Year : 2022 | Volume
: 67 | Issue : 4 | Page : 392--398
A review on cosmetics causing conatct urticaria
Merin Shaji, KA Merin, R Kameswaran
From the Department of Pharmacy Practice, J.K.K. Nattraja College of Pharmacy, Kumarapalayam, Tamil Nadu, India
Doctor of Pharmacy, Department of Pharmacy Practice, J.K.K. Nattraja College of Pharmacy, Kumarapalayam, Tamil Nadu
Physical appearance is more strongly pursued than ever in today's world and is considered to provide confidence, success and self-esteem. Cosmetics are the important product in beauty market and their growth is unstoppable. It is estimated that about 95% of women and 75% of men were daily using cosmetics. Despite the considerable use of cosmetics, most people are unaware of its adverse reactions. Urticaria is severe as well as the most common adverse reaction caused by cosmetics. Major cosmetics that cause urticaria include fragrance, preservatives, hair care products, lip plumbers, plant- and animal-derived products, bindi or kumkum, nail cosmetics, glycol peel, permanent makeup and tattoos, etc. This review provides a brief explanation of the cosmetic components that cause urticaria.
|How to cite this article:|
Shaji M, Merin K A, Kameswaran R. A review on cosmetics causing conatct urticaria.Indian J Dermatol 2022;67:392-398
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Shaji M, Merin K A, Kameswaran R. A review on cosmetics causing conatct urticaria. Indian J Dermatol [serial online] 2022 [cited 2023 Feb 6 ];67:392-398
Available from: https://www.e-ijd.org/text.asp?2022/67/4/392/360298
According to European legislation, cosmetics are substances or a mixture of substances used for application to external surfaces of the human body such as epidermis, hair, lips, and external genitalia, teeth or mucosa of the oral cavity with the only principle aim of cleaning, perfuming or modifying its appearance and or masking body odours. Cosmetics include personal hygiene products (e.g. gels and soaps) and moisturizers (e.g. creams, lotions), hair products (e.g. shampoos and lotions), toothpaste, make-up, nail products (e.g. nail polish and artificial nails), fragrances (e.g. deodorants and perfumes), hair removal products and sunscreens. These are divided into two as left on the skin and rinsed off the skin. Cosmetics that are left on the skin include lotions, creams, perfumes, etc. Rinsed off the skin cosmetics are shampoos and other detergents.
The extensive literature survey on the application of cosmetics shows that incidence of allergy to components of cosmetics is increasing in many countries. In the research conducted by Thyssen et al. among the citizens of Denmark shows that 56.7% of women and 33.6% of men have experienced adverse effects after using cosmetics at least once in their lifetime. It is also estimated that about 10% of the general population experiences side effects, urticaria, hypersensitivity or allergy-related irritation to cosmetics. The type of chemical exposure of cosmetic products and exposure time are the major reasons for these adverse reactions. Moreover, the use of cosmetics on irritated or inflamed skin increases the risk of side effects. The most common adverse effect caused by cosmetics is urticaria. It is mainly of two types, non-immunological contact urticaria and immunological urticaria. Non-immunological contact urticaria is without previous sensitisation, with skin lesions generally restricted to the site of contact, and systemic manifestation rarely being observed. Immunological contact urticaria is a type of hypersensitivity reaction in a previously sensitised individual. The pathogenesis is identical to that of other types of immediate hypersensitivity and it mainly involves the coupling of the absorbed antigen with specific IgE molecules on the surface of mast cells. The symptoms of immunological contact urticaria are due to the release of histamine.
Generalised reactions are frequent and are known as contact urticaria syndrome. There are four stages for the syndrome. Local symptoms include itching, tingling and burning sensation to wheal-and-flare responses, which are restricted to the area of contact and are common in the stage 1. Stage 2 consists of generalised urticaria following local cutaneous contact including angioedema. Extra cutaneous manifestations, which may include the respiratory, orolaryngeal or gastrointestinal tract are observed in the third stage. The last stage is anaphylaxis reactions.
