Technical Report-Ultraviolet Radiation: A Hazard to Children and Adolescents - American Academy ...
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FROM THE AMERICAN ACADEMY OF PEDIATRICS
Organizational Principles to Guide and Define the Child
Health Care System and/or Improve the Health of all Children
Technical Report—Ultraviolet Radiation: A Hazard to
Children and Adolescents
Sophie J. Balk, MD, and the COUNCIL ON ENVIRONMENTAL
HEALTH and SECTION ON DERMATOLOGY abstract
KEY WORDS Sunlight sustains life on earth. Sunlight is essential for vitamin D syn-
sun, ultraviolet radiation, children, skin cancer, skin-cancer
prevention, melanoma, vitamin D, prevention, sun protection, thesis in the skin. The sun’s ultraviolet rays can be hazardous, however,
sunscreen, tanning, artificial tanning because excessive exposure causes skin cancer and other adverse
ABBREVIATIONS health effects. Skin cancer is a major public health problem; more than
UVR—ultraviolet radiation 2 million new cases are diagnosed in the United States each year.
NMSC—nonmelanoma skin cancer
PABA—para amino benzoic acid
Ultraviolet radiation (UVR) causes the 3 major forms of skin cancer:
SPF—sun-protection factor basal cell carcinoma; squamous cell carcinoma; and cutaneous malig-
BCC—basal cell carcinoma nant melanoma. Exposure to UVR from sunlight and artificial sources
SCC—squamous cell carcinoma
early in life elevates the risk of developing skin cancer. Approximately
IARC—International Agency for Research on Cancer
FDA—Food and Drug Administration 25% of sun exposure occurs before 18 years of age. The risk of skin
UPF—ultraviolet protection factor cancer is increased when people overexpose themselves to sun and
NHANES—National Health and Nutrition Examination Survey
intentionally expose themselves to artificial sources of UVR. Public
AAP—American Academy of Pediatrics
25(OH)D—25-hydroxyvitamin D awareness of the risk is not optimal, compliance with sun protection is
This document is copyrighted and is property of the American inconsistent, and skin-cancer rates continue to rise in all age groups
Academy of Pediatrics and its Board of Directors. All authors have including the younger population. People continue to sunburn, and
filed conflict of interest statements with the American Academy of teenagers and adults are frequent visitors to tanning parlors. Sun
Pediatrics. Any conflicts have been resolved through a process
approved by the Board of Directors. The American Academy of
exposure and vitamin D status are intertwined. Adequate vitamin D is
Pediatrics has neither solicited nor accepted any commercial needed for bone health in children and adults. In addition, there is
involvement in the development of the content of this publication. accumulating information suggesting a beneficial influence of vitamin
The guidance in this report does not indicate an exclusive course of D on various health conditions. Cutaneous vitamin D production re-
treatment or serve as a standard of medical care. Variations, taking
quires sunlight, and many factors complicate the efficiency of vitamin
into account individual circumstances, may be appropriate.
D production that results from sunlight exposure. Ensuring vitamin D
adequacy while promoting sun-protection strategies, therefore, re-
quires renewed attention to evaluating the adequacy of dietary and
supplemental vitamin D. Daily intake of 400 IU of vitamin D will prevent
vitamin D deficiency rickets in infants. The vitamin D supplementation
amounts necessary to support optimal health in older children and
adolescents are less clear. This report updates information on the
relationship of sun exposure to skin cancer and other adverse health
effects, the relationship of exposure to artificial sources of UVR and
www.pediatrics.org/cgi/doi/10.1542/peds.2010-3502 skin cancer, sun-protection methods, vitamin D, community skin-
doi:10.1542/peds.2010-3502
cancer–prevention efforts, and the pediatrician’s role in preventing
skin cancer. In addition to pediatricians’ efforts, a sustained public
All technical report from the American Academy of Pediatrics
automatically expire 5 years after publication unless reaffirmed, health effort is needed to change attitudes and behaviors regarding
revised, or retired at or before that time. UVR exposure. Pediatrics 2011;127:e791–e817
PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).
Copyright © 2011 by the American Academy of Pediatrics BACKGROUND
Sunlight sustains life on earth. The sun provides warmth, is needed
for photosynthesis, drives biorhythms, and promotes feelings of
well-being, and sunlight is essential for vitamin D synthesis in
skin.
PEDIATRICS Volume 127, Number 3, March 2011 e791
Downloaded from www.aappublications.org/news by guest on August 13, 2021The sun emits electromagnetic ra- in winter, at midday than in morning or TABLE 1 Classification of Sun-Reactive Skin
Types5
diation that ranges from short- late afternoon, in places closer to the
Skin History of Sunburning or Tanning
wavelength, high-energy x-rays to long- equator, and at higher altitudes. Sand,
Type
wavelength, lower-energy radio waves. snow, concrete, and water can reflect
I Always burns easily, never tans
Ultraviolet (“above-violet”) radiation up to 85% of sunlight, thus intensifying II Always burns easily, tans minimally
(UVR) waves range from 200 to 400 nm. exposure.3 Water is not a good photo- III Burns moderately, tans gradually and
UVR waves are longer than x-rays and protectant, because UVR can pene- uniformly (light brown)
IV Burns minimally, always tans well
shorter than visible light (400 –700 trate to a depth of 60 cm, which results (moderate brown)
nm) and infrared (“below-red” or in a significant exposure. In contrast to V Rarely burns, tans profusely (dark brown)
“heat”) radiation (⬎700 nm). UVR is the variability of UVB radiation, UVA ra- VI Never burns, deeply pigmented (black)
subdivided into UVC (200 –290 nm), diation is relatively constant through-
UVB (290 –320 nm), and UVA (320 – 400 out the day and the year.
nm, further subdivided into UVA2 UVR can be produced by man-made expressed as the erythema “action
[320 –340 nm]) and UVA1[340 – 400 lamps (eg, sunlamps) and tools (eg, spectrum” (the rate of a physiologic
nm]). UVC rays possess the highest welding tools), but the sun is the pri- activity plotted against wavelength of
energy but do not penetrate the at- mary source of UVR for most people.4 light showing which wavelength of
mosphere. Thus, middle-wavelength UVR has been used for decades to treat light is most effectively used in a spe-
(UVB) and long-wavelength (UVA) skin diseases, especially psoriasis.1 cific chemical reaction). The action
UVR, visible light, and infrared radia- spectrum for erythema and sunburn is
tion have the greatest biological UVR EFFECTS ON THE SKIN mainly in the UVB range.6
significance. The skin is the organ most exposed to Tanning
Solar radiation that reaches the environmental UVR and to associated
earth’s surface constitutes approxi- sequelae. Exposure to UVR may result Tanning is a protective response to
mately 95% UVA and 5% UVB.1 Most UVB in erythema and sunburn, tanning, sun exposure.7 Immediate tanning (or
radiation is absorbed by stratospheric skin aging, photosensitivity, and carci- immediate pigment-darkening) re-
ozone, but ozone absorbs little or no nogenesis (nonmelanoma skin cancer sults from oxidation of existing mela-
UVA or visible light. The ozone layer [NMSC] and cutaneous malignant nin after exposure to visible light and
does not have uniform thickness; melanoma). UVA. Immediate pigment-darkening be-
ozone concentration tends to increase comes visible within several minutes
toward the poles but is thinning in Erythema and Sunburn and usually fades within 1 to 2 hours.
