Hair Dye Ingredients and Potential Health Risks from Exposure to Hair Dyeing (2024)

Given the worldwidepopularity of hair dyeing, there is an urgentneed to understand the toxicities and risks associated with exposureto chemicals found in hair dye formulations. Hair dyes are categorizedas oxidative and nonoxidative in terms of their chemical compositionand ingredients. For several decades, the expert panel’s CosmeticIngredient Review (CIR) has assessed the safety of many of the chemicalsused in hair dyes; however, a comprehensive review of hair dye ingredientsand the risk of exposure to hair dyeing has not been documented. Herein,we review the safety of the various chemicals in oxidative and nonoxidativehair dyes, toxicities associated with hair dyeing, and the carcinogenicrisks related to hair dyeing. While many compounds are consideredsafe for users at the concentrations in hair dyes, there are conflictingdata about a large number of hair dye formulations. The CIR expertpanel has ratified a number of coloring ingredients for hair dyesand banned a series of chemicals as carcinogenic to animals and unsafefor this application. The use of these chemicals as raw materialsfor producing hair dyes may result in the synthesis of other contaminantswith potential toxicities and increased risk of carcinogenesis. Itis an open question whether personal or occupational hair dyeing increasesthe risk of cancer; however, in specific subpopulations, a positiveassociation between hair dye use and cancer occurrence has been reported.To address this question, a better understanding of the chemical andmechanistic basis of the reported toxicities of hair dye mixturesand individual hair dye ingredients is needed. It is anticipated thatin-depth chemical and systems toxicology studies harnessing modernand emerging techniques can shed light on this public health concernin the future.

Table 1

2.1. Hair Dye Categories

The chemicalingredients of hair dyes vary among formulations that involve oxidativereactions to achieve coloring and those using nonoxidative processes.² Temporary and semipermanent hair dyes typicallyrely on nonoxidative processes, while permanent hair dyes rely onoxidative reactions (Table 1). Temporary hair dyes are composed of water-soluble acidicand basic dyes bearing azo or anthraquinone groups; they are generallyregarded as more benign because they are deposited on the hair surfaceand do not penetrate into the hair cortex. They do not require anoxidizing agent and are typically removed by a single shampooing.^3,4 Semipermanent hair dyes consist of acidic and basic dyes bearingazo groups, anthraquinones, triphenyl methanes, or nitro derivativesas chromophores. Ionic interactions or van der Waals forces are associatedwith the deposition of these low molecular weight compounds on hairstructures. The hair color from semipermanent dyes is generally retainedover several shampoo applications. Permanent hair dyes penetrate hairto change the natural hair color, and they are more frequently associatedwith adverse reactions and pose a higher risk to human health. Permanenthair dyes require three components: (1) precursor agents, that is,primary intermediates comprised of ortho- (o-) and para- (p-) aromaticamines substituted with amino groups and/or hydroxides; (2) couplingagents that are formed by aromatic compounds meta- (m-) substituted with electron-donating groups,such as m-phenylenediamines, resorcinol, naphthol,and other derivatives; and (3) oxidizing agents in alkaline media,predominantly hydrogen peroxide (H₂O₂) in thepresence of ammonia.

2.2. Hair Dye Ingredients: ChemicalCharacteristicsand Reported Toxicities

This section focuses on the physicaland chemical characteristics of widely used hair dye chemicals (Figure ​Figure11) and the chemicalbasis of their reported toxicities. Current knowledge regarding theirsafety (including their relevant hydrochloride and sulfate salts)is summarized in Table 2.⁶⁻²⁷

Open in a separate window

Figure 1

Chemicalstructures of hair dye ingredients. Chemical structuresof the following hair dye ingredients are shown: p-phenylenediamine 1 (PPD), N-monoacetyl-p-phenylenediamine 2 (MAPPD), N,N-diacetyl-p-phenylenediamine 3 (DAPPD), N-phenyl-p-phenylenediamine 4, N,N-bis(hydroxyethyl)-p-phenylenediamine 5, hydroxypropyl bis(N-hydroxyethyl-p-phenylenediamine) 6, 2-chloro-p-phenylenediamine 7, 4-methoxy-m-phenylenediamine 8, p-methylaminophenol 9, 2-methyl-5-hydroxyethylaminophenol 10, 2,4-diaminophenol 11, hydroquinone 12, t-butylhydroquinone 13, toluene-2,5-diamine (CAS no: 95-70-5) 14, toluene-3,4-diamine 15, Disperse Blue 7 16, Disperse Violet 1 17, Disperse Yellow 3 18, Acid Violet 43 19, Basic Blue 99 20, HC Blue no. 2 21, HC Yellow no. 5 22,HC Red no. 7 23, 3-nitro-p-hydroxyethylaminophenol 24, 4-amino-3-nitrophenol 25, 4-amino-2-hydroxytoluene 26, 1-naphthol 27, resorcinol 28, o-phenylenediamine 29, 4-chloro-o-phenylenediamine 30, 4-aminobiphenyl 31, and di-n-butyl phthalate 32. Only the core chemical structures are shown. The sulfate or hydrochloridesalts are omitted for simplicity.

