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Ultraviolet radiation (UVR) exposure has been linked to many adverse
effects, including malignant melanoma.
Photoprotection encompasses all methods of UVR blocking, including
sunscreens, protective clothing, and sunglasses. Sunscreens are widely
used to prevent sunburn and reduce the incidence of premature aging
and carcinogenesis, although clothing and avoiding direct sunlight offer
The use of tanning beds that use artificial ultraviolet A (UVA) has not
been shown to reduce long-term damage to the skin or to provide
protection from natural UVR. The use of tanning beds should be
minimized, and adherence to Food and Drug Administration (FDA)
recommendations on length of exposure should be encouraged.
Sunburn is a self-limiting condition, which is generally managed with
symptomatic treatment including oral analgesics, topical analgesics, and
topical anesthetics. Treatment beyond self-management is necessary if
the sunburn is accompanied by constitutionalsymptoms, involves
second- or third-degree burns, or is infected.
Phototoxicity and photoallergy are often drug- or chemical-induced
reactions to UVR exposure and account for up to 8% of adverse drug
Photodamaged skin is characterized as being wrinkled, yellowed, and
Topical retinoid therapy is most effective for patients of 50 to 70 years
of age with moderate-to-severe photoaging and for prophylactic use in
patients undergoing the initial changes of photoaging.
Most burn injuries are minor and can be managed in ambulatory settings. Case 42-6 (Question 1)
Major second- or third-degree burns should be immediately triaged to a
health system with a multidisciplinary team that can adequately manage
all of the potential complications.
Synthetic dressings and skin substitutes have expanded the options and
the desired outcomes for recovery.
ULTRAVIOLET RADIATION (UVR) EXPOSURE
Incidence, Prevalence, and Epidemiology
Changing lifestyles have considerably increased human exposure to sunlight: more
outdoor recreational activities, more emphasis on tanning, longer life spans, seasonal
population shifts to the Sunbelt, and an emphasis on improving vitamin D deficiency.
Epidemiologic evidence clearly implicates sunlight as a causative factor in many
skin diseases, and public attitudes toward tanning and sun exposure have slowly
begun to change. Skin cancer is the most common of all cancers and yet also one of
the most preventable. Squamous cell carcinoma (SCC) and basal cell carcinoma
(BCC), which together account for more than half of all malignancies in the United
States, are linked closely to exposure to ultraviolet radiation (UVR).
incidence rates have doubled from 1982 to 2011 in the United States, with 65,647
cases in 2011 and 9,128 deaths. Without intervention, the annual cost of treating
newly diagnosed melanomas is projected to triple by 2030, but the CDC estimates
that a comprehensive national skin cancer prevention program could potentially avert
In July 2014, the acting Surgeon General delivered “The
Surgeon General’s Call to Action to Prevent Skin Cancer.” The purpose of the call
was to unite various sectors of the nation to address skin cancer as a major public
health problem, increase awareness of skin cancer, and call for action to reduce
Sunburn, photoaging, immunologic changes in the skin, cataracts, photodermatoses,
phototoxicity, and photoallergy are other commonly encountered photosensitivity
reactions that occur after UVR exposure. Phototoxicity and photoallergy are often
drug- or chemical-induced reactions to UVR exposure and account for up to 8% of
4 The appropriate use of sunscreens or other photoprotective
behaviors can help mitigate the incidence of the adverse effects of UVR. Despite this
fact, sunscreen use remains low, with recent survey-based estimates showing that
fewer than 15% of men and 30% of women use sunscreen on both the face and the
exposed skin as recommended. Forty-two percent of men reported never using
ULTRAVIOLET RADIATION SPECTRUM
Ultraviolet radiation, the primary inducer of photosensitivity reactions in humans, is
divided into ranges according to the effects of four primary wavelengths: UVA1
(340–400 nm), UVA2 (320–340 nm), UVB (290–320 nm), and UVC (200–290 nm)
(Fig. 42-1; Table 42-1). UVA, with a wavelength of 320 to 400 nm, is closest in
6 UVA radiation levels have small fluctuations during the
day and are present from sunrise to sunset every day, all year round, even in the
winter and on cloudy days. UVA is considerably less likely than a comparable dose
of UVB to cause a similar degree of erythema.