Cosmetics and urticaria
Almost all the commonly used cosmetics have adverse reactions. Urticaria is one of the common adverse reactions. Commonly used cosmetics include soaps, creams, lipstick, foundation, sunscreens, perfumes, and eye, hair and nail cosmetics. It is estimated that 1–5.4% of the population is sensitised to cosmetics or cosmetic ingredients. These reactions are more common in women and about 80% of reactions occur in patients aged 20–60 years. It was observed that 23% of women and 18.8% of men experience some sort of adverse reaction to a personal care product over 1 year in an epidemiological survey conducted in the United Kingdom. Fragrance and aroma chemicals, dyes, preservatives, hair care products, antimicrobial agents, sunscreens, plant- and animal-derived cosmetics products, etc. are the agents causing urticaria, these are discussed in this review.
Fragrance is one of the basic ingredient used in the production or manufacture of materials because of their smell. The second most frequent cause of contact allergy in Spain after metals, are fragrance. They are the most frequent cause of cosmetics. The cosmetics most closely associated with sensitisation to fragrances are perfumes products, such as toilet waters, after-shave lotions and deodorants, but fragrance-containing skin-care products may also cause reactions, with leave-on products being more often responsible for allergy to fragrances than rinse-off products. The main skin sites affected are the face, neck, axillae and hands. M. pereirae (balsam of Peru) and fragrance mix (FM) I (a mixture of eight fragrance components in the baseline series (amyl cinnamal, cinnamal, cinnamyl alcohol, hydroxycitronellal, eugenol, isoeugenol, geraniol and Evernia prunastri [oakmoss] extract, all diluted 1% in petrolatum and emulsified with sorbitan sesquioleate) may elicit contact urticaria by both immunological and non-immunological mechanisms. Cinnamal the common ingredient to both, is probably the most important causal ingredient in this context. Mathias et al. has reported a case of lip swelling following its use in a mouthwash by a patient suffering from allergic rhinitis and asthma. A similar case was also observed caused by cinnamal-containing toothpaste and also by cinnamon in pastries.
A study of 10,000 patients with eczema was conducted in Denmark and it showed that 5.5% of respondents reported positive reaction after exposure to the fragrance mix. Among this mix oak moss causes the most common allergy, the second consecutive sensitising compound was isoeugenol, followed by the cinnamic aldehyde, cinnamic alcohol, eugenol, hydroxycitronellal, geraniol and finally amyl cinnamaldehyde. An allergy to oak moss and isoeugenol, is so common that both were prohibited to be added to the cosmetics in the European Union, which are part of deodorants and expensive perfume.
A case of immediate hypersensitivity to Cinnamonum cassia oil in toothpaste (as well as to sorbic acid, a preservative present in a shampoo) was explained by Rietschel. Facial oedema following the application of cosmetic products containing geraniol, another constituent of FMI, was also described; a 20-min closed test showed a wheel response, but no delayed hypersensitivity after 24–72 h. An immunological mechanism has been suggested because the patient had developed widespread urticaria and flare-up reactions on the face and neck by the day 3 reading of the patch test. Glaspole et al. revealed a case of anaphylaxis after an individual had used lemon-scented soap when showering; this patient also reported laryngeal oedema, generalised urticaria and asthma within minutes after ingestion of juice prepared from oranges, citrus seeds, peanuts and tree nuts.
Balsam of Peru is another addition of fragrance in many cosmetics, and its use is wide due to fixative properties. At least a dozen allergens are behind this product, and they include cinnamic aldehyde and acid, cinnamic cinnamon, cinnamon benzoate, benzyl benzoate, vanillin, vanillic acid, nerolidol and farnesol. Due to the existence of so many components, balsam of Peru has a high risk of cross-reactions.
Holmes et al. has reported regarding mint-flavoured toothpaste causing Type I allergy. The results of IgE-mediated allergy to mint or menthol include urticaria, rhinitis, asthma and/or anaphylaxis. It is estimated that the sensitivity to fragrance products occurs in 1–16% of unselected population. Hypersensitivity to fragrances usually occurs in the form of allergic contact dermatitis, contact urticaria and phototoxic reactions. These changes relate to various areas of the skin, including the face, neck, armpits or hands.
