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Risk factors/epidemiology

Skin Cancer Statistics and Issues Prevention Policy

Risk categories

Skin cancer risk is categorised into average risk, increased risk, and high risk by the Royal Australian College of General Practitioners, as described below.[1]

Melanocytic skin cancer

Individuals with medium/dark skin colour and no other risk factors are at average risk of melanocytic skin cancer.

Individuals with the following characteristics are at an increased risk of melanocytic skin cancer:

  • Family history of melanoma in first-degree relative (relative risk [RR] = 1.7)
  • Fair complexion, a tendency to burn rather than tan, the presence of freckles, high naevus count (>100), light eye colour, light or red hair colour
  • Presence of actinic damage (RR = 2)
  • Past history of non-melanocytic skin cancer (NMSC) (<40 years higher risk)
  • People with childhood high levels of ultraviolet (UV) exposure and episodes of sunburn in childhood (RR = 2)

Those at high risk (that is, those at greater than 6 times the average risk of melanocytic skin cancer) have have >5 atypical (dysplastic) naevi (atypically shaped moles) and/ora history of melanoma in themselves or a first-degree relative.[1]

Non-melanoma (keratinocytic) skin cancer

Individuals with fair to lighter than olive skin, and are less than 40 years of age without any risk factors are at an average risk of non-melanoma skin cancer. Individuals with the following characteristics are at increased risk:

  • fair complexion, a tendency to burn rather than tan, the presence of freckles, light eye colour, light or red hair
  • family history of skin cancer
  • aged >40 years
  • male
  • presence of multiple solar keratoses
  • high UV exposure (for example, outdoor workers)

Those at high risk will have characteristics associated with increased risk, as well as a previous history of non-melanoma skin cancer, past exposure to arsenic and/or immunosuppression.[1]


Melanoma is more common in older adults than younger people,[2][3] with the mean diagnosis age being 66 years among men and 62.3 years among women in 2018.[4] Older adults have had more cumulative sun exposure than younger people, with every additional decade of high sun exposure shown to further increase the risk of melanoma.[5][6] However, by limiting recreational sun exposure a person is likely to decrease their risk of melanoma, regardless of their age.[5]

Although early onset melanoma is comparatively rare, melanoma is the most commonly diagnosed cancer among Australians aged 15-29 years.[4] There were 1,225 new melanoma cases among those aged under 40 years in 2018 (estimated to be 1,169 in 2022).[4]

It is estimated that in 2015, just over two-thirds (68%) of NMSC treatments were provided to people aged 65 and over.[7]

Familial and personal skin cancer history

An individual’s skin cancer history is a risk factor for subsequent melanoma[1] (particularly following Lentigo maligna melanoma or nodular melanoma)[8] and non-melanoma skin cancer.[9] In retrospective studies, the percentage of melanoma patients that develop second primary melanoma ranges between 2% and 20%[10], varying according to the design and measures used.[11]

The risk of melanoma is increased in relatives of cutaneous malignant melanoma patients. Approximately 5% to 10% of cases of cutaneous melanoma occur in families with a hereditary predisposition.[12] Most cases of familial melanoma are due to shared sun exposure experiences among family members with susceptible skin types.[13] Meta-analysis of 60 studies assessing family history of skin cancer (melanoma diagnosed in a first-degree relative) estimated an almost 2-fold increase in melanoma risk.[14]

A prospective study by Ferrone and colleagues estimated a 19% cumulative five-year risk of a second primary tumour for patients who were diagnosed with a primary melanoma and also had a familial history of melanoma.[8]


Traits such as red or blond hair, light-coloured eyes, fair skin, sun sensitive skin (particularly Fitzpatrick type I skin) and propensity to freckle are genetic risk factors for developing melanoma and keratinocytic skin cancers when combined with UV exposure.[6][14]

Those with fair skin possess little epidermal eumelanin, which absorbs UV radiation and acts to neutralise UV radiation-generated free radicals, and are thus at greater risk of skin cancer.[15][16] However, it is the high pheomelanin to eumelanin ratio in the melanin of individuals with a red-hair and fair skin phenotype that greatly increases their melanoma risk. Mouse models suggest this genetic factor may be a UV radiation-independent carcinogen, with UV overexposure likely to exacerbate melanoma risk among this phenotype.[17]