Aromatic amines, such as p-phenylenediamine (PPD, 1) (Figures ​Figures11 and ​and2),2), constitute the main class of compoundsused as precursors in permanent hair dyes. The multiple toxicologicalproperties of PPD have been demonstrated in previous studies; forinstance, PPD induces apoptosis by increasing reactive oxygen species.²⁸ During hair coloring, PPD can penetrate theskin and be absorbed by the airway,²⁹ whereit can then be biotransformed into N-monoacetyl-p-phenylenediamine (MAPPD, 2) and N,N′-diacetyl-p-phenylenediamine (DAPPD, 3) (Figure ​Figure22). A study of the transformation of PPD to MAPPD and DAPPD usingreconstituted human epidermis showed that the metabolite levels produceddepend on the dose of PPD. At concentrations of 250–1000 μM,the formation of MAPPD was favored, while at doses below 250 μM,DAPPD was preferentially formed.³⁰ PPDinduces dendritic cell (DC) activation after in vitro exposure tooxygen in air, and a positive local lymph node assay (LLNA) responsein vivo, demonstrating its intracorporeal sensitizing potential. Thesensitizers produced by PPD oxidation in both cases induced immunestimulation. In contrast, MAPPD and DAPPD did not induce DC activationor give a positive LLNA response.³¹ Thebiotransformation of PDD to MAPPD or DAPPD and the formation of sensitizersfrom PPD oxidation are two distinct competing pathways. The formationof sensitizing agents is promoted when increased PPD concentrationsare present, leading to a series of PPD-related toxicities (Figure ​Figure22).

Open in a separate window

Figure 2

Mechanism of toxicityinduced by p-phenylenediamine.An increase in reactive oxygen species is associated with PPD 1-induced apoptosis. Dermal N-acetylationbiotransforms PPD toward MAPPD 2 and DAPPD 3; at concentrations up to 250 μM, it is beneficial to the MAPPDformation, and at the concentration of 250–1000 μM, itis beneficial to the DAPPD formation. MAPPD and DAPPD fail to activateDCs or cause a positive LLNA response, which are considered the markersof extracorporeal and intracorporeal sensitizing potential of chemicalcompounds. PPD can induce DC activation after exposure to oxygen inair in vitro, and creates an LLNA response in vivo. The sensitizingPPD oxidation provides some effective immune stimulation that is associatedwith PPD-induced toxicity. Abbreviations: ROS, reactive oxygen species.

N-Phenyl-p-phenylenediamine 4 (Figure ​Figure11, Table 2) is anothercommon aromatic amine present in hair dyes. It has been associatedwith toxic effects including body weight reduction as a function ofdose in rats, degeneration of the seminiferous tubules, skeletal malformation,and skin sensitization (Table 2).³² The EU Scientific Committeeon Consumer Products (SCCP) identified limitations in some of thesestudies, such as inadequate data inclusion and noncompliance withthe Organization for Economic Cooperation and Development guidelines,but confirmed the strong potential of N-phenyl-p-phenylenediamine to cause skin sensitization.³³ Exposure to the structurally related N,N-bis(hydroxyethyl)-p-phenylenediamine 5 (sulfate salt) is associated withreduction in body weight, darkening of thyroid glands, decrease inserum iron concentration, delayed hypersensitivity of guinea pig skin,and allergic contact dermatitis (ACD).^6,34 Exposure tohydroxypropyl bis(N-hydroxyethyl-p-phenylenediamine) hydrochloride salt 6 is linked toreduced body weight, decreased mean serum glucose, attenuated totalprotein levels, and reproductive and developmental problems,⁸ while exposure to 2-chloro-p-phenylenediamine 7 and its sulfate salt were linkedto skin irritation, reduced body weight and ocular irritation.¹⁰ It should be noted that 4-methoxy-m-phenylenediamine 8 and its hydrochloride and sulfatesalts are unsafe for use in cosmetic products due to their reportedcarcinogenicity in rats and mice (Table 2).⁹