In contrast to UVB, UVA penetrates
into the dermal layer and may cause harmful effects not caused by UVB.
100 times more UVA reaches the earth’s surface than UVB. Consequently, UVA may
contribute up to 15% of the erythemal response at midday.
erythemogenic and melanogenic of the three UVR bands.
blocked by the earth’s stratospheric ozone layer, and it is absorbed completely by the
In addition, UVB radiation can alter the immune
thereby increasing the incidence of certain cancers, including skin cancers.
The only known beneficial effect of UVR in humans is exposure to small amounts of
UVB, most commonly through sunlight, which converts 7-dehydrocholesterol to
). Vitamin D enhances calcium homeostasis and has direct
and indirect effects on cells involved with bone remodeling. As a result, vitamin D
can decrease the risk of rickets in childhood and fractures and osteomalacia in
The UVC wavelengths are absorbed completely by the earth’s stratospheric ozone
layer. Artificial sources of UVC have been used in the sterilization and preservation
of food and in minimizing bacterial growth in laboratories and hospital operating
rooms by germicidal lamps, which can cause erythema or cataracts if mishandled.
The amount of UVR that reaches the earth’s surface is influenced by many factors.
Concern has been focused on the implications of depletion of the ozone layer caused
by man-made pollutants such as chlorofluorocarbons (CFCs), nitrous oxide, and
other greenhouse gases (GHGs).
In the decade after this effect was first detected in
1983, ozone levels above the Antarctic had fallen to 50% of normal.
1990s, worldwide estimates from the Environmental Protection Agency (EPA)
predicted that for every 1% decrease in ozone, UVB radiation reaching the earth’s
surface would increase by 2% per year, possibly resulting in a 1% to 3% increase
per year in nonmelanoma skin cancer.
15 However, further research is needed to
determine whether this prediction has been realized.
16 As GHGs contribute to ozone
depletion, and because UVA is only slightly filtered by the ozone layer, any decrease
in the ozone layer would result in a disproportionate increase in UVB reaching the
Figure 42-1 Ultraviolet radiation (UVR) spectrum. *Erythrogenic and melanogenic bands of UVR.
Types of Ultraviolet Radiation and Characteristics
Radiation Wavelength (nm) Characteristics
340–400 Not absorbed by the ozone layer
Produces some tanning, photoaging, and skin
Lower carcinogenic potential than UVA2, but
harmful over long-term exposure
Levels remain relatively constant throughout the
UVA2 (short UVA) 320–340 Similar characteristics to UVA1, but greater
carcinogenic potential with erythema production
UVB (sunburn range of radiation) 290–320 Partially absorbed by the ozone layer before
Causes erythema, sunburn, tanning, wrinkling,
Daily and seasonal variation, with highest
Time of Day, Cloud Cover, and Surface Reflection
The time of day influences the amount of UVR reaching the earth’s surface; 20% to
30% of the total daily UVR is received from 11 AM to 1 PM, with 75% between 9 AM
and 3 PM. Cloud cover can decrease UV intensity by 10% to 80% and decreases
infrared radiation to an even greater extent. This greater attenuation of infrared
radiation by cloud cover can lead to an increased risk of UVR overexposure because
less infrared radiation will be absorbed by the body and transformed into heat,
resulting in less warning of overexposure to UVR. In general, whenever someone’s
shadow is shorter than his or her height, care should be taken; the shorter the shadow,
the more likely a sunburn will occur. Reflection of UVR by substances (e.g., sand,
water, snow) also may be important. For example, sand reflects about 25% of
incident UVB radiation; therefore, sitting under an umbrella at the beach may not
offer adequate protection. Fresh snow can reflect 50% to 95% of incident sunlight.