Light eye colour is also a significant risk factor for ocular melanoma.[18]


Those with particular genetic variants may be more sensitive to UV radiation than others, and may therefore only require modest levels of exposure to initiate development of melanoma.[19][20]

Common variations in at least twenty genes are known to influence melanoma risk in the population.[21] In 2020 Landi and colleagues identified 31 new genetic regions associated with melanoma risk.[22]

Polygenic risk scores (PRSs) aggregate the effects of many genetic variants across the genome into a single score aiming to reflect an individual’s genetic risk of disease. A 2022 study by Steinberg and colleagues derived newer melanoma PRSs from a larger, more diverse meta-analysis than had previously been undertaken, which was found to have. better risk prediction performance than an earlier PRS.[23]

Research is continuing in this area in order to further improve risk analysis for individuals.


The number of common naevi (moles) increases risk of cutaneous melanoma. A meta-analysis of 46 studies showed having between 101-120 naevi present a highly significant risk for melanoma - almost seven times greater (pooled relative risk of 6.89) than people with very few naevi (0-15 naevi).[24]

Figure 1: Dysplastic naevi

Images generously provided by Dr Alvin Chong, Skin & Cancer Foundation Victoria

The presence of dysplastic (atypical) naevi also indicates a high skin cancer risk.[1] Having more than five dysplastic naevi, as compared with having none, results in a melanoma RR (relative risk) of 6.36.[24] Furthermore, patients with a primary melanoma more than double their five-year risk of a second primary melanoma (24% cf. 11% increase in risk) if they have dysplastic naevi.[8]

Solar lentigines

Solar lentigines, also known as solar lentigo, are the result of actinic (sun) damage and have the appearance of small, tan-brown to black pigmented, flat or slightly raised spots. In particular, their presence is strongly associated with risk of lentigo malignant melanoma (LMM), Compared with zero solar lentigines on the arm, having more than 10 is associated with a fifteen-fold risk of LMM (compared with an almost five-fold risk of superficial spreading melanoma).[25]

Sun exposure

In Australia, up to 95% of melanomas are attributable to overexposure to UV radiation.[26][27] Skin exposure to UV radiation can result in DNA damage and mutations. These most commonly occur to the p53 suppressor gene through the formation of cyclobutane pyrimidine dimers (CPDs) UV-induced bonding between adjacent pyrimidines, such as thymine or cytosine DNA bases,[28] and other mutagenic photoproducts which are primarily caused by UVB radiation.[29] Cutaneous UV absorption also causes damage indirectly, due to the generation of excess reactive oxygen species (ROS) causing oxidative DNA damage (primarily UVA-induced).[29] However, this has been suggested as not being "sufficient to induce mutations in the normal skin genome".[30]

UV radiation is classified as a complete carcinogen because it causes mutations as well as general damage, and inducts and promotes tumour growth.[16] Excessive UV exposure increases the risk of both melanoma and keratinocytic skin cancers.[31]

Figure 1: UV-damaged, distorted DNA molecule showing cyclobutane pyrimidine dimers

Image retrieved from Wikimedia Commons

Both UVA and UVB radiation are independently associated with melanoma mortality according to an ecological study by Garland and colleagues, which links age-adjusted mortality rates with the spectrophotometric UV measurements of 45 countries (adjusting for population average skin pigmentation).[32] UVB radiation has been shown to be more carcinogenic than UVA in experimental induction of squamous cell carcinoma (SCC).[33] However, some research suggests that UVA may be more carcinogenic than previously thought. Data suggests that the basal skin layer is particularly vulnerable to UVA-induced damage.[34][35]

Skin cancer risk is not just related to the amount of sun exposure, but also to the pattern. Melanoma and basal cell carcinoma risk are particularly linked to habitual low sun exposure combined with high recreational sun exposure. For example, this is exactly the pattern of many indoor workers, with high sun exposure on sunny weekends or summer holidays. On the other hand, a more continuous pattern of exposure, such as that due to occupational exposure, is associated with increased SCC risk.[31][36]

