Editor's Note: Please click on the small image of the tables to see a larger version.
Dermatitis of the scalp is considered scalp irritation when caused by the contact of chemical, physical or biological agents.
Allergic Contact Dermatitis (ACD) is an important disease that notably affects 14.5 million Americans each year.1 The economic impact of this disease is high in terms of both patient morbidity and loss of income, school and work, not to mention significant expenditures for visits to healthcare providers and for medicaments.1 In the consultation of the patient, other key players, such as irritant contact dermatitis (ICD) and contact urticaria, may be identified as the clinical problem, as history (not patch testing) can point to these as the correct diagnosis for the patient. Unlike ACD, ICD is not immune mediated, but occurs secondary to contact with an irritating or abrasive substance.
In this column, we highlight ACD, explore top relevant allergens, discuss regional-based dermatitis presentations, explore entities in the differential diagnoses and provide clinical tips and pearls for diagnosis and treatment. This month’s focus is scalp irritation syndromes.
Scalp Irritation: Acute (Burn), Sensory, Non-Immunologic Contact Urticaria and Cumulative
Throughout the ages, society has influenced hairstyle trends — crew cut, mohawk, straight vs. curly hair, hair coloring, etc. — which leaves the scalp exposed to different chemicals (eg, dyes, highlights, straightening agents, etc.), hair styling gadgets (eg, blow dryers, curling or straightening irons, etc.) and hair-care products (“rinse-off” or “leave-on” preparations). All of this may lead to scalp irritation.2
Dermatitis of the scalp3 caused by the contact of chemical, physical or a biological agent is called scalp irritation. Endogenous factors, such as impaired barrier function and pre-existing dermatitis, may also play a role.4 Its four clinical entities are: 1) acute (burn); 2) sensory; 3) non-immunologic contact urticaria (NICU); and 4) cumulative.
Severe, Acute Irritant Scalp Dermatitis (Chemical Burn)
Hair procedures such as hair highlighting and relaxing utilize chemicals that are highly caustic and may cause scalp irritation.5,6 The clinical manifestations include mild signs from erythema and blister formation and symptoms such as burning and tingling scalp sensations to severe, acute scalp irritant dermatitis, ie scalp burn,2,5,6 also called cosmetic alopecia.3
Highlighting
Chan and Maibach reviewed eight cases of hair highlighting that resulted in scalp burn. The cases involved three adults and five pediatric patients.5 The authors found that the scalp burns in these cases could have been caused by 1) inadvertent spillage of the heated chemicals (the highlighting mixture); 2) contact between the heated aluminum foil and the scalp; 3) incorrect concentration of hydrogen peroxide – it was proposed that the concentration of hydrogen peroxide (H2O2) used was higher than usual (ie, greater than the European Union’s [EU] European Economic Community [EEC] cosmetics directives permissible concentration of H2O2 12%); and 4) the toxic reaction to the chemicals (H2O2 and the persulfates).5,7-12 The first three causes are presumed to be caused by, primarily, faulty practices of the hair dresser, including: 1) improper folding/positioning of the foil, resulting in spillage; 2) too much dye in the highlight mixture, resulting in over spillage; 3) improper positioning of the heated foil, thus allowing it to touch the scalp; 4) blow drying at a slightly higher temperature; 5) incorrect concentration of chemicals used; and/or 6) improper procedure.5,7-12 The fourth cause may be related to permissible levels of highlighting chemicals being set too high by the cosmetic regulatory bodies of the FDA and the EU EEC cosmetics directives.5
All cases were managed medically and surgically and resulted in scarring alopecia. It is noteworthy that, clinically, there is a psycho-social impact as well, as there was unnecessary pain and embarrassment to the eight patients, especially the five in the pediatric age group. Because hair dressers presumably play a role in the occurrence of scalp burns,13 it is of utmost importance that they be educated in not only the caustic nature of the highlighting chemicals but that they also receive proper hands-on training of technique.
