Sunscreen

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Sunscreen (also known as sunblock (US) or sun tan lotion (UK)) is a lotion, spray or other topical product that absorbs or reflects the sun's ultraviolet (UV) radiation, and protects the skin. Medical organizations such as the American Cancer Society recommend the use of sunscreen,[1] despite many epidemiological studies indicating an increased melanoma risk for the sunscreen user.[2][3][4][5][6][7][8][9] (see sunscreen controversy for a discussion of possible reasons)

Sunscreens contain one or more UV filters of which there are three main types[10] :

Contents

[edit] Dosing

The dose used in FDA sunscreen testing is 2 mg/cm² of exposed skin.[11] Provided one assumes an "average" adult build of height 5 ft 4 in (163 cm) and weight 150 lb (68 kg) with a 32 in (82 cm) waist, that adult wearing a bathing suit covering the groin area should apply 29 g (approximately 1 oz) evenly to the uncovered body area. Considering only the face, this translates to about 1/4 to 1/3 of a teaspoon for the average adult face.

Contrary to the common advice that sunscreen should be reapplied every 2–3 hours, some research has shown that the best protection is achieved by application 15–30 minutes before exposure, followed by one reapplication 15–30 minutes after the sun exposure begins. Further reapplication is only necessary after activities such as swimming, sweating, and rubbing.[12]

However, more recent research at the University of California, Riverside indicates that sunscreen needs to be reapplied within 2 hours in order to remain effective. Not reapplying could even cause more cell damage than not using sunscreen at all, due to the release of extra free radicals from those sunscreen chemicals which were absorbed into the skin.[13]

[edit] History

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The first effective sunscreen may have been developed by chemist Franz Greiter in 1938. The product, called Gletscher Crème (Glacier Cream), subsequently became the basis for the company Piz Buin (named in honor of the place Greiter allegedly obtained the sunburn that inspired his concoction), which today is a well-known marketer of sunscreen products. Some internet articles suggest that Gletscher Crème had a sun protection factor of 2, although a research citation is not readily available online.

The first widely used sunscreen was produced by Benjamin Greene, an airman and later a pharmacist, in 1944. The product, Red Vet Pet (for red veterinary petrolatum), had limited effectiveness, working as a physical blocker of ultraviolet radiation. It was a disagreeable red, sticky substance similar to petroleum jelly. This product was developed during the height of World War II, when it was likely that the hazards of sun overexposure were becoming apparent to soldiers in the Pacific and to their families at home.

Franz Greiter is credited with introducing the concept of Sun Protection Factor (SPF) in 1962, which has become a worldwide standard for measuring the effectiveness of sunscreen when applied at an even rate of 2 milligrams per square centimeter (mg/cm2). Some controversy exists over the usefulness of SPF measurements, especially whether the 2 mg/cm2 application rate is an accurate reflection of people’s actual use.

Newer sunscreens have been developed with the ability to withstand contact with water and sweat.

[edit] Measurements of sunscreen protection

[edit] Sunburn protection factor

The SPF of a sunscreen is a laboratory measure of the effectiveness of sunscreen; the higher the SPF, the more protection a sunscreen offers against UV-B (the ultraviolet radiation that causes sunburn). The SPF indicates the time a person can be exposed to sunlight before getting sunburn with a sunscreen applied relative to the time they can be exposed without sunscreen. For example, someone who would burn after 12 minutes in the sun would expect to burn after 2 (or more) hours (120 min) if protected by a sunscreen with SPF 10. In practice, the protection from a particular sunscreen depends on factors such as:

  • The skin type of the user.
  • The amount applied and frequency of re-application.
  • Activities in which one engages (for example, swimming leads to a loss of sunscreen from the skin).
  • Amount of sunscreen the skin has absorbed.