Preservative provides protection against the growth of bacteria and fungi that cause cosmetics to decay. Disinfectant properties of para-aminobenzoic acid esters (parabens), formaldehyde-releasing compounds, isothiazolinones and organic compounds of mercury (thiomersal) are commonly used in cosmetics. They are very important cosmetic allergens in water-based products such as cleansers, skincare products and makeup.
Phenoxyethanol is commonly used in cosmetics, often in combination with other preservatives such as parabens and formaldehyde releasers. A case of contact urticaria in a male patient, resulting from the use of an aftershave product containing phenoxyethanol was reported by Lujan et al. Similarly, three other cases of contact urticaria caused by cosmetics have been reported, but specific antibodies could not be identified, so the presence of immunological IgE-mediated reactions could not be confirmed. Sodium benzoate in toothpaste is a well-known cause of non-immunological contact urticaria. p-Chloro-m-cresol is present in a large number of topical preparations, and is a rare cause of allergic contact dermatitis and also contact urticaria. Triclosam is used in cosmetics, such as soaps, shampoos, mouthwashes and deodorants. A case of severe immunological contact urticaria and angioedema has been identified by the preservative tricolasm and owing to its presence in a metronidazole cream. Positive reactions occurring a few minutes following the application on a test chamber to the preservative agents benzoic acid, sodium benzoate and sorbic acid all of which are known to cause nonimmunological contact urticaria have been recognised.
Thiomersal, another preservative mainly found in cosmetics such as eye shadows, mascaras, lotions, contact lens solutions and ophthalmic preparations, which is also used in vaccines and many other products. Several studies clearly indicate that the incidence of positive patch test results with thiomersal is very high. Some studies have reported that about 18.5% of young people are affected by contact allergy and urticaria due to the use of thiomersal. Formalin (aqueous formaldehyde solution) and formaldehyde donors have high priority among the preservatives, which are present in allergy for cosmetics and also used in the production of plastics. Formaldehyde is a relatively potent contact allergen and numerous studies have reported that the proposed formaldehyde-releasing preservatives sometimes cause an allergic reaction, and in addition, there may be a concurrent adverse reaction including urticaria to formaldehyde. Remarkable preservatives are esters of para-hydroxybenzoic acid called parabens. For the study of allergy almost always three esters (methyl, ethyl and propyl) are considered. These compounds are present in almost all (99%) leave-on cosmetic products and in a large part (77%) of rinse-off cosmetics. Parabens are, however, relatively weak allergens and produce urticaria often as components of drugs, when applied on damaged skin.
Hair care products
p-phenylenediamine (PPD) and its derivatives, such as p-aminophenol and p-methylamino phenol and toluene-2,5-diamine are the important hair dye that causes immediate type hypersensitivity reaction. These reactions seem to occur only after oxidation by H2O2, and are attenuated when the antioxidant sodium sulphite is added to the mix. In a study, Haluk AH et al. has identified Brandowski base, an oxidation product of PPD as the main agent causing this reaction. It was observed that the natural permanent hair dye henna, derived from the leaves of the shrubs Lawsonia alba or Lawsonia inermis, is also a rare cause of rhinitis, conjunctivitis, sneezing, urticaria and asthmatic symptoms, it mainly occurs through inhalation of henna powder dispersed in the air. Most of the tattoos commonly used by teenagers, in addition to hair dyes, contain PPD. Tukenmez DG et al. reported a case of a 15-year-old adolescent female who had been sensitised to PPD from a black henna tattoo. She had angioedema-like reaction after her first exposure to hair dye. Delayed allergic reactions to PPD produce severe facial oedema thus mimicking type I immediate reactions.
Moreover, direct hair dyes, for example, Basic Blue 99 and Basic Brown 17, and patent blue dye, have been causes of contact urticaria, mainly acting through occupational exposure. Persulfate salts are widely used in the bleaching process and also make the hair easier to dye, which has high oxidising property. It is a potential cause of contact dermatitis, urticaria, rhinitis and asthma and some studies have shown specific binding of IgE to persulfates by two methods, namely, the immune spot test and radio allegro sorbent test (RAST); hence, the mechanism of immediate hypersensitivity seems to be IgE-mediated.