some areas.2 Ozone depletion has a Delayed tanning occurs when new mel-
Erythema and sunburn are acute reac- anin is formed after UVB exposure. De-
significant effect on the amount of UVB tions to excessive amounts of UVR. Ex-
that reaches the earth.2 Chlorofluoro- layed tanning becomes apparent 2 to 3
posure to solar radiation causes vaso- days after exposure, peaks at 7 to 10
carbons used as aerosol propellants dilatation and increases the volume of
and in refrigeration and air condition- days, and may persist for weeks or
blood in the dermis, which results in months. According to recent evidence,
ing can destroy ozone. erythema. The minimal erythema (or the tanning response means that DNA
UVR that passes through the strato- erythemal) dose (the amount of UVR damage has occurred in skin.8
sphere (10 –50 km above sea level) is exposure that will cause minimal ery-
scattered by molecules such as oxygen thema or slight pinkness of the skin) Skin-Aging (Photoaging)
and nitrogen. It then passes through the depends on factors such as (1) skin Chronic unprotected exposure to UVR
troposphere (0 –10 km above sea level), type, (2) skin thickness, (3) the amount weakens the skin’s elasticity and re-
where it is absorbed and scattered by of melanin in the epidermis, (4) mela- sults in sagging cheeks, deeper facial
pollutants, such as soot, and attenuated nin production after sun exposure, and wrinkles, and skin discoloration. Pho-
by clouds. Clouds reduce the intensity of (5) the intensity of the radiation. A clas- toaged skin is characterized by alter-
UVR but not to the same extent that infra- sification system of 6 skin types rang- ations of cellular components and of
red intensity is reduced; the sensation of ing from light to dark (Table 1) takes the extracellular matrix. There is accu-
heat is diminished, which results in the into account a person’s expected sun- mulation of disorganized elastin and of
potential for overexposure. burn and suntan tendency.5 fibrillin (its microfibrillar component
The intensity of UVB radiation varies; it The ability of UVR to produce erythema in the deep dermis) and a severe loss
has greater intensity in summer than depends on the radiation wavelength of interstitial collagens, the major
e792 FROM THE AMERICAN ACADEMY OF PEDIATRICS
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structural proteins of the dermal con- factor (SPF) when some light expo- than 50 years, and the incidence in this
nective tissue. These changes result sure is inevitable.12 age group is increasing rapidly.16–18
primarily from exposure to UVR- Plants that contain furocoumarins People with immune suppression, in-
generated reactive oxygen species may lead to phototoxic reactions or cluding organ transplant recipients,
that deplete and damage the skin’s en- phytophotodermatitis. These com- also are at higher risk. Genetically
zymatic and nonenzymatic antioxidant monly encountered plants include an- based conditions, such as basal cell
defense systems.9,10 ise, diseased celery, dill, fennel, fig, nevus syndrome, xeroderma pigmen-
lemon, lime, mustard, parsnip, pars- tosum (a condition in which there is a
Photosensitivity ley, and chrysanthemums. Phytophoto- genetically determined defect in the
Chemical photosensitivity refers to an dermatitis can occur through inges- repair of DNA damaged by UVR),19 and
adverse cutaneous reaction that re- tion of plants or, more commonly, albinism, are risk factors for the accel-
sults when certain chemicals or drugs erated development of NMSC. Treat-
through topical contact.13
are applied topically or taken systemi- ment with UVR for psoriasis also in-
Up to 80% of patients with lupus ery- creases risk.19 NMSC is extremely rare
cally at the same time that a person is thematosus have photosensitivity. The
exposed to UVR or visible radiation. in children in the absence of predis-
threshold UVR dose that triggers cuta- posing conditions.20
Phototoxicity is a form of chemical neous or systemic reactions is much
photosensitivity that does not depend The incidence of NMSC is increasing in
lower than that for sunburn. Many pa-
on an immunologic response; the reac- young adults. Researchers examined
tients are not aware of the association
tion can occur on first exposure to an the gender- and age-specific incidence
of flares with UVR exposure, because
agent. Most phototoxic agents are ac- of BCC and SCC in a young (⬍40-year-
the latency period between exposure
tivated in the range of 320 to 400 nm old), primarily white and middle-class
and skin eruptions can range from
(the UVA range). Drugs associated with population within Olmsted County,
several days to 3 weeks.14
phototoxic reactions include those Minnesota, by using comprehensive
commonly used by adolescents, such medical records available through
Carcinogenesis
as nonsteroidal anti-inflammatory the Rochester (MN) Epidemiology
agents; tetracyclines and tretinoin; Nonmelanoma Skin Cancer Project.21 Over the period of
other medications such as phenothia- NMSC includes basal cell carcinoma 1976 –2003, the incidence of BCC in-
zines, psoralens, sulfonamides, and (BCC) and squamous cell carcinoma creased significantly among young
thiazides; and para amino benzoic acid (SCC). In the US adult population, NMSC women, and the incidence of SCC in-
(PABA) esters.11 Photoallergy is an ac- is the most common malignant neo- creased significantly among both men
quired altered reactivity of the skin, plasm, with more than 2 million cases and women.
usually triggered by exposure to UVA, diagnosed each year. Most of these are A trend toward a greater number of
that depends on antigen-antibody or BCC, SCC occurs less often.15 The rate BCC cases occurring on the torso in
cell-mediated hypersensitivity. Pho- of NMSC has been increasing in the younger patients has been report-
toallergic reactions involve an immu- United States, but the exact number is ed.21–23 This change in location sup-
nologic response to a chemical or drug not precisely known, because physi- ports the possibility that excessive out-
that is altered by UVR. PABA-containing cians are not required to report NMSC door tanning, use of tanning booths, or
sunscreens, fragrances, sulfonamides, to cancer registries. NMSC is rarely fa- both give rise to BCC. Tanning-bed use
and phenothiazines are associated tal; nevertheless, it is estimated that has been shown to be a risk factor for
with photoallergic reactions.11 The each year, approximately 2000 people NMSC in young women.24
consequences of exposure to a pho- die of NMSC.15 Sun exposure is the main environmen-
tosensitizing agent can be uncom- In general, NMSC occurs in maximally tal cause of NMSC. Cumulative expo-
fortable, serious, or life-threatening. sun-exposed areas of fair-skinned peo- sure over long periods, which results
People who take medications or use ple. NMSC is uncommon in black peo- in photodamage, is considered impor-
topical agents known to be sensitiz- ple and people with increased natural tant in the pathogenesis of SCC.