Aminophenolsare another class of ingredients that are widely usedin hair dyes. They are chemically synthesized by the reduction ofnitrophenols and can be used as primary intermediates in manufacturingsulfur and azo dyes.¹¹ They typically undergoreactions with oxidants to produce corresponding imines that can chemicallyreact with coupling agents to produce indophenol dyes.¹² As a primary intermediate, p-methylaminophenol 9 (sulfate salt) reacts with hemoglobinat a more rapid rate than p-aminophenol to form methemoglobin,a form of oxidized hemoglobin, and slightly irritates rabbit skinbut is not considered a dermal sensitizer.¹² The coupling agent, 2-methyl-5-hydroxyethylaminophenol 10 is used in oxidative hair dyes at a concentration of ≤5%.It can be mutagenic, and exposure can cause skin irritation, and allergiccontact dermatitis.¹¹ The Food and DrugAdministration (FDA) concluded that the maximum allowable concentrationof 2,4-diaminophenol 11 and its dihydrochloride saltfor use in hair dyes is 0.2%. Exposure to this compound can lead toslight skin irritation, severe ocular irritation, and mutagenicity(Table 2).¹³ Hydroquinone 12 is used as an antioxidant,fragrance, reducing agent, and polymerization inhibitor in hair dyes,skincare products, and lipsticks.¹⁴ Humanskin absorbs hydroquinone from both aqueous and alcoholic preparations,and excretion of this compound involves the formation of glucuronideor sulfate conjugates.¹⁵ This chemicalmay cause nephrotoxicity, cytotoxicity, skin irritation, skin sensitization,skin depigmentation, and mutagenicity.¹⁴ The most noteworthy data are related to its reported animal carcinogenicity,in which an increased incidence of renal tubule cell tumors and leukemiawas observed in F344 rats; but so far, such adverse effects on humanshave not been described.¹⁵ The acid-catalyzedreaction of hydroquinone with isobutylene or t-butanolproduces a new crystalline solid, t-butyl hydroquinone 13, an ingredient which can cause mild to moderate toxicitysuch as reduced body weight and mutagenicity in rats when administeredorally or intraperitoneally (Table 2).¹⁶

Diaminotolueneis chemically prepared from dinitrotoluene via acatalytic hydrogenation procedure or from the reaction of iron, hydrochloricacid, and dinitrotoluene. The two isomers, toluene-2,5-diamine 14 and toluene-3,4-diamine 15, are primary intermediatesthat can impart different colors to permanent hair dyes.¹⁷ For example, toluene-2,5-diamine and its sulfatesalt can color hair black, brown, gold, or gray, and toluene-3,4-diaminemakes hair brown, red, or gold.¹⁷ Toluene-2,5-diamine 14 can be readily absorbed through the skin, but 90% willbe excreted within 24 h after absorption, with a half-time excretionof 8 h.¹⁹ These two compounds manifestedsome adverse effects such as extreme skin sensitization³⁵ and reproductive toxicity (Table 2); however, a maximum concentrationof 2% (calculated as free base) or 3.6% (calculated as sulfate salt)applied to the head was considered safe with regard to systemic toxicity.³⁵ An Ames test demonstrated that the presenceof toluene-2,5-diamine in an oxidative hair dye may cause mutagenicityin the TA98 test strain.³⁶ Further studiesare needed to determine the safety of toluene-3,4-diamine as a hairdye ingredient.

Many nonoxidative ingredients are used in temporaryand semipermanenthair dyes.²⁰⁻²⁷ The CIR concluded that there is insufficient data available regardingthe safety of Disperse Blue 7.²⁰ DisperseBlue 7 16 is an anthraquinone-based dye used as a hairingredient in a few selected hair dyes. Disperse Violet 1 17 is a diamino-anthraquinone dye used in temporary and semipermanenthair dyes at a maximum concentration of 1%. To date, the only toxicityreported is ocular irritation.²¹ Acid Violet43 19 can be used in any cosmetic product because itshowed no signs of significant toxicity.²³ Basic Blue 99 20 is the most frequently used chemicalproduct for hair tints.¹³ HC Blue no. 2 21 is exclusively used in hair dyes at a concentration of≤1.7%.²⁵ Although this compoundis mutagenic, no carcinogenic outcomes were observed in exposure studieswith rats and mice.²⁵ Formulations containingHC Yellow no. 5 22 are sold with a caution statementbecause of skin irritation. While some concern still exists, the availablesafety test data from the CIR expert panel demonstrated that HC Yellowno. 5 had no animal carcinogenicity as a hair dye ingredient at aconcentration of ≤1.6%; the oral LD₅₀ in rats is555.56 mg/kg.²⁶ HC Red no. 7 has been confirmedas suitable for use in hair dyes by the CIR expert panel up to concentrationsof 1% but may elicit skin irritation and mutagenicity (Table 2).²⁷

3.1. Contact Allergy and Hair Loss

Hairdyeing-induced contact allergies occur frequently, which may furtherlead to the occurrence of ACD and urticarial contact (Table 3).³⁷⁻⁴⁰ ACD commonly occurs on the scalp,face, and hands of hair dye users, manifesting as redness of the skinwith vesiculation or scaling (Table 3),^41,42 which reduces quality of lifein the affected individuals and can have negative socioeconomic impacts.The presence of contact allergies is closely attributed to the potentskin sensitizers contained in hair dyes, such as aromatic amines includingPPD, a prevalent hair dye ingredient.⁴³ However, using permanent hair dyes containing PPD at concentrations≤0.67% is unlikely to induce skin sensitization.⁴⁴ Recently, Goebel and co-workers⁴⁵ found that a methoxymethyl side chain introduced into PPDnot only reduced the sensitizing intensity and the risk of allergicinduction but also resulted in excellent hair coloring performance.

