Our bodies utilize a small quantity of UV-B radiation to act as a catalyst in the generation of Vitamin D (3). More specifically, the conversion of 7-dehydrocholesterol to vitamin D3 occurs in the skin, preventing rickets (4). Extensive amounts of UV-B radiation, however, can be detrimental to a variety of biological systems. Although the extent of DNA damage is variable, the duration of exposure and the susceptibility and resilience of the exposed are considered when evaluating exposure (3).
The Integumentary System
The human body is made up of several organ systems that combine to form one unit. The Integumentary System is comprised of our hair, skin, nails and sweat glands. More specifically, the skin consists of the outer epidermis derived from the embryonic ectoderm, and the inner dermis which develops from the mesoderm. Beneath the dermis is the hypodermis which anchors skin to underlying tissues. The skin and its appendages make up a complex set of organs that have several functions: 1) Protection and barrier against the outside, 2) Protection against dehydration, 3) Body Temperature Regulation, 4) Cutaneous Sensation, 5) Metabolic Functions, 6) Blood Reservoir and 7) Excretion (15).
The epidermis is a keratinized stratified squamous epithelium consisting of distinct cell types and distinct layers. Its thickness varies from 0.07-0.12 mm over most of the body to 0.8 mm on the palms, and 1.4 mm on the soles. Its surface layer is made up of dead cells and is rich in keratin, a protein which renders it dry and more or less waterproof. The epidermis also serves as a protective barrier against ultra-violet light, bacteria, chemicals and abrasion (15).
The Epidermal Cells
Keratinocytes compose most of the epidermis. They produce a protein, keratin, that helps waterproof the skin and that protects the skin and the underlying tissues from heat, microbes, abrasion and chemicals.
Merkel cells are sensory receptors. They associate with a disclike sensory nerve ending to form the Merkel disc.
Melanocytes synthesize the melanin pigments which protect the skin against ultraviolet damage.
The Langerhans cells are macrophages used in the defense against microorganisms (15).
The biological effects of UV radiation do not appear readily, so individuals who are often overexposed become aware of the damaging effects and the extent of damage over time. If exposure is sufficiently high, systematic effects such as nausea, fever and malaise may transpire. In cases of tremendous exposure, premalignant or malignant changes may ensue (2). Moreover, skin cancer, cataracts and immunosupression are the primary health effects associated with UV-B radiation exposure (3).
As mentioned in Harmful Effects of Ultraviolet Radiation section, the deleterious effects of UV-B radiation on individuals is related to prolonged, deliberate, and inadvertent sunlight exposure. In some individuals, this exposure leads to the development of one of the three major kinds of skin cancer:
- Basal-cell cancers (nonmelanoma)
- Squamous-cell cancers (nonmelanoma)
Basal-cell cancers (nonmelanoma)
Basal cell carcinoma begins in the lowest layer of the epidermis, called the basal cell layer. Basal cell skin cancer rarely metastasizes, or spreads, but it often damages nearby tissues, such as muscles or bones. Moreover, treatment for a basal cell cancer involves surgery to remove the lesion and, infrequently, topical chemotherapy or radiation therapy (16).
The signs and symptoms of basal-cell cancers may include:
- A small, fleshy bump with a smooth, pearly appearance.
- A scarlike lesion that is firm to the touch.
- A bump that bleeds, crusts over, and then repeats the cycle.
- A red, tender, flat spot that bleeds easily.
Squamous-cell cancers (nonmelanoma)
Squamous cell carcinomas develop in higher levels of the epidermis and account for about 20% of all skin cancers (16). Squamous cell cancers may rapidly develop into large masses and may spread to nearby lymph nodes (8). Treatment involves surgical removal of affected skin and may include radiation therapy or topical chemotherapy as well. When squamous cell skin cancer is properly treated, the cure rate is high (8).
Signs and symptoms of a squamous cell skin cancer may include:
- A firm red bump.
- A growth or patch of skin that feels scaly, bleeds, or develops a crust.
- A sore that does not heal (8).
Less common types of nonmelanoma skin cancer include:
- Kaposis sarcoma
- Cutaneous lymphoma
- Skin adnexal tumors
- Various types of sarcomas
- Merkel cell carcinoma
Together, these types account for less than 1% of nonmelanoma skin cancers (16).
Melanoma is a form of skin cancer that may affect the skin solely, or may spread through the blood or lymph systems to organs and bones. Melanoma can develop: 1) in an existing mole, 2) on another mark on the skin or 3) on unmarked skin. Most people with melanoma are treated with surgery to remove the lesion and are evaluated to determine if the cancer has metastasized. Prompt evaluation and treatment of a suspicious skin spot may prevent severe complications (6).
Early signs and symptoms of melanoma usually include changes in a mole or other colored skin spot:
- Color may turn dark, black or, less often, red, white, or blue. A part of the mole may lose color, or the mole may develop a mix of colors. Color may spread from the edge of a mole into surrounding skin.
- Size may rapidly increase. The mole is usually wider than a pencil eraser (6 mm or 1/4 inch) but may be smaller.