Because of carcinogenic and accelerated skin-aging effects of sunlight, sunscreens are increasingly used, not only in sunscreen products but also in other cosmetic products, including moisturizers. The major reactions to sunscreen chemicals are contact utricaria and allergic and photoallergic contact dermatitis reactions. Benzophenone-3 (INCI; syn. 2-hydroxy 4-methoxy benzophenone, oxybenzone), a common ultraviolet (UV) A/UVB sunscreen is an example for this type of reaction. Benzophenones are also added to protect against discolouration of cosmetics (textiles and plastics), which are exposed to sunlight. Contact urticaria and even contact-mediated anaphylaxis caused by benzophenones are, however, rare. The severity of clinical reaction tobenzophenones partly depends on the areas of exposed skin. Also, dibenzoylmethane derivatives have been recognised as important allergens and isopropyl dibenzoylmethane was withdrawn for this reason. On the other hand, methylbenzylidene camphor, cinnamates and phenylbenzimidazole sulfonic acid rarely cause cosmetic reactions. Octocrylene is increasingly reported as a contact allergen in children and frequently causes photo-contact allergic reactions. Also, it causes contact urticaria along with benzophenones, particularly in relation to photo-contact sensitisation by ketoprofen, a non-steroidal anti-inflammatory drug used to treat muscle pain. These reactions are most probably based on cross-reactivity.
Antioxidants are the minor group of cosmetic allergens. Propyl gallate, octyl gallate, which may cross-react with other gallates and be used as food additives, and t-butyl hydroquinone are some of the examples. Some antioxidants are used more specifically in sunscreen products and also in moisturising products to prevent ageing but are rare causes of allergic contact urticaria in such preparations. Also, sulphite allergy may explain reactions to certain cosmetic creams, cleansing products, as well as hair dyes, the number of contact urticaria reactions to oxidative-type hair dyes (PPD) and related compounds are common.
Chlorhexidine is a topical antiseptic and disinfectant with broad antimicrobial efficacy and has been increasingly used in instillation gels for urinary catheters, contact lens solutions and many cosmetic products. Urticaria following application to intact skin or mucosa, in some cases accompanied by dyspnoea, angioedema, syncope or anaphylaxis, has been identified. Polyaminopropyl biguanide (INCI; syn.polyhexanide, polyhexamethylene biguanide) is a widely used antiseptic, for example, in contact lens solutions, wound dressings and cosmetics have shown IgE-mediated reactions when it is present in wound-care products and wet wipes and may partly cross-react with chlorhexidine.
Plant- and animal-derived ingredients
The use of bonding glues that contain high concentrations of soluble (natural rubber) latex antigen has been increased for changing the length and style of hair. An anaphylactic death of a 28-year-old British fashion designer immediately following a hair extension procedure was explained by Pumphrey et al. The patient already had a history of nut allergy and inhalant atopy, and showed strong positive prick test reaction to natural rubber latex. Emollients and moisturizers are used in the cosmetic industry with plant protein derivatives (e.g. from soy, wheat, oat or sesame). Both allergic-contact dermatitis and immunological-contact uricaria resulting from the use of emollient creams containing oat extract have occurred. The patient later experienced an oral allergy syndrome when eating oat meal-containing biscuits and bread.
Many cases of IgE-mediated hypersensitivity to chestnut (Castanea sativa), a member of the Fagaceae family, were reported. Also, latex-fruit syndrome, in which ingestion of, for example, avocado, kiwi, banana [the latter a potential culprit in hair conditioners], and, less often, chestnut leads to urticaria and anaphylaxis in natural rubber latex-sensitised individuals. This syndrome is caused by cross-reactivity. A patient reacting to a cosmetic cream with delayed-type contact allergy to all dilutions of pure soybean extract, and also an immediate response to its 20% dilution, suggesting a possible type I hypersensitivity reaction was reported by Laurière M et al. Protein hydrolysates of collagen, keratin, elastin, milk, wheat, almond and silk, added to hair conditioners to 'repair' broken hair causes of contact urticaria. They produce reactions through a type 1 mechanism in atopic dermatitis patients. Leheron et al. even described IgE-mediated contact urticaria in a child caused by moisturising cream used by the mother, which contain hydrolysed wheat proteins and macadamia nuts.