ing should do their best to limit sun pigmentation. The head and neck re-
exposure and avoid UVA from artifi- gion is the most common site for BCC Melanoma
cial sources. They should wear fully and SCC; 80% to 90% of cases occur in Melanoma is primarily a disease of the
protective clothing and apply sun- this area in the general population. skin. Primary extracutaneous sites in-
screen with a high sun-protection NMSC is more common in people older clude the eye, mucous membranes,
PEDIATRICS Volume 127, Number 3, March 2011 e793
Downloaded from www.aappublications.org/news by guest on August 13, 2021gastrointestinal tract, genitourinary young women aged 15 to 39 years.31 EVIDENCE THAT UVR CAUSES SKIN
tract, leptomeninges, and lymph People at highest risk have light skin CANCER
nodes. Ninety-five percent of melano- and eyes and sunburn easily. Risk of In 1992, the International Agency for
mas occur in the skin.25 If detected developing melanoma is increased at Research on Cancer (IARC) reviewed
when the tumor is thin and small, cu- older ages, in people who have already the evidence for the carcinogenicity of
taneous malignant melanoma has an had melanoma, or in people who have solar radiation. They concluded that
excellent prognosis. However, meta- had a first-degree relative with mela- “[t]here is sufficient evidence in hu-
static melanoma has no successful noma. Melanomas frequently are mans for the carcinogenicity of solar
treatment options. Prevention and found in people with xeroderma pig- radiation. Solar radiation causes cuta-
early detection, therefore, are crucial mentosum and related disorders. In a neous malignant melanoma and non-
in this disease. large case-control study from the melanocytic skin cancer.1” Since that
Many authorities have stated that the Netherlands, the risk of developing time, evidence has strengthened the
incidence of cutaneous malignant mel- melanoma was increased in women link between sunlight exposure and
anoma (hereafter referred to as “mel- who had used estrogens (either as skin cancer.
anoma”) has reached epidemic pro- oral contraceptives or hormone-
portions. Possible factors contributing replacement therapy) for more than Cellular Studies
to the increased incidence of mela- half a year.32 UVB is absorbed by and can directly
noma include the decrease in the damage DNA, which ultimately leads to
Melanoma is rare in children, but it
earth’s protective ozone layer, chang- the development of skin cancer.38 The
does occur. Studies have documented
ing patterns of dress that favor more genotoxic effects of solar UVB radia-
an increase in the incidence in chil-
skin exposure, more opportunities tion are mainly mediated by direct ab-
for leisure activities in sunny areas, dren and adolescents, even in the ab-
sorption in the epidermis of photons
and increased exposure to artificial sence of predisposing conditions such
by DNA, which results primarily in cy-
sources of UVR for tanning purposes. as xeroderma pigmentosum. From
clobutane pyrimidine dimers (formed
1973 to 2001, the incidence of mela-
In the United States, melanoma is the between adjacent pyrimidine bases lo-
noma in US children younger than 20 cated on the same DNA strand) and py-
fifth most common cancer in men and
years increased 2.9% annually.33 An in- rimidine (6-4) pyrimidone photoprod-
the sixth most common in women.26
crease in incidence was noted in Swe- ucts.7 Incorrect repair of these lesions
The incidence of melanoma is increas-
den during 1973–1992,34 but incidence results in the formation of mutations
ing rapidly in the United States.27 In
1935, the lifetime risk for a person in then decreased.35 Ferrari et al36 re- in epidermal cells, which causes the
the United States developing invasive viewed a 25-year experience with 33 development of cancer.7,39
melanoma was 1 in 1500. In 2007, this Italian children with melanoma who
UVA penetrates more deeply into the
risk was 1 in 63 for invasive melano- were 14 years or younger at presenta-
skin than does UVB, including reaching
mas and 1 in 33 when in situ melano- tion. The children’s lesions were not the basal layer of the epidermis and
mas were included. Worldwide, mela- typical of melanoma lesions in adults. dermal fibroblasts.38 UVA causes oxi-
noma is increasing faster than any Melanoma lesions in adults gener- dative damage to DNA that is poten-
other malignancy.28 Melanoma repre- ally follow the “ABCDEs”: they are tially mutagenic.7
sents fewer than 5% of all skin cancers asymmetric (A), have irregular bor-
but is the cause of almost all skin- ders (B), variegated color (C), and Biological Evidence
cancer deaths. The American Cancer diameter (D) larger than 6 mm (the Biological evidence suggests that sun-
Society predicted that approximately size of a pencil eraser), and change light exposure is important in the
68 130 new melanoma cases would be or evolve (E).37 In the Ferrari et al36 pathogenesis of melanoma. Results of
diagnosed in 2010, with 8700 deaths.29 series, however, many lesions in chil- studies in opossums suggest that por-
Melanoma is more likely to occur in dren were amelanotic (pink, pink- tions of the UVA spectrum may play a
males and at older ages but also oc- white, or red) and tended to be role in the pathogenesis of melanoma40
curs in teenagers and young adults. It raised and to have regular borders. and that portions of the UVA and UVB
is the second most common cancer of The key to diagnosis for these chil- spectrums promote development of
women in their 20s and the third most dren was the recognition that the carcinomas in mice.41 Melanoma can
common cancer of men in their 20s.30 melanoma lesions were unlike any be induced by UVB and UVA radiation in
Melanoma incidence is increasing in other lesions on the child. certain fish.42 Research ethics make it
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impossible to determine directly variation in human skin appearance. History of Sun Exposure
which wavelengths result in skin can- Melanin that is genetically determined The pattern of sun exposure is impor-
cer in humans. is termed “constitutive” melanin pig- tant in the etiology of BCC, SCC, and
Melanoma has been induced in human mentation. When this basic pigmenta- melanoma skin cancers. Personal sun
newborn foreskins grafted onto immu- tion is increased by exposure to UVR, it exposure is usually characterized by
nologically tolerant animals exposed is termed “inducible” or “facultative” (1) total sun exposure, (2) occupa-
to UVR.43 Melanomas and NMSC are of- melanin pigmentation. Melanin is tional exposure (which signifies a
ten found in people with xeroderma thought to have evolved as an optical more chronic exposure), and (3) non-
pigmentosum and related disorders.44 and chemical photoprotective filter occupational or recreational exposure
