Left: the Star class has a long history of anchoring its classic annual events at the world’s best – as well as warmest – racing venues, including Nassau, Miami and southern California. Looking further back, the Bacardi Cup took place for many years in the big winds and waves of Havana (before some irritating domestic turbulence intervened). This may go some way to accounting for the class now being at the forefront when it comes to taking sun exposure seriously… though there is still work to do on the fashion front. Similarly this year’s Caribbean regattas (above) have also seen a steady trend towards more rigorous sun-protection among the crews who are taking part. There are clear parallels with skiing helmets – once the exception but now the rule (and in some countries the law)
(UVB) (280-320nm). UVA rays travel deeper into the skin and cause indirect DNA damage by free radicals, destroy collagen and whip up elastin which result in premature ageing (A for ageing). UVB rays stop short at the upper layer
of the skin and cause direct DNA muta- tion, sunburn (B for burning) and are the main cause of skin cancer. UVB penetra- tion is increased by thinning of the ozone layer and it has been estimated that a one per cent decrease in ozone layer increases melanoma mortality by around one to two per cent. UVC (200-280nm) does not reach the
surface of the earth as it is screened out by atmospheric oxygen as well as being absorbed by the ozone layer. UVR is responsible for a wide variety of
different acute and chronic effects on the skin. Acute responses of human skin to UVR include photodamage, erythema, mutation, immunosuppression, synthesis of Vitamin D and tanning. Chronic effects
include photoageing and photocarcinogen- esis, which is considered to be induced by mutation and immunosuppression. The World Health Organisation
(WHO) declared UV radiation carcino- genic in 2012 and a study in Australia showed that 65-90 per cent of melanomas and almost 100 per cent of keratinocyte cancers (basal cell carcinomas and squa- mous cell carcinomas) can be attributed to UV exposure. Accordingly, most ker- atinocyte cancers are found on sun- exposed areas and cancers on the lips and ears are at highest risk for spreading. Intermittent, high-intensity sun exposure
resulting in sunburn especially at a younger age is thought to be associated with melanoma and a large study showed that more than five severe sunburns between the age of 15 and 20 increase the risk of melanoma by 80 per cent. Skin incurs cumu- lative mutational damage also through repeated lower-intensity sun exposure, and that kind of longterm daily suberythemal
(just to make you a little pink) exposure is thought to cause precancers and the majority of keratinocyte cancers. Sailors certainly are at high risk. The
constant exposure of sun, wind and water, what I regard as the ‘triple threat’, wreaks havoc on the skin. Of course, these statis- tics fit mainly people with fair skin, those who always burn before they tan. In fact, people with fair skin are approximately 70 times more likely to develop skin cancer than those with black skin. Besides ‘being a sailor’, the inability to tan, or burning and freckling on sun exposure, having a lot of moles or atypical moles, extensive unprotected sun exposure or tanning bed use at early life and genetic predisposition can all increase skin cancer risk. Knowing your risk factors can be lifesaving. Dermatologists consider sailors a high-
risk population, so no wonder when I told my colleagues many years ago that I fell in love with a sailor called Peter Harken, the first question they asked was: ‘Does he
SEAHORSE 51
LAURENS MOREL
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