As far as plant-based hairdyes are concerned, although the publicperceives them as safe, they can cause minor allergic reactions. Forexample, a small number of case reports have documented rare casesof ACD in users of plant-based hair dyes that contain pure henna,black tea, and indigo powder (Table 3).⁴⁶⁻⁴⁸ There may be several explanations for this finding.First, pure henna, black tea, and indigo powder all contain about15% tannins, large complex polyphenolic molecules that could causethe observed ACD. Although allergens in tannins have not been identifiedto date, the tannin-induced allergenic response is associated withinhibition of IL-8, IL-6, and TNF-α secretion from stimulatedhuman mast cells.⁴⁹ The resulting colorintensity that can be achieved by some plant colorants, such as purehenna, is time dependent.⁴⁷ Some darkeningsubstances in proprietary formulas, such as lemon oil, vinegar, eucalyptusoil, or clove oil, may be added along with PPD to shorten the timeof application.

As hairdressers are exposed on a regular basisto hair dyes inall steps of the dyeing process,⁵⁰ theyface a significantly higher skin sensitization risk than personalhair dye users.^51,52 The use of protective glovesduring hair coloring and warnings on the product labels that a sensitivitytest is needed before application have decreased the incidence ofhair dye-induced allergies. With sufficient protection against localand systemic exposure to oxidative hair dyes, hair coloring is unlikelyto pose a serious risk to human health.^53,54 The adoptionof adequate protective measures during the use of hair dye as wellas appropriate education and training of hairdressers are crucialfor lowering occupational risks and preventing hair dye-induced skinsensitization.⁵⁵

Discoid lupus erythematosus(DLE) is an autoimmune skin diseasethat may be caused by ACD (Table 3); it is characterized by the development of autoantibodiesthat attack the skin at the interphase level.^56,57 Systemic lupus erythematosus (SLE) is another autoimmune diseasemanifesting multisystem disorders in addition to skin lesions. Althoughexposure to aromatic amines (such as PPD) may give rise to the occurrenceof lupus, several studies collectively confirm an insignificant associationbetween the use of hair dyes containing PPD and the increased riskof SLE.⁵⁸⁻⁶⁰ Nevertheless, skin exposure to hair dyes may induceother severe but rare contact allergies, including neck and facialswelling and angioedema (Table 3).⁶¹⁻⁶³ Angioedema is a type I hypersensitivity reactioncharacterized by edema of the skin and subcutaneous tissues that damagesthe airways and gastrointestinal tract and may even lead to life-threateninglaryngeal swelling.

Along with the increasing popularity ofhair dye use, growing complaintsabout hair dye-induced hair loss have been a concern of dermatologists.Isik et al.⁶² found that patients who experiencedhair loss after hair dyeing presented symptoms of ACD before or atthe time of hair loss, suggesting a close correlation between hairdye-induced ACD and hair loss (Table 3). H₂O₂, monoethanolamine, andPPD in hair dyes have been proposed as the main causative ingredientsof hair dyeing-induced hair loss.^64,65 Based on histologicalexamination conducted in animal tests, oxidative stress may be themechanism underlying hair-dye induced dermatitis.^64,65 H₂O₂ and monoethanolamine, in particular,were shown to synergistically induce oxidative stress and cytotoxicityin human keratinocytes, an observation that is consistent with thehistological data.^64,65

3.2. RespiratorySensitization, Allergies, AndOther Diseases

Asthma and allergic rhinitis are common diseasesthat can result in overwhelmingly negative socioeconomic impacts.⁶⁶ Hairdressers are at a high risk of occupationalrhinitis and asthma because, in daily work, they are frequently exposedto irritants and allergens such as persulfate and PPD in hair dyes.^67,68 A case-control study from Norway⁶⁹ showedthat hairdressers over 40 years of age were more likely to sufferasthma-like symptoms than nonhairdressers due to their long occupationalexposure to hair dye ingredients. Therefore, hairdressers and hairdressingapprentices should undergo continuous medical surveillance to monitorthe risk factors and reduce the chance of respiratory diseases linkedto occupational exposure.

