Skin-Cancer Risk with Soaring
It’s not soaring, exactly that’s the risk. It’s sunlight. But unless you assemble and stage under an awning, unless you only thermal in cloud shadow, it’s as risky as any other situation when the sun shines on your skin. Caucasians in Australia have much more sun and much more damaged skin than in northern Europe. Sun angle.
It’s important that one can own a canopy – even a clear canopy – with UV protection. Consider the extra cost to be health insurance. I remember flying one day in two gliders successively, each with a clear canopy. In one, my skin felt distinctly hot; in the other, it did not, so I discovered by experience what a blessing UV protection can be for comfort as well as protection.
What, actually, are the results of sun exposure?
First, genetics. Melanin absorbs ultraviolet light and is specifically protective. The more melanin your ancestors granted you, the lower your risk of light-damaged skin. Freckled pale redheads are the most vulnerable.
Light causes 3 conditions – actinic keratosis, squamous cell carcinoma, and basal cell carcinoma – and increases the risk of a 4th, melanoma. (Melanomas also occur internally and in shaded locations, about 10%. Melanoma is not common, about 1 to 6 per 1000 fair-skinned persons, depending on sunlight exposure.)
The sex of the skin-bearer influences the location of skin cancer. Women in our culture, especially during recreation, favor bare legs, so more commonly have lower-extremity skin cancers. Women also have head hair, while many men are bald, so scalp and facial skin cancers are more common with men.
It’s the cumulative light exposure that creates much of the risk, so the over-60 crowd has a lot more skin damage than the under-30 crowd. Yet skin cancer does take a long time to develop, so the risk of showing up with skin cancer while old is related (for example) to the number of blistering sunburns we had before age 20.
The difference between cancer cells and normal cells is that mutation of some sort has occurred. Two key things happen: one is that normal cells reproduction is stopped by contact with another cell: contact inhibition. This is lost, so that a lump of damaged cells may form. The other is that the abnormal cell continually reproduces. A normal skin cell rests for 2 weeks (in teens) to 8 weeks (in us geezers), then swiftly and efficiently reproduces in about one day. A damaged cell may not rest – its reproductive mechanisms are damaged, but it continually reproduces, though slowly.
A third abnormality may happen, in that a damaged cell may become motile. This can cause invasion or metastasis. In skin cancer, basal and squamous cell cancers commonly invades but seldom metastasize, melanomas more commonly metastasize.
Actinic keratosis is not a cancer because it neither invades nor metastasizes. It is important because it’s unsightly and because it sometimes transforms into squamous or basal cell cancer. Actinic keratosis is not permanent: avoiding sun exposure and using sunscreen permits lesions to resolve slowly (about 20% per year).
Actinic keratosis is common. About a third of US women and about half of US men have actinic keratosis by middle age. Skin cancer is “common” in the sense that about 1% of Caucasians in the US get basal cell or squamous cell skin cancer, mostly over 70 (about 50-300x more frequent over 75 than under 45).
What are the actual risks?
First, severe sunburn greatly increases the risk of skin cancer. For example, a French study including more than 1000 women with basal cell skin cancer versus more than 3600 controls found that a history of severe sunburn before the age of 25 years and after the age of 25 each independently doubled the risk of basal cell skin cancer.
At the benign end of the spectrum, actinic keratosis, the importance of melanin is illustrated by a study in Queensland, Australia. This compared fair skin, medium skin, and olive skin (vague but definite differences). This found that people with fair skin were 14x more likely and with medium skin were 6.5x more likely to develop actinic keratosis than olive-skinned people. Even a single episode of sunburn in childhood increases the risk for actinic keratosis.
Actinic keratosis is rare in people of African descent. (It is possible for Black people to sunburn: I recall an all-day canoe trip in my youth organized by a Black friend. The next day, we all had sunburns related to how well we’d protected ourselves. At breakfast, he said, “I can’t understand it! My skin hurts!” I said, “You’re sunburned!” He replied, “Really? What’s that?”)
Prevention:
Cover sun-exposed skin with clothing or sunscreen (SPF 30 or more) from childhood on.
Do not get sunburns, do not use tanning beds.
Diagnosis:
Actinic keratosis is scaly and often red. This is the cause of the blotchy faces of us elderly types. This is important as a sometimes precursor to skin cancer. It steadily worsens with continued sun exposure
Squamous and basal cell carcinoma are lumpy. If large, they may ulcerate. Melanoma is dark. Tiny charcoal-colored lumps or spreading dark spots with notched borders should be taken to a dermatologist (to get a sooner appointment, mail or email a closeup of the lesion with side lighting and say, “Could this be skin cancer?”)
Skin cancer diagnosis requires a small biopsy. If suspected melanoma, it’s important not to cut through the lesion; a clear border of more than 1 mm around and under the lesion is crucial. Not every doctor knows this.
Treatment:
That’s a long discussion. You can ask the Internet about choices (scholar.google.com is your friend). My favorite for actinic keratosis has for years been imiquimod, a tiny bit on the skin twice weekly for 16 weeks; the gentlest and least unsightly treatment, though not cheap.
Base photo by Bozena Michalowski
Dr Dan Johnson is a retired AME and internist flying gliders for about 30 years, living on the west coast of Wisconsin.