Relaxation Of The Hair
Another hair substance that may result in scalp burns is the hair relaxer, which is classified into two groups: “lye” (mostly sodium hydroxide) and “no-lye” (mostly guanidine hydroxide).6 Adverse effects of hair relaxers are irritant contact dermatitis14 and hair breakage with alopecia (with or without scarring).15-16
Khumalo et al reported the cases of five women of African descent with a history of scalp discomfort that started during or within minutes of a salon hair relaxation procedure. The discomfort lasted for a few days and healed with scarring alopecia, specifically central centrifugal cicatricial alopecia (CCCA).6 “No lye” hair relaxer was used for two women and “lye” containing relaxer was utilized for the other three. Poor skills of the hairdresser, such as relaxers that were applied for longer than recommended, and overuse of the products by clients, including having hair relaxed more frequently than the recommended period of 6 to 8 weeks, were found to be causative factors.6
Other etiologic factors for scarring alopecia during the relaxer procedure that have been discussed, but are much less likely, include: 1) irritant contact dermatitis;14 2) incorrect product formulation; and 3) poor salon facilities (eg, lack of running water). Public education is needed to help clarify the possibility of product-associated CCCA. The frequent correlation of insidious onset of CCCA and scalp burn to hair relaxers necessitates further investigation to establish a clear-cut pathogenesis of each condition.6 Because of the marked damage caused by acute scalp burns, detailed investigation is necessitated and should be able to be modeled in vitro.
Severe Scalp Allergic Dermatitis
Hair dye ingredients, such as the oxidative hair dyes, have been shown to cause irritation and have been regarded as “notorious allergens.”17 In fact, p-Phenylenediamine (PPD) has been documented to cause anaphylaxis in addition to ACD and ICD.18 Clinical manifestations include erythema, edema, vesicles and fissuring.19 Table 1 (left) lists the hair dye chemicals that can cause ACD. History can prove very useful in differentiating this entity from the scalp irritation syndrome group.
Sensory Irritation Of The Scalp
Itching, stinging, burning or tingling sensations of the scalp upon contact with certain chemicals in the absence of clinical signs describe sensory irritation. The subjective symptoms that occur within seconds to minutes of chemical exposure are reproducible.20 To date, a significant number 
of chemicals have been recalled by patients to be causative, with hair dyes leading the list. See Table 2. Even if the pathomechanism of sensory irritation is unknown, variables such as the quality of the chemical and concentration affect the outcome.20 Neural pathways may also play a role.20 The lactic acid stinging test (LAST) is used to study this type of irritation and is based on self-perceived assessment.20,21 Therefore, the threshold for this reaction differs between patients.20
The use of oxidative hair dyes such as hydrogen peroxide and strong alkalis has resulted in sensory irritation of the face and scalp.22 A self-assessment questionnaire was utilized by Fujita et al to measure sensory irritation in various regions of the body caused by two model hair-dye bases that contained different amounts of alkali agents without dyes.22 The occipital region was found as an alternative area of the scalp to test for sensory irritation of the hair dye bases. Scalp sensitivity in relation to skin properties such as stratum corneum water content, transepidermal water loss (TEWL), sebum level, surface temperature, current perception threshold (CPT), catalase activities in tape-stripped skin and sensory irritation score with the model hair-dye bases were evaluated. The hair-dye sensitive group showed higher TEWL, lower sebum, lower surface temperature and higher catalase activity than the insensitive group and was similar to that of damaged skin. This study suggests that sensory irritation caused by hair dye could occur easily on the damaged dry scalp, as it has previously been reported to be caused by skin cosmetics.22
Non-Immunologic Contact Urticaria (Nicu) Of The Scalp
A frequent type of immediate contact reaction that occurs without prior sensitization defines non-immunologic contact urticaria (NICU).23 Examples of compounds that have resulted in NICU are plant and animal products, food, medicaments, fragrances and preservatives.23,24 Symptoms vary according to different anatomic sites.23,34 One study reported marked variation in susceptibility to NICU agents, with the most sensitive area being the face, followed by the antecubital fossa, upper back, upper arm, volar forearm and lower back.25
The reactivity of the scalp, face and back to the non-immunologic urticants benzoic acid (BN) and hexyl nicotinate (HN) was compared by Zhai et al to ascertain relative responsiveness in 10 ‘bald’ men.26 Reactivity was assessed by visual scores (VS), visual analogue scale (VAS) and biophysical instruments at baseline, 15, 30 and 60 minutes post-application. Three concentrations each of BN and HN were applied to the nasolabial fold, back and scalp on one side, and placebo on the contralateral side. The upper back significantly (P<0.05) exceeded scalp in VS scores at 0.25% HN application; the back further showed a significantly (P<0.05) stronger reaction 60 minutes after application. On the other hand, at 2.5% BA site, VS of the face exhibited a significantly (P<0.05) higher reaction than the back at 15 minutes post-application. However, with 0.625% BA site, VS of the back was significantly (P<0.05) higher than the face. For the parametric data obtained from the biophysical measurements scoring for erythema, the a* was significantly (P<0.05) higher in the face. Percutaneous penetration studies might help explain these results, as different anatomic sites might have different diffusion pathways.27,28
Cumulative Irritation of the Scalp
Scalp irritation that occurs after repetitive application (days to weeks or even years) is referred to as cumulative irritation of the scalp.20 Relatively few studies have been performed to demonstrate cumulative irritancy potential of scalp products because the scalp does not readily show erythema. The authors suspect this arena justifies closer examination based on consumer complaints. The 21-day cumulative irritancy and comparative back-scalp studies might also yield insight into this neglected field.