3.3. Hair Dye Poisoning

Due to the easyavailability and high toxicity of PPD, people in the developing worldwho want to commit suicide may attempt it by consuming this agent.⁷⁰ Hair dye poisoning may trigger the occurrenceof some urgent and fatal outcomes, like pneumothorax, rhabdomyolysis,and acute kidney injury (AKI) (Table 3).⁷¹⁻⁷³ Orally ingesting PPD causes severe trauma to theairway and may lead to dyspnea, asphyxia, and other respiratory symptoms.If those ingesting PPD suffer respiratory distress and chest pain,then caution is needed regarding the occurrence of pneumothorax, whichcan be diagnosed by sonography or bedside X-ray. The pathologicalunderpinning of rhabdomyolysis involves calcium ions leaking fromthe smooth endoplasmic reticulum, resulting in prolonged muscle contractionand irreversible changes in muscle structure.⁷⁴ The most striking laboratory characteristic of rhabdomyolysis isa concentration of creatine phosphokinase in the plasma >10,000U/L.If patients do not receive aggressive treatment, they will eventuallydie. Globally, approximately 13.3 million humans suffer from AKI peryear, and more than 1 in 10 lose their life from this disease.⁷⁵ Individuals with AKI are also at a 9-fold riskof developing chronic kidney disease that can give rise to other organdysfunctions. The characterized pathological manifestations of AKIinclude glomerular hyperemia, acute tubular necrosis, intratubularcasts, and tubulointerstitial hemorrhages as well as mesangial hyperplasia.Hair dye-induced AKI occurs in a dose-dependent manner, but even withno intervention, the injured kidney may recover over time.⁷⁴

3.4. Reproductive Toxicity andDisruption of ThyroidHormone Synthesis

Zebrafish embryos are suitable animal modelsfor studying how hair dyes affect embryonic growth. Two studies byManjunatha et al.^76,77 demonstrated that exposure tohair dyes induced morphological and physiological abnormalities inzebrafish embryos, which provoked interest in determining whetherhair dyes could affect human embryo development. Abnormal birth weightin humans (live birth weight <2500 g or >4000 g) reflects thepoorhealth of the fetus and mother, which could contribute to the occurrenceof obesity, malnutrition, hypertension, cardiovascular diseases, andcancer in the child in the future.⁷⁸ Interms of hair dyeing, the risk of infantile abnormal birth weightis elevated when mothers have irregular menstruation or have usedhair dyes before pregnancy; the risk is increased if both factorsexist.⁷⁹

Resorcinol 28 is widely used as a component in hair dyes and cosmetics, and administrationto rodents at high doses (>520 mg/kg/d) over 2 years disruptedthyroidhormone synthesis and caused goitrogenic effects.⁸⁰ Dermatological clinical reports indicated that frequentexternal application of ointments containing a high concentrationof resorcinol (>34 mg/kg/d) to integrity-compromised human skinforseveral months to years can also induce thyroid side effects.⁸⁰ However, a risk assessment study concluded thatunder real-world conditions, exposure to resorcinol contained in hairdyes and cosmetics was unlikely to cause human thyroid dysfunction.⁸⁰

4.1. Bladder Cancer

Bladder cancer isthe most common urinary tract tumor and ranks 11th among the mostcommon malignant tumors worldwide.^81,82 Occupationalexposure to arylamines is frequently found in employees who engagein metal working, textile manufacture, driving, agriculture, construction,and rubber tire production and is the first identified cause of bladdercancer.⁸³ Hair dyes contain arylamines;⁸⁴ therefore, hairdressers and barbers are at riskof cancer from occupational exposure to arylamines. Findings demonstratethat individuals who pursue these occupations, particularly for longerthan 10 years, experience a significantly increased risk of bladdercancer.^82,85,86 On the contrary,some epidemiologic studies observed no evidence of a causal associationbetween occupational exposure to hair dyes and the increased riskfor bladder cancer among male hairdressers.^87,88 Permanent hair dyes may contain o-phenylenediamine⁸⁹29 and 4-chloro-o-phenylenediamine 30 (Figure ​Figure11),⁹⁰ which haveshown carcinogenicity in animal studies. These chemicals can leadto the formation of 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG)that is a marker of oxidative stress.⁹¹ These findings indicate that the carcinogenicity of o-phenylenediamines is related to the generation of oxidative DNAdamage, and 8-oxodG may be used as a biomarker to predict the associatedcarcinogenicity. Moreover, many permanent hair dyes contain 4-aminobiphenyl 31, which is produced during the production of hair dyes wherePPD is used as the primary intermediate.⁹² Airoldi and colleagues found that 4-aminobiphenyl was a human bladdercancer carcinogen and was positively associated with tumor grade.⁹³ Thus, it is a public health concern to determineif other contaminants formed during hair dye production may constitutean additional health risk to hair dye users.

