Homosalate absorbs the sun's UVB rays, preventing sunburn. It should be combined with a UVA absorber such as avobenzone or zinc oxide to ensure broad-spectrum protection


Grade Level of Evidence
A Multiple double-blind, controlled clinical trials.
B 1 double-blind, controlled clinical trial.
C At least 1 controlled or comparative clinical trial.
D Uncontrolled, observational, animal or in-vitro studies only.
Grade Effect Size of Effect Comments




Absorbs in the range 290-315 nm, which covers nearly the whole UVB spectrum. Alone, its SPF reaches a maximum of about 4 at a concentration of 6%.

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Scientific Research

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Table of contents:

1. Sources

Homosalate, also known as homomenthyl salicylate, is a clear, colourless to pale yellow liquid with a slight mint odour.[1] It has a long history of use as a UV filter in sunscreens, but a recent analysis of 100 sunscreen cosmetics found that it was used in only 4% of the products.[2]

Homosalate has also been detected in coastal plain aquifers in the United States,[3] in sediment collected from Japanese rivers and lakes,[4] and in fish from Spain.[5]

2. Skin penetration

Homosalate can penetrate through the skin, with an early study showing that 1.1% of the applied dose from a sunscreen containing 10% homosalate was absorbed through fresh dermatomed human abdominal skin. The proportion absorbed was substantially higher in rat skin, which had a mean total absorption of 8.7%.[1] A more recent study found that 4-6% of the applied dose in a gel became bioavailable in rats.[6]

However, one study in which 5% homosalate was applied to full-thickness human breast or abdominal skin showed that homosalate was absorbed only in the epidermis, and did not penetrate through the skin.[7] Another study demonstrated that penetration of homosalate from a sunscreen lotion containing 8% homosalate was minimal, with the vast majority retained in the stratum corneum.[8]

The choice of vehicle can influence the extent and amount of homosalate absorption. Homosalate in a gel accumulated in the stratum corneum and viable skin of rats between 3 to 10-fold more than homosalate in petrolatum, in a lotion or in an oily solution.[6] Similarly, an oil-in-water emulsion gel formulation of homosalate showed approximately 3-fold higher distribution into the stratum corneum of human skin than homosalate in petrolatum.[7]

It is assumed that homosalate is rapidly and completely metabolized to salicylic acid by esterases in the skin, despite the lack of actual experimental data.[1]

3. Effects on the skin

3.1 Photoprotection

Homosalate's absorbance range is between 290–315 nm.[9] It has 2 absorbance peaks at 238 and 306 nm.[1] The US FDA's standard sunscreen preparation, which contains 8% homosalate, has a sun protection factor (SPF) of 4.47 ± 1.279.[10] In a comparison of 18 sun filters all at their highest concentrations allowed by European legislation, homosalate ranked 9th in terms of efficacy. The authors also noted that the trend curve of SPF against homosalate concentration is asymptotic, with the SPF reaching a maximum value of about 4 as soon as concentration is at 6%.[11] Homosalate has a significant anti-inflammatory effect, which is thought to influence its in vivo SPF value.[12]

A photostable broad-spectrum sunscreen can be achieved by combining avobenzone and UVB sunscreens such as homosalate with the photostabilizer DESM.[13]

4. Stability

Homosalate is photostable as an emulsion and in various solvents. Its shelf life has been estimated to be at least 2-3 years.[1]

5. Safety

Homosalate is an approved sunscreen active ingredient in the US, where it can be included up to a concentration of 15%.[14] In Europe, the Scientific Committee on Consumer Products established in 2007 that homosalate at a maximum use concentration of 10% in cosmetic sunscreens does not pose a risk to the health of consumers.[1] This has formed the basis for its inclusion in the EU Cosmetics Directive.[15]

5.1 Skin irritation

Homosalate administered dermally to rabbits at a single dose of 5 g/kg body weight led to signs of skin irritation in the form of slight or moderate redness and edema.[1] Investigations using mice and guinea pigs revealed no photoallergic potential.[16][17] These results are in line with a quantitative structure-toxicity relationship model, which predicts that homosalate has weak sensitizing potential.[18]

Homosalate has also been tested for potential sensitization on human skin in a maximization test involving 25 volunteers. No signs of skin irritation or sensitization were observed. Numerous human repeated insult patch tests of cosmetic products containing 10-15% homosalate also found no clinically relevant potential for dermal irritation or sensitization.[1]

Photopatch tests on 118 patients with suspected photoallergic contact dermatitis revealed that none reacted to homosalate as a 5% preparation in petrolatum.[19] Moreover, there are only isolated cases reported concerning induction of skin sensitization or photoallergic reactions to homosalate, indicating that it has a negligible potential to induce adverse skin reactions in humans.[20][21][22][23]

5.2 Potential endocrine disruptor

Data on the estrogenicity of homosalate is conflicting. The earliest investigation found that homosalate induced proliferation in human breast cancer cells,[24] but important shortcomings have been identified in this study.[1][25] Other studies confirm that homosalate has estrogenic activity toward estrogen receptors in vitro,[26][27][28][29] but caution should be taken to avoid over-interpreting these data, since homosalate was not estrogenic in 2 in vivo experiments.[24][26]

Homosalate appears to be a potent antagonist of the human androgen receptor.[29][28] It has been demonstrated to suppress the dihydrotestosterone-induced activation of the androgen receptor in vitro,[30] though these preliminary results may not be relevant for the in vivo situation.

5.3 Enhanced absorption of a herbicide

A 5% homosalate has been shown to significantly increase the total penetration of 2,4-dichlorophenoxyacetic acid, a moderately lipophilic herbicide, in vitro, which may make it a risk to agricultural workers who use sunscreens as protection against UV-induced skin cancer.[31]

5.5 No genotoxic potential

Homosalate was not mutagenic in Salmonella assays with and without metabolic activation. It did not induce an increase structural chromosomal aberrations in Chinese hamster ovary cells either, indicating no clastogenic potential. As a result, the European Scientific Committee on Consumer Products concluded in 2007 that homosalate poses no genotoxic or mutagenic risk to humans.[1][32]

