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Editorial Author(s): Bruce Armstrong Source: Cancer Causes & Control, Vol. 7, No. 2 (Mar., 1996), pp. 195-196 Published by: Springer Stable URL: http://www.jstor.org/stable/3552808 . Accessed: 15/06/2014 01:46 Your use of the JSTOR archive indicates your acceptance of the Terms & Conditions of Use, available at . http://www.jstor.org/page/info/about/policies/terms.jsp . JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact [email protected]. . Springer is collaborating with JSTOR to digitize, preserve and extend access to Cancer Causes &Control. http://www.jstor.org This content downloaded from 195.34.78.245 on Sun, 15 Jun 2014 01:46:36 AM All use subject to JSTOR Terms and Conditions
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Page 1: Editorial

EditorialAuthor(s): Bruce ArmstrongSource: Cancer Causes & Control, Vol. 7, No. 2 (Mar., 1996), pp. 195-196Published by: SpringerStable URL: http://www.jstor.org/stable/3552808 .

Accessed: 15/06/2014 01:46

Your use of the JSTOR archive indicates your acceptance of the Terms & Conditions of Use, available at .http://www.jstor.org/page/info/about/policies/terms.jsp

.JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range ofcontent in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new formsof scholarship. For more information about JSTOR, please contact [email protected].

.

Springer is collaborating with JSTOR to digitize, preserve and extend access to Cancer Causes &Control.

http://www.jstor.org

This content downloaded from 195.34.78.245 on Sun, 15 Jun 2014 01:46:36 AMAll use subject to JSTOR Terms and Conditions

Page 2: Editorial

Cancer Causes and Control 1996, 7, pp. 195-196

Editorial

In contrast to linear relationships in North America and Australia,"2 melanoma incidence in Europe shows a U- shaped relationship with latitude with a minimum around latitude 520 north.3 This pattern is thought to be due to the interaction between gradients in ambient ultraviolet irradiance (increasing from north to south), cutaneous sensitivity to the sun (increasing from south to north), and intermittency of sun exposure (probably increasing from south to north). Thus, susceptibility to melanoma (as indicated by sun sensitivity) and the amount and pattern of sun exposure in southern Europe may be very different from those in northern Europe, the United States, and Australia where most case-control studies of melanoma have been conducted.

It is of particular interest, therefore, to read in this issue of Cancer Causes and Control the results of a case- control study of melanoma in the most southerly Eur- opean population so far studied, that of East Andalusia in southern Spain, situated between latitudes 36045' and 38025' north.4 They show a different pattern from what we have come to expect for the associations between mel- anoma and sun exposure- risk of melanoma increased with each of estimated lifetime occupational, recrea- tional, and total (ie., both occupational and recreational) exposure to the sun. The strengths of these associations were similar. In most case-control studies, estimated life- time total and occupational exposure to the sun have shown little if any positive association with melanoma and, in some, occupational exposure has even been asso- ciated negatively with melanoma.5'6 On the other hand, recreational exposure has been associated quite consis- tently with melanoma. A previous exception to these generalities, however, was another study from southern Europe - the south of France.7

Why might the pattern of associations between sun exposure and melanoma be different in a population in the far south of Europe than in populations farther north, or in populations of northern European origin liv- ing in other continents (sometimes as close or closer to the equator)?

First, artifact is a possibility. R6denas et a14 have not done a perfect study. Importantly, their control popula- tion (visitors to the hospital in Granada, Spain in which the cases were treated) was biased in favor of residents of the mainly urban province of Granada: 79.0 percent of controls and only 63.8 percent of cases were from Gran- ada. As a result of this bias, cases may have been more likely to work in rural occupations, and to be exposed

occupationally to the sun, than controls. It is said that control for place of residence did not alter the odds ra- tios; it would have been better, however, if the adjusted results had been presented. While there are other weak- nesses in the study, none appear likely to have produced artifactual relationships between melanoma and occupa- tional and total sun exposure.

Second, the site distribution of melanomas in the East Andalusia study was different from that in populations in which most case-control studies have been done. Forty percent of the melanomas in East Andalusia were on the more sun-exposed head and neck or upper limbs com- pared with a median value of about 34 percent for popu- lations in Scandinavia, the United Kingdom, USA, and Australia. Melanomas on exposed sites have been related more often to occupational sun exposure than those on other sites. It is doubtful, however, whether this moder- ate difference in site distribution could produce the ob- served difference in associations with occupational and total sun exposure between the East Andalusia study and most other studies.

Third, it may be that pattern of sun exposure (as re- flected in intermittency of exposure) is less important in determining risk of melanoma in less sun-sensitive popu- lations than it is in more sun-sensitive populations. If it is assumed that the effect of intermittency of exposure is mediated by the sun-exposure/sun-tanning cycle (i.e., that a person who is exposed intermittently is more likely to be exposed when his/her skin is untanned and more sensitive to the sun than a person who is more con- tinuously exposed) then a person whose skin is already protected substantially by stable, natural pigmentation may be less affected by intermittency than a person who requires sun exposure to develop any significant skin pig- mentation. Thus, while risk of melanoma in less sun-sen- sitive populations may still rise with increasing exposure to the sun, this association may be little modified by the pattern of exposure.