Melanoma risk is associated with cumulative, intermittent exposure to UV radiation.[31] A meta-analysis of 57 studies by Gandini and colleagues found a positive association between melanoma risk and intermittent sun exposure, but an inverse association for continuous over-exposure.[37]

Chronic exposure in later life has also been shown to be an important risk factor for BCC - risk is higher among outdoor compared with indoor workers according to a systematic review and meta-analysis by Bauer and colleagues.[38] Wu et al reported that chronic sun exposure in adulthood, as assessed by cumulative UV flux over long durations, were associated with substantially increased risks of BCC and SCC.[39]

Childhood exposure

High sun exposure in the first 10 years of life more than doubles melanoma risk,[5] while intense, intermittent sun exposure (number of sunburns and sunbathing vacations) during each decade up to 29 years of age increases risk of melanoma by more than one-and-a-half times.[6] Wu et al reported that melanoma risk is strongly associated with sun exposure in early life, as evidenced by the number of blistering sunburns between ages 15 and 20 years.[39]

Childhood is a critical period for melanoma risk because of sun exposure, as shown by ecological studies, and, less consistently, case-controlled studies.[40] Intensive childhood UV exposure increases the risk of developing BCC, while chronic childhood exposure increases the risk of SCC.[31]


While sunburn does not directly cause melanoma, it is often used as an indicator of melanoma risk. This is because it is memorable and is a marker of the type of sun exposure most associated with melanoma (intermittent intense exposure) combined with the type of skin that is most susceptible to melanoma (skin that is sensitive enough to UV to burn).[36][40] Recalling childhood sunburn is a good indication that an individual was over-exposed to UV and had sun-sensitive skin – two factors that increase melanoma risk. Reductions in the frequency of sunburn are also often used as a practical and appropriate short-term outcome measure to assess intervention programs, which are aimed at reducing excess sun exposure and ultimately preventing melanoma.[41][42][43]

A study by Pfahlberg and Kölmel found that having more than five sunburns doubled the risk of melanoma, with risk similar for childhood exposure before 15 years of age, and exposure after 15 years of age.[44] However, other studies found that childhood and youth were critical periods of increased melanoma risk due to sunburn. The number of recalled sunburns prior to 30 years of age was found to significantly increase melanoma risk - however the positive relationship with melanoma risk was weaker for sunburns incurred between the ages of 30-39, and not evident for 40-49 years of age.[6] Having a severe sunburn in childhood more than doubled melanoma risk in people aged 18-39 years in a case control study by Cust and colleagues.[45] Painful sunburns before the age of 20 are associated with increased risk of melanoma (1.4 times increase in risk), squamous cell carcinoma (1.5 times increase risk), and certain basal cell carcinoma subtypes (1.6 times increase in risk).[46] Savoye and colleagues[47] found severe sunburns under the age of 25 was associated with increased risk of all skin cancer types. However, severe sunburns obtained at age 25 or older were not associated with an increased melanoma risk, only BCC and SCC.

Solarium use

A systematic review has shown a dose-response relationship between sunbed use and melanoma risk. Sunbed use increases melanoma risk by 20%, with an increase of 59% if used before 35 years of age.[48] A study in the USA found that the more frequently people used solariums, the higher their risk of melanoma - regardless of the age at which they began using solariums.[49]

A meta-analysis by Wehner and colleagues found that indoor tanning increased risk of both SCC and BCC, with risk particularly high among people who had used indoor tanning before 25 years of age (SCC relative risk=2.02; BCC RR=1.40).[50] Indoor tanning is a strong risk factor for early-onset BCC among people under 40 years of age, particularly among women.[51]

Outdoor work

It is estimated that around 200 melanomas and 34,000 keratinocytic skin cancers per year are caused by occupational exposures in Australia.[52]

Outdoor workers receive between five to ten times the annual dose of UV than indoor workers.[53] Meta-analyses have found that the risk of SCC among outdoor workers is nearly double that of indoor workers[54] while risk of BCC is increased by almost 1.5 times.[38] These reviews conclude that outdoor work constitutes an independent and robust risk factor for the development of cutaneous SCC and BCC.[54][38]