that functions as a natural “sun- (which signifies intermittent expo-
Epidemiologic Evidence sure).46 SCC is significantly associated
screen” to regulate UVR penetration
Latitude or Estimated Ambient into skin. In early human evolution, the with estimated total sun exposure and
Solar UVR more highly melanized skins of people with occupational exposure. Chronic
The rates of BCC and SCC increase with indigenous to the tropics afforded bet- exposure to UVB is now considered the
increasing ambient solar UVR. There is ter protection against the deleterious main environmental cause of SCC. SCC
a direct relationship between the inci- effects of UVR. A dark epidermis pro- seems to be most straightforwardly
dence of NMSC and latitude; higher tected sweat glands from UVR-induced related to the total sun exposure: these
rates are found closer to the equator injury and ensured the integrity of so- tumors occur on skin areas that are
(where the amount of sunlight is matic thermoregulation. Highly mela- most regularly exposed (face, neck,
greater).28 The relationship of mela- nized skin also protected against and hands), and the risk rises with the
noma with latitude is not as clear as UVR-induced photolysis of folate, a me- lifelong accumulated dose of UVR.47
that for NMSC.28 tabolite essential for normal develop- BCC and melanoma are significantly
associated with intermittent sun expo-
Race and Pigmentation ment of the embryonic neural tube.45
sure (ie, sunburning or “brutal” expo-
As people migrated outside the trop-
BCC and SCC occur primarily in white sure), whereas SCC does not show
ics to northern areas, a lighter skin
people.15 Incidence and mortality rates this relationship. Melanoma is more
color was needed as an adaptation to
of melanoma are highest in white peo- strongly associated with intermittent
promote maintenance of UVR-
ple (Table 2).27 There is, in general, an sun exposures than is BCC.46
induced synthesis of vitamin D3 in ar-
inverse relationship between skin-
cancer incidence and the skin pigmen- eas of lower UVR exposure.45 As the Childhood Sun Exposure
tation of people in various countries in pace of human migrations quickened
Childhood and adolescence are often
the world. Superficial epidermal mela- in recent centuries, however, popu-
considered to contain “critical periods
nin decreases the transmission of lations have found themselves in
of vulnerability” when people are espe-
UVR, which may protect the deeper UVR-irradiation patterns to which cially susceptible to effects of toxic ex-
basal layer melanocytes and several they are poorly adapted. Cultural posures. Approximately 25% of lifetime
layers of keratinocytes from sunlight- practices, such as sunbathing and sun exposure occurs before 18 years
induced changes that lead to their ma- covering up for religious reasons, ex- of age.48 Sun exposure and blistering
lignant transformation.7 acerbate or mitigate the mismatch in sunburns during youth may be more
Melanin, a dark pigment produced by degree of melanin protection to UVR intense than later in life because of
melanocytes, accounts for most of the exposures.45 youths’ behavior. Exposure may result
in alteration of melanocyte DNA and an
increase in the risk of malignant de-
TABLE 2 Melanoma Incidence and Mortality Rates According to Race/Ethnicity27 generation in nevi as children age.
Race/Ethnicity Men, Rate per Women, Rate per Sunlight exposure during childhood
100 000 Men 100 000 Women
and adolescence is generally consid-
Incidence Mortality Incidence Mortality ered to confer increased risk of mela-
White 28.9 4.4 18.7 2.0 noma compared with exposure at
Black 1.1 0.5 1.0 0.4
Asian/Pacific Islander 1.6 0.5 1.3 0.3 older ages. This issue was reviewed in
American Indian/Alaska Native 3.9 1.6 2.8 0.9 an analysis of epidemiologic studies
Hispanic 4.6 0.9 4.7 0.6 categorized into 2 groups.49 The first
PEDIATRICS Volume 127, Number 3, March 2011 e795
Downloaded from www.aappublications.org/news by guest on August 13, 2021group contained 20 ecologic studies whether sunburn occurred during during the period of peak melanocytic
(ie, studies in which the unit of obser- childhood or adulthood. The summary activity. Populations exposed to high
vation is the population or community) odds ratios associated with sunburn sunlight levels in childhood will have
relating the risk of melanoma to during childhood and adulthood were more people with more initiated mela-
places of residence. These studies 1.8 (95% confidence interval: 1.6 –2.2) nocytes than populations of those who
were conducted on the basis of the fact and 1.5 (95% confidence interval: 1.3– experienced lower sunlight levels. This
that ambient solar radiation increases 1.8), respectively, although there was “melanoma potential” is retained
with proximity to the equator and in- significant heterogeneity among the when people move to a different
cluded studies of migrants to locations studies for the estimates of childhood environment.49
with markedly different levels of sun- sunburn. The authors underscored the
light. The second group consisted of lack of reliability of recalling personal Nevi
case-control studies in which mea- sun exposure as a reason for the in- Acute sun exposure is implicated in the
sures of sun exposure between people consistencies between the migrant development of nevi (moles) in chil-
with melanoma and those without and case-control studies and consid- dren. The number of nevi increases
were compared. ered the evidence from the migrant with age52; nevi occur with more fre-
In the first group, most studies re- studies to be of higher quality.49 In a quency on sun-exposed areas, and the
vealed that people who migrated from large multicenter case-control study, number of nevi on exposed areas in-
“low” to “high” areas of ambient solar the authors concluded that excessive creases with the total cumulative sun
radiation had decreasing melanoma UVR exposure later in life may be as exposure during childhood and ado-
risk with arrival at older ages, important a risk for melanoma as UVR lescence.53 Children with light skin who
whereas those who arrived in child- exposure earlier in life.50 There was a tend to burn rather than tan have
hood (younger than 10 years) or ado- similar upward gradient of melanoma more nevi at all ages, and children who
lescence (younger than 15 years) had risk related to sunburns during have more severe sunburns have more
similar risks as people who were childhood (defined as age ⱕ 15 years) nevi.52
native-born. The 1 study that investi- and adulthood (defined as age ⬎ 15 There is a relationship between the
gated age-specific “high-to-low” migra- years). More than 5 sunburns doubled number and type of melanocytic nevi
tion demonstrated higher risk in peo- the melanoma risk irrespective of and the development of melanoma.
