Richard F.
Edlich, M.D., Ph.D.
Distinguished Professor of
Plastic Surgery
and Professor of Biomedical
Engineering
University of Virginia
Health Systems
Charlottesville, VA
Since antiquity, the undesirable
effects of the sun have been appreciated, yet people continue to bask on the
beaches of the world to seek the benefits of heliotherapy. Scientific and
medical studies of the adverse reactions to the sun’s rays have evolved into
the field of clinical photobiology. The purposes of this paper are (1) to
describe the skin’s natural defenses, (2) to list common types of
sunlight-induced skin disorders in normal people, (3) to discuss
photosensitizing reactions, (4) to identify diseases aggravated by sunlight and
(5) to compare the effectiveness of various sun protective devices and drugs.
The sun’s electromagnetic (EM) radiation, which emanates from its internal thermonuclear reactions, consists of both waves and particles. Waves are oscillations that travel through space and can be described in terms of frequency and wavelength. All EM radiation travels at the speed of light and the frequency and wavelength are inversely related by the equation:
C = ν x l
where
C = velocity of light (3 x 1010 cm/sec),
ν = frequency (vibrations/sec),
and
l = wavelength (cm).
The
wavelengths emitted by the sun vary from an angstrom (Å) to hundreds of meters
and are classified into the special regions shown in Table 1.
|
|
Wavelength range |
|
Cosmic
rays |
0.005
Å |
|
Gamma
rays |
0.005-1.4
Å |
|
X-rays |
0.1-100
Å |
|
Vacuum
ultraviolet |
10-2000
Å |
|
Ultraviolet
C (UV-C) |
2000-2900
Å |
|
Ultraviolet
B (UV-B) |
2900-3200
Å |
|
Ultraviolet
A (UV-A) |
3200-4000
Å |
|
Visible
light |
4000-7400
Å |
|
Near
infrared |
7400
Å–1.5 n |
|
Middle
infrared |
1.5-5.6
n |
|
Far
infrared |
5.6-1000
n |
|
Microwaves
and radiowaves |
1000
n-550 m |
In addition to its transverse wave
properties, EM radiation exhibits particle-like behavior in the form of tiny
discrete packets of energy known as photons or quanta. The energy in a photon is directly
proportional to the frequency of the radiation by the equation E=hn.
Therefore, high frequency radiation directly corresponds to high photon
energy.
The earth is shielded by gases that
filter and attenuate the sun’s radiation, more commonly known as the ozone
layer. About one third of this energy
is either reflected, absorbed, or scattered by the atmosphere, allowing
wavelengths between 2900 and 18,000 Å to reach the earth. Of the EM waves that reach the earth, nearly
one half are in the visible light spectrum(4,000 to 7,400 Å). The remaining waves are in the invisible
ranges at either end of this spectrum.
Most of this radiation (80%) is infrared, with lower frequency and
longer wavelength than red light (7400 Å to 1.5 microns). The remaining 20% of the waves reaching the
Earth’s surface are in the ultraviolet range with waves of higher frequency and shorter wavelength than visible
light. Although ultraviolet light UV-L
constitutes only a small percentage of the sun’s total radiant energy, it
appears to be primarily responsible for cutaneous burns in human beings.
UV-L radiation is divided into three
categories: ultraviolet A (UV-A), ultraviolet B (UV-B), and ultraviolet C
(UV-C). Ninety-nine percent of the UV-L
received at the earth’s surface is UV-A.
Its radiation has a wavelength between 3200 and 4000 Å and causes melanogenesis
with relatively little reddening of the skin.
Approximately 50 to 70 joules/cm2 of UV-A is required to
produce minimal erythema, but since UV-A passes through window glass, it may
cause sunburn in people unwittingly exposed.