Pearls of Treatment
The cases of severe acute scalp irritant dermatitis (chemical burn) discussed above were treated medically and surgically.5,7-12 Medical treatments include proper wound care and controlling for infection by giving appropriate oral antibiotics.5,7-12 Surgical intervention was, at times, necessary to improve the cosmesis of the scarred area, including skin grafting and/or scalp reduction to the burnt area.5,7-12
As mentioned above, the LAST and the self-assessment questionnaire are the methods used to determine sensory irritation of the scalp.20,22 Because of the lack of objective signs, this clinical entity is quite difficult to assess.29 Patch testing of hair chemicals does not play a role. The best management is avoidance of substances that has previously caused sensory scalp irritation. That being said, since no objective signs are clinically evident in this state, topical ‘counter irritant’ agents such as benzoin resin, camphor, capsaicin and methyl salicilate (which may leave liniment residue) should be used with caution, as they could complicate the clinical picture by increasing erythema. Antihistamines have shown to be ineffective, as no increased levels of histamine were observed. The lower sebum amount and higher TEWL suggest damage to the skin, for which lipid emollient therapy could be of benefit; however, more studies are needed.
Although the mechanism of NICU reaction is not well understood, prostaglandin — and not histamine — was found to mediate NICU reactions.24 Aspirin and non-steroidal anti-inflammatory agents like ibrupofen inhibited the NICU agents such as dimethyl sulfoxide, benzoic acid, cinnamic acid, cinnamic aldehyde or methyl nicotinate.30 UV therapy was also found to be effective in inhibiting NICU reactions.31 UVA and UVB irradiation inhibits the NICU reaction for at least 2 weeks. This inhibition also includes areas of the skin that were sheltered from irradiation, suggesting a systemic effect.31
Lastly, cumulative irritation of the scalp is characterized by squamous plaques (thickening and scaling). Hence, it is best managed with the use of short-term interference of topical corticosteroids.2
Drs. Chan and Zhai are with the University of California San Francisco (UCSF) Department of Dermatology. Dr. Maibach is a Professor in the UCSF Department of Dermatology.
Dr. Jacob, the Section Editor of Allergen Focus, is Associate Clinical Professor of Medicine and Pediatrics WOS (Dermatology) at the University of California, San Diego.
Disclosure: Dr. Jacob is the principal investigator for Smartchoice USA PREA-2 trial.
Editor's Note: Please click on the small image of the tables to see a larger version.
Dermatitis of the scalp is considered scalp irritation when caused by the contact of chemical, physical or biological agents.
Allergic Contact Dermatitis (ACD) is an important disease that notably affects 14.5 million Americans each year.1 The economic impact of this disease is high in terms of both patient morbidity and loss of income, school and work, not to mention significant expenditures for visits to healthcare providers and for medicaments.1 In the consultation of the patient, other key players, such as irritant contact dermatitis (ICD) and contact urticaria, may be identified as the clinical problem, as history (not patch testing) can point to these as the correct diagnosis for the patient. Unlike ACD, ICD is not immune mediated, but occurs secondary to contact with an irritating or abrasive substance.
In this column, we highlight ACD, explore top relevant allergens, discuss regional-based dermatitis presentations, explore entities in the differential diagnoses and provide clinical tips and pearls for diagnosis and treatment. This month’s focus is scalp irritation syndromes.
Scalp Irritation: Acute (Burn), Sensory, Non-Immunologic Contact Urticaria and Cumulative
Throughout the ages, society has influenced hairstyle trends — crew cut, mohawk, straight vs. curly hair, hair coloring, etc. — which leaves the scalp exposed to different chemicals (eg, dyes, highlights, straightening agents, etc.), hair styling gadgets (eg, blow dryers, curling or straightening irons, etc.) and hair-care products (“rinse-off” or “leave-on” preparations). All of this may lead to scalp irritation.2
Dermatitis of the scalp3 caused by the contact of chemical, physical or a biological agent is called scalp irritation. Endogenous factors, such as impaired barrier function and pre-existing dermatitis, may also play a role.4 Its four clinical entities are: 1) acute (burn); 2) sensory; 3) non-immunologic contact urticaria (NICU); and 4) cumulative.
