Updated sunscreen advice: SPF30.
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Biomedical subjects
Publications and source records attributed to M A Weinstock.
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Skin cancer prevention is increasingly a focus of public health campaigns. The most important avoidable cause of skin cancer is ultraviolet radiation from the sun, but sunscreens are often used in a suboptimal manner, compromising their effectiveness. People may "compensate" for the use of sunscreen by increasing their time in the sun, which can have adverse effects on health. Epidemiologic studies of sunscreen use have suffered from important methodologic limitations. A clearer picture of the impact of sunscreens is emerging from randomized trials that have recently been published or presented. The available evidence supports the current recommendation to "Slip! Slop! Slap!" when in the sun.
The authors examined the relation of constitutional factors and sun exposure to risk of basal cell carcinoma of the skin (BCC) in a prospective cohort of 44,591 predominantly Caucasian US male health professionals, 40-75 years of age and free of cancer at enrollment in 1986. During 8 years of follow-up, 3,273 cases of self-reported BCC were documented. The following variables were each associated with an elevated risk of BCC: having red hair; green, hazel, or blue eyes; a tendency to sunburn; and north European ancestry. The lifetime number of blistering sunburns was also positively associated with BCC risk (p trend < 0.0001). Compared with men who as teenagers had been outside less than once a week, men who had been outside weekly (relative risk (RR) = 1.30; 95% confidence interval (CI): 1.14, 1.47) and daily (RR = 1.42; 95% CI: 1.24, 1.63) had an elevated risk of BCC. Living in a region of residence with high solar radiation as an adult was also associated with an increased risk of BCC (RR = 1.48; 95% CI: 1.36, 1.60), whereas living in such a region only in childhood did not increase BCC risk. These results confirm the role of constitutional factors and suggest that adult sun exposure increases BCC risk.
BACKGROUND: The authors sought to evaluate trends in survival among a population-based group of patients with mycosis fungoides, in response to informal evidence of improved prognosis and concerns about the influence of detection bias on incidence data. METHODS: Data used in this study were drawn from the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute, which includes 9 population-based cancer registries. Together, these registries cover approximately 10% of the U.S. population and have tracked the survival of all mycosis fungoides patients who were registered during the years 1973-1992. Data included follow-up through 1994. RESULTS: There was a total of over 10,000 person-years of follow-up for the 1633 patients studied. Relative survival changed little after 11 years, at which point it was 66%. Advanced age and black race were associated with poorer survival. The prognoses of Asian and Hispanic patients were slightly but not significantly worse than those of whites, and there were no significant geographic differences related to prognosis. The survival of married women was superior to that of other gender and marital-status groups. Prognosis did improve substantially over the 20-year period of study. CONCLUSIONS: Mycosis fungoides is usually not a fatal disease, although the mortality risk is substantial. The authors quantified various prognostic factors and documented an improved prognosis over the 20-year period of study. The data from this study raise concern about possible detection bias in incidence data. These data are also consistent with the concept that beyond 11 years after diagnosis, this disorder has relatively little impact on the risk of death.
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Ultraviolet adiation is an important cause of melanoma, so the use of sunscreen lotions has been advocated for melanoma prevention. Several arguments have been raised in opposition to this inference. Sunscreen use may interfere with cutaneous vitamin D synthesis, which some have hypothesized may lower melanoma risk. Sunscreen users may compensate for their sunscreen use by staying out much longer in the sun, or may use sunscreen lotions inconsistantly. Published melanoma case-control studies have not consistantly demonstrated a protective effect of sunscreens; however, these studies do not provide strong evidence, ultraviolet radiation is a known cause of melanoma, and ultraviolet B may be particularly potent, so on balance the evidence supports continued advocacy of sunscreen lotion use as part of an overall sun-protection regimen. Uncertainty will remain, however, until the action spectrum of melanoma is convincingly demonstrated or the methodologic limitations of existing epidemiologic evidence are overcome. The latter may require another decade or more of experience with sunscreen use.
Sun care products containing sunscreens are widely used, but consumers are generally unaware of the important differences in the ability of these lotions to block exposure to the ultraviolet A (UVA) portion of the solar spectrum. The purpose of this study was to determine the transmittance spectra, with particular emphasis on the UVA portion of the spectrum, for a variety of commercially available sun care products, to determine Commission Internationale d'Eclairage (CIE) erythema effectiveness spectra and to compare these with information in the product label. The transmittance spectra for a sample of sun care products were measured spectrophotometrically. These values were convoluted with the CIE erythema action spectrum and the sunlight spectra determined for solar noon on June 21 at 0 degrees and 50 degrees N latitude to produce CIE effectiveness spectra. The UVA transmitted through the sun care products that claimed UVA protection on the bottle label varied from as little as 6% to as much as 52%. In addition, it was determined from the CIE effectiveness spectra that any erythema induced following application of the tested lotions would be caused by the UVA portion of the solar spectrum for all, but one, of the products examined. The results of this study emphasize the necessity for better guidance to the consumer as to the ability of sun care products to provide protection against UVA exposure.
