Because of this, sun exposure should be limited to 90 to 120 minutes for each outing
after appropriate sunscreen application. Further, environmental factors, such as
elevated atmospheric humidity, and inadequate application techniques, may reduce
photoprotection by as much as half.
Relative Ultraviolet Protection Factor (UPF) by Ultraviolet Ray (UVR)
UVR Transmitted (%) UVR Absorbed (%) UPF Protection Category
10 90.0 10 Moderate protection
3.3 96.7 30 Very high protection
2.5 97.5 40 Extremely high protection
<2.0 >98.0 50 Maximal protection
Sunscreen formulations with SPF as high as 50 can be made using combinations of
chemical and physical sunscreen agents.
Individuals who are extremely sensitive to
the sun may benefit from formulations with higher SPF, but the average fair-skinned
person gains adequate protection for sunbathing or for average daily exposure from a
Protection from sunburn increases with higher SPF; however, it is important to
remind J.J. that this protection does not correlate to the extent of skin damage from
UVA rays. One study reported less sunburn in patients who applied SPF 85
compared with those who applied SPF 50 and spent a similar amount of time in
In the FDA amendment that went into effect in 2012, SPF ratings
were limited to a maximum of 50+ due to lack of evidence for greater efficacy at
57 J.J. should also be reminded that the SPF is only accurate if he
correctly applies the sunscreen in the adequate amount.
CASE 42-1, QUESTION 9: Recommend appropriate protective eyewear for R.J. and J.J.’s family while
R.J. and J.J. should wear sunglasses when outdoors to decrease their lifelong
exposure to solar radiation and while at the beach to prevent high exposure of UVR
and possible photokeratitis or conjunctivitis. Many manufacturers of sunglasses label
their products according to three categories: cosmetic, general purpose, and special
purpose. Cosmetic sunglasses block at least 70% of UVB, at least 20% of UVA, and
less than 60% of visible light and are appropriate for casual wear when high
exposure to UVR is unlikely. General-purpose sunglasses block at least 95% of
UVB, at least 60% of UVA, and 60% to 92% of visible light and are appropriate for
most activities in sunny environments.
107 Special-purpose sunglasses block at least
99% of UVB, at least 60% of UVA, and at least 97% of visible light and are
appropriate for very bright environments, such as ski slopes or tropical beaches.
Special- or general-purpose sunglasses are appropriate recommendations for R.J.,
J.J, and their children to wear while on vacation.
Most tanning beds, booths, or salons use an artificial light source that emits about
95% UVA with minimal (i.e., 1%–5%) UVB.
It was originally thought that UVA
is much less likely to produce photoaging and photocarcinogenic changes of the skin
than UVB; however, UVA has now been found to cause many of the same effects on
the skin as UVB, including immunologic, degenerative, and neoplastic changes, as
well as damage to DNA and the formation of reactive oxygen species.
contributes to cataract formation and the activation of herpetic lesions.
doses of UVA received during a tanning session, as well as increasing cumulative
UVA doses over time, raise great concern about the long-term effects of UVA.
addition, UVA may augment the photocarcinogenic effect of UVB,
evidence indicates a relationship between indoor tanning and melanoma.
bed use dramatically increased from less than 1% of Americans in 1988 to 27% of
113 However, results from the National Health Interview Survey
noted a decrease in adults who frequented tanning salons from 5.5% in 2010 to just
over 4.2% in 2013. The decrease is hypothesized to be due to increased awareness
regarding the harms of tanning. Concern still exists about the number of Americans
choosing to tan, especially within the adolescent population.
2013 Youth Risk Behavior Survey conducted by the CDC reported that about 13% of
high school students, including 20% of high school girls, had used an indoor tanning
device one or more times during the last year.
115 This issue is compounded by
evidence that suggests that excessive UV exposure, particularly tanning beds, may
have a behavioral component similar to other substance-related disorders, which
may be related to an endogenous release of opioids secondary to exposure to UV
116 As many as 10% to 53% of young adults meet the criteria for having an
addictive component to indoor tanning behavior.
epidemic of use in young people, the FDA reclassified ultraviolet lamps to be class
II medical devices in 2014 and include a black box warning indicating that they
should not be used by minors 18 years old or younger.
more regulation on tanning booths, concern has been raised that regulating tanning
equipment as medical devices implies that they offer a therapeutic benefit, and is not
commensurate with other products that are known carcinogens with very little to no
With a skin type III, B.P. may be able gradually to achieve a moderate tan with
minimal burning, thus providing some protection from UVR because of increased
melanization of the skin. This UVA-induced tan, however, may not be as protective
as a tan achieved under normal sunlight conditions because UVA does not thicken the
118 An artificially produced tan plus subsequent sun exposure has not
been found to provide any net reduction in long-term damage to the skin when
compared with the same amount of tan obtained by sunbathing alone.
reasons, B.P. should not use the tanning booth to obtain a protective tan, and she
should use appropriate photoprotective measures during her trip.
CASE 42-2, QUESTION 2: What precautions would you recommend if she decides to visit a tanning salon?
If B.P. decides to artificially tan despite your recommendation, she should
undertake some precautions. The FDA has recommended exposure schedules for
first-time users based on skin type, which determines a person’s minimal erythemal
dose (MED) of UV radiation. The MED is determined by the amount of UV exposure
necessary to produce any visible reddening of the skin 24 hours after exposure. This
policy suggests that exposure be limited to no more than 0.75 MED 3 times the first
week, followed by a gradual increase to maintenance doses of a maximum of 4.0
MED delivered weekly or biweekly.
It is important to remember that MED is
specific to an individual, and therefore will be different depending on his or her skin
type. Correlating the FDA’s policy into time limits for an individual is therefore
dependent on skin type as well as the amount of UV exposure provided by the tanning
apparatus the individual will use. To minimize cataract development, B.P. should
always wear protective eye wear that absorbs all UVA, UVB, and visible light up to
500 nm; simply closing her eyes or wearing regular sunglasses provides no
protective effect against eye damage.
CASE 42-2, QUESTION 3: B.P. decides to accept your recommendations to avoid tanning beds; however,
photoprotection for B.P. against sunburn?
Sunless tanner is a commercial term that denotes a product that provides a tanned
appearance without exposure to the sun or other sources of UVR. One commonly
used ingredient in these products is dihydroxyacetone (DHA), a color additive that
darkens the skin to orange brown by reacting with amino acids in the stratum
corneum. The term bronzer is used to describe a variety of products intended to
achieve a temporary tanned appearance. For example, among the products marketed
as bronzers are tinted moisturizers and brush-on powders. These produce a
temporary effect, similar to other types of makeup, and wash off over time. Some
products are marketed with other ingredients in addition to DHA to provide a tanned
appearance. Generally, neither sunless tanners nor bronzers provide any protective
activity to UV exposure by themselves, unless specifically listed with a SPF rating
As previously described, the FDA now requires that all suntanning preparations that
do not contain sunscreen ingredients are required to carry a warning statement on the
label that they do not protect against sunburn.
Tanning pills are promoted for tinting the skin by ingesting massive doses of color
additives, usually canthaxanthin. At large doses, canthaxanthin is deposited in
various organs, including skin, imparting an orange-bronze color. This color varies
from individual to individual. This colorization is not the result of an increase in the
skin’s supply of melanin. Although canthaxanthin is approved by the FDA for use as a
retinopathy, nausea, gastrointestinal cramping, diarrhea, pruritus, and urticaria. None
of the above noted unapproved agents should be recommended for use.
QUESTION 1: G.B., a 31-year-old man with skin type IV, returned a few hours ago from an afternoon of
medications. What treatment recommendations would you give G.B. for his sunburn?
Sunburn is a self-limiting condition, and treatment is usually symptomatic.
Suggested treatments that G.B. can try for his first-degree burn are oral (e.g.,
compresses (tap water, saline, or aluminum acetate solution [Burow solution])
applied to the skin, or cool protectant baths (e.g., colloidal oatmeal). Nonsteroidal
anti-inflammatory drugs (NSAIDs), such as aspirin or ibuprofen, may be preferred
over acetaminophen because of blockade of the inflammatory prostaglandin-mediated
sunburn process; however, although offering symptomatic relief, corticosteroids,
NSAIDs, antioxidants, antihistamines, or emollients offer only mild improvement at
decreasing the time to recovery.
Topical anesthetics, such as benzocaine or lidocaine, provide only transient
analgesia for up to 15 to 45 minutes. These topical agents should not be used in large
quantities or applied more than 3 or 4 times a day. In addition, they should not be
used on raw, blistered, or abraded skin. Benzocaine has minimal systemic toxicities,
but is commonly associated with contact sensitization.
associated with a low incidence of contact sensitization.
have been shown to provide minimal clinical benefit when applied after UV
If G.B. wants to try a topical agent, application or administration is
recommended when the pain is particularly bothersome, such as at bedtime. Oral
antihistamines may help control pruritus associated with sunburn, as well as aid with
sleep, if taken at bedtime; however, no definitive studies have shown benefit in
reducing symptoms or benefit of one agent over another.
Treatment beyond self-management is generally unnecessary unless the sunburn is
extensive with constitutional symptoms (i.e., fever, chills, nausea, vomiting),
involves second- or third-degree burns (particularly if on the eyes or genitalia), or
becomes infected. In such cases, referral of the patient to his or her healthcare
provider is indicated as a short course (i.e., up to 3 days) of an oral corticosteroid
may need to be given (e.g., 1 mg/kg of prednisone or equivalent, given once daily).
Clinical Application of Phototoxicity or Photoallergy
Phototoxic photosensitivity reactions are dose dependent and occur in almost any
person who takes or applies an adequate amount of the offending agent. The dose
necessary to produce such a reaction varies from person to person and depends on
such factors as complexion, hair and eye color, usual ability to tan, and type and
amount of UVR exposure. Phototoxic photosensitivity reactions are not
immunologically mediated or true allergic reactions; they can occur on first exposure
to the agent and generally show no cross-sensitivity to chemically related agents.
A phototoxic reaction usually has a rapid onset, often within several hours after
UVR exposure, and presents as an exaggerated or intensified sunburn with erythema,
pain, and prickling or burning. Blistering, desquamation, and hyperpigmentation can
27,28 Symptoms generally peak 24 to 48 hours after the initial
exposure and are usually limited to the areas of UVR-exposed skin. Because
phototoxicity reactions do not involve the immune system, prior exposure to the
photosensitizer is unnecessary for this reaction to occur. Common drug classes
known to be phototoxic include fluoroquinolone, tetracycline, and sulfonamide
antibiotics, diuretics, sulfonylureas, nonsteroidal anti-inflammatory agents.
Clinically, photoallergy differs from phototoxicity in that it produces an intensely
pruritic, eczematous form of dermatitis.
28 The rash is preceded by pruritus and may
subside within an hour. In 5% to 10% of cases, persistent hypersensitivity to light
occurs, even after the offending chemical has been eliminated.
reactions are not dose-related, and eruptions can also be caused by chemically
related agents via cross-sensitivity or cross-allergenicity. As a type of delayed
hypersensitivity reaction, time is required to develop an immune response, and the
onset of a photoallergic reaction is often delayed for 1 to 3 days. These reactions can
present as macular, bullous, or purpuric lesions. Acute urticaria can occur within
minutes after UVR exposure. Recovery is slower than from a phototoxic reaction, and
it can persist after the offending product has been removed. These reactions may
present with erythema and possible edema secondary to the inflammation, but are
most commonly found to be eczematous, characterized by erythema; pruritus
(possible severe); and papules, vesicles, or both, with weeping, oozing, and crusting.
Scaling, lichenification, and pigmentation may occur later.
information do you need to know before making treatment recommendations?
Because D.L. is reporting symptoms that differ from previous sun exposures,
further questions should be asked regarding the history of the current scenario.
Information that may be important in the history of the condition include the temporal
relationship between sun exposure and onset of symptoms; the nature and duration of
symptoms; recent ingestion or topical application of medications; possible exposure
to photosensitizers, chemical irritants, or plants that can cause allergic contact
dermatitis (e.g., poison ivy); and the potential for arthropod bites. Information that
may be important from the physical examination includes the distribution and
morphology of the reaction, as well as areas of the body spared of the reaction.
A drug-induced photosensitivity reaction most commonly appears as a sunburn of
greater severity than would normally be expected or as a rash in areas exposed to the
sun or tanning apparatus. These reactions can be secondary to oral medications;
however, it is important to remember that chemicals with photosensitization potential
are found in cosmetics, shampoos, moisturizing lotions, hair dyes or tints, soaps, and
other topically applied medications and agents.
Drug-induced photosensitivity reactions can be subdivided into phototoxic and
photoallergic reactions. The same medication or agent may produce both phototoxic
and photoallergic reactions, and it may at times be difficult to differentiate clinically
between the two types of reactions.
CASE 42-4, QUESTION 2: On further questioning, you discover that D.L. first experienced painful
causes of his exaggerated sunburn reaction?
The most likely explanation for D.L.’s exaggerated sunburn reaction is
phototoxicity, secondary to contact with psoralen-like chemicals from the plants at
his job at the outdoor garden and greenhouse. Photoallergy is another possible cause
of D.L.’s symptoms. Although much less common than phototoxicity, photoallergy
requires prior or prolonged exposure to the photosensitizing compound.
Presumably, D.L. came into contact with psoralen-containing plants and
simultaneous exposure to sunlight. With an unusual distribution of lesions on his
hands, forearms, neck, and face and the lack of lesions on areas not contacted by the
plants or sunlight, the temporal relationship between the exposure and onset of
symptoms places phototoxicity higher in the differential diagnosis. D.L. is unlikely to
have a photoallergic reaction because of the lack of a delayed temporal relationship
between the onset of symptoms and combined exposure to a psoralen-containing plant
and sunlight. Unlike phototoxicity reactions, photoallergic reactions can spread to
areas that have not been exposed to sunlight; however, D.L.’s lesions were limited to
areas of skin exposed to sunlight.
CASE 42-4, QUESTION 3: What nonprescription remedies might you recommend for D.L. at this time?
General recommendations for the management of phototoxicity and photoallergy
reactions are focused on the removal of exposure to the potential photosensitizer and
reduced exposure to the sun. Patients should be counseled not to take any
medications, orally or topically, without first consulting with their healthcare
provider to minimize exposure to other photosensitizers. D.L. should try wearing
long-sleeved shirts, pants, and gloves when working to limit exposure to plant
photosensitizers. He also may try applying a broad-spectrum sunscreen to protect his
skin from UVB and UVA radiation. If these measures do not prevent further
photosensitivity reactions, D.L. should consider a different type of employment. His
presenting symptoms should be managed in a manner similar to that for an
Incidence, Prevalence, and Epidemiology
Photoaging, or premature aging of the skin, involves skin changes that differ from
those associated with normal chronologic aging.
130,131 Aside from advancing age, risk
factors that have been associated with photoaging include fair skin, male gender, high
115,132 Because recognizing photoaging and photodamage
may prevent the progression or development of skin cancer, it is important that they
are recognized as real medical problems, not just cosmetic or aesthetic concerns.
Normal aging of the skin involves fine wrinkling of the skin, atrophy of the dermis,
and a decrease in the amount of subcutaneous adipose tissue, all of which lead to a
state of hypocellularity of the skin.
131 Photoaging involves a chronic inflammatory
state induced by long-term exposure to UVA radiation from reactive oxygen species
(ROS), leading to a hypermetabolic state of the skin.
characterized histologically by an accumulation of excessive quantities of thickened,
degenerated elastic connective tissue fibers (elastosis).
predominates in normal skin, but in photodamaged skin, type III collagen increases
about fourfold, and the mature matrix of type I collagen slightly decreases.
degenerative changes in connective tissue may be caused by hyperactive fibroblasts
or by enzymatic degradation via cellular infiltrates in inflamed skin.
connective tissue then replaces the collagen in the upper parts of the dermis.
ground substance, composed of proteoglycans and glycosaminoglycans, also is
increased considerably in photoaged skin.
6 Capillaries in the dermis become dilated
and tortuous, resulting in telangiectasias, ecchymosis, and purpura.
thickens, and epidermal cells become hyperplastic and possibly neoplastic. Large
cumulative doses of UVA, UVB, and possibly infrared radiation during the course of
a lifetime are strongly implicated as the cause of these changes in photoaged skin.
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