Severe, Acute Irritant Scalp Dermatitis (Chemical Burn)
Hair procedures such as hair highlighting and relaxing utilize chemicals that are highly caustic and may cause scalp irritation.5,6 The clinical manifestations include mild signs from erythema and blister formation and symptoms such as burning and tingling scalp sensations to severe, acute scalp irritant dermatitis, ie scalp burn,2,5,6 also called cosmetic alopecia.3
Highlighting
Chan and Maibach reviewed eight cases of hair highlighting that resulted in scalp burn. The cases involved three adults and five pediatric patients.5 The authors found that the scalp burns in these cases could have been caused by 1) inadvertent spillage of the heated chemicals (the highlighting mixture); 2) contact between the heated aluminum foil and the scalp; 3) incorrect concentration of hydrogen peroxide – it was proposed that the concentration of hydrogen peroxide (H2O2) used was higher than usual (ie, greater than the European Union’s [EU] European Economic Community [EEC] cosmetics directives permissible concentration of H2O2 12%); and 4) the toxic reaction to the chemicals (H2O2 and the persulfates).5,7-12 The first three causes are presumed to be caused by, primarily, faulty practices of the hair dresser, including: 1) improper folding/positioning of the foil, resulting in spillage; 2) too much dye in the highlight mixture, resulting in over spillage; 3) improper positioning of the heated foil, thus allowing it to touch the scalp; 4) blow drying at a slightly higher temperature; 5) incorrect concentration of chemicals used; and/or 6) improper procedure.5,7-12 The fourth cause may be related to permissible levels of highlighting chemicals being set too high by the cosmetic regulatory bodies of the FDA and the EU EEC cosmetics directives.5
All cases were managed medically and surgically and resulted in scarring alopecia. It is noteworthy that, clinically, there is a psycho-social impact as well, as there was unnecessary pain and embarrassment to the eight patients, especially the five in the pediatric age group. Because hair dressers presumably play a role in the occurrence of scalp burns,13 it is of utmost importance that they be educated in not only the caustic nature of the highlighting chemicals but that they also receive proper hands-on training of technique.
Relaxation Of The Hair
Another hair substance that may result in scalp burns is the hair relaxer, which is classified into two groups: “lye” (mostly sodium hydroxide) and “no-lye” (mostly guanidine hydroxide).6 Adverse effects of hair relaxers are irritant contact dermatitis14 and hair breakage with alopecia (with or without scarring).15-16
Khumalo et al reported the cases of five women of African descent with a history of scalp discomfort that started during or within minutes of a salon hair relaxation procedure. The discomfort lasted for a few days and healed with scarring alopecia, specifically central centrifugal cicatricial alopecia (CCCA).6 “No lye” hair relaxer was used for two women and “lye” containing relaxer was utilized for the other three. Poor skills of the hairdresser, such as relaxers that were applied for longer than recommended, and overuse of the products by clients, including having hair relaxed more frequently than the recommended period of 6 to 8 weeks, were found to be causative factors.6
Other etiologic factors for scarring alopecia during the relaxer procedure that have been discussed, but are much less likely, include: 1) irritant contact dermatitis;14 2) incorrect product formulation; and 3) poor salon facilities (eg, lack of running water). Public education is needed to help clarify the possibility of product-associated CCCA. The frequent correlation of insidious onset of CCCA and scalp burn to hair relaxers necessitates further investigation to establish a clear-cut pathogenesis of each condition.6 Because of the marked damage caused by acute scalp burns, detailed investigation is necessitated and should be able to be modeled in vitro.
Severe Scalp Allergic Dermatitis
Hair dye ingredients, such as the oxidative hair dyes, have been shown to cause irritation and have been regarded as “notorious allergens.”17 In fact, p-Phenylenediamine (PPD) has been documented to cause anaphylaxis in addition to ACD and ICD.18 Clinical manifestations include erythema, edema, vesicles and fissuring.19 Table 1 (left) lists the hair dye chemicals that can cause ACD. History can prove very useful in differentiating this entity from the scalp irritation syndrome group.