Water reflects approximately 5% of erythemal UVR, whereas 75% of the radiation is
transmitted through 2 m of water, offering swimmers little protection.
changes, geographic latitude, and altitude also influence the amount of UVR reaching
The UV Index/Global UV Index (http://www.epa.gov/sunwise/uvindex.html),
developed by the EPA, the National Weather Service, and the Centers for Disease
Control and Prevention, is a public health education service that is calculated on a
next-day basis for every ZIP code across the United States, and worldwide.
index, with a scale from 1 (low exposure) to 11+ (extremely high exposure),
forecasts the probable intensity of skin-damaging UVR expected to reach the surface
during the noon hour when the sun is highest in the sky. Theoretically, the UV Index
can range from 0 (e.g., during the night) to 15 or 16 (in the tropics at high elevations
The amount of UVR exposure needed to damage an individual’s skin is affected by
the elevation of the sun in the sky, the amount of ozone in the stratosphere, and the
amount of clouds present. Clear skies transmit 100% of UVR to the earth’s surface,
with scattered clouds transmitting 89%, broken clouds, 73%, and overcast clouds,
32%. The darker an individual’s skin tone, the longer (or the more UVR) it takes to
ERYTHEMA, SUNBURN, AND TANNING
Erythema and Oxygen Free Radicals
Excessive exposure of the epidermal and dermal layers of the skin to UVR can result
in an inflammatory erythematous reaction. Excess UVA and UVB cause the release of
vasodilatory mediators (e.g., histamine, prostaglandins, cytokines), resulting in
increased blood flow, erythema, tissue exudates, swelling, increased sensation of
warmth, and a characteristic sunburn.
6,10 Severe UVR exposure, primarily UVB, can
cause blister formation, desquamation, fever, chills, weakness, and shock. Erythema
caused by UVB begins within 3 to 5 hours after exposure, is maximal after 12 to 24
hours, and usually resolves during the ensuing 3 days.
by UVA begins immediately, plateaus between 6 and 12 hours, and remains for 24
hours. UVA-induced changes in the dermis are characterized by greater damage to the
vasculature and dense cellular infiltrates that penetrate to deeper levels of the skin.
The dermis also may be damaged when endogenous components of the skin absorb
UVR energy and subsequently interact with oxygen to form tissue-damaging oxygen
The skin undergoes adaptive changes in response to UVR exposure.
When keratinocytes in the epidermis are damaged and lose their typical
organization, both the epidermis and the stratum corneum thicken and attempt to serve
as a barrier to UVR, particularly to UVB.
9 The skin’s normal protective immune
response, however, is altered with exposure to UVR. Metalloproteinase proteins act
as proteolytic enzymes that are produced from low-dose UVR
exposure, causing degradation of collagen and elastin in the dermal matrix.
Langerhans cells (i.e., antigen-presenting cells in the skin) are decreased in number
and function even after small doses of UVB.
18 These cells abnormally activate
suppressor T lymphocytes and lose their ability to activate normal effector pathways
Immediate Pigment Darkening and Delayed Tanning
Tanning is an adaptive mechanism of the skin to UVR. Tanning occurs by two
different mechanisms: immediate pigment darkening (Meirowsky phenomenon) and
delayed tanning. The primary cell involved in tanning is the melanocyte, which
produces the radiation-absorbing protein melanin.
begins during the actual exposure to UVA and certain bands of visible light,
oxidation of existing melanin in the epidermis transiently turns the skin grayish
brown. The degree of immediate pigment darkening depends on the duration and
intensity of exposure, the extent of previous tanning (or amount of preexisting
melanin), and the skin type of the individual.
Immediate pigment darkening is not
protective against UVB erythema.
Delayed tanning occurs 48 to 72 hours after exposure to either UVA or UVB. It is
most intense 7 to 10 days after UV exposure and can last for weeks to months.
Delayed tanning is the result of increased production of melanin, an increase in the
size of dendritic processes, increased melanization of melanosomes, and an increase
in the rate of transfer of melanosomes (particulate bodies of melanin) to
6,9 The keratinocyte, now pigmented with melanosomes, migrates to the
epidermis, producing the characteristic suntan. Delayed tanning caused by UVA is
less protective against sunburn than delayed tanning caused by UVB, because
epidermal thickening is not induced by UVA.
Squamous Cell and Basal Cell Carcinoma
The association between skin cancer in humans and UVR exposure is based primarily
on clinical and epidemiologic evidence. Nonmelanoma skin cancers, such as SCC
and BCC, occur most commonly on areas that are maximally exposed to sunlight
(e.g., the face, neck, arms, back of the forearms, and hands).
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