UV-B comprises the remaining 1% of
UV-L received on earth. Its wavelengths
range from 2900 to 3200 Å and stimulate tanning of the skin as well as
sunburn. UV-B is 1000 times more
erythemogenic than UV-A and accounts for most of the damage done to the skin
even though 10 times more UV-A reaches the earth’s surface. Studies on the cutaneous effects of
simultaneous irradiation with UV-A and UV-B are limited, and there is
disagreement as to whether their combined effects are simply additive or
synergistic. Window glass blocks UV-B,
but water, even at a depth of ten feet, transmits 50% of the UV-B and most
UV-A, making swimmers and snorkelers susceptible to sunburn. UV-C (2000 to 2900 Å) does not reach the
earth’s surface.
The intensity of solar radiation
received at any point on the earth’s surface is primarily a function of the
distance to the sun. This is determined
by the longitude, latitude, and altitude of the specific site as well as the
season of the year. In general,
radiation in the northern hemisphere is most intense in June, or the other
summer months, and at sea level; UV-L energy is strongest between 10:00 A.M.
and 3:00 P.M., peaking at noon. During
this time, the surface of the earth receives approximately two thirds of its
daily supply of UV-L energy. For every
1000 feet above sea level, the intensity of UV-L energy increases by 5%.
The most intense radiation is
received at the equator, and the intensity decreases with increasing
distance. For example, in June, the
length of time required to produce minimal erythema in New Jersey (40ºN latitude)
is 21 minutes as compared with only 10 minutes in the Florida Keys (24ºN). Blistering sunburn occurs after 165 minutes
exposure in New Jersey and after only 120 minutes in the Florida Keys.
Atmospheric phenomena, such as smog
or clouds, reflect and absorb radiation and serve to reduce UV-L energy
received in direct proportion to their density. Light cloud cover may lessen the appearance of the sun’s energy
yet, is deceptive as it blocks few of the harmful UV-L rays. Even clothing transmits UV-L energy, and a
thin white shirt, if wet, will transmit UV-L light, particularly that of longer
wavelengths.
In addition to direct solar
radiation, scattered and reflected light also can be erythemogenic. Snow is an excellent reflector of UV-L
energy, being 85% efficient, and accounts for skiers’ sunburn. While white sand is a poor reflector (15%
efficient), it may account for sunburn, despite the protection of a beach
umbrella. The reflection of UV-L energy
off water varies with the time of day; at noon, only 5% is reflected, but as
the angle of incidence of the sunlight decreases, reflectivity increases,
reaching 100% efficiency at sunrise and sunset.
The human body has evolved several
means to protect itself from UV-L radiation.
The two most important are the thickening of the stratum corneum and the
formation of melanin in melanocytes.
Following exposure to UV-L radiation, the stratum corneum thickens by as
much as three times in the biological phenomenon of epidermal hyperplasia. This thickening occurs even in amelanotic
skin and is associated with increased tolerance to subsequent exposure. These thick cell layers absorb, reflect, and
scatter radiation. Consequently, the
thick epidermal layers of the palms and soles display a greater tolerance to
sun exposure than do the thinner epidermal layers that cover other anatomic
regions. Tanning acquired by sunless
tanning agents does not offer this thickness or melanin production and should
not be relied on for protection from the sun.
Upon exposure to solar radiation,
the melanocytic system undergoes two distinct changes. The first process, immediate pigment
darkening (IPD), results from photooxidation of existing melanin. This UV-A produced tan fades within four
hours and contributes little to the development of a lasting tan, while also
reducing the skin’s tolerance for UV-L energy.
IPD does not offer any future photoprotection. The more important response of the pigmentary system is delayed
tanning (DT), or true melanogenesis. DT
is the most effective protection against solar radiation and appears within 72
hours of exposure. In DT, the amount of
melanin/melanocyte increases in a genetically determined capacity stimulated by
UV-B radiation. This response is less
well developed in children, and they are consequently more susceptible to
sunburn.