Currently availableepidemiological data are controversial regarding whether hair dyeuse is a carcinogenic risk factor for bladder cancer. One population-based,case-controlled study found a positive association between the useof permanent hair dyes and enhanced bladder cancer risk,⁹⁴ while the results of other large-scale studiesand a meta-analyses did not corroborate this conclusion (Table 4).⁹⁵⁻¹⁰⁰ Studies investigating other confounding factors, like duration ofuse, frequency of use, age at first use, sex, and dye color, did notfind a significant association between hair dye use and bladder cancer.^101−104 In addition, the New England Bladder Cancer Study¹⁰⁵ found no significant association between permanent hairdye use and increased bladder cancer risk in studies with female participants,but suggested that female users with a college degree had a greaterrisk of bladder cancer than nonusers (OR = 3.3; 95% CI, 1.2–8.9).This study also found that bladder cancer risk was higher among womenwith the NAT2 slow acetylation phenotype comparedto those with the NAT2 rapid/intermediate acetylationphenotype (OR = 7.3; 95% CI, 1.6–32.6). A population-basedstudy from the United States¹⁰⁶ involving363 non-Asian women demonstrated a 2.9-fold increased risk of bladdercancer among women with the NAT2 slow acetylationphenotype and a 2.5-fold increased risk among those with the CYP1A2 slow phenotype who exclusively used permanent hairdyes, perhaps due to a slower detoxification capacity (Table 4). Significant positive frequency-and duration-related dose–response associations were reportedin individuals with the NAT2 and/or CYP1A2 slow phenotypes. A follow-up study from Sweden¹⁰⁷ involving 38,866 female and 6824 male hairdressers andanalyzing their malignancies over a period of 39 years demonstratedthat the risk of bladder cancer among male hairdressers graduallydecreased with follow-up time, albeit at the highest standardizedincidence ratio (SIR) of 2.56 (95% confidence interval [CI], 1.36–4.39)in the 1960s. In recent decades, this risk has disappeared, with anSIR of 1.04 (95% CI, 0.74–1.40), suggesting that modern haircolorants do not exert an occupational bladder cancer risk in malehairdressers. However, there is another explanation for the nonapparentcarcinogenic risk of bladder cancer from modern hair dyes: Aromaticamine-induced human urothelial cancers typically have a latency timelonger than 20 years,¹⁰⁸ so the neoplasticonset time has not yet arrived. With the currently available data,bladder cancer risk due to exposure to hair dyes should be assessedon a case-by-case basis and the toxicological profile and individualexposure should be taken into consideration.

4.2. Breast Cancer

Breast cancer is oneof the most common malignant tumors among women and the second leadingcause of cancer death in the world.^109,110 The presentevidence is inconclusive describing the link between personal hairdye use and breast cancer risk. Several epidemiological case-controlstudies^111−115 have indicated that hair dyeing does not increase the risk of breastcancer in women, even in those with benign breast diseases. In contrast,several case-control studies,^116−118 a prospective study,¹¹⁹ and two meta-analyses^1,120 reported that personal hair dye use was related to the carcinogenicrisk of breast cancer (Table 4). Early age at menarche is associated with an increased riskfor breast cancer.¹²¹ Each 2-year delayin onset of menstruation decreases this risk by approximately 10%.¹²² The early exposure to menstruation and ovulation-associatedhormones, linked with an earlier menstruation onset, has been proposedas an etiological factor for increased breast cancer risk.^123,124 Higher estrogen levels have been reported in individuals that experiencedearly menstruation onset, for several years after menarche.^125,126

Endocrine disrupting chemicals (EDCs) are exogenous agentsthat interact with estrogen receptors or estrogen signaling pathways,disrupting the physiological function of the endocrine system andthe development of the mammary tissue. This heterogeneous group ofchemicals includes parabens, bisphenols, and phthalates, widely usedsubstances in cosmetic and personal care products, and are presentin hair dyes.^127,128 EDCs can be transported fromthe bloodstream to breast milk via passive diffusion and are theningested by infants through breast-feeding. The hormone levels inthe infants can be affected, and the growth of their germ cells canbe disrupted.¹²⁹ Exposure to hair dyescontaining EDCs in childhood may increase breast cancer risk, by loweringthe age at menarche but most likely without affecting breast density.¹³⁰ Indeed, a study by Llanos et al.¹³¹ demonstrated that the use of hair dyes containingEDCs is correlated with an elevated risk of estrogen receptor-positivebreast cancer. Adolescent use of hair dyes containing EDCs may increasethe risk of premenopausal breast cancer.¹³² Di-n-butyl phthalate 32 is an EDCthat is present in several hair dyes and personal-care products. Invitro studies revealed a large group of genes associated with fertility(inhibin, placental growth factor), the immune response (tumor necrosisfactor-induced proteins), and antioxidant status (glutathione peroxidase)in normal human mammary epithelial cells were altered after exposureto di-n-butyl phthalate,¹³³ suggesting that these genes may be potential biomarkers for predictingreproductive problems associated with hair dye use.

The previouslymentioned meta-analysis¹²⁰ concluded thatthe use of hair dyes, especially temporary and permanenthair dyes, increased breast cancer risk. However, an overall correlationbetween hair dyes and breast cancer risk as a function of race, timingof use, and dye color was not found. A case-control study from westernWashington¹¹⁵ found that young women usinga single type of dyeing method (i.e., temporary, semipermanent orpermanent dyes, straightener, and bleaching following dyeing or frosting)did not experience an increase in breast cancer risk (relative risk[RR] = 1.10; 95% CI, 0.90–1.30), but those who used two ormore methods did have an increased risk (RR = 1.90; 95% CI, 1.40–2.50),indicating that reproductive-age women who used just one type of dyeingmethod avoided the increased risk of breast cancer (Table 4). These conflicting conclusionsare likely explained by differences in individual subjects’molecular phenotypes, ages, and hair dyeing methods.