A meta-analysis by Gandini and colleagues did not find an association between high occupational sun exposure and melanoma.[37] However there is evidence that melanomas of the head and neck are associated with chronic sun exposure.[55] Melanoma risk is particularly linked to habitual low sun exposure combined with high recreational sun exposure.[36]

Melanoma risk at different body sites is associated with different patterns of sun exposure at different latitudes. Recreational (i.e. intermittent) sun exposure is a strong predictor of melanoma on the trunk and limbs at all latitudes, whereas occupational exposure appears to predict melanoma on the head and neck - albeit weakly - predominately at low latitudes. Total sun exposure is associated with melanoma on the limbs at low latitudes.[56]

Risk factors for second primary melanoma or keratinocytic skin cancer

A prospective study by Ferrone and colleagues estimated the cumulative five-year risk of a second primary tumour for patients diagnosed with a primary melanoma is 11%, with almost half that risk within the first year. Risk of a second primary melanoma increased to 19% for patients with a family history of melanoma, and 24% for patients with dysplastic naevi[8] In 2020 Villani and colleagues conducted a retrospective study and found the risk to be 8.2%.[11] Phenotypic characteristics (fair skin and inability to tan) also increased risk of second primary melanomas.[57]

First primary lentigo or nodular melanomas had higher risks of multiple melanomas compared with the more common superficial spreading melanoma.[57] High exposure to UV radiation (childhood exposure and lifetime recreation sun exposure) was also shown to increase risk of multiple primary melanomas.[5]

Registry-linked data shows the cumulative incidence of second primary melanomas varies across populations, and is estimated at 6.4% at 10 years after diagnosis in Queensland[58] - higher than in Switzerland or the US.[59]

A meta-analysis of 17 studies by Marcil and Stern estimated that of patients with a history of non-melanoma skin cancer 44% would develop a subsequent basal cell carcinoma and 18% a squamous cell carcinoma within 3 years. The risk of developing a BCC from a prior SCC or BCC were similar, but the risk of developing a SCC following a BCC diagnosis was relatively low.[9]

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Last modified: 5 August 2022