An individual’s skin color is determined genetically
by a constitutive factor, the amount of melanin the skin contains, and a
facultative factor, the ability of the skin to produce more melanin. The amount of melanin pigment in the skin
determines the photosensitivity and, consequently, dark-skinned individuals
generally are more resistant to sunburn than people with light complexions,
though they are not entirely protected from the harmful effects of UV-L radiation. Approximately 15% of white people do not
produce sufficient melanin to protect them against sunburn. Upon exposure to the sun, distinct sites of
hyperpigmentation (freckles) develop, leaving the remaining skin susceptible to
burn. The Food and Drug Administration
(FDA) has organized a chart with skin types and tanning history (Table 2).
|
Skin Type |
Response to Suna |
Sensitivity |
|
Ib |
Always
burns easily; never tans |
sensitive |
|
IIb |
Always
burns easily; tans minimally |
sensitive |
|
III |
Burns
moderately; tans gradually (light brown) |
normal |
|
IV |
Burns
minimally; tans well (moderate brown) |
normal |
|
Vc |
Rarely
burns; tans profusely (dark brown) |
insensitive |
|
VI |
Never
burns (black) |
insensitive |
a After 35-40 minutes on
previously unexposed skin.
b Light-skinned, blue-eyed
redheads, and some persons with dark brown hair and blue or green eyes.
c Darker-skinned persons
(e.g., those of Mediterranean or Asian descent).
The adverse cutaneous and systemic
reactions to sunlight in normal, healthy skin are classified into two types:
the immediate type or acute sunburn, and the delayed type long term effects
that occur following chronic exposure to light.
ACUTE
SUNBURN
After 48 hours of sun exposure, the UV-L energy
absorbed at different levels of the skin results in cell damage in the
dyskerototic cells of the stratum malpighi and stratum corneum. Erythema induced by vasodilation, increased
blood flow, and edema ensues. An inflammatory
infiltrate develops in the underlying papillary dermis and is thought to be
mediated by histamine, serotonin, and kinins.
Prostaglandins (PG) and related derivatives recently have been
implicated in the development of erythema, and increased levels of PG have been
found in human tissue exposed to UV-L energy.
These substances of low molecular weight are synthesized by microsomal
enzymes in all mammalian cells, and the biosynthesis of PG can be inhibited by
nonsteroidal anti-inflammatory compounds, such as indomethacin or aspirin. When administered either topically or
intradermally, indomethacin delays the onset and intensity of UV-L-induced
erythema.
Depending on the skin type and
duration of exposure, sunburn can range in severity from a mild asymptomatic
erythema to a more intense skin reaction that includes exquisite tenderness,
pain, swelling, and blistering. The
most serious sunburn includes systemic signs such as fever, chills, nausea, and
prostration.
TREATMENT
Treatment of acute sunburn includes (1) restoring
any loss in intravascular volume, (2) suppressing UV-L-induced erythema, and
(3) providing analgesics. When skin is
burned by solar radiation, intravascular fluids extravasate into the burned
tissue thereby reducing intravascular volume.
In severe sunburn injuries, this reduction of vascular volume may be
sufficient to produce hypotension. In
such cases, the intravascular volume must be replaced with a crystalloid
solution.
Most studies substantiate that
synthesis and release of PG may be the primary mechanism in the production of
erythema. PG synthetase inhibitors
administered systemically or topically are highly efficient suppressors of UV-L
erythema, but have no apparent preventative effect on the ultimate damage to
the skin. Topical and systemic steroids
have also been advocated in the treatment of sunburn erythema. However, when steroid treatment was
evaluated by means of random, double-blind studies, there were no significant
differences in responses between the steroid treated groups and the controls.
The basic form of benzocaine is
bioactive and penetrates the intact and damaged sunburned skin and limits the
sensation of pain, burning, and itching.
When properly formulated in concentrations between 5 and 20%, benzocaine
is an effective and safe topical analgesic, anesthetic, and antipruritic agent
on the intact skin. Among the
benzocaine preparations that are commercially available, those consisting of
20% benzocaine base in propylene glycol are most effective. Relief is obtained
for periods of four to six hours. The
lack of efficacy of some of the manufactured preparations is most commonly
related to insufficient concentrations of the active ingredient (less than 5%
benzocaine).
Epidemiologic data on allergy,
irritancy, and other reactions to benzocaine do not support the contention that
it is a potent sensitizer. It has been
and is still one of the safest topical anesthetic agents. Because it has a low degree of water
solubility, the quantities of absorbed benzocaine are relatively insignificant,
and plasma levels that cause systemic
reactions characterized by the soluble “caine” type drugs do not occur with
this drug. The convulsions and cardiac
depression, characteristic of the “caine” type drugs, do not occur with this
drug, and reports of such drug-related reactions are nonexistent. A 1% solution of lidocaine hydrochloride
exaggerates rather than relieves the pain associated with sunburn.
DELAYED
REACTIONS
Repeated exposure to solar radiation, particularly
for individuals with skin types I, II, and III who do not use sunscreens, can
lead to aging of the skin. Lighter skin
types allow the photons of UV-L radiation to penetrate deeper into the skin,
causing more lasting damage, such as elastosis, eye damage, and cutaneous
neoplasia. Premature aging of the skin
also results from prolonged exposure to the sun, which may damage both the
epidermal and dermal layers of the skin.
The epidermis becomes thickened and develops actinic keratoses. In the dermis, elastic tissues become a
tangled shapeless mass without flexibility.
Mature collagen levels decrease, and the small blood vessels are dilated
to an extreme. These effects lead to a
leathery appearance of the skin.
Studies have shown that areas protected from the sun, such as the
buttocks, do not show these changes.
Skin moisturizers and toners cannot reverse these signs of premature
aging.
In the United States, sun-induced carcinomas, which
occur most frequently on the face, ears, hands and feet, are the most common of
all forms of cancer, accounting for an estimated 30% of all cancer cases. It is estimated by the Center for Disease
Control and Prevention that malignant melanoma claimed 9,200 lives in 1999. Nonmelanomatic cancers may be precursors to
the more serious malignant forms of basal cell and squamous cell
carcinoma. Basal cell carcinomas occur
more frequently in men and in three forms:
nodular, morpheaform, and superficial.
Squamous cell carcinoma, typically found on the face or other areas
affected by intense UV-L radiation, are small craters with raised edges. Typically basal cell carcinomas remain
localized and do not metastasize, while squamous cells metastasize at a 5%
rate. Surgical excision removes both
types of lesions.
Malignant melanoma also result from sun exposure. Four types of melanoma are known to exist: superficial spreading melanoma, nodular melanoma, lentigo malignant melanoma, and acral-lentiginous melanoma. The two most common are the superficial spreading melanoma, which generally appears on the back and legs, and lentigo malignant melanoma. The latter arises from cumulative sun exposure and rarely metastasizes. The former stems from intermittent sunburn experiences and metastasizes at a rate of 20%. If diagnosed early, melanoma may be excised, but a late diagnosis requires treatment with chemotherapy, immunotherapy, or radiation.
UV-B acts as a carcinogen by
suppressing the immune system. The
radiation changes the function of Langerhan’s cells located in the epidermis
from triggering immunity to suppressing immunity. The cells can no longer present antigen to the immune system and
more readily allow cancer formation.
A photosensitizing reaction is a
sunburn that appears unexpectedly after a limited exposure to sunlight
following the parenteral administration of a chemical. Adverse photosensitivity reactions may be
phototoxic or photoallergic. Phototoxic
reactions can be elicited in any normal healthy individual when appropriate
concentrations of an offending agent are either applied topically (contact) or
given orally (systemic) (Table 3).
After exposure to light, the agent leads to a sunburn reaction that
occurs 5 to 18 hours after exposure to the sun and is usually maximum at 36 to
72 hours. Desquamation,
hyperpigmentation, or hypopigmentation may also occur. Furocoumarins, encountered in Persian lime
juice or in cosmetic agents containing plant extracts or other essential oils,
frequently produce phototoxic reactions that are manifested clinically by
hyperpigmentation that is confined to the anatomic site where the agent is
applied.
|
Systemic
Photosensitizers |
Contact
Photosensitizers |
|
Sulfonamides |
Plants:
Ragweed and furocoumarins (i.e., figs, limes, etc.) |
|
Chlorothiazides |
Soaps:
Halogenated phenolic soaps |
|
Phenothiazides |
Drugs:
Sulfa, tar |
|
Antibiotics |
Dyes:
Rose Bengal, fluorescein |
|
Estrogens
and progesterones |
Cosmetics:
Furocoumarin compounds (i.e, oil of lime and oil of Bergamot) |
Systemic photosensitizers are
chemicals in the body that under certain circumstances can induce a phototoxic
reaction. An immediate type reaction occurs upon exposure to sunlight following
the oral or parenteral administration of a variety of different drugs (i.e.,
demeclocycline hydrochloride, sulfonamides, phenothiazines, tolbutamide,
chlorothiazide diuretics, halogenated phenolic compounds).
The photoallergic reaction is a
cell-mediated immune response that may develop in any normal person following
repeated contact with a sensitizing chemical substance. The absorbed light seems to promote a
photochemical reaction between the drug and skin protein. The drug acts to form a haptenic group and
either combines directly with the protein to form a photoantigen or is altered
by the absorbed energy, after which it reacts with the protein to form an
antigen. All first allergic reactions
include a latent period of at least ten days, before the allergic reaction
occurs. After that, under the same
conditions of the photosensitizing chemical interacting with sunlight, the
interval between the time of contact with the sensitizing agent and the
allergic reaction is within 24 hours.
Close examination of the skin reaction shows that it differs distinctly
from sunburn, with either wheal (hives) or dermatitis that simulates
eczema. Much smaller quantities of
chemical sensitizers are capable of reproducing the photoallergic effect than
phototoxic reactions. The most common
photoallergic drugs are halogenated salicylanilides, phenols, and carbanilides.
Sensitivity can be so exquisite that
minute amounts of residual chemical in the skin along with exposure to
artificial light will be sufficient to maintain an active state of disease in
the absence of the sensitizer. The
sensitized patient, a persistent light reactor, will often display thickened,
hyperpigmented, and hypopigmented skin with fissuring.
TREATMENT
Therapy of acute phototoxic reactions, induced by
the topical or systemic agent, consists of removing the agent and avoiding
exposure to the sun. Clinical
phototesting can aid in making the diagnosis.
In theory, any lesion in which sunlight plays an etiologic role should
be reproducible using artificial light sources and the offending agent. Topical steroids, such as 0.1% triamcinolone
cream, lotion, or spray, two or three times a day are usually adequate to
relieve skin reactions. It is important
to avoid persistent or repeated use of the more potent steroids, such as
fluocinonide and fluocinolone acetonide, when areas such as the face are
involved, because prolonged use can lead to skin atrophy and striae. When photosensitive reactions are severe, a
seven-day tapering course of oral prednisone, starting with 40 mg orally on the
first day, is often beneficial.
Antihistamines suppress symptoms in
some patients with photoallergic reactions.
In most patients, the eruption associated with chemical photosensitivity
subsides within a week or two of avoiding the chemical and sunlight. Exposure to sun should be avoided especially
between the hours of 10 A.M. and 3 P.M.
When exposure is unavoidable, sunscreens with a high sun protection
factor (SPF) should be used.
Certain diseases are aggravated or
induced by sunlight. The most classical
reaction of this type is seen in various types of porphyria. In these diseases, the photosensitizing
reactions are due to the overproduction of proto-, uro- or coproporphyrins and
their precursors. The wavelengths for
elicitation of cutaneous reactions are mainly in the visible-light spectrum
(4000 to 7000 Å) and correspond to the rays that are strongly absorbed by
porphyrin in vitro (4000 to 6000
Å). Vesiculobulbous, urticarial, or
eczematous reactions are seen in different types of porphyria. Postinflammatory atrophic and pigmentary
changes may also be present in these reactions. The most disabling types of photosensitivity reactions are found
in erythropoietic (congenital) porphyria, also known as Gunther’s disease, and
in erythropoietic protoporphyria.
Congenital erythropoietic porphyria is characterized by several skin
mutilating effects, such as vesicles and bullae, which lead to scarring. These dramatic effects are only seen upon
cutaneous exposure to the sun.
Erythropoietic protoporphyria is a disease distinguished by the lack of
an enzyme necessary to catalyze the incorporation of iron into protoporphyrin,
which manifests itself as a stinging sensation, and is much more common than
the congenital form. Symptoms and signs
of this sensitivity to sunlight occur in childhood. The adverse reactions to sunlight in most patients with
erythropoietic protoporphyria have been eliminated by the oral ingestion of b-carotene.
The mechanism of light-induced reactions in the rare
genetic disease, xeroderma pigmentosum, has also been recently elucidated. This disorder is due to ineffective excision
or post-replication repair of deoxyribonucleic acid (DNA) following exposure to
UV-L. Patients with xeroderma
pigmentosum exhibit extreme sun-sensitivity by age 1 and generally develop skin
cancer by age 8.
Certain other diseases predispose
patients to increased sensitivity to sunlight, but the mechanism in most of
these disorders is unknown.
Sun-sensitivity in collagen-vascular diseases is well known. One third to one half of the patients with
systemic lupus erythematosus (SLE) are photosensitive. The pathogenic role of UV-L radiation in SLE
is uncertain, although both UV-A and UV-B have been implicated. Irradiated DNA appears to bind an antigen
leading to SLE, while unirradiated DNA does not. Noxious stimuli other than UV-L radiation can elicit cutaneous
lesions in patients with SLE.
Polymorphous light eruption (PLE) is an erythematous, macular, sometimes
urticarial eruption that develops in the sun-exposed area in the spring. It may be pruritic, and typically lasts
through the summer into the fall, eventually disappearing in the winter only to
recur the following spring. There are
no associated systemic symptoms.
Other sun-sensitive disorders include
phenylketonuria, pellagra, and carcinoid.
Diseases, which are exacerbated on exposure to the sun, include herpes
simplex, varicella, lymphogranuloma, venereum, and other dermatologic disorders
(i.e, psoriasis, lichen planus, keratosis follicularis, pityriasis rubra
pilaris, pemphigus erythematosus, erythema multiforme, sarcoid, and
lymphocytoma).
The goal of any form of
photoprotection, in normal or abnormal skin, is to limit the UV-L penetration
to the viable skin layer by scattering, absorption, or reflection. Sunscreens accomplish protection on a
cellular level by inhibiting DNA mutagenesis, and on a larger scale by stopping
irreversible processes, such as photoaging and wrinkling. Several forms of barriers, natural,
physical, and chemical exist, none of these barriers possess the ability to
prevent completely sunburn, but instead serve to prolong the exposure time for
erythema to occur.
A combination of more than one type
of photoprotection barrier, along with avoiding the powerful mid-day sun, is
the most promising way to avoid sun damage.
Natural barriers to the sun’s harmful rays include the ozone layer and
shaded areas, while physical barriers include clothing, hats, sunglasses, and opaque
substances, like zinc oxide. The last
form of protection, chemical agents, contains UV-L-absorbing molecules that
form an impenetrable film on the skin.
Emulsions, oils, gels, and sprays,
constitute the general forms of vehicles for sunscreening agents. Emulsions are most popular and may be either
creams or gels, depending upon their viscosity. Oils provide poor protection due to their interaction with the
sunscreening chemicals they contain, and gels typically wash off or cause
stinging sensations for the users.
Today’s sunscreens offer non-toxic,
invisible, waterproof, sweat-proof UV-L radiation protection. Protection aimed at absorbing a specific
portion of the UV-B spectrum typically arises from solutions containing
para-aminobenzoic acid (PABA), a PABA ester, or non-PABA chemicals, such as
cinnamates, salicylates or benzophenones.
Even though the PABA chemicals have shown to produce an extremely
effective barrier, they possess the drawbacks of producing a stinging
sensation, dryness of skin, and the staining of clothing. Solutions containing one or more of these
agents provide a most powerful UV-B defense
.
Most chemical agents have been
proven to block UV-B radiation only, as it was originally believed to be the
more harmful portion of the UV-L-spectrum.
The hazards of UV-A exposure now known have culminated in the formation
of UV-A absorbing agents. The most
active of these ingredients include dioxybenzone, oxybenzone, sulisobenzone,
methyl anthranilate, octocylene, and octyl methoxycinnamate. While each of these blocks only a specific
portion of the UV-A spectrum, only one agent has shown to block the entire
range: Parsol 1789. This agent, containing avobenzone, was
approved in 1997 for use in 2-3% concentrations, with the belief that its
benefits of protection far outweigh any drawbacks of allergy. Unfortunately, the chemicals that are
stronger blockers of UV-A radiation tend to be yellow in color and this
cosmetically unappealing characteristic limits their use.
Sun protection offers a varying
degree of substantivity, or adherence to the skin after sweating, swimming, or
washing. Sunscreens tend to dissolve
more quickly in fresh water than sea water, and those containing PABA
derivatives bind aggressively to skin.
New developments in photoprotection research offer an even greater
amount of substantivity. Hydrophobic
silica particles have been created which provide resistance to sweating or
other interactions with skin oils. When
silica reacts with an organosilicon, it becomes hydrophobic and inhibits the
movement of the chemical agents in the sunscreen. This inhibited movement causes the protective agents to remain on
the skin when most would be washed away.
The newest form of sunscreen adherence comes in the form of tiny glass
beads encasing the photoprotective agents. CoppertoneÒ (Schering-Plough Healthcare Products,
Memphis, TN), uses this new ingredient, which is called C10-30 alkyl acrylate
crosspolymer in their waterproof and sweatproof skin products. This ingredient
allows higher concentrations of sunscreens to be used and prevents chemical
interactions that may limit the sunscreen’s effectiveness. The most effective water resistant sunscreen
product to use would be any labeled waterproof with a high SPF. CoppertoneÒ Ultra Sweatproof SPF 48 is both waterproof
and sweatproof, and provides a high SPF rating of 48. To test for substantivity, the FDA requires testing in an indoor
pool with the temperature and air humidity recorded. To achieve the water-resistant label, the label SPF must be the
same as the SPF after 40 minutes of fresh water immersion. The label waterproof is given to those
maintaining SPF after 80 minutes of immersion.
Sunscreen strength is measured by
the SPF. SPF can be mathematically
described as the ratio of the minimal erythemal dose (MED) of protected skin to
that of unprotected skin. The amount of
energy required to produce minimally perceptible redness in 24 hours is termed
the MED. To determine the SPF value for
a specific sunscreen, volunteers with skin types I-III who are not taking
medications known to produce abnormal sunlight responses or who do not have
phototoxic or photoallergic responses are exposed to natural or artificial
light before and after a standard application of the sunscreen. An area between the beltline and shoulder
blade of 50 cm2 is marked off and application of sunscreen is 2
mg/cm2. A waiting period of
15 minutes between application and exposure is allowed.
This method does not always produce
reliable results for several reasons.
The subject’s skin type and amount of sweat produced may not be taken
into account. The UV-L intensity of the
light source, artificial or natural, is not reported, and the concentration of
the sunscreen and thickness of application may not be held constant. The thickness necessary to transmit only 10%
incidence radiation is referred to as the critical film thickness and typically
lies between 0.02 and 0.05 mm. The
environment also plays a great role in the effectiveness of protection with
factors such as humidity, altitude, and the degree of reflection of sand and
snow.
The FDA gained control of sunscreens
when they became classified as drugs instead of cosmetics. The release of several regulations regarding
the labels of sunscreens is aimed to correct these problems. The terms “sunscreen” and “water –resistant”
may replace those of “sunblock”, “water-proof”, and “all day protection”. In addition, only three degrees of SPF are
specified (Table 4).
Minimum 2-11
High 30 and above
The system hopes to make the actual SPF closer to the reported SPF. Underapplication of sunscreen, which has a simple solution, along with sweating and the inability of most sunscreens to block UV-A radiation remain the major factors in reducing the actual SPF. Sunscreens should be applied in a thickness of 2 gm/cm2 and at least 30 minutes prior to sun exposure. For the safest exposure, reapplication should occur every 90 minutes.