Sensory Irritation Of The Scalp
Itching, stinging, burning or tingling sensations of the scalp upon contact with certain chemicals in the absence of clinical signs describe sensory irritation. The subjective symptoms that occur within seconds to minutes of chemical exposure are reproducible.20 To date, a significant number 
of chemicals have been recalled by patients to be causative, with hair dyes leading the list. See Table 2. Even if the pathomechanism of sensory irritation is unknown, variables such as the quality of the chemical and concentration affect the outcome.20 Neural pathways may also play a role.20 The lactic acid stinging test (LAST) is used to study this type of irritation and is based on self-perceived assessment.20,21 Therefore, the threshold for this reaction differs between patients.20
The use of oxidative hair dyes such as hydrogen peroxide and strong alkalis has resulted in sensory irritation of the face and scalp.22 A self-assessment questionnaire was utilized by Fujita et al to measure sensory irritation in various regions of the body caused by two model hair-dye bases that contained different amounts of alkali agents without dyes.22 The occipital region was found as an alternative area of the scalp to test for sensory irritation of the hair dye bases. Scalp sensitivity in relation to skin properties such as stratum corneum water content, transepidermal water loss (TEWL), sebum level, surface temperature, current perception threshold (CPT), catalase activities in tape-stripped skin and sensory irritation score with the model hair-dye bases were evaluated. The hair-dye sensitive group showed higher TEWL, lower sebum, lower surface temperature and higher catalase activity than the insensitive group and was similar to that of damaged skin. This study suggests that sensory irritation caused by hair dye could occur easily on the damaged dry scalp, as it has previously been reported to be caused by skin cosmetics.22
Non-Immunologic Contact Urticaria (Nicu) Of The Scalp
A frequent type of immediate contact reaction that occurs without prior sensitization defines non-immunologic contact urticaria (NICU).23 Examples of compounds that have resulted in NICU are plant and animal products, food, medicaments, fragrances and preservatives.23,24 Symptoms vary according to different anatomic sites.23,34 One study reported marked variation in susceptibility to NICU agents, with the most sensitive area being the face, followed by the antecubital fossa, upper back, upper arm, volar forearm and lower back.25
The reactivity of the scalp, face and back to the non-immunologic urticants benzoic acid (BN) and hexyl nicotinate (HN) was compared by Zhai et al to ascertain relative responsiveness in 10 ‘bald’ men.26 Reactivity was assessed by visual scores (VS), visual analogue scale (VAS) and biophysical instruments at baseline, 15, 30 and 60 minutes post-application. Three concentrations each of BN and HN were applied to the nasolabial fold, back and scalp on one side, and placebo on the contralateral side. The upper back significantly (P<0.05) exceeded scalp in VS scores at 0.25% HN application; the back further showed a significantly (P<0.05) stronger reaction 60 minutes after application. On the other hand, at 2.5% BA site, VS of the face exhibited a significantly (P<0.05) higher reaction than the back at 15 minutes post-application. However, with 0.625% BA site, VS of the back was significantly (P<0.05) higher than the face. For the parametric data obtained from the biophysical measurements scoring for erythema, the a* was significantly (P<0.05) higher in the face. Percutaneous penetration studies might help explain these results, as different anatomic sites might have different diffusion pathways.27,28
Cumulative Irritation of the Scalp
Scalp irritation that occurs after repetitive application (days to weeks or even years) is referred to as cumulative irritation of the scalp.20 Relatively few studies have been performed to demonstrate cumulative irritancy potential of scalp products because the scalp does not readily show erythema. The authors suspect this arena justifies closer examination based on consumer complaints. The 21-day cumulative irritancy and comparative back-scalp studies might also yield insight into this neglected field.
Pearls of Treatment
The cases of severe acute scalp irritant dermatitis (chemical burn) discussed above were treated medically and surgically.5,7-12 Medical treatments include proper wound care and controlling for infection by giving appropriate oral antibiotics.5,7-12 Surgical intervention was, at times, necessary to improve the cosmesis of the scarred area, including skin grafting and/or scalp reduction to the burnt area.5,7-12
As mentioned above, the LAST and the self-assessment questionnaire are the methods used to determine sensory irritation of the scalp.20,22 Because of the lack of objective signs, this clinical entity is quite difficult to assess.29 Patch testing of hair chemicals does not play a role. The best management is avoidance of substances that has previously caused sensory scalp irritation. That being said, since no objective signs are clinically evident in this state, topical ‘counter irritant’ agents such as benzoin resin, camphor, capsaicin and methyl salicilate (which may leave liniment residue) should be used with caution, as they could complicate the clinical picture by increasing erythema. Antihistamines have shown to be ineffective, as no increased levels of histamine were observed. The lower sebum amount and higher TEWL suggest damage to the skin, for which lipid emollient therapy could be of benefit; however, more studies are needed.