This third proposition depends on the assumption that the East Andalusian population is substantially less sun-sensitive, on average, than other populations in which case-control studies have been done. Few previous case-control studies have used the same skin-type classi- fication as R6denas et al, and fewer have reported the distribution of controls by skin type. Elwood et alt classified 10 percent of controls in Western Canada into a 'burn only' (type I) category; 34 percent into a'burn then tan' (probably mainly type II); 10 percent into a 'tan with

? 1996 Rapid Science Publishers ancer Causes andControl.Vol7.1996 195

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Page 3: Editorial

Editorial

protection' category (probably types III and IV); and 47

percent into a 'tan, no burn' category (probably types IV and V). A rough comparison, then, between the western Canada and East Andalusian4 populations gives the fol-

lowing: skin types I and II - western Canada, 44 percent, East Andalusia, six percent; skin type III-western Canada, 10 percent, East Andalusia 40 percent; skin types IV and V - western Canada, 47 percent, east Andalusia, 54

percent.The apparent difference in proportions with types I and II skin is as expected; the apparent lack of difference in proportions with types IVand Vskin is not. However, as we have discussed previously,8 the classification of skin

type based on subjective responses to questions about ten-

dency to burn and ability to tan may be highly dependent on past experience of intense sun exposure. Those who have experienced intense sun exposure may be more likely to report burning and less likely to report ready tanning than those who have not. Thus, it probably is true that the east Andalusian population is less sun-sensitive than the

mainly northern European populations in which other case-control studies of melanoma have been done.

The third proposition suggests a different interaction between sun sensitivity and the amount and pattern of sun exposure in increasing risk of melanoma than has been proposed previously.'0 It was proposed that those who tanned readily would be most affected by pattern of exposure and those who tanned poorly would be least affected; the results from east Andalusia suggest that the

opposite may be true. Be that as it may, these new results

emphasize again the lack of any adequate empirical ac- count of the interaction between sun sensitivity and pat- tern and amount of sun exposure in causing melanoma. A large, multicenter study covering populations at differ- ent latitudes and with differing sun sensititivies and in-

cluding accurate quantitative measures of sun sensitivity and amount and pattern of sun exposure is the only way that the necessary empirical data will be obtained.0 Without such a study, it will remain impossible to advise different populations and individual people accurately about the approaches they should change to their sun ex- posure to reduce their risk of melanoma.

Bruce Armstrong Cancer Control Information Centre

NSW Cancer Council New South Wales, Australia

References

1. Scotto J, Fears TR. The association of solar ultraviolet and skin melanoma incidence among Caucasians in the Uni- ted States. Cancer Invest 1987; 5: 275-83.

2. Jones ME, Shugg D, Dwyer T, Young B, Bonett A. Inter- state differences in incidence and mortality from melano- ma: a re-examination of the latitudinal gradient. Med J Aust 1992; 157: 373-7.

3. Armstrong BK. Melanoma of the skin. Br Med Bull 1984; 40: 346-50.

4. R6denas JM, Delgado-Rodriguez, Herranz MT, Tercedor J, Serrano S. Sun exposure, pigmentary traits, and risk of cutaneous malignant melanoma: a case-control study in a Mediterranean population. Cancer Causes Control 1996; 7: 275-83.

5. International Agency for Research on Cancer. Solar and Ultraviolet Radiation. Lyon, France: IARC, 1992; IARC Monogr Eval Carcinog Risks Humans, Vol. 55.

6. Armstrong BK, English DR. Cutaneous malignant mela- noma. In: Schottenfeld DR, Fraumeni JF Jr, eds. Cancer Epidemiology and Prevention, Second Edition. New York, NY (USA): Oxford University Press, in press.

7. Grob JJ, Gouvernet J, Aymar D, et al. Count of benign melanocytic nevi as a major indicator of risk of nonfami-

iial nodular and superficial spreading melanoma. Cancer 1990; 66: 387-95.

8. Kricker A, Armstrong BK, Jones ME, Burton RC. Health, Solar UV Radiation and Environmental Chang'. Lyon, France: International Agency for Research on Can- cer, 1993; IARC Tech. Rep. No. 13.

9. Elwood JM, Gallagher RP, Hill GB, Spinelli JJ, Pearson JCG, Threlfall W. Pigmentation and skin reaction to sun as risk factors for cutaneous melanoma: Western Canada Melanoma Study. Br MedJ 1984; 288: 99-102,

10. Armstrong BK. The epidemiology of melanoma: Where do we go from here? In: Gallagher RP, Elwood JM, eds. Epidemiological Aspects of Cutaneous Malignant Melano- ma. Boston, MA (USA): Kluwer Academic Publishers, 1994: 307-23.

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