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OBJECTIVES: Patterns of mycosis fungoides incidence and associated mortality in the United States were evaluated. METHODS: Data were taken from the Surveillance, Epidemiology, and End Results cancer registry program and the National Center for Health Statistics. RESULTS: The incidence rate from 1973 through 1992 was 0.36/10(5) person-years. The age-adjusted incidence rate ratio of Blacks to Whites was 1.7; that of Asians to Whites was 0.6. There was no evidence of increasing incidence rates during the period 1983 through 1992. Mortality rates declined steadily from 1979 to 1991 and were less heterogeneous geographically than incidence rates. Mortality rate patterns with age, sex, and race were similar to the corresponding incidence patterns. CONCLUSIONS: The incidence rate of mycosis fungoides has stabilized and the mortality rate has declined. For unknown reasons, the disorder varies greatly among demographic and geographic subgroups.
Sun exposure histories were obtained from a series of patients age 35 or younger following diagnosis and removal of a basal cell carcinoma (BCC). The DNA was extracted from tumor biopsy samples derived from BCC of 10 patients who reported that they did not use sunscreens during youth (age 18 or younger) and 10 patients who routinely employed sunscreens during this age period. Exons 5-9 of the p53 gene were then amplified in three fragments from these samples using a nested polymerase chain reaction (PCR) approach and screened for mutations using an RNA heteroduplex assay. All PCR products displaying evidence of a mutation were sequenced. It was found that 6 of the 10 patients who were not routine sunscreen users displayed mutations in these p53 exons. All of the mutations were located at dipyrimidine sites, five of the six were C-->T transitions and one mutation was a tandem double mutation, consistent with a role for solar UVB in BCC formation. In contrast, only one p53 mutation was detected in the group of 10 patients who routinely employed sunscreens during childhood and adolescence. Hence, a significantly (P = 0.029) lower level of p53 mutations was detected in the BCC obtained from sunscreen users compared with tumors derived from nonusers. These findings suggest that the mechanisms involved in the etiology of skin carcinogenesis differ in sunscreen users compared with people who did not routinely employ sunscreens. These data are also indicative of a protective effect associated with sunscreen use against the formation of p53 mutations. It is possible that the patients who were diagnosed with BCC despite their use of sunscreens possessed a genetic susceptibility for skin cancer formation and developed BCC through a p53-independent pathway. Alternatively, solar UVA wavelengths, that were generally not blocked by the suncare products employed by the sunscreen users, may have played a significant role in BCC development through induction of a mutation(s) in an oncogene and/or a tumor suppressor gene, other than p53, for these patients.
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The reported incidence of cancers typically diagnosed in the outpatient setting may underestimate their true frequency, but the validity of mortality estimates from many of these causes has not been studied in detail. The authors sought to evaluate the validity of mortality estimation from death certificates for two such cancers, melanoma and mycosis fungoides (a cutaneous lymphoma), using routinely collected cancer registry data for 1973-1994 from the Surveillance, Epidemiology, and End Results program. Their method estimates that 93% of the deaths attributable to melanoma were certified as due to melanoma but that only 60% of the deaths attributable to mycosis fungoides were so certified. Evaluation of the accuracy of cause-of-death certification in this manner is helpful in the interpretation of mortality statistics.
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Sun exposure is a known cause of melanoma, and there are several reasons for concern that tanning lamp use may also cause melanoma, especially because of the spectral output of the lamps,the similarity of tanning lamp use to natural sun exposure (particularly sunbathing), the reported association of melanoma with PUVA therapy, and the positive results in several case-control studies of melanoma risk and tanning lamp use. We have reviewed the epidemiologic literature relevant to the relation between tanning lamp use and melanoma and have discussed methodologic issues that should be considered in interpreting these reports and designing improved studies. Although several investigations have found a positive relation between tanning lamp use and melanoma, in some instances including dose-response or duration-response effects, the methodologic limitations preclude any firm conclusion regarding a causative relation. Meta-analysis of existing data may provide better information, but several limitations could only be overcome by new studies collecting more precise exposure data. The popularity of tanning lamp use, especially in young persons, adds urgency to the quest for elucidation of the relation between the use of these devices and melanoma risk.
Malignant melanoma imposes a considerable public health burden. Both incidence and mortality have increased many fold over the past several decades, although current trends suggest possible change in the prior patterns. Etiologic factors have been established, of which the most important is intense sun exposure. Primary prevention and early detection are both potentially critical in reducing the burden of melanoma. Much remains to be clarified in our management of this disorder on a population basis, and methodologic difficulties are plentiful. The potential for substantial reductions in melanoma mortality requires that we address the difficulties so that maximally effective public health initiatives may be undertaken.
Family history of melanoma is an important risk factor for both melanoma and, it is thought, dysplastic nevi. However, assessment of family history of melanoma in epidemiologic investigations has typically been limited to interview of the proband. As part of a case-control study of dysplastic nevi, we attempted to confirm family histories. We disproved about half of the reported family histories of melanoma among first-degree relatives, and confirmed them by medical records in only 17%. Few family histories pertaining to other relatives could be confirmed. We documented the association of melanoma family history with dysplastic nevus risk, and we further documented a substantially greater odds ratio for this association when history was based on confirmation by medical records, compared to confirmation by proband interview only. The bias thus documented must be considered in evaluating the many published epidemiologic studies of melanoma and related disorders. Future research should attempt to confirm family histories of melanoma whenever possible, despite the practical difficulties.
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