The SPF is an imperfect measure of skin damage because invisible damage and skin aging is also caused by the very common ultraviolet type A, which does not cause reddening or pain. Conventional sunscreen does not block UVA as effectively as it does UVB, and an SPF rating of 30+ may translate to significantly lower levels of UVA protection according to a 2003 study. According to a 2004 study, UVA also causes DNA damage to cells deep within the skin, increasing the risk of malignant melanomas.[14] Even some products labeled "broad-spectrum UVA/UVB protection" do not provide good protection against UVA rays.[15] The best UVA protection is provided by products that contain zinc oxide, avobenzone, and ecamsule. Titanium dioxide probably gives good protection, but does not completely cover the entire UV-A spectrum.[16]

Owing to consumer confusion over the real degree and duration of protection offered, labeling restrictions are in force in several countries. In the United States in 1999, the Food and Drug Administration (FDA) decided to institute the labelling of SPF 30+ for sunscreens offering more protection, and a similar restriction applies in Australia. This was done to discourage companies from making unrealistic claims about the level of protection offered (such as "all day protection"),[17]. In the EU sunscreens are limited to SPF 50+, indicating a SPF of 60 or higher.[18]

UV-B sunlight spectrum (on a summer day in the Netherlands), along with the CIE Erythemal action spectrum. The effective spectrum is the product of the former two.
UV-B sunlight spectrum (on a summer day in the Netherlands), along with the CIE Erythemal action spectrum. The effective spectrum is the product of the former two.

The SPF can be measured by applying sunscreen to the skin of a volunteer and measuring how long it takes before sunburn occurs when exposed to an artificial sunlight source. In the US, such an in vivo test is required by the FDA. It can also be measured in vitro with the help of a specially designed spectrometer. In this case, the actual transmittance of the sunscreen is measured, along with the degradation of the product due to being exposed to sunlight. In this case, the transmittance of the sunscreen must be measured over all wavelengths in the UV-B range (290–350 nm), along with a table of how effective various wavelengths are in causing sunburn (the erythemal action spectrum) and the actual intensity spectrum of sunlight (see the figure). Such in vitro measurements agree very well with in vivo measurements.[19]

Mathematically, the SPF is calculated from measured data as

\mathrm{SPF} = \frac{\int A(\lambda) E(\lambda)d\lambda}{\int A(\lambda) E(\lambda)/\mathrm{MPF}(\lambda) \, d\lambda},

where E(λ) is the solar irradiance spectrum, A(λ) the erythemal action spectrum, and MPF(λ) the monochromatic protection factor, all functions of the wavelength λ. The MPF is roughly the inverse of the transmittance at a given wavelength.

The above means that the SPF is not simply the inverse of the transmittance in the UV-B region. If that were true, then applying two layers of SPF 5 sunscreen would be equivalent to SPF 25 (5 times 5). The actual combined SPF is always lower than the square of the single-layer SPF.

[edit] Measurements of UVA protection

Persistent Pigment Darkening (PPD), Immediate Pigment Darkening (IPD), Boots Star System, Japanese PA system

The Persistent Pigment Darkening (PPD) method is a method of measuring UVA protection, similar to the SPF method of measuring UVB light protection. Originally developed in Japan, and is the preferred method used by manufacturers such as L'Oreal.

Instead of measuring erythema or reddening of the skin, the PPD method uses UVA radiation to cause a permanent darkening or tanning of the skin.Theoretically, a sunscreen with a PPD rating of 10 should allow you to endure 10 times as much UVA as you would without protection. The PPD method is an in vivo test like SPF. In addition Colipa has introduced a method which is claimed can measure this in vitro and provide parity with the PPD method

As part of revised guidelines for sunscreens in the EU, a requirement to provide the consumer with a minimum level of UVA protection in relation to the SPF. This should a UVA PF of at least 1/3 of the SPF to carry the UVA seal. The implementation of this seal is in its phase-in period, so a sunscreen without may already offer this protection.[20]

[edit] Star rating system

In the UK and Ireland, the Boots star rating system is a proprietary method used to describe the ratio of UVA to UVB protection offered by sun screen creams and sprays. Invented by Dr Diffey of the Boots Company in Nottingham UK, it has been adopted by most companies marketing these products in the UK. The logo and methodology of the test are freely licenced to any manufacturer or brand of sunscreens that wishes to place product on the UK market. It should not be confused with SPF which is measured with reference to burning and UVB. One star products provide the least ratio of UVA protection, five star products are the best. The method has recently been revised in light of the Colipa UVA PF test, and with the new EU recommendations regarding UVA PF. The method still uses a spectrophotometer to measure absorption of UVA vs UVB, The difference stems from a requirement to pre-irradiate samples (where this was not previously required) to give a better indication of UVA protection, and of photostability when the product is used

[edit] Active ingredients

The principal ingredients in sunscreens are usually aromatic molecules conjugated with carbonyl groups. This general structure allows the molecule to absorb high-energy ultraviolet rays and release the energy as lower-energy rays, thereby preventing the skin-damaging ultraviolet rays from reaching the skin. So, upon exposure to UV light, most of the ingredients (with the notable exception of avobenzone) do not undergo significant chemical change, allowing these ingredients to retain the UV-absorbing potency without significant photo-degradation.[11] A chemical stabilizer is included in sunscreens containing avobenzone to slow breakdown. Avobenzone is also the only ingredient that blocks only UVA.

Some sunscreens also include enzymes like photolyase, which are able to repair UV-damaged DNA.[21]

[edit] FDA allowable ingredients

The following are the FDA allowable active ingredients in sunscreens:

UV-filter other names maximum concentration permitted in these countries Results of safety testing
p-Aminobenzoic acid PABA 15% EC, USA, AUS Mixed[22][23][24]
Padimate O OD-PABA, octyldimethyl-PABA, σ-PABA 8% EC, USA, AUS not tested
Phenylbenzimidazole sulfonic acid Ensulizole, Eusolex 232, PBSA, Parsol HS 4%(US,AUS) 8%(EC) EC,USA, AUS Genotoxic in bacteria[25]
Cinoxate 2-Ethoxyethyl p-methoxycinnamate 3%(US) 6%(AUS) USA, AUS not tested
Dioxybenzone benzophenone-8 3% USA, AUS not tested
oxybenzone benzophenone-3, Eusolex 4360, Escalol 567 6%(US) 10%(AUS) EC, USA, AUS not tested
Homosalate Homomethyl salicylate, HMS 10%(EC) 15%(US,AUS) EC, USA, AUS not tested
Methyl anthranilate Methyl-aminobenzoate, meradimate 5% USA, AUS not tested
Octocrylene Eusolex OCR, 2-cyano-3,3diphenyl acrylic acid, 2-ethylhexylester 10% EC,USA, AUS Increases ROS
Octyl methoxycinnamate Octinoxate, EMC, OMC, Ethylmethoxycinnamate, Escalol 557, 2-ethylhexyl-paramethoxycinnamate, Parsol MCX 7.5%(US) 10%(EC,AUS) EC,USA, AUS Protects against skin tumors in mice[26]
Octyl salicylate Octisalate, 2-Ethylhexyl salicylate, Escalol 587, 5% EC,USA, AUS not tested
Sulisobenzone 2-Hydroxy-4-Methoxybenzophenone-5-sulfonic acid,

3-benzoyl-4-hydroxy-6-methoxybenzenesulfonic acid, BENZ-4, Escalol 577

 5%(EC) 10%(US, AUS) EC,USA, AUS Protects against skin tumors in mice [26]
Trolamine salicylate Triethanolamine salicylate 12% USA, AUS not tested
Avobenzone 1-(4-methoxyphenyl)-3-(4-tert-butylphenyl)propane-1,3-dione, Butyl methoxy dibenzoylmethane, BMDBM, Parsol 1789, Eusolex 9020 3%(US) 5%(AUS) EC, USA, AUS Not available[27]
Ecamsule Mexoryl SX, Terephthalylidene Dicamphor Sulfonic Acid 10 EC, USA, AUS Protects against skin tumors in mice[28][29][30]
Titanium dioxide 25% EC,USA, AUS not tested
Zinc oxide 25%(US) 20%(AUS) (EC)Not listed as sunscreen, Still under SCCP review EC,USA, AUS Protects against skin tumors in mice[28][26]

Other ingredients approved within the EU[31] and other parts of the world:[32]

UV-filter other names maximum concentration permitted in Results of testing
4-Methylbenzylidene camphor Enzacamene, Parsol 5000, Eusolex 6300, MBC 4% EC, AUS not tested
Tinosorb M Bisoctrizole, Methylene Bis-Benzotriazolyl Tetramethylbutylphenol,MBBT 10% EC, AUS not tested
Tinosorb S Bis-ethylhexyloxyphenol methoxyphenol triazine, Bemotrizinol, BEMT, anisotriazine 10% EC, AUS not tested
Neo Heliopan AP Bisdisulizole Disodium, Disodium phenyl dibenzimidazole tetrasulfonate, bisimidazylate, DPDT 10% EC, AUS not tested
Mexoryl XL Drometrizole Trisiloxane 15% EC, AUS not tested
Uvinul T 150 Octyl triazone, ethylhexyl triazone, ET 5% EC, AUS not tested
Uvinul A Plus Diethylamino Hydroxybenzoyl Hexyl Benzoate 10% (EC) EC
UVAsorb HEB Iscotrizinol, Diethylhexyl butamido triazone, DBT 10% EC not tested
Parsol SLX Dimethico-diethylbenzalmalonate, Polysilicone-15 10% EC, AUS not tested
Isopentenyl-4-methoxycinnamate Isoamyl p-Methoxycinnamate, IMC, Neo Heliopan E1000, Amiloxate 10% EC, AUS not tested

Many of the ingredients not approved by the FDA are relatively new and developed to absorb UVA.[33]

[edit] Possible adverse effects

Main article: Sunscreen controversy

Adverse health effects may be associated with some synthetic compounds in sunscreens.[34]

[edit] Absorption into the skin

Sunscreen is a topically applied cosmetic product. According to Mavon, et al. (2007), it is desirable that sunscreen "should remain at the skin surface or impregnate the first layers of the stratum corneum only"[35] However, a fraction of some active ingredients can penetrate through the epidermal barrier to deep layers of skin, to potentially come into contact with living tissue and the bloodstream. For example, benzophenone-3, octyl-methoxycinnamate, and 3-(4-methylbenzylidene) camphor penetrate these layers well, while methylene bis-benzotriazoyl tetramethylbutylphenol penetrates poorly, and titanium dioxide does not penetrate.[35][36][37]

  • Treffel and Gabard have determined that 6 hours after application to human skin, the percentage of sunscreen that came into contact with the epidermis is 4% (benzophenone-3), 9% (ethylmethylmethoxycinnamate) and 7% (ethylhexylsalicylate).[38]
  • Hayden et al investigated the amount of sunscreen found in the urine after topical application.[36] Nine volunteers applied a commercially available SPF15+ sunscreen (Ingredients: oxybenzone, octylmethoxycinnamate, octyl salicylate and octocrylene), and then their urine samples were collected for 48 hours. They estimated that within 10 hours between 1 and 2% of the applied benzophenone-3 was absorbed into the body.
  • Jiang et al. found that after 8 hours 10% of the chemical UV-filter benzophenone-3 has passed through the skin into the body.[39]

[edit] Reactive oxygen species

Three commonly used ultraviolet (UV) filters -- octylmethoxycinnamate, benzophenone 3, and octocrylene -- eventually soak into the deeper layers of the skin after their application, leaving the top skin layers vulnerable to sun damage.[13] UV rays absorbed by the skin can generate harmful compounds called reactive oxygen species (ROS), which may cause skin cancer and premature aging. One study concluded that once the chemicals in sunscreen soak into the lower layers of skin, the chemicals react with UV light to create ROS.[13] To reduce ROS generation and damage, the researchers recommended reapplying the sunscreen often, which will replenish the sunscreen which has penetrated the skin. Future possibilities may include the development of sunscreens which stay at the surface of the skin, or mixing sunscreens with antioxidants that can neutralize ROS.[40]

[edit] Photomutagens, photogenotoxins, and photocarcinogens

Photomutagenic compounds are those which cause changes in DNA or RNA in either lab animals, tissue samples, cells, bacteria, or on isolated DNA molecules in solution when exposed to light.[26] In contrast, photocarcinogenic compounds are those which have been shown in laboratory animals to cause cancer when exposed to light. Photocarcinogenicity testing is usually conducted on hairless mice.[26] However most sunscreen ingredients have not been tested for a possible photocarcinogenic effect by the authorities because they were introduced before such testing became compulsory.[28] Whether a photomutagenic compound is photocarcinogenic or not depends on its ability to penetrate the stratum corneum and to be absorbed into the deeper layers of the skin.

Photocarcinogenicity testing is not done under "realistic use" conditions, with the following differences: in real use, only 75% of the skin surface is treated with sunscreen, sunscreens are lost during swimming, sweating, and transfer to clothing, people generally only apply one-quarter the amount used in these studies, and most people usually use sunscreen for 3 to 4 weeks out of a year, which is less than the amount of time the mice are exposed.[26]

[edit] FDA-mandated testing of sunscreen ingredients

In 1978, The United States became the first (and only) country to make photocarcinogenicity testing compulsory for sunscreen ingredients.[28][26] After this more demanding requirement had been introduced no new sunscreen ingredient has reached the US-market until the year 2000. Between 2000 and 2007 three new sunscreen absorbers were admitted to the US-market: avobenzone, zinc oxide, and ecamsule.[28]

[edit] Results of sunscreen testing

PABA, phenylbenzimidazole sulfonic acid, and avobenzone have photomutagenic or photogenotoxic effects.

In photocarcinogenicity tests, 4 compounds (Meroxyl SX, 2-ethylhexyl-paramethoxycinnamate, 3-benzoyl-4-hydroxy-6-methoxybenzenesulfonic acid, and titanium dioxide), have been found to protect against the development of cancer in hairless mice.[26]

No sunscreen ingredient has been found to be photocarcinogenic. [26]

[edit] Correlation between malignant melanoma and sunscreen use

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Although sunscreen use prevents sunburn and other skin damage caused by direct DNA damage, studies by Bastuji-Garinit et al and Marshall et al. indicate it may be correlated with conditions that are caused by indirect DNA damage like malignant melanoma.[41][42] The majority of epidemiological studies indicates a positive correlation between sunscreen use and melanoma (sunscreen users have more melanoma)[3][4][5][6][7][8][9] and some show a negative correlation.[43][44][45] (See also Epidemiology of melanoma and sunscreen.)

Philippe Autier et al. performed a case-control study with 418 melanoma cases and 438 healthy controls in France Belgium and Germany.[4] They investigated groups of people who had sunburns in their childhood and those who did not. They found that people with melanoma were more likely to have used sunscreen.

Westerdahl et al.[3] performed a case-control study on 571 patients with malignant melanoma and 913 healthy controls. All the patients and controls were asked about their history of sunburn, hair color, sunbathing habits (how long, how often) and use of sunscreen. Several adjustments were made with respect to the history of sunburns, hair color and other factors. The study found that those patients with malignant melanoma were more likely to have used sunscreen regularly.

[edit] Lawsuits against sunscreen manufacturers

The results from the epidemiological studies have lead to lawsuits against sunscreen manufacturers because of the absence of UV-A filters.[46][47][48][49][50][51]

[edit] Other adverse effects

Some individuals can have mild to moderate allergic reactions to certain ingredients in sunscreen, particularly the chemical benzophenone, which is also known as phenyl ketone, diphenyl ketone, or benzoylbenzene.

A significant reduction in sun exposure inhibits the production of vitamin D. The use of sunscreen with a sun protection factor (SPF) of 8 inhibits more than 95% of vitamin D production in the skin.[52] However, excessive sun exposure has been conclusively linked to some forms of skin cancer and signs of premature aging. Season, geographic latitude, time of day, cloud cover, smog, skin type, and sunscreen all have an effect on vitamin D production in the skin.[53] Fifteen minutes per day of direct exposure to the sun (i.e. without sunscreen) is a generally accepted guideline to follow for optimum vitamin D production.[54]

Hubertus et al have conducted a study in which one sunscreen ingredient is suspected of being an endocrine disruptor.[55]

[edit] Allowable health claims for sunscreen

In August 2007, The United States FDA proposed to disallow manufacturer claims on bottles that using sunscreens prevents cancer and to change SPF to refer to Sunburn Protection Factor instead of Sun Protection Factor (FDA proposed changes). This was done due to the epidemiological results in conjunction with some mechanistic studies which show that sunscreens prevent inflammation only and not necessarily the causes of melanoma.

[edit] See also

[edit] References

  1. ^ [1] What You Need To Know About Skin Cancer
  2. ^ Garland C, Garland F, Gorham E (1992). "Could sunscreens increase melanoma risk?". Am J Public Health 82 (4): 614-5. PMID 1546792. 
  3. ^ a b c Westerdahl J; Ingvar C; Masback A; Olsson H (2000). "Sunscreen use and malignant melanoma.". International journal of cancer. Journal international du cancer 87: 145-50. 
  4. ^ a b c Autier P; Dore J F; Schifflers E; et al (1995). "Melanoma and use of sunscreens: An EORTC case control study in Germany, Belgium and France". Int. J. Cancer 61: 749-755. 
  5. ^ a b Weinstock, M. A. (1999). "Do sunscreens increase or decrease melanoma risk: An epidemiologic evaluation.". Journal of Investigative Dermatology Symposium Proceedings 4: 97-100. 
  6. ^ a b Vainio, H., Bianchini, F. (2000). "Cancer-preventive effects of sunscreens are uncertain.". Scandinavian Journal of Work Environment and Health 26: 529-31. 
  7. ^ a b Wolf P, Quehenberger F, Müllegger R, Stranz B, Kerl H. (1998). "Phenotypic markers, sunlight-related factors and sunscreen use in patients with cutaneous melanoma: an Austrian case-control study.". Melanoma Res. 8 (4): 370-378. doi:10.1097/00008390-199808000-00012. PMID 9764814. 
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  10. ^ Shaath, N. (2005). "The Chemistry of Ultraviolet Filters," in Regulations and Commericial Development 3rd edition, edited by N. Shaath, Taylor and Francis Press, New York. 954pp, 2005.
  11. ^ a b http://www.fda.gov/ohrms/dockets/dailys/00/Sep00/090600/c000573_10_Attachment_F.pdf
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  17. ^ http://www.fda.gov/bbs/topics/ANSWERS/ANS00955.html
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  20. ^ http://www.colipa.com/site/index.cfm?SID=15588&OBJ=26368&back=1
  21. ^ Dagmar Kulms, Birgit Pöppelmann, Daniel Yaroshdagger, Thomas A. Luger, Jean KrutmannDagger and Thomas Schwarz (1999). Nuclear and cell membrane effects contribute independently to the induction of apoptosis in human cells exposed to UVB radiation PNAS 96(14):7974-7979
  22. ^ H Flindt-Hansen; P. Thune, T. Eeg-Larsen (1990). "The inhibiting effect of PABA on photocarcinogenesis". Archives of Dermatological Research 282: 38-41. 
  23. ^ H Flindt-Hansen; P. Thune, T. Eeg-Larsen (1990). "The effect of short-term application of PABA on photocarcinogenesis". Acta Derm Venerol. 70: 72-75. 