ple born in a sunny area or having had whether those sunburns occurred in The presence of congenital melano-
more than 1 year living in a sunny area childhood or adulthood.50 cytic nevi (CMN) (pigment cell malfor-
before 10 years of age.49 The results of There is biological plausibility to sup- mations formed during gestation and
most studies of the age of migration, port the heightened susceptibility of visible at or shortly after birth) in-
therefore, supported the “critical- young melanocytes. Peak melanocytic creases melanoma risk. In a review of
period” hypothesis. activity occurs in early life as demon- 14 studies— case series with adequate
Ten case-control studies that exam- strated by the steady acquisition of follow-up periods—investigators found
ined melanoma risks associated with nevi during childhood and adoles- an overall risk of melanoma arising in
personal sun exposure during 2 or cence. Freckling is also prominent at CMN of 0.7%, which was lower than ex-
more age periods were evaluated in these ages; freckles in children often pected. Melanoma risk strongly de-
the second group. Findings of these appear abruptly after high-dose sun pended on the size of the CMN and was
studies differed widely without consis- exposure and are thought to represent highest in nevi designated as garment
tent associations with childhood sun clones of mutated melanocytes. The nevi (defined as nevi situated on the
exposure. Three studies reported sig- presence of freckles is associated with trunk that measure ⬎40 cm in largest
nificantly increased risks of mela- an increased risk of melanoma.7 Young diameter or expected to reach this
noma associated specifically with melanocytes may be especially vulner- size in adulthood). The mean age at
episodes of sunburns during child- able to the adverse effects of solar ra- melanoma diagnosis (15.5 years)
hood, whereas 1 Swedish study found diation. Sunlight may have both early and median age of diagnosis (7
no effect of childhood sunburn but re- and late effects on the development of years) underscored the maximum
ported significantly higher risks asso- melanoma (akin to cancer “initiation,” risk in childhood and adolescence.54
ciated with adulthood sunburns. The “promotion,” and “progression”51), Dysplastic melanocytic nevi typically
remaining 5 studies reported similar and the biological effectiveness of sun- are 5 mm or larger in diameter; usu-
risks of melanoma regardless of light in initiating melanoma is greatest ally have fuzzy, irregular borders; and
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have variegated color. Dysplastic nevi traocular malignant neoplasm in of white recipients in Western coun-
are considered precursor lesions that adults, is associated with light skin tries and 70% to 80% of those in Aus-
increase melanoma risk.55 The familial color, blond hair, and blue eyes. There tralia will have developed at least 1
dysplastic nevus syndrome is a disor- is contradictory evidence regarding NMSC (mostly SCC).66 People who have
der with the following features: (1) a the role of UVR in causing uveal had renal transplants also have an in-
distinctive appearance of abnormal melanoma.63,64 creased incidence of melanoma.67 Be-
melanocytic nevi; (2) unique histologic cause ongoing immunosurveillance
features of the nevi; (3) autosomal UVR EFFECTS ON THE IMMUNE has been lacking, skin cancers in peo-
dominant pattern of inheritance; and SYSTEM ple who have received organ trans-
(4) hypermutability of fibroblasts and Exposure to UVR contributes to immu- plants are likely to behave aggres-
lymphoblasts. Fibroblasts and lympho- nosuppression, which is increasingly sively with a higher rate of local
blasts from patients with this syn- recognized as important in the devel- recurrence and a greater tendency to
drome are abnormally sensitive to UV opment of skin cancer. UVR exposure be invasive and metastatic.66
damage, and people with this syn- is thought to have 2 effects: skin-
drome are at markedly higher risk cancer induction and immune sup- ARTIFICIAL SOURCES OF UVR
of developing melanoma.56 Certain pression.65 Experiments in mice chron- People may be exposed to artificial
families with germ-line mutations in ically exposed to UVR have shown that sources of UVR in several ways, includ-
CDKN2A, CDK4, and other genes are at
tumors induced by UVR are highly an- ing as treatment for medical condi-
increased risk of developing dysplas-
tigenic and are recognized and re- tions (such as psoriasis), in occupa-
tic nevi and melanoma.57
jected by animals with normal immune tional settings (such as welding), and
History of Exposure to Artificial UVR systems. The tumors grow progres- for cosmetic purposes. Sunlamps and
Exposure to tanning beds and sun- sively, however, when transplanted tanning beds are the main sources of
lamps, which produce primarily UVA, is into mice with immune systems that artificial UVR used for deliberate pur-
associated with increased risk of de- are compromised.65 UVR exposure in- poses.68 Artificial tanning is a relatively
veloping BCC, SCC, and melanoma. duces “systemic” immune suppres- new phenomenon that results in po-
sion so that exposure on 1 body site tentially large exposures to UVA and
UVR EFFECTS ON THE EYE suppresses the immune response UVB. The “tanning industry” has grown
In adults, more than 99% of UVR is ab- when the antigen is introduced at a quickly; it takes in $5 billion in annual
sorbed by the anterior structure of the distant site that was not irradiated. revenue, up from $1 billion in 1992.69
eye, although some of it reaches the Soluble factors implicated in sys- Each day, more than 1 million people
retina.58 Acute exposure to UVR can re- temic immune suppression include tan in one of 50 000 tanning facilities in
sult in photokeratitis.59 Gazing directly platelet-activating factor (PAF), pros- the United States.69 Indoor tanning also
into the sun (as can occur during an taglandin E2 (PGE2), cis-urocanic is popular in northern Europe and is
eclipse) can cause focal burns to the acid, histamine, interleukin 4, interleu- gaining popularity in Australia.68
retina (solar retinopathy).60 kin 10, and ␣-melanocyte-stimulating Artificial tanning is a common practice
Exposure to solar UVB radiation is as- hormone.65 among teenagers. In a national sample
sociated with an increased risk of cat- Skin cancers are common in people ex- of non-Hispanic white teenagers 13 to
aracts.61 UVR can contribute to the posed to immunosuppressive agents, 19 years of age in the United States,
development of pterygium, corneal de- which further illustrates the role of the 24% of respondents—representing
generative changes, and cancer of the immune system. In people who have 2.9 million teenagers—reported using
skin around the eye.58 There is evi- had renal transplants, lifelong immu- a tanning facility at least once in their
dence for a probable relationship be- nosuppressive treatment needed for lives.70 In another national survey, 10%
tween UVR exposure and squamous adequate graft function leads to a re- of youth 11 to 18 years of age reported
intraepithelial neoplasms of the con- duction of immunosurveillance and an using indoor tanning beds or sun-
junctiva or cornea, but there is insuffi- increased risk of various cancers. With lamps in the previous year.71 Women