Animal-derived protein allergens in cosmetics are also common. An immediate-type reaction to a fish-derived elastin-containing cosmetic cream in a patient with a history of respiratory distress when inhaling smoke from grilled fish, and a case of rhinitis, choking and systemic urticaria following the ingestion of egg in a patient who treated her hair weekly with a homemade egg-white-based mask are main examples in this perspective. Moreover, a case of immunological urticaria caused by a-lactalbumin from mare's milk containing cosmetic cream has also been reported. Katayama et al. reported the first case of contact urticaria syndrome (CUS) stage 3 caused by the use of honey for skincare treatment. Subiza et al. (143) presented seven hay fever patients who suffered from conjunctivitis; two of them also had angioedema of the lids after washing their eyes with chamomile tea, a folk remedy used to treat conjunctivitis and other ocular reactions. A similar case was reported by Foti et al., also with a positive prick test reaction to German chamomile (Matricaria chamomilla). Also, one case of contact utricaria caused by multiple components in a cosmetic skin mask was reported by West and Maibach; immediate open testing showed an extensive wheal-and-flare reaction to the whole egg.
Bindi or Kumkum
In India, due to various cultural and religious practices and traditional medicines, skin disorders are common. Bindi- or Kumkum-induced dermatitis is the most important among them. The terms kumkum and bindi overlap somewhat but are not synonymous. Kumkum is always applied with paste or powder and can cover the face or other parts of the body. Whereas a bindi can be paste or a sticker and is worn only between the eyes. Self-adhesive bindis (sticker bindis) are disposable substitutes for older liquid bindis, and are easy to apply. Kumkum is made of turmeric and slaked lime with colour-enhancing dyes. A study conducted by Ashwini et al., among 18 patients to identify the allergens causing kumkum-induced allergic contact dermatitis revealed that 14 patients had patch test positivity to kumkum and four had a negative reaction to kumkum. Patch test with other suspected contact allergens showed a positive reaction to turmeric in four patients, Sudan-1 in three patients and 4-aminoazobenzene in two patients. Among the allergens of the Indian Standard Series, positivity to nickel and fragrance mix was seen in five and two patients, respectively. Positive reaction to PPD, chlorocresol and parthenium was seen in one patient each.
Most allergic reactions to nail cosmetics are caused by toluene sulfonamide formaldehyde resin used in nail varnishes. Some of the other ingredients in nail varnishes, such as formaldehyde, nitrocellulose and other resins, among others, may also be a cause of dermatitis and urticaria although much less frequently.
Lip plumbers are used to increasing lip volume within minutes to days following their application. They act by vasodilatation secondary to either irritant contact dermatitis or non-immunological contact urticaria. Common ingredients used in the preparation are essential oils of cinnamon and cayenne pepper, which are classified as both irritants and urticants. Lee Wong M et al. reported a case of a young boy who developed an urticarial plaque of rapid onset on the right cheek. This was caused following a kiss from his mother after she had applied a lip plumper 1 h earlier. The active ingredients of this included benzyl nicotinate and C. frutescens resin.
Glycol peel are other cosmetic component that causes urticaria. Post-inflammatory hyperpigmentation, infections, scarring, allergic reactions, milia, persistent erythema and textural changes are its various complications. A case of contact urticaria limited to the area of contact with the glycolic acid peel in a patient with a history of severe acne vulgaris was revealed by Vishal et al.
Excipients, emulsifiers, surfactants and humectants
These are mainly used in topical pharmaceutical and cosmetic products. The contact allergens reported were rare cosmetic allergens, such as wool alcohols, fatty alcohols (e.g., cetyl alcohol) and propylene glycol. Also, dicaprylyl maleateisononyl isononanoate and trioley phosphate and the humectants butylenes glycol and pentylene glycol are considered to be more irritant and allergenic. Cocamidopropylbetaine is considered to be more irritant than allergenic though, and alkyl glucosides, that is, condensation products of fatty alcohols with glucose such as coco-and lauryl glucosides, which are often used as mild surfactants and cleansing agents, as well as emulsifiers, particularly cetearyl- and decyl glucoside, a hidden allergen in sunscreens causes contact urticaria. Moreover, other copolymers present in nail lacquers, and skin-care and sunscreen products have been reported as a cause of contact urticaria.
