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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-.


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SUNSCREENS AND PHOTOPROTECTION

Sarah Gabros; Trevor A. Nessel; Patrick M. Zito.

Author Information and Affiliations

AUTHORS

Sarah Gabros1; Trevor A. Nessel2; Patrick M. Zito3.



AFFILIATIONS

1 Rowan University SOM
2 MSU College of Osteopathic Medicine
3 University of Miami; Miller School of Medicine

Last Update: July 17, 2023.

Go to:


CONTINUING EDUCATION ACTIVITY

Photoprotection is indicated for the reduction of ultraviolet (UV)
radiation-induced skin damage and skin cancers. Photoprotection includes
sunscreens, clothing, hats, makeup, sunglasses, and windshields. The damaging
effects of UV radiation include photoaging and photocarcinogenesis. Photoaging
can manifest as sagging and wrinkling, while photocarcinogenesis is due to the
damage of cells and DNA. This activity outlines the indications, mechanism of
action, methods of administration, important adverse effects, contraindications,
and monitoring, of various photoprotective agents, so providers can direct
patient therapy in treating indicated disorders as part of the interprofessional
team.

Objectives:

 * Identify the mechanism of action of various classes of UV blocking agents.
 * Review the benefits of using sunscreens and photoprotection to block UV rays.
 * Summarize the adverse events associated with various sun-blocking products.
 * Explain the importance of improving care coordination among the
   interprofessional team to enhance care delivery for patients who can benefit
   from therapy with sunscreens and photoprotective agents.

Access free multiple choice questions on this topic.



Go to:


INDICATIONS

Photoprotection is indicated for the reduction of ultraviolet (UV)
radiation-induced skin damage and skin cancers.[1][2] Photoprotection includes
sunscreens, clothing, hats, makeup, sunglasses, and windshields.[3] The damaging
effects of UV radiation include photoaging and photocarcinogenesis. Photoaging
can manifest as sagging and wrinkling, while photocarcinogenesis is due to the
damage of cells and DNA. Recurrent and severe sunburns are a risk factor for
nonmelanoma skin cancer.[2] The FDA regulates sunscreen as an over-the-counter
medication. Currently, 16 UV filters are listed, 14 organic filters, and two
nonorganic filters, including zinc oxide and titanium dioxide. The FDA has
changed its guidelines to address broad-spectrum sunscreen use, which involves
UVA and UVB coverage; water resistance, to indicate the time duration the
sunscreen is effective; and sun protection factor (SPF). SPF-15 or higher is the
recommended blocking strength, and manufacturers can label it as reducing the
risk of skin cancer and early skin aging.[4]

Go to:


MECHANISM OF ACTION

UV radiation greatly affects the skin, causing aging, sunburns, precancerous and
cancerous lesions, and immunosuppression.[5] UV radiation has an
immunosuppressive effect on the antigen-presenting cells within the epidermis
and contributes to the likelihood of skin cancer.[4] There are three types of UV
radiation: UVC, UVB, and UVA. The ozone layer absorbs 100% of UVC, 90% of UVB,
and a minimal amount of UVA. For this reason, the depletion of the ozone layer
increases UV transmission. UVA is associated with aging and pigmentation. It
penetrates deep into the skin layer and produces free radical oxygen species,
indirectly damaging DNA. UVA increases the number of inflammatory cells in the
dermis and decreases the number of antigen-presenting cells.[6] UVB causes
sunburn and DNA strand breaks. It causes pyrimidine dimer mutations, which are
associated with nonmelanoma skin cancers.[7] 

Photoprotection involves both primary and secondary protective factors. Primary
factors are sunscreens; these include physical barriers that reflect and scatter
light and chemical barriers that absorb light. Secondary factors include
antioxidants, osmolytes, and DNA repair enzymes, which help to limit skin damage
by disturbing the photochemical cascade that occurs with UV sunlight.[5] 

