Table 5. Meta-Analysis Results: Intermittent and Chronic Sun Exposure and Melanoma Risk continued...
Data from Connecticut have shown that cumulative lifetime exposure to ultraviolet-B (UVB) radiation does not differ between melanoma cases and controls; rather, intermittent sun exposure is the more important risk factor. The risks related to intermittent sun exposure are even greater if this pattern is experienced both early in life and later in life. These data can also be interpreted as suggesting that sun exposure patterns are rather consistent and stable throughout one's lifetime (i.e., that individuals who receive a great deal of intermittent sun exposure during early life are also likely to receive a great deal of intermittent sun exposure during later life). Nonetheless, an intermittent pattern of sun exposure over many years appears to significantly increase melanoma risk.
The relationship between sun exposure, sunscreen use, and the development of skin cancer is also complex. It is complicated by "negative confounding" (i.e., subjects who are extremely sun sensitive deliberately engage in fewer activities in direct sunlight, and they are more likely to wear sunscreen when they do). These subjects are genetically susceptible to the development of skin cancer by virtue of their cutaneous phenotype and thus may develop skin cancer regardless of the amount of sunlight exposure or the sun protection factor of the sunscreen.[12,13]
Other environmental factors
There are a number of additional environmental factors that are important to melanoma development (see Table 6).
Table 6. Environmental Exposures Other Than Sunlight Associated with Melanomaa
|Study Citation||Subjects||Time and/or Place||Point Estimate|
|Cl = confidence interval; OR = odds ratio; PCB = polychlorinated biphenyls; PVC = polyvinyl chloride; RR = relative risk; SIR = standardized incidence ratio; SMR = standard mortality rate.|
|a Adapted from Gruber et al.|
|Wennborg et al.||Cohort (N = 23,718)||1970–1994; Sweden||RR = 2.7 (95% CI, 1.1–5.6)|
|Ron et al.||Various cohorts (N = 80,000)||Hiroshima, Japan||Excess RR per Sievert = 2.1 (95% CI, <0.01–12)|
|Sigurdson et al.||U.S. Radiologic Technologists cohort (N = 90,305)||United States||SIR = 1.59 (95% CI, 1.38–1.80)|
|Telle-Lamberton et al.||French Atomic Energy Commission workers (N = 58,320)||France||SMR = 1.50 (90% CI, 1.04–2.11) among males|
|Sont et al.||(N = 3,737)||Canada||SIR = 1.16 (90% CI, 1.04–1.30)|
|Airline Flight Crews|
|Pukkala et al.||Male pilots (N = 10,032)||Scandinavia||SIR = 2.3 (95% CI, 1.7–3.0)|
|Tynes et al.||(N = 807 cases, 1,614 controls)||1980–1996; Norway||OR = 1.87 (95% CI, 1.23–2.83)|
|Lundberg et al.||Men in PVC processing plants (N = 717)||Sweden||SMR = 3.4 (95% CI, 1.1–7.9)|
|Landgård et al.||Workers exposed to PVC (N = 428)||Norway||SIR = 2.06, (95% CI, 1.36–6.96)|
|Loomis et al.||Occupational cohort of men exposed to PCBs (N = 138,905)||United States||RR = 1.29 (95% CI, 0.96–1.82), 5% increase per 2,000 h of exposure|