Sensitization and Allergies

Fragrance allergies affect two to 11 percent of the general population.[1],[2] This translates to tens of millions of people globally affected by fragrance. Fragrance chemicals can become major sensitizers through air oxidation, photo-activation, or skin enzyme catalysis or cross-sensitizing – a process by which a person becomes sensitized to substances different from the substance to which the person is already sensitized.[3] Once sensitized, the only way to prevent the development of a severe, irreversible allergy is to avoid further exposure.

Medical literature estimates that more than one percent of the general population suffers from fragrance ingredient allergies.[4] And according to the American Academy of Dermatology (AAD), fragrances are considered the leading cause of cosmetic contact dermatitis.[5] Reactions to both natural and synthetic fragrance ingredients can range from contact dermatitis (characterized by redness, swelling, and irritation of the skin) to sneezing, coughing, or eye irritation. In total, the European Union’s Scientific Committee on Consumer Safety has identified 82 fragrance substances as “established contact allergens in humans,” including popular fragrance chemicals like cinnamal, eugenol, and citral[6] and 26 currently have to be listed on the label in EU products that contain them.

Respiratory Diseases and Irritation

Since fragrance ingredients are volatile, they easily enter the air as gases and expose the eyes and naso-respiratory tract. For asthmatics, the effect of exposure may be more severe. Like second hand smoke[7], even low concentrations of fragrance ingredients can provoke asthmatic episodes.[8] Inhalation exposure to common sanitizing agents called quaternary ammonium compounds (QACs) has been linked to occupational asthma.[9] Other common fragrance ingredients such as benzyl salicylate, benzyl benzoate, butoxyethanol are known skin, eye, nose and throat irritants which can cause severe symptoms such as a burning sensation, nausea, vomiting and damage to the liver and kidneys.[10],[11],[12] European Union’s Scientific Committee on Consumer Safety has identified the fragrance ingredients cinnamal and citral as “established contact allergens in humans.”[13]


In 2011, the International Fragrance Association (IFRA) published a list of 2,339 possible fragrance materials used by IFRA affiliated members, including fragrance suppliers, who use chemicals from this list or “palette” of ingredients to formulate fine fragrances and fragranced cosmetics and personal care products.[14] The IFRA list of possible fragrance ingredients includes chemicals listed as carcinogens by California’s Prop 65 Program and the National Toxicology Program (NTP) such as pyridine, benzophenone, methyleugenol and styrene.[15]

Endocrine Disrupters

In a 2010 study, 17 tested fragrances contained an average of four hormone-disrupting ingredients each, including synthetic musks and diethyl phthalate.[16] Synthetic musks mimic and displace natural hormones, which can potentially disrupt important endocrine and biological processes. [17],[18],[19],[20],[21],[22] High levels of musk ketone and musk xylene in women’s blood may also be associated with gynecological abnormalities such as ovarian failure and infertility.[23] These findings provide human evidence for findings that suggest endocrine disruption in other species.[24] In another example of endocrine disruption, diethyl phthalate has been linked to unusual reproductive development in baby boys and sperm damage in adult men.[25],[26],[27]

Neurotoxic Chemicals

In 1986, the National Academy of Sciences targeted fragrance as one of the six categories of chemicals that should be given priority for neurotoxicity testing.[28] Since then, animal studies have linked fragrance ingredient p-cymene to headache, weakness, and irritability, along with the reduction in number and density of brain synapses.[29] In addition, research has shown that the synthetic musks tonalide and galaxolide induce brain cell degeneration, which can lead to degenerative disorders such as Parkinson’s disease.[30]

Environmental Toxicants

Fragrance represents a serious threat to the environment. Synthetic musks end up in wastewater, drinking water, soil, and indoor air. Musk also bio-accumulates in the fatty tissue of aquatic wildlife, and travels through the food chain into salmon and shrimp.[31] In a 2010 study of fragranced products, each product emitted volatile organic compounds that have been identified as toxic or hazardous under federal law. Despite releasing compounds like chloromethane and methylene into the air, fragrance remains unregulated.[32] The continual contamination of our air, soil and water resources has even identified some fragrance chemicals as persistent organic pollutants (POPs).


[1] Schnuch, A., Lessmann, H., Geier, J., Frosch, P.J., and Uter, W. (2004) Contact allergy to fragrances: Frequencies of sensitization from 1996 to 2002. Results of the IVDK. Contact Dermatitis. Vol. 50. pp. 65-76. 2004. & Schafer, T., Bohler, E., Ruhdorfer, S., Weigl, L., Wessner, D., Filipiak, B., Wichmann, H.E., and Ring, J. (2001) Epidemiology of contact allergy in adults. Allergy. Vol. 56. pp: 19992- 1996.

[2] Cheng, J., and Zug, K. (2014). Fragrance Allergic Contact Dermatitis. Dermatitis, 25(5), pp. 232-245.

[3] Scientific Committee on Consumer Safety. (2012) Opinion on Fragrance Allergens in Cosmetic Products. European Commission. pp. 33-38.

[4] Cheng J, Zug K. (2014) Fragrance Allergic Contact Dermatitis. Dermatitis, 25(5), pp. 232-245.

[5] Contact dermatitis. American Academy of Dermatology.—d/contact-dermatitis/who-gets-and-causes.