Sunscreen established its roots during WWII when an airman and future pharmacist Benjamin Green helped develop a sun protective formula for soldiers. In 1944, Green used his invention as the basis for CoppertoneÒ Suntan Cream – the very first consumer sunscreen product. This mixture of cocoa butter and jasmine was concocted on his wife’s stove and tested on his own baldhead.
Placing a priority on research and development enables Schering-Plough Healthcare Products, the maker of the CoppertoneÒ brand, to innovate new products in each suncare category. The CoppertoneÒ brand is credited with some extremely important benchmarks in the study of suncare. Through the CoppertoneÒ Solar Research Center, the SPF System for the U.S. was developed to determine the proper amount of sun protection. In the early 1970’s, the CoppertoneÒ Solar Research Center worked closely with the FDA to define standards and measures for suncare products. The FDA continues to look to Schering-Ploughman Healthcare Products for information in the field of suncare research.
The Coppertone SportÒ Ultra Sweatproof SPF 48 is the number one selling product in suncare products. It features the following:
§ high-performance protection for the active adult,
§ three convenient formulas; lotion, spray, and stick,
§ patented ultra-sweatproof formula that bonds to the skin so it won’t run in your eyes and cause stinging,
§ non-greasy application won’t affect your grip,
§ UVA/UVB protection, and
§ waterproof.
Another company named Fallene, Ltd., (King of Prussia, PA), has developed products that allow for even the photosensitive to come into the light. Fallene was co-founded by a cosmetic plastic surgeon and a pharmaceutical chemist with the goal of developing cosmoceutical grade personal skin care products with unique advantages.
Total BlockÒ (Fallene, Ltd), is a unique, complete block for UVB/UVA, visible and infrared, offering full-spectrum protection for photosensitive individuals. It does not contain PABA, but is made with a mixture of eight highly reflective, micronized particles and a mixture of five active ingredients. These ingredients include avobenzone, benzophenone-3, octylmethoxycinnamate, titanium dioxide, and zinc oxide. It counteracts free-radical damage with antioxidants and trace elements to increase protection against UV and acute oxidation damage.
Total BlockÒ comes in both a foundation/cover-up or clear sunblock lotion. The Total BlockÒ SPF 60 Foundation/Cover-up Sunblock Lotion acts as a protective liquid make-up to cover up hyper-pigmented skin. It has been found especially useful for covering up erythema resulting from laser treatment, and it is also useful with other pigmentation irregulatities
.
Total BlockÒ SPF 65 Clear Sunblock Lotion offers people the choice of total protection from light in a formulation that dries invisible on the skin.
Both of the Total BlockÒ lotions are used for the following:
§ skin cancer protection,
§ post-laser surgery,
§ drug-photosensitivity,
§ lupus photosensivity,
§ facial trauma,
§ post-radiation therapy, and
§ post-transplant chemotherapy.
All sunscreen products produced by Fallene, Ltd. are not waterproof.
An individual’s sensitivity to UV-L energy determines the choice of sunscreen. In general, individuals who burn readily (skin type I) should use a sunscreen of SPF 30+, or high SPF, and individuals with darker skin may use lesser degrees of protection. For swimmers, the sunscreen with a high SPF must also be labeled waterproof. People, who are active in sports, should select a sunscreen that is sweatproof, waterproof, and SPF 30+ or higher. Selection of the most appropriate agent can help mitigate the harmful effects of UV-L radiation. In addition, individuals should avoid mid-day sun exposure, wear hats, sunglasses, and other protective clothing.
Bibliography
Black HS, deGruijl FR, Forbes PD, Cleaver JE. Photocarcinogenesis: an overview. Photochem Photobiol 1997;40:29-47. This article provides an excellent review of the role of sunlight as a carcinogenic agent.
Sunscreen
drug products for over-the –counter human use; tentative final monographs:
proposed rule, the code of federal regulations. Washington (DC): Food and Drug Administration: 1998; 21CFR Part
352; 28-33. The FDA continues to take a
leadership role as it regulates sunscreen agents.