cient evidence to determine if there is increased duration of transplantation, and girls represent the majority of
a relationship between UVR exposure skin cancer is now one of the common- people who artificially tan. Of the 1 mil-
and the development of macular de- est causes of death in renal transplant lion people daily who are tanning-
generation.62 Melanoma of the uveal recipients. Twenty years after trans- salon customers, 70% are females 16
tract, the most common primary in- plantation, approximately 40% to 50% to 49 years of age.69 Twenty-eight per-
PEDIATRICS Volume 127, Number 3, March 2011 e797
Downloaded from www.aappublications.org/news by guest on August 13, 2021cent of white US teenaged girls inter- tured that ultraviolet light exposure re- nature and is a new phenomenon in
viewed in 1996 had used tanning sa- sults in induction of cutaneous endor- people.78
lons 3 or more times during their phins; thus, endorphin release may Artificial UVR exposure has been
lives.70 Tanning-bed use increases with play a role in driving UVR-exposure be- shown repeatedly to induce erythema
age, from 7% among 14-year-old girls havior. If cutaneous endorphins are in- and sunburn. Erythema or burning ef-
to 16% among 15-year-old girls and to duced, an endorphin blockade would fects were reported by 18% to 55% of
35% among 17-year-old girls.72 be expected to block the effect.76 A re- users of indoor tanning equipment in
Tanning-bed use by adolescent girls is cent study assessed the prevalence of Europe and North America.68 Although
often associated with other unhealthy addiction to indoor tanning among col- UVB is much more potent than UVA in
behaviors. In 1 study, frequent tanning- lege students and its association with causing sunburn, high fluxes of UVA
bed use was associated with smok- substance use and symptoms of anxi- can cause erythema in people who are
ing cigarettes, binge-drinking, being ety and depression. Two written sensitive to sunlight. In people who tan
highly concerned about weight, and measures, the CAGE (cut down, an- easily, exposure to tanning appliances
other risk behaviors.73 noyed, guilty, eye-opener) Question- will lead first to immediate pigment-
naire, used to screen for alcoholism, darkening. A more permanent tan will
Evidence That Tanning and the Diagnostic and Statistical occur with accumulated exposure, de-
May Be Addictive Manual of Mental Disorders, Fourth pending on individual tanning ability
Exposure to UVR from sunlight or tan- Edition, Text Revision (DSM-IV-TR) crite- and the amount of UVB present in the
ning parlors may be addictive. Beach- ria for substance-related disorders light spectrum of the tanning lamps.
goers aged 18 years and older in were modified to evaluate study partic- Immediate pigment-darkening has no
Galveston, Texas, were interviewed us- ipants for addiction to indoor tanning. photoprotective effect against UVR-
ing questions to evaluate dependence Self-report measures of anxiety, de- induced erythema or sunburn. In addi-
on tanning. Subjects completed sur- pression, and substance use were ad- tion, the permanent tan induced by
ministered. Among the 229 study par- UVA and UVA-induced skin-thickening
veys that included a tanning-specific
ticipants who had tanned indoors, 70 provides little photoprotection.
modification of a screening instru-
ment for alcoholism and questions to (30.6%) met CAGE criteria and 90 Other frequently reported effects of ar-
evaluate criteria for tanning-specific (39.3%) met DSM-IV-TR criteria for ad- tificial tanning include skin dryness,
substance-related disorder. Of 145 diction to indoor tanning. Indoor tan- pruritus, nausea, photodrug reac-
subjects, 26 (18%) screened positive ners reported significantly greater tions, disease exacerbation (eg, sys-
on both measures, and 63 (43%) symptoms of anxiety and greater use temic lupus erythematosus), and dis-
screened positive on 1 measure. The of alcohol, marijuana, and other sub- ease induction (eg, polymorphous
authors concluded that those who stances than those who did not meet light eruption). Long-term health ef-
chronically and repeatedly expose these criteria. Depressive symptoms fects include skin-aging, effects on the
themselves to UVR to tan may have did not significantly vary according to eye (eg, cataract formation), and
a type of UVR substance-related indoor-tanning-addiction status.77 carcinogenesis.
disorder.74 In a study of 14 adults, tan- In 1992, the IARC1 classified the “use
ners overwhelmingly preferred UVR- Effects of Artificial UVR on Human of sunlamps and sunbeds” as “prob-
emitting beds when asked to choose Skin ably carcinogenic to humans.” In
blindly between UVR-emitting and Tanning beds primarily emit UVA radi- 2000, the National Institutes of Health
non–UVR-emitting tanning beds. A ation, although a small amount (⬍5%) stated that “exposure to sunlamps or
more relaxed and less tense mood was is in the UVB range.68 In terms of bio- sunbeds is known to be a human car-
reported after UVR exposure com- logical activity, the intensity of UVA ra- cinogen, based on sufficient evi-
pared with after non-UVR exposure.75 diation produced by large, powerful dence of carcinogenicity from stud-
In another study, the opioid antagonist tanning units may be 10 to 15 times ies in humans, which indicate a
naloxone was given to 8 frequent salon higher than that of the midday sun. causal relationship between expo-
tanners and 8 people who were infre- Frequent indoor tanners may receive sure to sunlamps or sunbeds and hu-
quent tanners. Withdrawal-like symp- 1.2 to 4.7 times the annual dose of UVA man cancer.”79
toms were induced in 4 of 8 frequent than is received from the sun, in addi- A case-control study demonstrated a
salon tanners; no symptoms occurred tion to doses from sun exposure.68 This significant association between using
in the 8 infrequent tanners. It is conjec- intensity of exposure is not found in any tanning device and the incidence
e798 FROM THE AMERICAN ACADEMY OF PEDIATRICS
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of SCC and BCC.80 A prospective cohort artificial tanning. The Indoor Tanning province of New Brunswick, Canada.87
study of 106 379 women in Scandinavia Association, an industry group founded Currently (as of February 2011), more
examined melanoma risk in females in 1999, promotes “a responsible mes- than 60% of US states regulate tanning
who reported having used a sunbed or sage about moderate tanning and sun- facilities for minors.88 Some states
sunlamp. A 55% increase in melanoma burn prevention.”82 Their mission is to completely ban salon access to chil-
risk was found in women who reported “protect the freedom of individuals to dren younger than 14 years, whereas
having used a tanning device at least acquire a suntan, via natural or artifi- other states ban access to adolescents
once per month in at least 1 of the 3 cial light.”83 The Indoor Tanning Associ- 15 or 16 years of age. Some states re-
decades between 10 and 39 years of ation claims that “controlled” salon quire written parental consent or writ-
age, compared with those who had tanning is safer than “uncontrolled” ten consent with the parent present at
never or rarely used a tanning device beach tanning; this concept is not sup- the facility or a doctor’s prescription.