Chemical sunscreens are known as organic sunscreens. Their mechanism of action
is based on their chemical structure involving an aromatic compound conjugated
with a carbonyl group. This structure allows high-energy UV rays to be absorbed,
causing the molecule to achieve an excited state. As the molecule returns to the
ground state, it will release the lower energy of longer wavelengths. The
specific range of wavelength a sunscreen absorbs will vary. Chemical sunscreens
consist of UVA and UVB blockers. UVB filters absorb the entire spectrum of UVB
radiation (290 to 320 nm). UVA filters do not cover the entire spectrum of UVA
radiation. Uva radiation is divided into UVA I (340 to 400 nm) and UVA II (320
to 340nm). Broad-spectrum sunscreens absorb UV radiation from both the UVA and
UVB portions.[8]

UVB Blockers

 * Aminobenzoates
 * Cinnamates
 * Salicylates
 * Octocrylene
 * Ensulizole
 * Camphor derivatives

Aminobenzoates are the most potent UVB absorber but do not absorb UVA. Their use
has declined due to para-aminobenzoic acid (PABA) sensitivity. PABA is a very
effective UVB filter; however, it was reportedly the most common photoallergen
and contact allergen. For this reason, it has limited use in sunscreen. Padimate
O is the most commonly used PABA derivative; it has a good safety profile and is
an effective UVB filter.[3]

Cinnamates have replaced PABA as the next most potent UVB absorber and
include octinoxate (OMC) and cinoxate.[5] Octinoxate is the most commonly used
UVB filter in the United States. It is not as potent a UVB absorber as padimate
O; for this reason, other UVB absorbers are used in combination to increase the
SPF. Octinaxate is not very photostable and degrades in the presence of sunlight
after a short period. Cinnoxate is a less common choice.[3]

Salicylates are used in high concentrations as they are weak UVB absorbers. They
are also used to increase the effect of other UVB filters. Two salicylates that
are FDA listed are homosalate and octisalate. They function to decrease the
photodegradation of other UV filters, such as oxybenzone and avobenzone. A
water-soluble salicylate is trolamine salicylate.[3]

Octocrylene is a very safe chemical associated with a decreased likelihood of
irritation, phototoxicity, and photoallergic potential.[9] When combined with
other UV absorbers, it can increase the SPF formula.[5]

Ensulizole is a pure UVB filter and does nothing that affects UVA. It is a
water-soluble compound commonly used in cosmetics for a lighter, less oily
feel.[5] 

Camphor derivatives are not FDA-listed but are moderately effective UVB filters.
A camphor derivative that is also a broad UVA filter is terephthalyidene
dicamphor sulfonic acid.[3]

UVA Blockers

 * Benzophenones
 * Anthranilates
 * Avobenzones
 * Ecamsule

Typical benzophenones absorb mostly UVB; however, oxybenzone is considered a
broad spectrum absorber as it can absorb UVA II as well.[5] It is the most
commonly used benzophenone.[3] However, out of all the sunscreens, oxybenzone
has the greatest likelihood of inducing contact or photo contact dermatitis.
Oxybenzone is not considered photostable, and although not scientifically proven
yet, there is a concern about carcinogenic and endocrine adverse
effects.[5] Other FDA-listed benzophenones include sulisobenzone and
dioxybenzone.[3] 

Anthranilates are very weak UVB and UVA filters and are less effective than
benzophenones. As a result, clinicians rarely use them.[3]

Avobenzones are considered broad-spectrum and have high efficacy against UVA I
(>380 nm); however, they are very photo-unstable and lose from 50% to 90% of
their particles after 1 hour of UV exposure. There are also reports that they
degrade the UV filter octinoxate. UV absorbers such as octocrylene,
benzophenones, salicylates, camphor derivatives, and micronized zinc oxide or
titanium dioxide are used in combination to increase photostability.[3]

Ecamsule contains terephthalyidene dicamphor sulfonic acid, a very photostable
product that is water-resistant with low systemic absorption. In animal studies,
it prevented UVA-induced photoaging.[3]

Broad-spectrum sunscreens include methylene-bis-benzotriazolyl
tetramethylbutylphenol (MBBT) and bis- ethylhexyloxyphenol methoxyphenyl
triazine (BEMT). MBBT is advantageous as it is a large molecule that decreases
the likelihood of systemic absorption or endocrine effects. It works as a
combination of organic and inorganic filters, ultimately absorbing, scattering,
and reflecting UV radiation. It decreases UVA transmission more than UVB. BEMT
also does not affect the endocrine system and is photostable.[5]  

The mechanism of action of a physical sunscreen has its basis on the reflection
and scattering of UV light in much the same way as clothing. The reflective
properties determine the effectiveness of the sunscreens. These properties
include the reflective index, the size of the particles, the film thickness, and
the dispersion of the base—the higher the reflective index, the better the UV
filter. Decreasing the size of the particles to a micronized form (10 to 50 nm)
is more cosmetically appealing but leads to the protection of shorter
wavelengths and increases the risk of systemic absorption.[8] A thick coating
increases the degree of reflection but is cosmetically less appealing. Iron
oxide can be an additive to increase absorption and improve UVA protection.
Physical sunscreens consist of zinc oxide and titanium dioxide.[3]

Microfine zinc oxide protects against a wide range of UVA, including UVA 1 (340
to 400 nm). It is very photostable and does not react with other UV filters. It
is more effective than titanium dioxide for UVA protection; however, it is less
efficient against UVB radiation.[3][5]

Microfine titanium dioxide protects against UVA 2 (315 to 340 nm) and UVB but
does not protect against UVA 1, as does zinc oxide.[5] It has a smaller particle
size and higher refractive index than zinc oxide, causing it to appear white and
making it cosmetically less appealing. Photochemical reactions cause zinc oxide
and titanium dioxide to become less effective as a sunscreen. For this reason,
silica and dimethicone coat these particles, stabilizing these inorganic
filters.[3] 

As mentioned above, secondary photoprotection includes antioxidants, osmolytes,
and DNA-repair enzymes, which help to limit skin damage by disturbing the
photochemical cascade that occurs with UV sunlight. The mechanism of action of
antioxidants is to reduce the reactive oxygen species (ROS) produced from UVA
radiation. Naturally, these ROS become neutralized by antioxidants found
naturally within the body, such as superoxide dismutase and catalase. These
enzymes can become saturated within an overproduction of reactive oxygen
species, resulting in a deficiency of antioxidants and damage to proteins and
DNA. Topical antioxidants function from within the cell to decrease the shortage
of antioxidants and can remain active for several days after
application.[10][5]  

Many sunscreens include antioxidants such as vitamin C, vitamin E, silymarin,
and green tea polyphenols. Vitamin C acts to protect against UV- damage, which
results in sunburn and erythema.[5][11] Vitamin E has many protective actions,
such as decreasing immunosuppression, erythema, photoaging, and
photocarcinogenesis.[5][12][13][14] Silymarin comes from milk thistle plants,
functioning to prevent lipid and lipoprotein oxidation and acting as a scavenger
of reactive oxygen species. Topical application results in a decrease in
UVB-induced sunburn cells and a reduction in the amount of UVB-induced
pyrimidine dimers. In mice, it has been shown to reduce the amount of
UVB-induced tumors.[15] Green tea polyphenols contain antioxidants that are more
potent than vitamin C and E. They are anti-inflammatory and anti-carcinogenic.
They function to scavenge singlet oxygen, superoxide radicals, hydroxyl
radicals, peroxyl radicals, and hydrogen peroxide.[16]

Osmolytes are small molecules that stabilize the cell in stressful conditions by
regulating hydration. Taurine and ectoine are osmolytes that protect against
many UV effects and are components in many sunscreens.[5][17][18]

Go to:


ADMINISTRATION

Sunscreen should be applied topically. Correct administration is key to the
effectiveness of use. A liberal uniform film of sunscreen should be applied, and
the application should be 15 minutes before sun exposure. The adequate amount to
apply is 2 mg/cm^2, equivalent to 30 mL/ body application. Sunscreen should be
reapplied every 2 hours and after sweating or swimming.[2]