Although the mechanism of NICU reaction is not well understood, prostaglandin — and not histamine — was found to mediate NICU reactions.24 Aspirin and non-steroidal anti-inflammatory agents like ibrupofen inhibited the NICU agents such as dimethyl sulfoxide, benzoic acid, cinnamic acid, cinnamic aldehyde or methyl nicotinate.30 UV therapy was also found to be effective in inhibiting NICU reactions.31 UVA and UVB irradiation inhibits the NICU reaction for at least 2 weeks. This inhibition also includes areas of the skin that were sheltered from irradiation, suggesting a systemic effect.31
Lastly, cumulative irritation of the scalp is characterized by squamous plaques (thickening and scaling). Hence, it is best managed with the use of short-term interference of topical corticosteroids.2
Drs. Chan and Zhai are with the University of California San Francisco (UCSF) Department of Dermatology. Dr. Maibach is a Professor in the UCSF Department of Dermatology.
Dr. Jacob, the Section Editor of Allergen Focus, is Associate Clinical Professor of Medicine and Pediatrics WOS (Dermatology) at the University of California, San Diego.
Disclosure: Dr. Jacob is the principal investigator for Smartchoice USA PREA-2 trial.
Editor's Note: Please click on the small image of the tables to see a larger version.
Dermatitis of the scalp is considered scalp irritation when caused by the contact of chemical, physical or biological agents.
Allergic Contact Dermatitis (ACD) is an important disease that notably affects 14.5 million Americans each year.1 The economic impact of this disease is high in terms of both patient morbidity and loss of income, school and work, not to mention significant expenditures for visits to healthcare providers and for medicaments.1 In the consultation of the patient, other key players, such as irritant contact dermatitis (ICD) and contact urticaria, may be identified as the clinical problem, as history (not patch testing) can point to these as the correct diagnosis for the patient. Unlike ACD, ICD is not immune mediated, but occurs secondary to contact with an irritating or abrasive substance.
In this column, we highlight ACD, explore top relevant allergens, discuss regional-based dermatitis presentations, explore entities in the differential diagnoses and provide clinical tips and pearls for diagnosis and treatment. This month’s focus is scalp irritation syndromes.
Scalp Irritation: Acute (Burn), Sensory, Non-Immunologic Contact Urticaria and Cumulative
Throughout the ages, society has influenced hairstyle trends — crew cut, mohawk, straight vs. curly hair, hair coloring, etc. — which leaves the scalp exposed to different chemicals (eg, dyes, highlights, straightening agents, etc.), hair styling gadgets (eg, blow dryers, curling or straightening irons, etc.) and hair-care products (“rinse-off” or “leave-on” preparations). All of this may lead to scalp irritation.2
Dermatitis of the scalp3 caused by the contact of chemical, physical or a biological agent is called scalp irritation. Endogenous factors, such as impaired barrier function and pre-existing dermatitis, may also play a role.4 Its four clinical entities are: 1) acute (burn); 2) sensory; 3) non-immunologic contact urticaria (NICU); and 4) cumulative.
Severe, Acute Irritant Scalp Dermatitis (Chemical Burn)
Hair procedures such as hair highlighting and relaxing utilize chemicals that are highly caustic and may cause scalp irritation.5,6 The clinical manifestations include mild signs from erythema and blister formation and symptoms such as burning and tingling scalp sensations to severe, acute scalp irritant dermatitis, ie scalp burn,2,5,6 also called cosmetic alopecia.3
Highlighting
Chan and Maibach reviewed eight cases of hair highlighting that resulted in scalp burn. The cases involved three adults and five pediatric patients.5 The authors found that the scalp burns in these cases could have been caused by 1) inadvertent spillage of the heated chemicals (the highlighting mixture); 2) contact between the heated aluminum foil and the scalp; 3) incorrect concentration of hydrogen peroxide – it was proposed that the concentration of hydrogen peroxide (H2O2) used was higher than usual (ie, greater than the European Union’s [EU] European Economic Community [EEC] cosmetics directives permissible concentration of H2O2 12%); and 4) the toxic reaction to the chemicals (H2O2 and the persulfates).5,7-12 The first three causes are presumed to be caused by, primarily, faulty practices of the hair dresser, including: 1) improper folding/positioning of the foil, resulting in spillage; 2) too much dye in the highlight mixture, resulting in over spillage; 3) improper positioning of the heated foil, thus allowing it to touch the scalp; 4) blow drying at a slightly higher temperature; 5) incorrect concentration of chemicals used; and/or 6) improper procedure.5,7-12 The fourth cause may be related to permissible levels of highlighting chemicals being set too high by the cosmetic regulatory bodies of the FDA and the EU EEC cosmetics directives.5
All cases were managed medically and surgically and resulted in scarring alopecia. It is noteworthy that, clinically, there is a psycho-social impact as well, as there was unnecessary pain and embarrassment to the eight patients, especially the five in the pediatric age group. Because hair dressers presumably play a role in the occurrence of scalp burns,13 it is of utmost importance that they be educated in not only the caustic nature of the highlighting chemicals but that they also receive proper hands-on training of technique.