  1. The Royal Australian College of General Practitioners. Guidelines for preventive activities in general practice. 9th edn. East Melbourne, Australia; 2016.
  2. Lasithiotakis KG, Petrakis IE, Garbe C. Cutaneous melanoma in the elderly: epidemiology, prognosis and treatment. Melanoma Res 2010 Jun;20(3):163-70 Available from:
  3. Australian Institute of Health and Welfare. Skin cancer in Australia. Cat. no. CAN 96. Canberra, Australia: AIHW; 2016 [cited 2016 Oct 5] Available from:
  4. Australian Institute of Health and Welfare. Cancer data in Australia. [homepage on the internet] Canberra, Australia: AIHW; 2022 Jul 1 [cited 2022 Jul 27]. Available from:
  5. Kricker A, Armstrong BK, Goumas C, Litchfield M, Begg CB, Hummer AJ, et al. Ambient UV, personal sun exposure and risk of multiple primary melanomas. Cancer Causes Control 2007 Apr;18(3):295-304 Available from:
  6. Veierød MB, Adami HO, Lund E, Armstrong BK, Weiderpass E. Sun and solarium exposure and melanoma risk: effects of age, pigmentary characteristics, and nevi. Cancer Epidemiol Biomarkers Prev 2010 Jan;19(1):111-20 Available from:
  7. Fransen M, Karahalios A, Sharma N, English DR, Giles GG, Sinclair RD. Non-melanoma skin cancer in Australia. Med J Aust 2012 Nov 19;197(10):565-8 Available from:
  8. Ferrone CR, Ben Porat L, Panageas KS, Berwick M, Halpern AC, Patel A, et al. Clinicopathological features of and risk factors for multiple primary melanomas. JAMA 2005 Oct 5;294(13):1647-54 Available from:
  9. Marcil I, Stern RS. Risk of developing a subsequent nonmelanoma skin cancer in patients with a history of nonmelanoma skin cancer: a critical review of the literature and meta-analysis. Arch Dermatol 2000 Dec;136(12):1524-30 Available from:
  10. Lallas A, Apalla Z, Kyrgidis A, Papageorgiou C, Boukovinas I, Bobos M, et al. Second primary melanomas in a cohort of 977 melanoma patients within the first 5 years of monitoring. J Am Acad Dermatol 2020 Feb;82(2):398-406 Available from:
  11. Villani A, Fabbrocini G, Costa C, Greco V, Scalvenzi M. Second primary melanoma: incidence rate and risk factors. J Eur Acad Dermatol Venereol 2020 Apr 21 Available from:
  12. Hansson J. Familial melanoma. Surg Clin North Am 2008 Aug;88(4):897-916, viii Available from:
  13. Goldstein AM, Tucker MA. Genetic epidemiology of cutaneous melanoma: a global perspective. Arch Dermatol 2001 Nov;137(11):1493-6 Available from:
  14. Gandini S, Sera F, Cattaruzza MS, Pasquini P, Zanetti R, Masini C, et al. Meta-analysis of risk factors for cutaneous melanoma: III. Family history, actinic damage and phenotypic factors. Eur J Cancer 2005 Sep;41(14):2040-59 Available from:
  15. Markovic SN, Erickson LA, Rao RD, Weenig RH, Pockaj BA, Bardia A, et al. Malignant melanoma in the 21st century, part 1: epidemiology, risk factors, screening, prevention, and diagnosis. Mayo Clin Proc 2007 Mar;82(3):364-80 Available from:
  16. D'Orazio J, Jarrett S, Amaro-Ortiz A, Scott T. UV Radiation and the Skin. Int J Mol Sci 2013 Jun 7;14(6):12222-48 Available from:
  17. Mitra D, Luo X, Morgan A, Wang J, Hoang MP, Lo J, et al. An ultraviolet-radiation-independent pathway to melanoma carcinogenesis in the red hair/fair skin background. Nature 2012 Nov 15;491(7424):449-53 Available from:
  18. Vajdic CM, Kricker A, Giblin M, McKenzie J, Aitken J, Giles GG, et al. Eye color and cutaneous nevi predict risk of ocular melanoma in Australia. Int J Cancer 2001 Jun 15;92(6):906-12 Available from:
  19. Olsen CM, Pandeya N, Law MH, MacGregor S, Iles MM, Thompson BS, et al. Does polygenic risk influence associations between sun exposure and melanoma? A prospective cohort analysis. Br J Dermatol 2019 Nov 20 Available from:
  20. McMeniman EK, Duffy DL, Jagirdar K, Lee KJ, Peach E, McInerney-Leo AM, et al. The interplay of sun damage and genetic risk in Australian multiple and single primary melanoma cases and controls. Br J Dermatol 2019 Dec 3 Available from:
  21. Mann, G, A/Prof Anne Cust, Damian, D, Paul Fishburn, Kelly, J, Victoria Mar MBBS, FACD, PhD, Soyer, P, Cancer Council Australia Melanoma Guidelines Working Party. Guidelines:Genetic determinants of high risk for new primary melanoma. In: Clinical practice guidelines for the diagnosis and management of melanoma. [homepage on the internet] Sydney, Australia: Melanoma Institute Australia.; [cited 2022 Aug 5; updated 2019 Mar 13]. Available from:
  22. Landi MT, Bishop DT, MacGregor S, Machiela MJ, Stratigos AJ, Ghiorzo P, et al. Genome-wide association meta-analyses combining multiple risk phenotypes provide insights into the genetic architecture of cutaneous melanoma susceptibility. Nat Genet 2020 May;52(5):494-504 Available from:
  23. Steinberg J, Iles MM, Lee JY, Wang X, Law MH, Smit AK, et al. Independent evaluation of melanoma polygenic risk scores in UK and Australian prospective cohorts. Br J Dermatol 2022 May;186(5):823-834 Available from:
  24. Gandini S, Sera F, Cattaruzza MS, Pasquini P, Abeni D, Boyle P, et al. Meta-analysis of risk factors for cutaneous melanoma: I. Common and atypical naevi. Eur J Cancer 2005 Jan;41(1):28-44 Available from:
  25. Kvaskoff M, Siskind V, Green AC. Risk factors for lentigo maligna melanoma compared with superficial spreading melanoma: a case-control study in Australia. Arch Dermatol 2012 Feb;148(2):164-70 Available from:
  26. Whiteman DC, Webb PM, Green AC, Neale RE, Fritschi L, Bain CJ, et al. Cancers in Australia in 2010 attributable to modifiable factors: introduction and overview. Aust N Z J Public Health 2015 Oct;39(5):403-7 Available from:
  27. Armstrong BK, Kricker A. How much melanoma is caused by sun exposure? Melanoma Res 1993 Dec;3(6):395-401 Available from:
  28. Rigel DS. Epidemiology of melanoma. Semin Cutan Med Surg 2010 Dec;29(4):204-9 Available from:
  29. Pfeifer GP, Besaratinia A. UV wavelength-dependent DNA damage and human non-melanoma and melanoma skin cancer. Photochem Photobiol Sci 2012 Jan;11(1):90-7 Available from:
  30. Ikehata H, Ono T. The mechanisms of UV mutagenesis. J Radiat Res 2011;52(2):115-25 Available from:
  31. Leiter U, Garbe C. Epidemiology of melanoma and nonmelanoma skin cancer--the role of sunlight. Adv Exp Med Biol 2008;624:89-103 Available from:
  32. Garland CF, Garland FC, Gorham ED. Epidemiologic evidence for different roles of ultraviolet A and B radiation in melanoma mortality rates. Ann Epidemiol 2003 Jul;13(6):395-404 Available from:
  33. de Gruijl FR. Photocarcinogenesis: UVA vs. UVB radiation. Skin Pharmacol Appl Skin Physiol 2002 Sep;15(5):316-20 Available from:
  34. Agar NS, Halliday GM, Barnetson RS, Ananthaswamy HN, Wheeler M, Jones AM. The basal layer in human squamous tumors harbors more UVA than UVB fingerprint mutations: a role for UVA in human skin carcinogenesis. Proc Natl Acad Sci U S A 2004 Apr 6;101(14):4954-9 Available from:
  35. Tewari A, Sarkany RP, Young AR. UVA1 induces cyclobutane pyrimidine dimers but not 6-4 photoproducts in human skin in vivo. J Invest Dermatol 2012 Feb;132(2):394-400 Available from:
  36. Armstrong BK. How sun exposure causes skin cancer: An epidemiological perspective In: Hill D, Elwood JM, English D. Prevention of Skin Cancer. Dordrecht, The Netherlands: Kluwer Academic Publishers; 2004. p. 89-116.
  37. Gandini S, Sera F, Cattaruzza MS, Pasquini P, Picconi O, Boyle P, et al. Meta-analysis of risk factors for cutaneous melanoma: II. Sun exposure. Eur J Cancer 2005 Jan;41(1):45-60 Available from:
  38. Bauer A, Diepgen TL, Schmitt J. Is occupational solar ultraviolet irradiation a relevant risk factor for basal cell carcinoma? A systematic review and meta-analysis of the epidemiological literature. Br J Dermatol 2011 Sep;165(3):612-25 Available from:
  39. Wu S, Han J, Laden F, Qureshi AA. Long-term Ultraviolet Flux, Other Potential Risk Factors, and Skin Cancer Risk: A Cohort Study. Cancer Epidemiol Biomarkers Prev 2014 May 29 Available from:
  40. Whiteman DC, Whiteman CA, Green AC. Childhood sun exposure as a risk factor for melanoma: a systematic review of epidemiologic studies. Cancer Causes Control 2001 Jan;12(1):69-82 Available from:
  41. Hill D, White V, Marks R, Borland R. Changes in sun-related attitudes and behaviours, and reduced sunburn prevalence in a population at high risk of melanoma. Eur J Cancer Prev 1993 Nov;2(6):447-56 Available from:
  42. Elwood M, Makin J, Sinclair C, Burton RC. Prevention and screening In: Balch C, Houghton A. N, Sober A. G, Soong SJ, Atkins MB, Thompson JF. Cutaneous Melanoma 5th edition. St Louis Quality Medical Publishing; 2009. p. 107-32.
  43. Tabbakh T, Volkov A, Wakefield M, Dobbinson S. Implementation of the SunSmart program and population sun protection behaviour in Melbourne, Australia: Results from cross-sectional summer surveys from 1987 to 2017. PLoS Med 2019 Oct;16(10):e1002932 Available from:
  44. Pfahlberg A, Kölmel KF, Gefeller O, Febim Study Group. Timing of excessive ultraviolet radiation and melanoma: epidemiology does not support the existence of a critical period of high susceptibility to solar ultraviolet radiation- induced melanoma. Br J Dermatol 2001 Mar;144(3):471-5 Available from:
  45. Cust AE, Jenkins MA, Goumas C, Armstrong BK, Schmid H, Aitken JF, et al. Early-life sun exposure and risk of melanoma before age 40 years. Cancer Causes Control 2011 Jun;22(6):885-97 Available from:
  46. Kennedy C, Bajdik CD, Willemze R, De Gruijl FR, Bouwes Bavinck JN, Leiden Skin Cancer Study. The influence of painful sunburns and lifetime sun exposure on the risk of actinic keratoses, seborrheic warts, melanocytic nevi, atypical nevi, and skin cancer. J Invest Dermatol 2003 Jun;120(6):1087-93 Available from:
  47. Savoye I, Olsen CM, Whiteman DC, Bijon A, Wald L, Dartois L, et al. Patterns of Ultraviolet Radiation Exposure and Skin Cancer Risk: the E3N-SunExp Study. J Epidemiol 2018 Jan 5;28(1):27-33 Available from:
  48. Boniol M, Autier P, Boyle P, Gandini S. Cutaneous melanoma attributable to sunbed use: systematic review and meta-analysis. BMJ 2012 Jul 24;345:e4757 Available from:
  49. Lazovich D, Vogel RI, Berwick M, Weinstock MA, Anderson KE, Warshaw EM. Indoor tanning and risk of melanoma: a case-control study in a highly exposed population. Cancer Epidemiol Biomarkers Prev 2010 Jun;19(6):1557-68 Available from:
  50. Wehner MR, Shive ML, Chren MM, Han J, Qureshi AA, Linos E. Indoor tanning and non-melanoma skin cancer: systematic review and meta-analysis. BMJ 2012 Oct 2;345:e5909 Available from:
  51. Ferrucci LM, Cartmel B, Molinaro AM, Leffell DJ, Bale AE, Mayne ST. Indoor tanning and risk of early-onset basal cell carcinoma. J Am Acad Dermatol 2012 Oct;67(4):552-62 Available from:
  52. Fritschi L, Driscoll T. Cancer due to occupation in Australia. Aust N Z J Public Health 2006 Jun;30(3):213-9 Available from:
  53. Gies P, Wright J. Measured solar ultraviolet radiation exposures of outdoor workers in Queensland in the building and construction industry. Photochem Photobiol 2003 Oct;78(4):342-8 Available from:
  54. Schmitt J, Seidler A, Diepgen TL, Bauer A. Occupational ultraviolet light exposure increases the risk for the development of cutaneous squamous cell carcinoma: a systematic review and meta-analysis. Br J Dermatol 2011 Feb;164(2):291-307 Available from:
  55. Whiteman DC, Stickley M, Watt P, Hughes MC, Davis MB, Green AC. Anatomic site, sun exposure, and risk of cutaneous melanoma. J Clin Oncol 2006 Jul 1;24(19):3172-7 Available from:
  56. Chang YM, Barrett JH, Bishop DT, Armstrong BK, Bataille V, Bergman W, et al. Sun exposure and melanoma risk at different latitudes: a pooled analysis of 5700 cases and 7216 controls. Int J Epidemiol 2009 Jun;38(3):814-30 Available from:
  57. Siskind V, Hughes MC, Palmer JM, Symmons JM, Aitken JF, Martin NG, et al. Nevi, family history, and fair skin increase the risk of second primary melanoma. J Invest Dermatol 2011 Feb;131(2):461-7 Available from:
  58. McCaul KA, Fritschi L, Baade P, Coory M. The incidence of second primary invasive melanoma in Queensland, 1982-2003. Cancer Causes Control 2008 Jun;19(5):451-8 Available from:
  59. Psaty EL, Scope A, Halpern AC, Marghoob AA. Defining the patient at high risk for melanoma. Int J Dermatol 2010 Apr;49(4):362-76 Available from: