Photodermatitis is an abnormal skin response to ultraviolet (UV) rays,
particularly sunlight. It can be acute or chronic. UV rays are classified by
wavelength and the greater the wavelength, the greater the risk of developing
photodermatitis. UVB rays range from 290 to 320 nm and may cause sunburn,
tanning, aging, or cancer-causing changes to the skin. UVA rays range from 320
to 400 nm and may cause reactions to light even through window glass. Ninety
percent of the UV radiation from sunlight comes from UVA rays, 10% from UVB.
Photoreactions from UV rays depend upon the amount of light reaching the earth.
This is influenced by the season or time of year, latitude, thickness of the
ozone layer, and topography.
Signs and Symptoms
Itchy bumps, blisters, or raised areas
Lesions that resemble eczema
Hyperpigmentation (darkened discoloration compared to one's normal
Outbreaks in areas of skin exposed to light
Pain, redness, and swelling
Chills, headache, fever, and nausea
Less severe symptoms after repeated
What Causes It?
Certain chemical agents and drugs may predispose an individual to sunburn, an
eczema-like reaction, or hives in reaction to UV rays. In the United States
alone, there are more than 115 chemical agents and drugs that are ingested or
applied to the skin that may elicit photodermatitis. The reaction may be related
to an allergy or it may be a direct toxic effect from the substance. Below are
examples of agents or circumstances that may trigger one or the other type of
Direct toxic effect:
Tetracycline and sulfonamides, medications used for bacterial
Griseofulvin, used for fungal infections
Coal tar derivatives and psoralens, such as methoxsalen and
trioxsalen, used for psoriasis
Tretinoin and other medications containing retinoic acid used for acne
Nonsteroidal anti-inflammatory drugs (NSAIDs), such as
Chemotherapy agents used to treat cancer, such as 5-fluorouracil and
Sulfonylureas, such as glyburide and glipizide, oral medications used
Quinine and other medications used to treat malaria
Thiazide diuretics, such as hydrochlorothiazide
Desipramine and other medications used for depression (known as
Phenothiazines, a class of medications used for psychosis
Benzodiazepines, such as alprazolam and tetrazepam, medications used
for anxiety disorders
Fragrances containing, for example, musk ambrette and
Sunscreens with p-aminobenzoic acid (PABA) esters
Industrial cleaners that contain
Photodermatitis may also result from some immune-related disorders such as
systemic lupus erythematosus (SLE) or certain states of nutrient deficiencies,
including pellagra, which is caused by niacin (vitamin B3)
Who's Most At Risk?
Skin type may influence the likelihood of a photodermatitis reaction.
Those with fair to light skin, or those with red or blond hair, and green or
blue eyes tend to be most sensitive, regardless of their racial or ethnic
background. This is categorized as skin type I.
Exposure to UV rays for 30 minutes to several hours increases risk of
photodermatitis (outbreaks in spring and summer months are common)
Exposure to UV rays from 11 a.m. to 2 p.m. also increases risk of
photodermatitis since 50% of UV radiation is emitted during this
What to Expect at Your Provider's Office
A physical exam and a detailed history of exposure to sensitizers (see
section entitled What Causes It?) and UV rays are important for
diagnosis. A review of all body systems, including blood and urine tests, helps
detect any related disease. Allergy tests may help identify substances that
trigger or worsen the condition.
These measures may help prevent photodermatitis:
Limit skin exposure to sun, especially intense midday sun.
Use sunscreens that protect against UVA and have a sun protection
factor (SPF) of 30 to 50.
Cover up with a long-sleeved shirt, long pants, and a wide-brimmed
Beware of using any product that causes sun sensitivity. (If you are
already taking a prescription medication, however, do not stop taking it without
consulting your healthcare provider.)
For blisters or weepy eruptions, apply cool, wet dressings. With certain
types of photodermatitis, doctors may actually use phototherapy (controlled
exposure to light for treatment purposes) to desensitize the skin or to help
For extremely sensitive patients, doctors may prescribe azathioprine to
suppress the immune system. Short-term use of glucocorticoids may help control
eruptions. For those who cannot be treated with phototherapy, doctors may
prescribe hydroxychloroquine, thalidomide, beta-carotene, or nicotinamide (see
section entitled Nutrition for details regarding the latter two).
Note: Thalidomide causes severe birth defects and therefore should never
be used by women who either are or wish to become pregnant.
Complementary and Alternative
Particular nutritional deficiencies can contribute to photosensitivity.
Pellagra, for example, is caused by a niacin deficiency. Recent research results
suggest that antioxidant nutrients, including beta-carotene, may help lessen the
severity of photodermatitis.
Beta-carotene and Other Carotenoids: Despite the fact that
beta-carotene is considered part of standard treatment for photodermatitis, the
results of studies regarding this supplement have been mixed. One study of the
effect of beta-carotene supplements on sunburns in humans showed no significant
protection. In another trial, though, 20 healthy subjects received either
carotenoids alone, mainly from beta-carotene, or carotenoids plus vitamin E.
Both groups improved significantly. Vitamin E did not appear to add to the
benefits of the carotenoids alone.
Fish Oil/Omega-3 Fatty Acids: In one study, 13 patients with a
particular type of photodermatitis received supplements of fish oil, which
contains omega-3 fatty acids, for three months. Tests afterward showed that the
patients were significantly less sensitive to UV rays. Similarly, case reports
of three children with hydroa vacciniforme, a rare scarring photosensitivity
disorder, found that omega-3 supplements lessened symptoms for two of the three
children. Photosensitive patients could consider eating a diet rich in omega-3
fatty acids, such as from cold water fish.
Protein: Actinic prurigo, a form of photosensitivity marked by
ongoing outbreaks of itchy bumps during hot weather, is seen mainly in
malnourished individuals. Research suggests that the condition is related to a
diet deficient in protein or a specific amino acid (the building blocks of
protein). Patients treated with a high-protein diet have improved but tend to
relapse a few weeks after returning to their standard diet.
Vitamin B3: Nicotinamide (a form of niacin, or
vitamin B3) may make a photosensitive reaction less likely. In a
pilot study, 42 people with photodermatitis were given nicotinamide; despite
extensive sun exposure, 25 of these people did not develop
Vitamins C and E: Antioxidants, including vitamins C and E,
help remove free radicals, harmful by-products that result from cells' use and
generation of energy. Free radicals are linked to skin damage. Oral supplements
of vitamins C and E seem to work together to possibly reduce UV-induced skin
Vitamin D: In animal studies, vitamin D helped trigger the
effects of an antioxidant protein found in skin cells of rats. This protein
helps to protect against damage from UVB rays. It is not clear yet whether
vitamin D supplements may help protect humans in the same
Green Tea: The antioxidant properties in green tea (Camellia
sinensis) may provide protection against reddening of the skin caused by UV
light. Epigallocatechin-3-gallate (EGCG), an active component of green tea has
demonstrated photoprotection in animal studies. In a human study, tests on skin
samples showed that EGCG does not block the absorption of UVB light but it does
appear to inhibit redness, some cell damage, and other changes normally
associated with UVB rays.
Calendula: Although not studied scientifically, this herb has
been used clinically for skin conditions including sunburn. It may also be used
as a homeopathic remedy at doses consistent with that kind of therapy.
Similar to photosensitizing medications, certain herbs can trigger
photodermatitis; such herbs include St. John's wort (Hypericum
perforatum), angelica seed or root (Angelica archangelica), celery
stems (Apium graveolens), rue (Rutae folium), and lime oil/peel (
While scientific studies of homeopathy specifically addressing
photodermatitis have not been conducted to date, individual reports suggest that
homeopathic remedies may be a useful adjunct for the prevention and treatment of
photodermatitis. An experienced homeopath considers each individual case and may
recommend treatments tailored to address both the underlying condition and any
Most photosensitivity reactions go away on their own and cause no permanent
harm. However, symptoms can be severe when associated with a systemic disorder
or when the exposure has been severe. Some photosensitivity reactions can
continue for years after exposure ends.
Complications may include:
Ongoing photosensitivity, resulting in chronic
Hyperpigmentation or dark discoloration compared to normal skin tone
even after inflammation has resolved
Premature aging of the skin
Squamous cell or basal cell skin cancer or
Patients who need steroids to treat photosensitivity reactions must be
monitored closely. In addition, anyone with a history of photodermatitis or
photoreactivity should keep track of the frequency and duration of symptoms.
This information can help determine the cause and appropriate treatment.
Abramowitz AI, Resnik KS, Cohen KR. Margarita photodermatitis [letter]. N
Engl J Med. 1993;328(12):891.
Adamski H, Benkalfate L, Delaval Y, et al. Photodermatitis from non-steroidal
anti-inflammatory drugs. Contact Dermatitis. 1998;38(3):171-174.
American Academy of Pediatrics. Ultraviolet light: a hazard to children.
Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic
Guide to Herbal Medicines.Boston, Mass: Integrative Medicine Communications;
1998:35-36; 214-215; 245-249.
Callen JP. Photodermatitis in a 6-year-old child. Arthritis Rheum.
Darr D, Dunston S, Faust H, Pinnell S. Effectiveness of antioxidants (vitamin
C and E) with and without sunscreens as topical photoprotectants. Acta Derm
Venereol (Stockh). 1996;76(4):264-268.
Durán MM, Ordoņez CP, Prieto JC, Bernal J. Treatment of actinic prurigo in
Chimila Indians. Int J Dermatol. 1996;35(6):413-416.
Eberlein-König B, Placzek M, Przybilla B. Protective effect against sunburn
of combined systemic ascorbic acid (vitamin C) and d-alpha-tocopherol (vitamin
E). J Am Acad Dermatol. 1998;38(1):45-48.
Enta T. Dermacase. Contact photodermatitis. Can Fam Physician.
Enta T. Dermacase. Photodermatitis reaction to chlorothiazide. Can Fam
Physician. 1994;40:1269, 1276.
Fernandez de Corres L, Diez JM, Audicana M. Photodermatitis from plant
derivatives in topical and oral medicaments. Contact Dermatitis.
Freedberg IM, Eisen AZ, Wolff K. Fitzpatrick's Dermatology in General
Medicine. Vol. 1. 5th ed. New York, NY: McGraw-Hill; 1996:1573-1586.
Fuchs J, Kern H. Modulation of UV-light-induced skin inflammation by
D-alpha-tocopherol and L-ascorbic acid: a clinical study using solar simulated
radiation. Free Radic Biol Med. 1998;25(9):1006-1012.
Garmyn M, Ribaya-Mercado JD, Russell RM, Bhawan J, Gilchrest BA. Effect of
beta-carotene supplementation on the human sunburn reaction. Exp
Hadshiew I, Stäb F, Untiedt S, Bohnsack K, Rippke F, Hölzle E. Effects of
topically applied antioxidants in experimentally provoked polymorphous light
eruption. Dermatology. 1997;195(4):362-368.
Hanada K, Sawamura D, Nakano H, Hashimoto I. Possible role of
1,25-dihydroxyvitamin D3-induced metallothionein in photoprotection against UVB
injury in mouse skin and cultured rat keratinocytes. J Dermatol Sci.
Kamat JP, Devasagayam TP. Methylene blue plus light-induced lipid
peroxidation in rat liver microsomes: inhibition by nicotinamide (vitamin B3)
and other antioxidants. Chem Biol Interact. 1996;99(1-3):1-16.
Katiyar SK, Matsui MS, Elmets CA, Mukhtar H. Polyphenolic antioxidant
(-)-epigallocatechin-3-gallate from green tea reduces UVB-induced inflammatory
responses and infiltration of leukocytes in human skin. Photochem Photobiol.