Permanent makeup and tattoos
Tattoos and permanent makeup are becoming popular in the modern world. The inks used in the tattoos have high prevalence in causing immediate skin reactions. A case of anaphylaxis with an immediate skin reaction to purple and blue ink was reported by Lee-Wong et al.
This review confirms that various cosmetic components cause contact urticaria with or without systemic symptoms. It includes fragrance, preservatives, hair care products, lip plumber, plant- and animal-derived products, nail cosmetics, glycol peel, permanent makeup and tattoos, etc. However, cases of contact urticaria might be more common but patients probably lack awareness. Therefore physicians should continue to look out for new possible causes. Anaphylactic reactions provoked by patch testing with the allergen are rare, but, in patients with a severe history of contact urticaria symptoms, the emergency measures remain necessary. The cosmetic components that cause contact urticaria should be monitored. Once the specific allergens causing urticaria are identified, the patient should be informed on which products can be safely used in the future.
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Conflicts of interest
There are no conflicts of interest.
|1||White IR, de Groot AC. Cosmetic and skin care products. In: Frosch PJ, Menné T, Lepoittevin JP, editors. Contact Dermatitis. 4th ed. Berlin: Springer; 2006. p. 493-506.|
|2||Lunder T, Kansky A. Increase in contact allergy to fragrances: Patch-test results 1989-1998. Contact Dermatitis 2000;43:107-9.|
|3||Thyssen JP, Linneberg A, Menné T, Nielsen NH, Johansen JD. The prevalence and morbidity of sensitization to fragrance mix I in the general population. Br J Dermatol 2009;161:95-101.|
|4||Wolf R, Wolf D, Tüzün B, Tüzün Y. Cosmetics and contact dermatitis. Dermatol Ther 2001;14:181-7.|
|5||Klimańska M, Żmudzińska M, Jenerowicz D, Czarnecka-Ope racz M. The importance of exposure to contact allergens in patients with allergic contact dermatitis. Postep Derm Alergol 2011;28:203-11.|
|6||Lathi A. Nonimmunologicalurticaria. In: Kanerva L, Elsner E, Wahlberg JE, Maibach HI, editors. Handbook of Occupational Dermatology. 1st ed, Chapter 26. Springer Verlag, Berlin-Heidelberg-New York; 2000. p. 221–4.|
|7||Ismail M, Maibach HI. Theclinical significance of immunological contact urticaria to processed grains. Contact Dermatitis 2012;78:591–4.|
|8||Aalto-Korte K, Mäkinen-Kiljunen S. Specific immune globulin E in patients with immediate persulfate hypersensitivity. Contact Dermatitis 2003;49:22–5.|
|9||Maibach HI, Engasser PG. Dermatitis due to cosmetits. Contact Dermatitis 1986;1:368-93.|
|10||Orton DI, Wilkinson JD. Cosmetic allergy: Incidence, diagnosis, and management. Am J Clin Dermatol 2004;5:327–37.|
|11||Uter W, Aberer W, Armario-Hita JC, Fernández-VozmedianoJM, Ayala F, Balato A, et al. Current patch test results withthe European baseline series and extensions to it from the European Surveillance System on Contact Allergy network, 2007-2008. Contact Dermatitis 2012;67:9-19.|
|12||Goossens AE. Sensitizing substances. In: Loden M, Maibach HI, editors. Dry Skin and Moisturizers: Chemistry and Function. Boca Raton, Fla, USA: CRC Press; 2006. p. 515–22.|
|13||Cancian M, Fortina AB, Peserico A. Contact urticaria syndrome from constituents of balsam of Peru and fragrance mix in a patient with chronic urticaria. Contact Dermatitis 1999;41:300.|