  24. ^ P. J. Osgood; S. H. Moss, D. J. Davies (1982). "The sensitization of near-ultraviolet radiation killing of mammalian cells by the sunscreen agent para-aminobenzoic acid". Journal of Investigative Dermatology 79 (6): 354-357. doi:10.1111/1523-1747.ep12529409. 
  25. ^ Mosley, C N; Wang, L; Gilley, S; Wang, S; Yu, H (2007). "Light-Induced Cytotoxicity and Genotoxicity of a Sunscreen Agent, 2-Phenylbenzimidazol in Salmonella typhimurium TA 102 and HaCaT Keratinocytes". International Journal of Environmental Research and Public Health 4 (2): 126-131. 
  26. ^ a b c d e f g h i Nohynek G. J.; Schaefer H (2001). "Benefit and Risk of Organic Ultraviolet Filters". Regulatory Toxicology and Pharmacology 33 (3): 285-299. doi:10.1006/rtph.2001.1476. PMID 11407932. 
  27. ^ Nash,JF (2006). "{{{title}}}". Dermatologic Clinics 24: 35-51. 
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  29. ^ Benech-Kieffer F, Meuling WJ, Leclerc C, Roza L, Leclaire J, Nohynek G (Nov-Dec 2003). "Percutaneous absorption of Mexoryl SX in human volunteers: comparison with in vitro data". Skin Pharmacol Appl Skin Physiol 16(6): 343-55. PMID 14528058. 
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  31. ^ http://eur-lex.europa.eu/LexUriServ/site/en/consleg/1976/L/01976L0768-20060809-en.pdf
  32. ^ http://www.tga.gov.au/docs/pdf/argom_10.pdf
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  38. ^ Treffel, P.; Gabard, B. (1996). "Skin penetration and SPF of ultraviolet filters from two vehicles.". Pharm. Res. 13: 770-774. doi:10.1023/A:1016012019483. 
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  40. ^ http://www.newsroom.ucr.edu/cgi-bin/display.cgi?id=1399
  41. ^ S. Bastuji-Garin; T.L. Diepgen (2002). "Cutaneous malignant melanoma, sun exposure, and sunscreen use: epidemiological evidence.". The British journal of dermatology 146 (1): 24-30. 
  42. ^ Stephen W. Marshall, Charles Poole, Anna E Waller, (2003). "SUNSCREEN USE AND MALIGNANT MELANOMA RISK: THE JURY IS STILL OUT". American Journal of Public Health 93 (1). 
  43. ^ Espinosa Arranz J, Sanchez Hernandez JJ, Bravo Fernandez P, Gonzalez-Baron M, Zamora Auñon P, Espinosa Arranz E, Jalon Lopez JI, Ordoñez Gallego A. (1992). "Cutaneous malignant melanoma and sun exposure in Spain.". Melanoma Res. 9 (2): 199-205. PMID 10380943. 
  44. ^ Holly EA, Aston DA, Cress RD, Ahn DK, Kristiansen JJ. (1995). "Cutaneous melanoma in women. I. Exposure to sunlight, ability to tan, and other risk factors related to ultraviolet light.". Am J Epidemiol. 141 (10): 923-933. PMID 7741122. 
  45. ^ Ródenas JM, Delgado-Rodríguez M, Herranz MT, Tercedor J, Serrano S. (1996). "Sun exposure, pigmentary traits, and risk of cutaneous malignant melanoma: a case-control study in a Mediterranean population.". Cancer Causes Control. 7 (2): 275-283. doi:10.1007/BF00051303. PMID 8740740. 
  46. ^ Link to documents of legal firm representing sunscreen users in class-action lawsuit
  47. ^ Sunscreen Makers Lie, Suits Charge
  48. ^ Lawsuit Filed Against Sunscreen Makers
  49. ^ Snake Oil
  50. ^ Sunscreen Labels & Lawsuits - Whose Fault Is It?
  51. ^ http://www.peoplespharmacy.com/archives/editorial/do_sunscreens_create_a_false_sense_of_security.asp Do Sunscreens Create a False Sense of Security
  52. ^ Holick M (2004). "Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease". Am J Clin Nutr 80 (6 Suppl): 1678S-88S. PMID 15585788. 
  53. ^ Holick M (1995). "Environmental factors that influence the cutaneous production of vitamin D". Am J Clin Nutr 61 (3 Suppl): 638S-645S. PMID 7879731. 
  54. ^ Dietary Supplement Fact Sheet: Vitamin D. National Institutes of Health. Retrieved on 2006-06-10.
  55. ^ [3]

[edit] External links

* FDA monograph on sunscreen
* FDA monograph on dosing, mechanism of action, and photodegradation of sunscreen (PDF file)