Leroy D, Dompmartin A, Szczurko C, Michel M, Louvet S. Photodermatitis from
ketoprofen with cross-reactivity to fenofibrate and benzophenones.
Photodermatol Photoimmunol Photomed. 1997;13(3):93-97.
Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in
Food, Drugs and Cosmetics. 2nd ed. New York, NY: Wiley and Sons; 1996.
Magaņa-Garcia M, Magaņa M. Actinic prurigo. The possible etiologic role of an
amino acid in the diet. Med Hypotheses. 1993;41(1):52-54.
Murata Y, Kumano K, Ueda T, Araki N, Nakamura T, Tani M. Photosensitive
dermatitis caused by pyridoxine hydrochloride. J Am Acad Dermatol.
1998;39(2 pt 2):314-317.
Neumann R, Rappold E, Pohl-Markl H. Treatment of polymorphous light eruption
with nicotinamide: a pilot study. Br J Dermatol. 1986;115(1):77-80.
Newall CA, Anderson LA, Philpson JD. Herbal Medicines: A Guide for
Health-care Professionals. London: The Pharmaceutical Press; 1996.
Pigatto PD, Legori A, Bigardi AS, et al. Multicenter study of allergic
contact photodermatitis: epidemiological aspects. Am J Contact Dermat.
Quinones D, Sanchez I, Alonso S, et al. Photodermatitis from tetrazepam.
Contact Dermatitis. 1998;39(2):84.
Rhodes LE, Durham BH, Fraser WD, Friedmann PS. Dietary fish oil reduces basal
and ultraviolet B-generated PGE2 levels in skin and increases the threshold to
provocation of polymorphic light eruption. J Invest Dermatol.
Rhodes LE, White SI. Dietary fish oil as a photoprotective agent in hydroa
vacciniforme. Br J Dermatol. 1998;138(1):173-178.
Ross JB, Moss MA. Relief of the photosensitivity of erythropoietic
protoporphyria by pyridoxine. J Am Acad Dermatol. 1990;22(2 pt
Scholzen TE, Brzoska T, Kalden DH, et al. Effect of ultraviolet light on the
release of neuropeptides and neuroendocrine hormones in the skin: mediators of
photodermatitis and cutaneous inflammation. J Invest Dermatol Symp Proc.
Stahl W, Heinrich U, Jungmann H, Sies H, Tronnier H. Carotenoids and
carotenoids plus vitamin E protect against ultraviolet light-induced erythema in
humans. Am J Clin Nutr. 2000;71(3):795-798.
Tanaka M, Niizeki H, Shimizu S, Miyakawa S. Photoallergic drug eruption due
to pyridoxine hydrochloride. J Dermatol. 1996;23(10):708-709.
Tierney LM, McPhee SJ, Papadakis MA. Current Medical Diagnosis and
Treatment 2000. New York, NY: Lange Medical Books/McGraw-Hill;
Review Date: December 2000
Reviewed By: Participants in the review process include: Robert A. Anderson, MD,
President, American Board of Holistic Medicine, East Wenatchee, WA; Constance
Grauds, RPh, President, Association of Natural Medicine Pharmacists, San Rafael,
CA; Jacqueline A. Hart, MD, Department of Internal Medicine, Newton-Wellesley
Hospital, Harvard University and Senior Medical Editor Integrative Medicine,
Boston, MA; Leonard Wisneski, MD, FACP, George Washington University, Rockville,
The publisher does not accept any responsibility for the accuracy of
the information or the consequences arising from the application, use, or misuse
of any of the information contained herein, including any injury and/or damage
to any person or property as a matter of product liability, negligence, or
otherwise. No warranty, expressed or implied, is made in regard to the contents
of this material. No claims or endorsements are made for any drugs or compounds
currently marketed or in investigative use. This material is not intended as a
guide to self-medication. The reader is advised to discuss the information
provided here with a doctor, pharmacist, nurse, or other authorized healthcare
practitioner and to check product information (including package inserts)
regarding dosage, precautions, warnings, interactions, and contraindications
before administering any drug, herb, or supplement discussed