4.3. Hematopoietic Cancer

Hematopoieticcancers comprise a group of malignant tumors that occur in peripheralblood, bone marrow, and the lymphohematopoietic system, includingleukemia, multiple myeloma (MM) and lymphoma. The etiology of somedisorders is still unclear to date. Lymphomas originate from the lymphohematopoieticsystem and are classified into Hodgkin’s lymphoma (HL) andnon-Hodgkin’s lymphoma (NHL) according to the lymphocyte typein the tumor tissues.

Although two population-based case-controlstudies determined^134,135 that hair dye use is a riskfactor for primary myelodysplastic syndrome, a large number of studieshave not identified a significant association between personal hairdye use and an overall increased risk of leukemia, HL, NHL, or MM(Table 4).^136−142 Because the data are conflicting regarding the potential carcinogeniceffect of hair dye on the hematopoietic system, further studies shouldbe performed to assess risk, for example, evaluating instances wherehair dyes applied have very low concentrations of oxidative chemicals.If the duration of use is prolonged and the frequency of use is increased,the risk of hair dye-induced leukemia and other malignant lymphatictumors is elevated.^96,143−145 Moreover, it was reported that the lymphoma risk of hair dye userscompared to nonusers was elevated by 19%, and further increased by26% when the frequency of use was >12 times per year.¹⁴²

The incidence of NHL has increased globallyin recent decades.¹⁴⁶ Occupational exposureto hair dyes may increasethe risk of diffuse large B cell lymphoma, a subtype of NHL. A Shanghaihospital-based case-control study¹⁴⁷ revealedthat personal hair dye use was not associated with an elevated riskof NHL or any NHL subtypes. In contrast, a population-based case-controlstudy from the United States¹⁴⁸ showeda positive correlation between the use of permanent hair dyes andan increased risk of NHL, which became stronger for longer durationof use and earlier age of first use. Furthermore, several long-termcase-control studies^149−153 found that hair dye use correlated with NHL risk and that this riskwas significantly enhanced in users who dyed their hair prior to 1980,but not in those who used hair dyes in or after 1980 (Table 4). One possible explanationfor this observation could be from the changes in hair dye formulationand the duration of use differences before and after 1980.

4.4. Maternal Hair Dyeing-Induced Childhood Tumors

As hairdyes contain EDCs, maternal hair dyeing during the monthbefore pregnancy, during pregnancy, or during breastfeeding is considereda risk factor for offspring health. Childhood tumors are the secondmost common cause of childhood death in developed countries,¹⁵⁴ in which leukemia accounts for approximately35.8% and ranks first.¹⁵⁵ Maternal hairdye use in the first trimester of pregnancy increases the risk ofchildhood acute lymphoblastic leukemia (ALL), and breastfeeding elevatesthe risk of childhood acute myeloid leukemia (AML). However, if childrenexhibited MLL (mixed lineage leukemia) gene rearrangementsand their mothers were previously exposed to hair dye chemicals duringpregnancy, an elevated risk of ALL or AML was not observed.¹⁵⁶ Gao and colleagues¹⁵⁷ found that the risk of maternal hair dyeing-induced childhood leukemiawas reduced by breastfeeding, and if the breastfeeding duration reached7–9 months, the reduction effect was more pronounced.

Neuroblastoma is the most common extracranial cancer in infants underthe age of 12 months, corresponding to approximately 6–10%of global childhood tumors.¹⁵⁴ If hairdye use takes place a month before pregnancy or during pregnancy,the neuroblastoma risk in children is slightly increased, regardlessof the type of hair dye used, and this effect was doubled by maternalsemipermanent hair dye use.^158,159 Intriguingly, it wasreported that mothers’ use of temporary hair dye was linkedto a greater neuroblastoma risk in children than maternal use of permanenthair dye.¹⁵⁴

Testicular germ celltumor (TGCT) is a rare human tumor with anestimated incidence of 8/100,000 and predominately occurs in malesaged between 15 and 44 years.^160,161 Development of TGCTsis hypothesized to be due to a hormonal etiology related to EDCs.The United States Servicemen’s Testicular Tumor Environmentaland Endocrine Determinants study¹⁶² indicatedthat pregnant women frequently using personal care products (e.g.,face lotion) containing EDCs during their pregnancy or breast-feedingmay increase the risk of TGCTs in their sons. Similarly, a study byChen et al.¹⁶³ suggested that maternalhair dyeing during the month before pregnancy and during breastfeedingincreased the risk of malignant germ cell tumors (MGCTs) in theirsons and that breastfeeding also led to an elevated MGCT risk fortheir daughters (Table 4).^164,165,166

•

Dr. Lin He published 15 SCI papersas first or co-firstauthor during the past five years. He is an oncologist in the AnhuiProvincial Maternal and Child Health Hospital.