|14||Diba VC, Statham BN. Contac turticaria from cinnamal leading to anaphylaxis. Contact Dermatitis 2003;48:119.|
|15||Mathias T, Chappler R, Maibach HI. Contact urticaria from cinnamic aldehyde. Arch Dermatol 1980;116:74–6.|
|16||Johansen J, MenneT. The fragrance mix and its constituents: A 14-year material. Contact Dermatitis 1995;32:15-23.|
|17||Hendriks S, Ginkel C. Evaluation of the fragrance mix in the European Standard Series. Contact Dermatitis 2000;41:161-4.|
|18||Yamamoto A, Morita A, Tsuji T, Suzuki K, Matsunaga K. Contact urticaria fromgeraniol. Contact Dermatitis 2002;46:52.|
|19||Glaspole IN, deLeon MP, Rolland JM, O'Hehir RE. Anaphylaxis to lemon soap: Citrusseed and peanut allergen cross-reactivity. Ann Allergy Asthma Immunol 2007;98:286–9.|
|20||Rastogi S, Johansen J, Menne T. Natural ingredients based cosmetics. Content of selected fragrance sensitizers. Contact Dermatitis 1996;34:423.|
|21||Holmes G, Freeman S. Cheilitis caused by contact urticaria to mint flavoured toothpaste. Aust J Dermatol 2001;42:43–5.|
|22||Heydorn S, Johansen JD, Andersen KE, Bruze M, Svedman C, White IR, et al. Fragrance allergy in patients with hand eczema – A clinical study. Contact Dermatitis 2003;48:317-23.|
|23||Kiec-Świerczyńska M, Kręcisz B, Świerczyńska-Machura D. Contact allergy to para-(amino) compounds in European Standard Series [Polish]. Przegl Dermatol 2008;3:287-92.|
|24||Uter W, Yazar K, Kratz EM, Mildau G, Lidén C. Coupled exposure to ingredients of cosmetic products: preservatives. Contact Dermatitis 2014;70:219–26.|
|25||Lujan D, Hernandez-Machin B, Peñate Y, Borrego L. Contact urticaria due to phenoxy ethanolinan after shave. Dermatitis 2009;20:E10.|
|26||Birnie AJ, English JS. 2-Phenoxyethanol-inducedcontact urticaria. Contact Dermatitis 2006;54:349.|
|27||Munoz FJ, Bellido J, Moyano C, Alvarez M, Fonseca JL. Perioral contact urticaria from sodium benzoate in a toothpaste. Contact Dermatitis1996;35:51.|
|28||Walker SL, Chalmers RJ, Beck MH. Contact urticaria due to p-chloro-m-cresol. Br J Dermatol 2004;151:936–7.|
|29||Özkaya E, Bozkurt PK. An unusual case of triclosan-induced immunological contact urticaria. Contact Dermatitis 2013;68:117–28.|
|30||Śpiewak R. Contact allergy – diagnosis and treatment [Polish]. Alergia Astma Immunologia 2007;3:109-26.|
|31||Tanglertsampan C. Allergic contact dermatitis from formaldehyde with initially negative repeated open application test. Contact Dermatitis 2003;48:171-2.|
|32||Kiec-Świerczyńska M, Kręcisz B, Świerczyńska-Machura D. Contact allergy to para-(amino) compounds in European Standard Series [Polish]. Przegl Dermatol 2008;3:287-92.|
|33||Haluk Akar H, Adatepe S, Tahan F, Solmaz I. Hair dyes and temporary tattoos are areal hazard for adolescents? Eur Ann Allergy Clin Immunol 2014;46:35–7.|
|34||Tukenmez Demirci G, Kivanc Altunay I, Atis G, Kucukunal A. Allergic contact dermatitis mimicking angioedema due to paraphenylendiamine hypersensitivity: A case report. Cutan Ocul Toxicol 2012;31:250–2.|
|35||Vanden Broecke K, Bruze M, Persson L, Deroo H, Goossens A. Contact urticaria syndrome caused by direct hair dyes in a hairdresser. Contact Dermatitis 2014:71:108–28.|
|36||Estrada Rodríguez JL, Gozalo Reques F, Cechini Fernandez C, Rodríguez Prieto MA. Contact urticaria due to potassium persulfate. Contact Dermatitis 2001:45:177.|