Clothing is a form of photoprotection, which can be measured using the UV
protection factor.[5] This metric measures the transmission of UVA and UVB
through a given fabric. In animal studies, research showed a UPF over 30 to
protect against erythema and premalignant lesions. Whether the fabric is wet or
dry may increase or decrease UPF based on the type of fabric. Light-colored
fabrics have decreased UPF compared to dark-colored fabrics.[3]  Overall,
clothing provides a balanced amount of protection against both UVA and UVB, and
a loose-fitting colored fabric is the best form of photoprotection.[5]

Hats are a variable form of photoprotection dependent on the brim width,
material, and weaving. A hat with a brim width of more than 7.5 cm has an SPF of
7 for the nose, 5 for the neck, 3 for the cheeks, and 2 for the chin. A hat with
a brim width of 2.5 to 7.5 cm has an SPF of 3 for the nose, 2 for the neck and
cheek, and 0 for the chin. A hat with a brim of less than 2.5 cm has an SPF of
1.5 for the nose and a minimal amount for the chin and neck.[3]

The pigment content of makeup provides an SPF of 3 to 4, even if there is no
sunscreen included; however, this photoprotective effect is lost 4 hours after
application. Many foundations now include UV filters to provide
photoprotection.[3] 

Sunglasses are a form of photoprotection for the eyes. Sun exposure can result
in many eye conditions, such as cataracts, which direct result from sun
exposure, specifically UVB radiation. Chronic exposure results in the formation
of cataracts and eye cancer. Sunglasses should absorb 99% to 100% of the full UV
spectrum. Contact lenses can also provide photoprotection for the ocular
lens; however, they do not protect the anterior portion of the eye.[3] 

Car windshields offer UV protection. The Federal Motor Vehicle Safety Standard
No. 205 mandates that the tinted glass in cars provide no less than 70%
transmission of visible radiation. The windshields of cars contain zinc, chrome,
nickel, and other metals which block UV radiation. The windshield of the vehicle
is more photoprotective than the side window glass of the automobile.[3]

Go to:


ADVERSE EFFECTS

Adverse effects of sunscreen include four types of contact dermatitis: irritant,
allergic, phototoxic, and photoallergic.[8] In Germany, a 15-year study of patch
and photo patch testing demonstrated that the most common reaction to sunscreen
is a nonimmune-based irritant response.[2] The most common UV filters that cause
adverse effects are benzophenones and dibenzoylmethanes, with the most common
photoallergen being benzophenone-3 (BP-3), as it is a derivative of PABA. For
this reason, benzophenone 3 is not used frequently in the United States.[2] 
Some studies have associated sunscreen use with melanoma due to the users' false
sense of security, which may increase the duration in the sun, resulting in UVA
formation and malignant changes.[8] Phototoxic and allergic contact dermatitis
are usually the results of UVA (320 to 400 nm) and visible light ranges (400 to
800 nm). UVA is capable of penetrating the reticular dermis and is the cause of
most photosensitivity reactions.[19]

An American study revealed that UV filters are the most common cause of positive
photo patch testing.[20] Risk factors that can lead to sunscreen allergy are
unknown but are more likely to be sex, prior photodermatosis, use of sunscreen
on damaged skin, working outdoors, and atopy. It was previously a concern that
regular sunscreen use would result in vitamin D deficiency; however, vitamin D
levels are not significantly affected by the regular use of sunscreen.[2]

The adverse effects of physical sunscreen are due to the usage of nanoparticles,
which have a more beneficial cosmetic effect. The increased surface area of
nanoparticles can result in a greater level of catalytic reactions, increasing
the production of free radicals and damage to DNA and proteins. These smaller
particles can form complexes with the protein that can behave as haptens,
inducing autoimmune conditions.[5][21]

Three observations led to the review of animal and human studies regarding the
adverse effects of UV filters:

 * An increase in sunscreen use
 * An increase in the incidence of malignant melanoma
 * An increase in experimental studies demonstrating UV filters have adverse
   endocrine effects

In vivo and in vitro animal studies have shown multiple potential adverse
effects of UV filters within sunscreen. These adverse effects include endocrine
dysfunction of the reproductive and developmental systems. The UV filters of
concern include BP-3, 4-MBC, and OMC. An anti-estrogenic effect was strongly
associated with BP-3 as well as 3-BC, 4 MBC, and OMC. This finding was based on
the uterine weight of immature rats. UV filters demonstrated the anti-estrogenic
effect of HMS, OD-PABA, and PABA in yeast expressing human estrogen receptor a.
After exposure to UV filters, 3-BC, and 4—MBC, there was a delay in male puberty
and reduced prostate weight. The mechanism of action behind the reproductive
toxicity may be due to alterations in proteins of the gene expression of
estrogen receptor, androgen receptor, progesterone receptor, insulin-like growth
factor I, complement proteins, nuclear receptor co-repressor, and steroid
receptor coactivator 1 in the uterus and prostate. In a 90-day study with BP-3,
fertility was affected in male mice. This finding was demonstrated by decreased
sperm density in a dose-related manner following dermal exposure in mice and
oral exposure in mice and rats.[20]

Experimental studies in humans have demonstrated an increased permeability of
the UV filters BP-3, 4 MBC, and OMC. Levels were detectable in the plasma 1 to 2
hours after exposure. The study also demonstrated a difference in concentration
based on gender. Male urine and plasma concentration samples were higher than
female samples. A Swiss study of human breast milk revealed that 85% of the
sample contained UV filters. Bisphenol and BP-3 share a similar chemical
structure. Bisphenol can cross the blood-placenta barrier, so the assumption is
that BP-3 can also cross the placenta. An increased concentration of BP-3 in a
mother's urine was associated with decreased birth weight in girls and increased
birth weight and head circumference in boys.[20]

Go to:


CONTRAINDICATIONS

Although photoprotection is indicated in all age groups, the 1999 FDA Sunscreen
Final Monograph recommended that parents of children under the age of 6 months
should consult a physician before sunscreen administration in this age
group. This recommendation is due to the lack of infant metabolism development
and excretion of the chemically absorbed agents within sunscreen. If sunscreen
is necessary, it should be limited and infrequently used on sun-exposed areas of
the body only.[3]

Go to:


MONITORING

The FDA regards and regulates sunscreen as an over-the-counter medication. The
efficacy of sunscreen is determined by UVB protection, which is measured by the
sun protection factor (SPF) and substantivity. SPF is the ratio of the smallest
dose of UVB radiation required to produce minimal erythema on
sunscreen-protected skin compared to the necessary dose of UVB to produce the
same amount of erythema on non-protected skin. SPF is a better predictor of
protection against UVB since it is 1000 times more erythemagenic than UVA. An
SPF-15 can block 94% of UVB radiation, while an SPF-30 can block 97% of UVB
radiation.[3] Substantivity is the ability of a sunscreen to withstand adverse
conditions such as water and sweat. The FDA has defined terminology to label
substantivity. Water-resistant refers to a 40 minute time interval of maintained
photoprotection with water immersion and moderate activity. Very water-resistant
refers to effectiveness for 80 minutes. Both terms can qualify as
sweat-resistant.[5]

Go to:


TOXICITY

Regarding contact dermatitis, the first step is to avoid the causative agent.
Patch testing can help identify the etiologic agent. The results of patch
testing can be listed on the American Contact Dermatitis Society website, which
can provide patients with a list of non-allergenic products that can be used.
Treatment includes topical steroids for local reactions. Severe reactions
require the use of systemic steroids. If oral steroids are ineffective,
immunosuppressants such as oral cyclosporine, methotrexate, or mycophenolate
mofetil a. For mild-to-moderate dermatitis, calcineurin inhibitors,
pimecrolimus, and tacrolimus are options.[8]

With photoallergy and phototoxicity, UVA radiation is usually a requirement to
precipitate the reaction. The patient should avoid the etiologic agent, but if
avoidance is not possible, the patient should avoid direct sunlight and tanning
beds and wear protective clothing and non-allergenic sunscreen.[8]

Barrier creams and high-lipid moisturizers can help to prevent and improve
irritant contact dermatitis.[8]

Go to:


ENHANCING HEALTHCARE TEAM OUTCOMES

An estimated 1 million new cases of nonmelanoma skin cancer occur every year.
The numbers have increased significantly over the last 20 years within the
United States and Europe. A research survey completed in 2005 revealed limited
awareness of nonmelanoma skin cancer and prevention in the U.S., Australia, and
Europe. For most individuals, healthcare providers are not the primary source of
information for sun protection measures. The media plays a significantly
influential role; however, there is minimal long-term behavioral change. These
findings support the importance of engaging healthcare professionals to increase
patient education regarding photoprotection and its role in preventing
nonmelanoma skin cancer.[22] 

This is where a coordinated interprofessional effort from the interprofessional
healthcare team, including clinicians, nurses, and pharmacists, can help
patients avoid UV exposure and protect their skin. Since retail pharmacists are
uniquely positioned where sun protection products are sold and can also see if
the patient is taking any medications with potential phototoxicity, they can
exert a significant influence in this regard. Nurses can also counsel patients,
and all team members should be aware of patients with fair skin, who present
with significant or frequent burns, or who have a high level of UV exposure
because of work. WIth a coordinated interprofessional effort, patients can
achieve the best outcomes with the fewest adverse events. [Level 5]

Go to:


REVIEW QUESTIONS

 * Access free multiple choice questions on this topic.
 * Comment on this article.

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REFERENCES

1.
Rai R, Srinivas CR. Photoprotection. Indian J Dermatol Venereol Leprol. 2007
Mar-Apr;73(2):73-9. [PubMed: 17456910]
2.
Moloney FJ, Collins S, Murphy GM. Sunscreens: safety, efficacy and appropriate
use. Am J Clin Dermatol. 2002;3(3):185-91. [PubMed: 11978139]
3.
Kullavanijaya P, Lim HW. Photoprotection. J Am Acad Dermatol. 2005
Jun;52(6):937-58; quiz 959-62. [PubMed: 15928611]
4.
Latha MS, Martis J, Shobha V, Sham Shinde R, Bangera S, Krishnankutty B, Bellary
S, Varughese S, Rao P, Naveen Kumar BR. Sunscreening agents: a review. J Clin
Aesthet Dermatol. 2013 Jan;6(1):16-26. [PMC free article: PMC3543289] [PubMed:
23320122]
5.
Rai R, Shanmuga SC, Srinivas C. Update on photoprotection. Indian J Dermatol.
2012 Sep;57(5):335-42. [PMC free article: PMC3482794] [PubMed: 23112351]
6.
Lavker RM, Gerberick GF, Veres D, Irwin CJ, Kaidbey KH. Cumulative effects from
repeated exposures to suberythemal doses of UVB and UVA in human skin. J Am Acad
Dermatol. 1995 Jan;32(1):53-62. [PubMed: 7822517]
7.
Rhodes LE. Topical and systemic approaches for protection against solar
radiation-induced skin damage. Clin Dermatol. 1998 Jan-Feb;16(1):75-82. [PubMed:
9472436]
8.
Heurung AR, Raju SI, Warshaw EM. Adverse reactions to sunscreen agents:
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Disclosure: Sarah Gabros declares no relevant financial relationships with
ineligible companies.

Disclosure: Trevor Nessel declares no relevant financial relationships with
ineligible companies.

Disclosure: Patrick Zito declares no relevant financial relationships with
ineligible companies.

 * Continuing Education Activity
 * Indications
 * Mechanism of Action
 * Administration
 * Adverse Effects
 * Contraindications
 * Monitoring
 * Toxicity
 * Enhancing Healthcare Team Outcomes
 * Review Questions
 * References

Copyright © 2023, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons
Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) (
http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to
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Bookshelf ID: NBK537164PMID: 30725849


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Gabros S, Nessel TA, Zito PM. Sunscreens and Photoprotection. [Updated 2023 Jul
17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;
2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537164/
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