Scientific References

  1. Scientific Committee on Consumer Products. Opinion on homosalate. SCCP. (2007)
  2. Liu T, Wu D. Simultaneous determination of some ultraviolet-absorbing chemicals in sunscreen cosmetics using a high-performance liquid chromatography method. Int J Cosmet Sci. (2011)
  3. Del Rosario KL, et. al. Detection of pharmaceuticals and other personal care products in groundwater beneath and adjacent to onsite wastewater treatment systems in a coastal plain shallow aquifer. Sci Total Environ. (2014)
  4. Kameda Y, Kimura K, Miyazaki M. Occurrence and profiles of organic sun-blocking agents in surface waters and sediments in Japanese rivers and lakes. Environ Pollut. (2011)
  5. Gago-Ferrero P, Díaz-Cruz MS, Barceló D. An overview of UV-absorbing compounds (organic UV filters) in aquatic biota. Anal Bioanal Chem. (2012)
  6. Kim TH, et. al. Percutaneous absorption, disposition, and exposure assessment of homosalate, a UV filtering agent, in rats. J Toxicol Environ Health A. (2014)
  7. Chatelain E, Gabard B, Surber C. Skin penetration and sun protection factor of five UV filters: effect of the vehicle. Skin Pharmacol Appl Skin Physiol. (2003)
  8. Sarveiya V, Risk S, Benson HA. Liquid chromatographic assay for common sunscreen agents: application to in vivo assessment of skin penetration and systemic absorption in human volunteers. J Chromatogr B Analyt Technol Biomed Life Sci. (2004)
  9. Patel NP, Highton A, Moy RL. Properties of Topical Sunscreen Formulations: A Review. J Dermatol Surg Oncol. (2013)
  10. US Food and Drug Administration. CFR - Code of Federal Regulations Title 21, Part 352, Subpart D, Section 352.70. Code of Federal Regulations. (2013)
  11. Couteau C, et. al. Study of the efficacy of 18 sun filters authorized in European Union tested in vitro. Pharmazie. (2007)
  12. Couteau C, et. al. UV filters, ingredients with a recognized anti-inflammatory effect. PLOS ONE. (2012)
  13. Chaudhuri RK, et. al. Design of a photostabilizer having built-in antioxidant functionality and its utility in obtaining broad-spectrum sunscreen formulations. Photochem Photobiol. (2006)
  14. US Food and Drug Administration. CFR - Code of Federal Regulations Title 21, Part 352, Subpart B, Section 352.10. Code of Federal Regulations. (2013)
  15. European Commission. List of UV filters allowed in cosmetic products. Cosmetics Directive. (2011)
  16. Gerberick GF, Ryan CA. A predictive mouse ear-swelling model for investigating topical photoallergy. Food Chem Toxicol. (1990)
  17. Gerberick GF, Ryan CA. Contact photoallergy testing of sunscreens in guinea pigs. Contact Dermatitis. (1989)
  18. Enslein K, et. al. A quantitative structure-toxicity relationships model for the dermal sensitization guinea pig maximization assay. Food Chem Toxicol. (1997)
  19. Pollock B, Wilkinson SM. Photopatch test method: influence of type of irradiation and value of day-7 reading. Contact Dermatitis. (2001)
  20. Menz J, Muller SA, Connolly SM. Photopatch testing: a six-year experience. J Am Acad Dermatol. (1988)
  21. González E, González S. Drug photosensitivity, idiopathic photodermatoses, and sunscreens. J Am Acad Dermatol. (1996)
  22. Fischer T, Bergström K. Evaluation of customers' complaints about sunscreen cosmetics sold by the Swedish pharmaceutical company. Contact Dermatitis. (1991)
  23. Rietschel RL, Lewis CW. Contact dermatitis to homomenthyl salicylate. Arch Dermatol. (1978)
  24. Schlumpf M, et. al. In vitro and in vivo estrogenicity of UV screens. Environ Health Perspect. (2001)
  25. Bolt HM, Guhe C, Degen GH. Comments on "In vitro and in vivo estrogenicity of UV screens". Environ Health Perspect. (2001)
  26. Schreurs R, et. al. Estrogenic activity of UV filters determined by an in vitro reporter gene assay and an in vivo transgenic zebrafish assay. Arch Toxicol. (2002)
  27. Gomez E, et. al. Estrogenic activity of cosmetic components in reporter cell lines: parabens, UV screens, and musks. J Toxicol Environ Health A. (2005)
  28. Schreurs RH, et. al. Interaction of polycyclic musks and UV filters with the estrogen receptor (ER), androgen receptor (AR), and progesterone receptor (PR) in reporter gene bioassays. Toxicol Sci. (2005)
  29. Jiménez-Díaz I, et. al. Simultaneous determination of the UV-filters benzyl salicylate, phenyl salicylate, octyl salicylate, homosalate, 3-(4-methylbenzylidene) camphor and 3-benzylidene camphor in human placental tissue by LC-MS/MS. Assessment of their in vitro endocrine activity. J Chromatogr B Analyt Technol Biomed Life Sci. (2013)
  30. Ma R, et. al. UV filters with antagonistic action at androgen receptors in the MDA-kb2 cell transcriptional-activation assay. Toxicol Sci. (2003)
  31. Pont AR, Charron AR, Brand RM. Active ingredients in sunscreens act as topical penetration enhancers for the herbicide 2,4-dichlorophenoxyacetic acid. Toxicol Appl Pharmacol. (2004)
  32. Zeiger E, et. al. Salmonella mutagenicity tests: III. Results from the testing of 255 chemicals. Environ Mutagen. (1987)