Sunday, July 15, 2007

Sunburns, Sunscreens, and Skin Cancer

Summertime and the living's easy. Easy enough, for instance, to fall asleep in the sun and wake up medium rare. As our parents taught us, before hitting the water we should slap on the sunscreen, lest we become extra crispy, or worse, we get skin cancer.

We put on sunscreen to block out one particularly vicious element of sunlight: ultraviolet (UV) rays. These are waves of light that are a higher frequency than visible violet rays, and are known for their ability to damage the DNA of our cells, for instance creating a bond between two Thymidines in our DNA known as a Thymidine dimer or introducing free radicals that can then damage the cell. When too much damage is dealt to a cell's DNA, it triggers a type of abort sequence and that cell undergoes programmed cell death, or apoptosis. When UV light hits your skin, it can injure the cells that populate the epidermis, or outermost layer, of the skin: commonly, keratinocytes and melanocytes. By then undergoing cell death, the epidermis becomes inflammed and reddened in the phenomenon known as sunburn, or solar erythema. If too many cells die the epidermis may seperate from the dermis underneath it, resulting in the blistering so common to second degree burns.

Actually, in some ways the sunburn is a good sign: it means that the cells that have been damaged by the sun are dying. On the other hand, if damage is not "caught" and the skin cells don't die by apoptosis, certain DNA injuries may cause malignant changes. The most common skin cancers (95%) are basal cell and squamous cell carcinomas, which stem from keratinocytes. Melanocyte (pigment cell) cancers, or melanomas, only make up 5% of skin cancers but are responsible for 75% of the mortality associated with skin cancer. This can be a brutal illness, often metastasizing to the liver, lungs, bone, and brain. The interesting thing is that there appears to be an association between the type of UV light and the type of cancer. UVB light, which has long been associated with sunburns, creates Thymidine dimers, which are more easily seen by the cell and usually cause cell death, but may also cause cancer. This was the light normally blocked by most sunscreens. There is also UVA light, which is a longer wavelength and does not nomally cause burns. However, it may cause sub-lethal mutations in your skin cells, particularly melanocytes, which can mean cancerous change. So while your sunscreen blocks UVB, it may let UVA through with deleterious results.

The bottom line: have fun in the sun but be safe. Make sure you use a sunblock that works against both UVA and UVB light. And, as an article on sunscreen from The New York Times last week discusses, make sure that you use it correctly. A shotglass of sunscreen for the body and a teaspoon for the face, reapplying every few hours. Don't let a sunburn (or worse) get in the way of your summer fun.

Wednesday, July 11, 2007

Poison Ivy and Hypersensitivity Reactions

It is a common summer scene: you are on a camping trip, or looking for a lost ball in the woods, or finding some impromptu private thicket in order to take care of "business." Suddenly, a glance down and thoughts of concern course through your mind: was that...poison ivy?!? Did I step in it? Is that a rash? Do I feel itchy? I feel a little itchy, I must have touched it!

Poison Ivy enacts its damage by a chemical called urushiol, which is a catechol molecule that is part of the oily sap. This oil is in all parts of the plant: leaves, stems, roots, and berries. When human skin is exposed to the oil the catechols may combine with skin proteins and the response is the typical itching rash from a mechanism called a type IV hypersensitivity reaction. Understanding this is crucial to understanding what is, and what isn't, caused by a brush with poison ivy, oak, or sumac.

A type IV hypersensitivity reaction, also called a delayed type hypersensitivity reaction, is a type of allergic reaction that is mediated by the T cells of your immune system rather than antibodies, the mediator of other allergic reactions. This is important because an adverse response requires two encounters with the offending agent, be it a chronic bacteria (such as tuberculosis) or an environmental contact like poison ivy. During the first encounter, macrophages engulf the invading agent and present this to your T cells, which become sensitive to that specific antigen. When you are re-exposed, the T cells can interact directly with the antigen (the urushiol in this case) and elicit an aggressive immune response.

Basically, the first time you see the poison ivy you educate your T cells, which takes roughly three weeks. Then, the second time you are exposed, the memory T cells are ready in waiting and can immediately start responding. This isn't the fastest of allergic responses: since actual cells are responding, and not just an antibody, it takes time for them to divide and signal for others to go to the site of the lesion. The peak response will be 2 days following encounter with the antigen (the same reason a PPD test for TB takes 2 days to read); therefore if you are in the woods and suddenly get a poison ivy-like rash, you must have touched the plant 2 days prior.

Poison ivy will cause a rash, or contact dermatitis, that often starts as little red bumps and later blisters and may crust or ooze. Keep in mind that leakage of blisters does NOT spread the rash, only lingering oils on skin and clothing or tools. If you have been exposed the best treatment is to try and remove the oil within 10 minutes; rubbing alcohol can break it up and help in this process. The FDA recommends you first use rubbing alcohol, and then rinse generously with water; don't use soap yet because it may spread the oil. After this, take a shower with soap and water if possible. Of course, avoiding poison ivy in the first place is the best medicine: if you see "leaves of three, let it be."