Relaxation Of The Hair
Another hair substance that may result in scalp burns is the hair relaxer, which is classified into two groups: “lye” (mostly sodium hydroxide) and “no-lye” (mostly guanidine hydroxide).6 Adverse effects of hair relaxers are irritant contact dermatitis14 and hair breakage with alopecia (with or without scarring).15-16
Khumalo et al reported the cases of five women of African descent with a history of scalp discomfort that started during or within minutes of a salon hair relaxation procedure. The discomfort lasted for a few days and healed with scarring alopecia, specifically central centrifugal cicatricial alopecia (CCCA).6 “No lye” hair relaxer was used for two women and “lye” containing relaxer was utilized for the other three. Poor skills of the hairdresser, such as relaxers that were applied for longer than recommended, and overuse of the products by clients, including having hair relaxed more frequently than the recommended period of 6 to 8 weeks, were found to be causative factors.6
Other etiologic factors for scarring alopecia during the relaxer procedure that have been discussed, but are much less likely, include: 1) irritant contact dermatitis;14 2) incorrect product formulation; and 3) poor salon facilities (eg, lack of running water). Public education is needed to help clarify the possibility of product-associated CCCA. The frequent correlation of insidious onset of CCCA and scalp burn to hair relaxers necessitates further investigation to establish a clear-cut pathogenesis of each condition.6 Because of the marked damage caused by acute scalp burns, detailed investigation is necessitated and should be able to be modeled in vitro.
Severe Scalp Allergic Dermatitis
Hair dye ingredients, such as the oxidative hair dyes, have been shown to cause irritation and have been regarded as “notorious allergens.”17 In fact, p-Phenylenediamine (PPD) has been documented to cause anaphylaxis in addition to ACD and ICD.18 Clinical manifestations include erythema, edema, vesicles and fissuring.19 Table 1 (left) lists the hair dye chemicals that can cause ACD. History can prove very useful in differentiating this entity from the scalp irritation syndrome group.
Sensory Irritation Of The Scalp
Itching, stinging, burning or tingling sensations of the scalp upon contact with certain chemicals in the absence of clinical signs describe sensory irritation. The subjective symptoms that occur within seconds to minutes of chemical exposure are reproducible.20 To date, a significant number of chemicals have been recalled by patients to be causative, with hair dyes leading the list. See Table 2. Even if the pathomechanism of sensory irritation is unknown, variables such as the quality of the chemical and concentration affect the outcome.20 Neural pathways may also play a role.20 The lactic acid stinging test (LAST) is used to study this type of irritation and is based on self-perceived assessment.20,21 Therefore, the threshold for this reaction differs between patients.20
The use of oxidative hair dyes such as hydrogen peroxide and strong alkalis has resulted in sensory irritation of the face and scalp.22 A self-assessment questionnaire was utilized by Fujita et al to measure sensory irritation in various regions of the body caused by two model hair-dye bases that contained different amounts of alkali agents without dyes.22 The occipital region was found as an alternative area of the scalp to test for sensory irritation of the hair dye bases. Scalp sensitivity in relation to skin properties such as stratum corneum water content, transepidermal water loss (TEWL), sebum level, surface temperature, current perception threshold (CPT), catalase activities in tape-stripped skin and sensory irritation score with the model hair-dye bases were evaluated. The hair-dye sensitive group showed higher TEWL, lower sebum, lower surface temperature and higher catalase activity than the insensitive group and was similar to that of damaged skin. This study suggests that sensory irritation caused by hair dye could occur easily on the damaged dry scalp, as it has previously been reported to be caused by skin cosmetics.22
Non-Immunologic Contact Urticaria (Nicu) Of The Scalp
A frequent type of immediate contact reaction that occurs without prior sensitization defines non-immunologic contact urticaria (NICU).23 Examples of compounds that have resulted in NICU are plant and animal products, food, medicaments, fragrances and preservatives.23,24 Symptoms vary according to different anatomic sites.23,34 One study reported marked variation in susceptibility to NICU agents, with the most sensitive area being the face, followed by the antecubital fossa, upper back, upper arm, volar forearm and lower back.25
The reactivity of the scalp, face and back to the non-immunologic urticants benzoic acid (BN) and hexyl nicotinate (HN) was compared by Zhai et al to ascertain relative responsiveness in 10 ‘bald’ men.26 Reactivity was assessed by visual scores (VS), visual analogue scale (VAS) and biophysical instruments at baseline, 15, 30 and 60 minutes post-application. Three concentrations each of BN and HN were applied to the nasolabial fold, back and scalp on one side, and placebo on the contralateral side. The upper back significantly (P<0.05) exceeded scalp in VS scores at 0.25% HN application; the back further showed a significantly (P<0.05) stronger reaction 60 minutes after application. On the other hand, at 2.5% BA site, VS of the face exhibited a significantly (P<0.05) higher reaction than the back at 15 minutes post-application. However, with 0.625% BA site, VS of the back was significantly (P<0.05) higher than the face. For the parametric data obtained from the biophysical measurements scoring for erythema, the a* was significantly (P<0.05) higher in the face. Percutaneous penetration studies might help explain these results, as different anatomic sites might have different diffusion pathways.27,28
Cumulative Irritation of the Scalp
Scalp irritation that occurs after repetitive application (days to weeks or even years) is referred to as cumulative irritation of the scalp.20 Relatively few studies have been performed to demonstrate cumulative irritancy potential of scalp products because the scalp does not readily show erythema. The authors suspect this arena justifies closer examination based on consumer complaints. The 21-day cumulative irritancy and comparative back-scalp studies might also yield insight into this neglected field.