during those 3 decades.81 ported by laboratory, behavioral, or In California, where tanning-salon use is
In 2006, the IARC published an updated epidemiologic data.78 Another com- banned for children younger than 14
analysis of studies of the carcinogenic- monly held misconception is that getting years, recent legislation made annual
ity of artificial UVR with regard to mel- a “prevacation tan”—when people visit signed parental consent required for
anoma, SCC, and BCC.68 On the basis of tanning salons to prepare skin for a tanning-facility use by adolescents 14 to
19 studies, any previous use of sun- sunny vacation—will protect against 17 years of age.89 During the 2010 legis-
beds was positively associated with subsequent skin damage during the va- lative session, 20 states introduced
melanoma (summary relative risk: cation. This practice actually leads to ex- bills to regulate tanning facilities for
1.15 [95% confidence interval: 1.00 – tra radiation exposure not only before minors.88,*
1.31]), although there was no consis- the vacation but also afterward, because The Indoor Tanning Association has
tent evidence of a dose-response re- people use fewer sun-protection precau- fought against legislative initiatives
lationship. First exposure to sunbeds tions during the vacation because of a and stated that legislation will harm
before 35 years of age significantly in- mistaken belief that the tan will protect business90 and that tanning is an issue
creased the risk of melanoma on the them.69 A prevacation tan results in min- of parental rights: “When it involves a
basis of 7 studies (summary relative imal protection (an SPF of 3),78 which suntan, the State has no business in-
risk: 1.75 [95% confidence interval: provides virtually no protection against serting itself between child and par-
1.35–2.26]). The summary relative risk sun-induced DNA damage.68 ent. This notion that government knows
of 3 studies of SCC showed an in- more about child rearing than parents is
creased risk. Studies did not support Antitanning Legislation and preposterous.”89 Pediatric health advo-
an association for BCC. The evidence Recommendations cates have countered this argument by
did not support a protective effect of Because of mounting evidence about the stating that laws to limit minors’ access
the use of sunbeds against damage carcinogenicity of artificial UVR, support to tanning parlors should be thought of
to the skin from subsequent sun for regulations to limit teenagers’ ac- in the same way as laws that limit youth
exposure. cess to tanning facilities has been wide- access to tobacco.87,89 All states prohibit
spread. The World Health Organization,84 the purchase of tobacco products by
Biological evidence supports the epi-
the American Medical Association,85 and those younger than 18 years; some pro-
demiologic studies. The skin of volun-
the American Academy of Dermatology86 hibit tobacco sales to those younger
teers exposed to UVA lamps used in
all support legislation to ban the use of than 19 years.87 Tanning legislation is of-
tanning appliances showed DNA dam-
artificial tanning devices by people ten not enforced.91
age.68 The IARC concluded that young
adults should be discouraged from us- younger than 18 years. The IARC review Artificial Tanners (Spray Tans and
ing indoor tanning equipment and that concluded that young adults should be Sunless Tanning Lotions)
restricted access to sunbeds by mi- discouraged from using indoor tanning
Several organizations have suggested
nors should be strongly considered. equipment and that restricted access to
that people who wish to obtain the look
sunbeds by minors should be strongly
of a tanned skin use artificial (or “sun-
Tanning-Industry Response considered.68
less”) tanning products to substitute
The tanning industry has fought vigor- France has banned indoor tanning for
ously to allow teenagers access to tan- people younger than 18 years since *For more information on current state laws that
restrict the use of tanning beds by children and
ning salons and promotes the pur- 1997; indoor tanning for those younger teenagers, please contact the AAP Division of State
ported health benefits and safety of than 18 years also is prohibited in the Government Affairs.
PEDIATRICS Volume 127, Number 3, March 2011 e799
Downloaded from www.aappublications.org/news by guest on August 13, 2021for tanning obtained by going outside ucts that contain added sunscreen 3. Seek shade.
or at tanning salons. Sunless tanners provide UVR protection only during the 4. Use extra caution near water, snow,
contain dihydroxyacetone, a chemical first few hours after application and and sand.
that reacts with amino acids in the that additional sun protection must be
5. Apply sunscreen.
stratum corneum to form brown-black used during the duration of the artifi-
compounds—melanoidins—that de- cial tan. 6. Wear sunglasses.
posit in skin. Dihydroxyacetone is a Clothing and Hats
mutagen that induces DNA strand PREVENTION
breaks in certain strains of bacteria; it Clothing can be an excellent UVR bar-
The incidence of skin cancer continues
has not been shown to be carcinogenic rier, because it offers a simple and
to rise despite public health efforts
in animal studies.92 practical means of sun protection. In
to increase awareness of sun-safety
contrast to sunscreens, the photopro-
Dihydroxyacetone is the only color ad- measures. Children and teenagers
tection afforded by clothing does not
ditive approved by the US Food and continue to sunburn: in 1 large study of
diminish throughout the day unless
Drug Administration (FDA) for use as more than 10 000 white teenagers 12
the clothing becomes wet. Infants and
a tanning agent.93 Dihydroxyacetone- to 18 years of age, most respondents
children may be dressed in cool, com-
containing tanning preparations may (83% [n ⫽ 8355]) reported sunburning
fortable clothing and wear hats with
be applied to the consumer’s bare skin at least once, and 36% of children re-
brims. One study revealed that wear-
by misters at sunless tanning booths. ported 3 or more burns during the pre-
ing clothing decreases the develop-
Bronzers are water-soluble dyes that vious summer.72 Only one-third of re-
ment of nevi.103 Protective factors in
temporarily stain the skin. Bronzers spondents reported routine use of
clothing include fabric type, thickness,
are easily removed with soap and sunscreen during the past summer.
color, and chemical enhancement.2
water. Sunburning during the summer was
Wool and synthetic materials such as
The prevalence of sunless tanner use reported in a nationwide survey of
polyester are more protective, whereas
in Australia has ranged from 9% to youth, although many reported using
cotton, linen, acetate, and rayon are less
22%94; 28% of women between 18 and sunscreen before their most serious
protective. A tighter weave lets in less
24 years of age reported using sunless sunburn.96 Among adolescents 16 to 18
sunlight than a looser weave. Darker col-
tanners.95 A survey of young adults 18 years of age, the prevalence of sun-
ors are more protective than lighter
to 24 years of age in the United States burn and the average number of days
ones. Clothes that cover more of the
revealed that 22% had used sunless spent at the beach increased be-
body provide more protection; sun-
tanners in the previous 12 months, and tween surveys conducted in 1998 and
protective styles cover to the neck, el-
2004.97
another 22% who had not used these bows, and knees. Treating fabrics with
products would consider doing so in It has been estimated that sun avoid- chemical absorbers or washing them
the next 12 months.94 Sunless-tanning- ance could reduce the number of life- with optical brighteners increases UVR
product users were more likely to be time NMSC cases by almost 80%.98 protectiveness.