- The edges of the mole may turn jagged or scalloped (irregular borders).
- A flat mole may thicken or raise up.
- The mole may become scaly, wear down (erode), ooze, bleed, or become crusted.
- Skin around the mole may turn red or swollen or develop new patches of color.
- The spot may itch, tingle, or burn.
- Pieces of skin may become too soft and break off easily (friability).
- Later signs and symptoms of melanoma include the following:
- A sorelike pit (ulcer) may develop.
- A mole or colored skin spot may become painful or bleed (6).
ABCDs of Melanoma
Asymmetry: One half of the growth doesn't match the other half.
Border irregularity: The edges of the growth are ragged, notched, or blurred.
Color: The pigmentation of the growth is not uniform. Shades of tan, brown, and black are present. Dashes of red, white, and blue also may appear.
Diameter: Any growth greater than 6 millimeters (about the size of a pencil eraser) is cause for concern (12).
The eye has many components. Our eyelids hold our lashes, keep the eye moist, and shield it from intense light. The conjunctiva is a membrane that covers most of the eyeball and allows the lids to gently glide over the eye. The clear cornea covers the iris, and works like a watch-face for the eye. It allows a small amount of light to enter the eye through the pupil. Then along with the natural lens, it acts like a camera-lens and focuses the image onto the retina. The retina is like the film in your "ocular" camera. It lines the inside of the eye, and is mostly clear. The retina has very few blood vessels which would disturb the retinal picture. Since the retina has so few blood vessels and does a lot of work, it needs to be nourished by a blood vessel layer beneath it, called the choroid or uvea (17).
Not only does the choroid feed the retina, but it also contains pigment cells called melanocytes. These cells and their product "melanin" absorbs any extra light which might distort the retinal picture. Melanocytes are the cells which can lose control, and grow into a malignant melanoma (17).
Possible eye damage, particularly to the cornea, can result from high doses of UV Radiation (5). Chronic eye exposure to UV radiation may increase the incidence of 'cataract,' which is a clouding of the eye lens; 'pterygium,' in which a fleshy membrane covers the eye; and possibly 'macular degeneration,' or the development of spots that could result in blindness (12).
Excessive UV-B exposure interferes with the functioning of immune systems in animals and human beings (14). UV radiation also triggers another distinct immunological effect - systemic immunosuppression. Although tumors appear on the surface of skin, there is also an effect being experienced by the body. It has been hypothesized that the initial event in immune suppression is UV-B absorption by urocanic acid (UA), the most abundant substance found in the outer layer of skin. Researchers have also found that urocanic acid switches from a trans to cis geometry at exactly the wavelength that triggers immune suppression.
Although it is not clear how t-UA goes on to suppress immunity, many hypotheses have been studied. One researcher hypothesized that the active t-UA may hamper the ability of Langerhans cells, dendritic cells stationed in the epidermis which are believed to play a part in immune "surveillance and recruit killer T-cells to the lymph nodes. Killer T-cells are cells that are responsible for destroying foreign antigens by literally "blowing them up"(14).
As research in this area continues, damage to the immune system also has several implications for an individual's health: increased risk of the incidence and severity of infectious disease, increased risk of malignant melanoma, and diminished efficacy of vaccinations (14).
2. Moeller, D. (1998). Environmental Health. (Rev.ed.). Cambridge, Mass: Harvard University Press.
3.CIESIN Thematic Guides. Overview of Health Effects from Increased Ultraviolet-B Exposure due to Ozone Depletion. Center for International Earth Science Information Network, Columbia University.
4. National Research Council. (1979). Human health effects. Chapter 3 in Protection against depletion of stratospheric ozone by chlorofluorocarbons, 74-119. Washington, D.C.: National Academy of Sciences.
5. NAS System Division Educational Resources. (1999). Stratospheric Ozone Depletion: Ultraviolet Radiation. Acessed 11/12/03.
6. Wed MD and AOL Health. (2003). Protecting Your Skin from Ultraviolet Radiation and Skin Cancer: Melanoma . Accessed 12/02/03.
7. Web MD and AOL Health. (2003). Basal Skin Cancer: Nonmelanoma Skin Cancer. Accessed 12/01/03.
8. Web MD and AOL Health (2003). Squamous cell skin cancer: Nonmelanoma Skin Cancer. Accessed 11/30/02.
12. SunWise School Program. (1999). Staying Healthy in the Sun. Environmental Protection Agency. Accessed 11/12/03.
14. Lohr, Y. (1999). A Chemical Perspective on the Mechanisms of UV-induced Skin Cancer. Accessed 11/30/03.
15. The University of Western Australia (2003). School of Anatomy and Human Biology Blue Histology Integumentary System. Accessed 12/01/03
16. National Council on Skin Cancer Prevention (October 2003). Detailed Guide:
Skin Cancer-Nonmelanoma. Newslink Issue #11. Accessed 12/02/03
17. Finger, Paul T. Eye Cancer Network: Ocular Oncology, diseases treatment and research. Accessed 12/03/03.
Return to top of page