|37||Yesudian PD, King CM. Severe contact urticaria and anaphylaxis from benzophenone-3 (2-hydroxy4-methoxy benzophenone). Contact Dermatitis 2002:46:55–6.|
|38||Saraswat A. Contact allergy to topical corticosteroids and sunscreens. Indian J Dermatol Venereol Leprol 2012;78:552-9.|
|39||Sasseville D, Moreau L, Al-Sowaidi M. Allergic contact dermatitis to idebenone used as an antioxidant in an antiwrinkle cream. Contact Dermatitis 2007;56:117–8.|
|40||Opstrup MS, Johansen JD, Bossi R, Lundov MD, Garvey LH. Chlorhexidine in cosmetic products – A marketsurvey. Contact Dermatitis 2015;72:55–8.|
|41||Pumphrey RS, Duddridge M, Norton J. Fatall at ex allergy. J Allergy Clin Immunol 2001;107:558.|
|42||Boussault P, Léauté-Labrèze C, Saubusse E, Maurice-Tison S, Perromat M, Roul S, et al. Oat sensitization in children with atopic dermatitis: Prevalence, risks and associated factors. Allergy 2007;62:1251–56.|
|43||Pecquet C, Lauriere M, Huet S, Leynadier F. Is the application of cosmetics containing protein-derived products safe? Contact Dermatitis 2002;46:123.|
|44||Laurière M, Pecquet C, Bouchez-Mahiout I, Snégaroff J, Bayrou O, Raison-Peyron N, et al. Hydrolysed wheat proteins present in cosmetics can induce immediate hypersensitivities. Contact Dermatitis 2006;54:283–9.|
|45||Leheron C, Thierry B, Marialice A, Giovannini C. Immediate contact urticaria caused by hydrolysed wheat proteins in a child via maternal skin contact sensitization. Contact Dermatitis 2016;68:379-80.|
|46||Katayama M, Inomata N, Inagawa N, Fukuro H, Aihara M. A case of contact urticaria syndrome stage 3 after honey ingestion, induced by epicutaneous sensitization during skin care with honey. Contact Dermatitis 2016;74:189-91.|
|47||Subiza J, Subiza J L, Alonso M. Allergic conjunctivitis to chamomile tea. Annals of Allergy 1990; 65:127– 32.|
|48||Fotis C, Nettis E, Panebianco R, Cassano N. Contact urticaria from Matricaria chamomilla. Contact Dermatitis 2000;42:360-61.|
|49||Verhulst L, Kerre S, Goossens A. The unsuspected power of mare's milk. Contact Dermatitis 2016;74:376–7.|
|50||Gupta D, Thappa DM. Dermatoses due to Indian cultural practices. Indian J Dermatol 2015;60:3-12.|
|51||Ashwini A, Priya S, Srinivas CR. Kumkum induced allergic contact dermatitis: Are we missing the actual culprit? 2018;84:153-6.|
|52||Constandt L, Hecke EV, Naeyaert JM, Goossens A. Screening for contact allergy to artiﬁcial nails. Contact Dermatitis 2005;52:73–7.|
|53||Lee-Wong M, Karagic M, Silverberg N. Anaphylactic reaction to permanent tattoo ink. Ann Allergy Asthma Immunol 2009;103:88–9.|
|54||Vishal B, Rao SS, Pavithra S, Shenoy MM. Contact urticaria to glycolic acid peel. J Cutan Aesthet Surg 2012;5:58–9.|
|55||Hervella M, Yanguas JI, Iglesias ME, Larrea M, Ros C, Gallego M. Alergia de contacto a 3-dimetilaminopropilaminay cocamidopropil betaína. Actas Dermosiﬁliogr 2006;97:189-95.|
|56||Schnuch A, Lessmann H, Geier J, Uter W. Is cocamidopropyl betaine a contact allergen? Analysis of network data and short review of the literature. Contact Dermatitis 2011;64:203-11.|
|57||Wakelin SH. Contact urticaria. Clin Exp Dermatol 2001;26:132–6.|
|58||Doutre MS. Occupational contact urticaria and protein contact dermatitis. Eur J Dermatol 2005;15:419–24.|
|59||Verhulst L, Goossens A. Cosmetic components causing contact urticaria: A review and update. Contact Dermatitis 2016;75: 333–44.|