[6] Scientific Committee on Consumer Safety. (2012) Opinion on Fragrance Allergens in Cosmetic Products. European Commission. pp. 7-9.

[7] Institute of Medicine. (2000) Clearing the Air, Asthma and Indoor Air Exposures, Executive Summary. p. 9.

[8] Kumar P., Caradonna-Graham V.M., Gupta S., Cai X., Rao P.N., and Thompson, J. (1995) Inhalation challenge effects of perfume scent strips in patients with asthma. Annals of Allergy Asthma Immunology, 75, pp. 429-433.

[9] Purohit, A., Kopferschmitt-Kubler, M.C., Moreau, C., Popin, E., Blaumeiser, M., and Pauli, G. (2000) Quaternary ammonium compounds and occupational asthma. International archives of occupational and environmental health, 73(6), 423-427.

[10] Opinion concerning fragrance allergy in consumers. Scientific Committee on Cosmetic Products and Non-Food Products Intended for Consumers. European Commission. (1999)

[11] Toxnet. Benzyl Benzoate. Toxicology Data Network. (2003)

[12] CDC. Butoxyethanol. NIOSH Pocket Guide to Chemical Hazards. (2015)

[13] Opinion on Fragrance Allergens in Cosmetic Products. Scientific Committee on Consumer Safety. European Commission. (2012) pp. 7-9.

[14] IFRA Ingredients. (2015)

[15] Report on Carcinogens, Thirteenth Edition. NTP (National Toxicology Program). U.S. Department of Health and Human Services, Public Health Service. (2014)

[16] Not So Sexy: Hidden Chemicals in Perfume and Cologne. EWG. (2010)

[17] Petersen, K., and Tollefsen, K. (2011) Assessing combined toxicity of estrogen receptor agonists in a primary of culture of rainbow trout (Oncorhynchus mykiss) hepatocytes. Aquatic toxicology, 101, pp. 186-195.

[18] Gomez E, et al. (2005) Estrogenic activity of cosmetic components in reporter cell lines: parabens, UV screens, and musks. Journal of Toxicology and Environmental Health, 68, pp. 239-251.

[19] Simmons D, Marlatt V, Trudeau V, Sherry J, Metcalfe C. (2010) Interaction of Galaxolide® with the human trout estrogen receptor-α. Science of the Total Environment, 408(24), pp 6158-6164.

[20] Yamauchi R, Ishibashi H, Hirano M, Mori T, Kim J-W, Arizono K. (2008) Effects of synthetic polycyclic musks on estrogen receptor, vitellogenin, pregnane X receptor, and cytochrome P450 3 A gene expression in the livers of male medaka (Oryias latipes). Aquatic Toxicology, 90, pp. 261-268.

[21] Witorsch R, Thomas J. (2010). Personal care products and endocrine disruption: a critical review of the literature. Critical Reviews in Toxicology, 40(S3), pp. 1-30.

[22] Schreurs R, Sonneveld E, Jansen J, Seinen W, van der Burg B. (2005). Interaction of polycyclic musks and UV filters with the estrogen receptor (ER), androgen receptor (AR), and progesterone receptor (PR) in reporter gene bioassays. Toxicological Sciences, 83, pp. 264-272.

[23] Eisenhardt S, Runnebaum B, Bauer K, Gerhard I. (2001). Nitromusk compounds in women with gynecological and endocrine dysfunction. Environmental Research Section A, 87, pp. 123-130.

[24] Carlsson G, Om S, Andersson P, Soderstrom H, Norrgren L. (2000) The impact of musk ketone on reproduction in zebrafish (Danio rerio). Marine Environmental Research, 50(1-5), pp. 237-241.

[25] Washington Toxics Coalition. (2008). Earliest Exposures. Retrieved from web.

[26] Hauser, R., Meeker, J. D., Singh, N. P., Silva, M. J., Ryan, L., Duty, S., & Calafat, A. M. (2007). DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Human reproduction, 22(3), 688-695.

[27] Swan, S. H. (2008). Environmental phthalate exposure in relation to reproductive outcomes and other health endpoints in humans. Environmental research, 108(2), 177-184.

[28] Congress, U. S. (1990). Office of Technology Assessment, Neurotoxicity: Identifying and controlling poisons of the nervous system. OTA-BA-436. Washington, DC: US Government Printing Office.

[29] Lam HR, Ladefoged O, Ostergaard G, Lund SP, Simonsen L. (1996). Four weeks’ inhalation exposure of rats to p-cymene affects regional and synaptosomal neurochemistry. Pharmacol Toxicol, 79(5), pp. 225-30.

[30] Ayuk-Takem L, Amissah F, Aguilar B, Lamango N. (2014). Inhibition of polyisoprenylated methylated protein methyl esterase by synthetic musks induces cell degeneration. Environmental Toxicology, 29(4), pp. 466-477.

[31] Bridges, B (2002). Fragrance: emerging health and environmental concerns. Flavour and Fragrance Journal, 17, pp. 368–369.

[32] Steinemann AC, et al. (2010). Fragranced consumer products: Chemicals emitted, ingredients unlisted. Environ Impact Asses Rev, doi:10.1016/j.eiar.2010.08.002.