female, to be younger, and to report Although other risk factors (eg, pre-
In 1996, Australia and New Zealand es-
having sunburned during the previous cursor lesions, older age, race, previ-
tablished standards for the UVR pro-
summer than potential users or ous melanoma, and family history) are
tectiveness of clothing. The United
nonusers. more closely associated with mela-
States developed standards in 2001.
noma than sunburns, exposure to UVR
Dihydroxyacetone-induced tans be- The ultraviolet protection factor (UPF)
is the only risk factor that is avoidable.
come apparent within 1 hour; maximal measures a fabric’s ability to block
Leading organizations (the American
darkening occurs within 8 to 24 hours. UVR from passing through the fabric
Cancer Society,99 Centers for Disease
Most users report that color disap- and reaching the skin. The UPF is clas-
Control and Prevention,100 Healthy Peo-
pears over 5 to 7 days. Because neither sified from 15 to ⱖ50 as follows: 15 to
ple,101 National Council on Skin Cancer
dihydroxyacetone nor melanoidins af- 24 is rated as “good”; 25 to 39 is rated
Prevention102) have recommended
ford any significant UV protection, con- as “very good”; and 40 to ⱖ50 is rated
sun-safe behaviors. UVR-protective
sumers must be advised that sunburn as “excellent.” Although garments with
messages include:
and sun damage may occur unless a UPF above 50 may be labeled “UPF
they use sunscreen and other sun- 1. Do not burn; avoid suntanning and 50⫹,” these garments may not offer
protection methods. Consumers must tanning beds. substantially more protection than
also be warned that any sunless prod- 2. Wear protective clothing and hats. those with a UPF of 50. Any garment
e800 FROM THE AMERICAN ACADEMY OF PEDIATRICS
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with a UPF lower than 15 should not be TABLE 3 FDA-Approved Sunscreens110,115
labeled as “sun protective” or “UV pro- Sunscreen Range of Comments
tective.”104 Denim provides a UPF of protection
1700.2 Typical summer cotton T-shirts Organic
PABA derivatives UVB —
provide a UPF of 5 to 9. The UPF of fab- PABAa
rics can be increased by shrinking and Padimate O (octyl dimethyl PABA)
decreased by stretching. If cotton fab- Cinnamates UVB —
Octinoxate (octyl
rics get wet, the UPF decreases. The methoxycinnamate)
US Federal Trade Commission moni- Cinoxate
tors advertising claims about sun- Salicylates UVB —
Octisalate (octyl salicylate)
protective clothing.105 Homosalate
Hats provide variable sun protection Trolamine salicylatea
Benzophenones UVB, UVA2 Penetrates skin; estrogenicity in animal
for the head and neck, depending on
Oxybenzone (benzophenone 3) studies
the brim width, material, and weave. A Sulisobenzone (benzophenone 4)
wide-brimmed (3-in) hat provides an Dioxybenzone (benzophenone 8)a
SPF of 7 for the nose, 3 for the cheek, 5 Others
Octocrylene UVB In combination with other sunscreen agents,
for the neck, and 2 for the chin. improves product photostability
Medium-brimmed (1- to 3-in) hats pro- Ensulizole (phenylbenzimidazole UVB —
vide an SPF of 3 for nose, 2 for the sulfonic acid)
Avobenzone (butyl methoxybenzoyl UVA1, UVA2 Photolabile; efficacy decreases by ⬃60%
cheek and neck, and none for the chin. methane, Parsol 1789) after 60 min of exposure
A narrow-brimmed hat provides an Ecamsule (terephthalylidene UVB, UVA2 Photostable; particularly effective for UVA2;
SPF of 1.5 for the nose but little protec- dicamphor sulfonic acid) approved by the FDA in 2007
Meradimate (menthyl UVA2 —
tion for the chin and neck.2 anthranilate)a
Inorganic
Shade Titanium dioxide UVB, UVA2/UVA1 —
Zinc oxide UVB, UVA2/UVA1 —
Infants younger than 6 months should Note that other agents are approved for use in the European Union.
be kept out of direct sunlight. When- a These agents are rarely used in sunscreen formulations.
ever possible, children’s outdoor activ-
ities should be planned to minimize
peak-intensity midday sun (10 AM to 4 sunburn. Most FDA-approved sun- tection from full-spectrum UVR.3 Table
PM). Seeking shade is somewhat useful, screen agents are organic chemicals 3 lists the FDA-approved sunscreen
but people can still sunburn, because that absorb various wavelengths of agents.
light is scattered and reflected. A fair- UVR, primarily in the UVB range; others SPF is a grading system developed to
skinned person sitting under a tree are effective in the UVA range.110 Some quantify the degree of protection from
can burn in less than an hour. Shade agents are not photostable in the UVA erythema provided by using a sun-
provides relief from heat and possibly range and degrade with sun exposure. screen; the higher the SPF, the greater
provides a false sense of security Combinations of chemicals are needed the protection. For example, a person
about UVR protection. Clouds decrease to provide broad-spectrum protection who would normally experience sun-
UVR intensity but not to the same ex- and increase photostability.110 burn in 10 minutes can be protected
tent that they decrease heat intensity The 2 FDA-approved inorganic physical up to approximately 150 minutes (10 ⫻
and, thus, may promote a mispercep- sunscreens are zinc oxide and tita- 15) with an SPF-15 sunscreen. SPF per-
tion of protection.6 nium dioxide, which prevent penetra- tains only to UVB. The SPF is deter-
tion of skin by UVB, UVA1, and UVA2. mined indoors according to a stan-
Sunscreen Physical sunscreens are usually white dard protocol that uses artificial light
Sunscreen is the main form of protec- or tinted after application; some sources and application of a defined
tion used by the population, including newer formulations are less visible on amount of sunscreen (2 mg/cm2). An
parents who use sunscreen to protect the skin but may be less effective.110 SPF-2 sunscreen applied at this thick-
children.106–109 Sunscreens reduce the Physical sunscreens are useful for ness blocks approximately 50% of UVB
intensity of UVR affecting the epider- people with photosensitivity disorders radiation; an SPF-10 blocks 90%; an
mis, thus preventing erythema and and other conditions that require pro- SPF-15 blocks 94%; and an SPF-30
PEDIATRICS Volume 127, Number 3, March 2011 e801
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