Pearls of Treatment
The cases of severe acute scalp irritant dermatitis (chemical burn) discussed above were treated medically and surgically.5,7-12 Medical treatments include proper wound care and controlling for infection by giving appropriate oral antibiotics.5,7-12 Surgical intervention was, at times, necessary to improve the cosmesis of the scarred area, including skin grafting and/or scalp reduction to the burnt area.5,7-12
As mentioned above, the LAST and the self-assessment questionnaire are the methods used to determine sensory irritation of the scalp.20,22 Because of the lack of objective signs, this clinical entity is quite difficult to assess.29 Patch testing of hair chemicals does not play a role. The best management is avoidance of substances that has previously caused sensory scalp irritation. That being said, since no objective signs are clinically evident in this state, topical ‘counter irritant’ agents such as benzoin resin, camphor, capsaicin and methyl salicilate (which may leave liniment residue) should be used with caution, as they could complicate the clinical picture by increasing erythema. Antihistamines have shown to be ineffective, as no increased levels of histamine were observed. The lower sebum amount and higher TEWL suggest damage to the skin, for which lipid emollient therapy could be of benefit; however, more studies are needed.
Although the mechanism of NICU reaction is not well understood, prostaglandin — and not histamine — was found to mediate NICU reactions.24 Aspirin and non-steroidal anti-inflammatory agents like ibrupofen inhibited the NICU agents such as dimethyl sulfoxide, benzoic acid, cinnamic acid, cinnamic aldehyde or methyl nicotinate.30 UV therapy was also found to be effective in inhibiting NICU reactions.31 UVA and UVB irradiation inhibits the NICU reaction for at least 2 weeks. This inhibition also includes areas of the skin that were sheltered from irradiation, suggesting a systemic effect.31
Lastly, cumulative irritation of the scalp is characterized by squamous plaques (thickening and scaling). Hence, it is best managed with the use of short-term interference of topical corticosteroids.2
Drs. Chan and Zhai are with the University of California San Francisco (UCSF) Department of Dermatology. Dr. Maibach is a Professor in the UCSF Department of Dermatology.
Dr. Jacob, the Section Editor of Allergen Focus, is Associate Clinical Professor of Medicine and Pediatrics WOS (Dermatology) at the University of California, San Diego.
Disclosure: Dr. Jacob is the principal investigator for Smartchoice USA PREA-2 trial.
Hair dye ingredients, such as the oxidative hair dyes, have been shown to cause irritation and have been regarded as “notorious allergens.”17 In fact, p-Phenylenediamine (PPD) has been documented to cause anaphylaxis in addition to ACD and ICD.18 Clinical manifestations include erythema, edema, vesicles and fissuring.19 Table 1 (left) lists the hair dye chemicals that can cause ACD. History can prove very useful in differentiating this entity from the scalp irritation syndrome group.
of chemicals have been recalled by patients to be causative, with hair dyes leading the list. See Table 2. Even if the pathomechanism of sensory irritation is unknown, variables such as the quality of the chemical and concentration affect the outcome.20 Neural pathways may also play a role.20 The lactic acid stinging test (LAST) is used to study this type of irritation and is based on self-perceived assessment.20,21 Therefore, the threshold for this reaction differs between patients.20
