] |
| Ionizing radiation | Ionizing radiation causes BCC in humans and animals. The latency period is 20–30 years. | Patients that have been exposed to 1 Gy (gray) of radiation had a greater risk of developing cancer. In individuals that have been exposed to 35 Gy of radiation, the risk was 40x greater compared to the general population. | [20, 21] |
| Chemical substances | A large majority of chemical carcinogens cause SCC and not BCC. There are exceptions, such as arsenic in people and 3-methylcholanthrene and antramine in rats. | BCC developed 30–40 years after chronic arsenic exposure, as a consequence of contaminated food, water, seafood, and so forth. | [22] |
|
| SCC | | | |
| Extrinsic factors | | | |
| Ultraviolet light | UV light is one of the most important factors. The most common sites of SCC are the head, neck, and the dorsal side of arms. People with type 1 skin according to Fitzpatrick are particularly at risk. | SCC incidence increases nearer to the Equator. It doubles per 10° latitude towards the Equator. | [11, 12] |
| Ionizing radiation | Gamma, Grenz, and X-rays are well known carcinogens. | The incidence of cancer due to radiation increases linearly by 5,5% per 1 Sv. | [23] |
| HPV | HPV infection presents a risk for cervical SCC development, as well as certain genital and skin variants of SCC | Cervical, anal, and oropharyngeal cancers are almost always etiologically connected to a HPV infection. Together with UVA, they are thought to be cocarcinogens for skin cancer. | [24] |
| Chemical substances | Hydrocarbons, arsenic, and tobacco are well known carcinogens. | Hydrocarbons were important etiological factors in certain professions (e.g., chimney sweeps). Skin lesion development correlates to arsenic exposure. | |
| Intrinsic factors | | | |
| Genodermatoses | Those with Xeroderma Pigmentosum (XP) are more susceptible to UVA radiation, which leads to skin and eye degeneration and the development of skin SCC, BCC, and MM | In individuals with XP, the incidence of cancer before the age of 20 is 2000X greater than in the general population. | [25, 26] |
| Immunosuppression | Chronic immunosuppression (e.g., long-term corticosteroid immunosuppression therapy or posttransplant therapy) increases skin cancer incidence. | (i) In Netherlands and Norway, the incidence in patients after heart or kidney transplant is 65 to 250 times greater.
(ii) In the USA 35% of individuals within 10 years of a heart transplant developed some form of skin cancer. | [27–29] |
| Actinic keratosis (AK) | (i) These lesions are the most common premalignant conditions.
(ii) Bowen’s disease and Erythroplasia of Queyrat are forms of SCC in situ that can sometimes develop into an invasive form. | They represent one of the most common reasons for a dermatologist visit in the USA. In the USA, AK were present in 55% of fair skinned men and 37% of fair skinned women between the ages of 65 and 74. | [30, 31] |
| Other skin lesions | SCC often develops in scar tissue (e.g., healed burns). Similarly, it also arises in areas of chronic inflammation, such as ulcers, sinus tracts, and inflammatory dermatoses. | Approximately 1% of skin cancer develops in chronically irritated skin. In 95% it is SCC. | |
|
| Malignant melanoma | | | |
| Constitutional factors (race, pigmentation, and genetic predisposition) | (i) Skin type and sunlight are the main factors that influence MM incidence.
(ii) The incidence of MM and other types of skin cancer is greater in patients with XP and albinism. | (i) On average, MM is 3-4 times more common in less pigmented races, compared to more pigmented ones.
(ii) The number of melanocytic nevi that a person has on their skin is a good indicator of MM risk. | [32] |
| Ultraviolet light | (i) The main environmental factor for MM and other skin cancer development is short wavelength UV light present in sunlight.
(ii) The prominent effects of UV radiation are pyrimidine dimer formation, DNA base and nucleoprotein crosslinking, and polynucleotide chain disruption. | Incidence increases nearer to the Equator, where the UVB dose in sunlight is highest. UVA also have carcinogenic effects. | [32, 33] |
| Other factors | Multiple factors were proposed; occupation, diet, smoking, oral contraceptives, endometriosis, Parkinson's disease, TNF inhibitors, and so forth. | Statistically significant links with the disease have not been found for most factors, with the exception of endometriosis and Parkinson’s disease. Correlation with MM has been found there. | [34, 35] |
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