•

Dr. Freideriki Michailidou is a Collegium ResearchFellow at ETH Zurich. Her current research encompasses biocatalysisand protein engineering, sustainable production, and safety assessmentof fragrance ingredients.

•

Dr. HaileyGahlon is a Group Leader in the Laboratoryof Toxicology at ETH Zurich. Her current research focuses on understandingmechanisms of mitochondrial genome instability and strategies to circumventanticancer drug resistance.

•

Dr.Weibin Zeng is the Group Leader of the Collegeof Animal Science and Technology, Shihezi University. His currentresearch centers on animal reproduction and biotechnology.

• Gera R.; Mokbel R.; Igor I.; Mokbel K.Does the Use of HairDyes Increase the Risk of Developing Breast Cancer? A Meta-analysisand Review of the Literature. Anticancer Res.2018, 38 (2), 707–716. 10.21873/anticanres.12276. [PubMed] [CrossRef] [Google Scholar]
• Hedberg Y. S.; Uter W.; Banerjee P.; Lind M. L.; SkovvangSteengaard S.; Teo Y.; Lidén C.Non-oxidativehair dye products on the European market: What do they contain?. Contact dermatitis2018, 79 (5), 281–7. 10.1111/cod.13074. [PubMed] [CrossRef] [Google Scholar]
• Piérard G. E.; Goffin V.; Piérard-Franchimont C.Corneosurfametry:apredictive assessment of the interaction of personal-care cleansingproducts with human stratum corneum. Dermatology(Basel, Switzerland)2004, 189 (2), 152–6. 10.1159/000246820. [PubMed] [CrossRef] [Google Scholar]
• Diamante C.; Bergfeld W. F.; Belsito D. V.; Klaassen C. D.; Marks J. G. Jr; Shank R. C.; Slaga T. J.; Snyder P. W.; Alan Andersen F.Final reporton the safety assessment of Basic Violet1, Basic Violet 3, and Basic Violet 4. Int.J. Toxicol.2009, 28 (6 Suppl2), 193S–204S. 10.1177/1091581809354649. [PubMed] [CrossRef] [Google Scholar]
• Zhang Y.; Birmann B. M.; Han J.; Giovannucci E. L.; Speizer F. E.; Stampfer M. J.; Rosner B. A.; Schernhammer E. S.Personaluse of permanent hair dyes and cancer risk and mortality in US women:prospective cohort study. BMJ.2020, 370, m2942. 10.1136/bmj.m2942. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Final Report on theSafety Assessment of N,N-Bis(Hydroxyethyl)-p-Phenylenediamine Sulfate. Int. J. Toxicol.1992, 11 (1), 129–142. 10.3109/10915819209141994. [CrossRef] [Google Scholar]
• Andersen F. A.Final reporton the safety assessment of N-Phenyl-p-Phenylenediamine, N- Phenyl-p-Phenylenediaminehydrochloride, and N-Phenyl-p-Phenylenediamine sulfate. Journal of the American college of toxicology1994, 13 (5), 374–394. 10.3109/10915819409140613. [CrossRef] [Google Scholar]
• Becker L. C.; Bergfeld W. F.; Belsito D. V.; Hill R. A.; Klaassen C. D.; Liebler D. C.; Marks J. G. Jr; Shank R. C.; Slaga T. J.; Snyder P. W.; Andersen F. A.Safety Assessmentof Hydroxypropyl Bis(N-Hydroxyethyl-p-Phenylenediamine) HCl as Usedin Cosmetics. Int. J. Toxicol.2016, 35 (2 suppl), 5s–11s. 10.1177/1091581816659258. [PubMed] [CrossRef] [Google Scholar]
• Skinner J. P.Final reporton the safety assessment of 4-Methoxy-m-Phenylenediamine, 4-Methoxy-m-Phenylenediaminesulfate, and 4-Methoxy-m-Phenylenediamine-HCl. Journal of the American college of toxicology1992, 11 (4), 381–422. 10.3109/10915819209141882. [CrossRef] [Google Scholar]
• Willis L.Final reporton the safety assessment of 2-Chloro-p-Phenylenediamine and 2-Chloro-p-PhenylenediamineSulfate. Journal of the American college oftoxicology1992, 11 (4), 521–530. 10.3109/10915819209141890. [CrossRef] [Google Scholar]
• Final Report on theSafety Assessment of 2-Methyl-5-Hydroxyethylaminophenol. Int. J. Toxicol.1990, 9 (2), 185–202. 10.3109/10915819009078733. [CrossRef] [Google Scholar]
• Final Report on theSafety Assessment of p-Methylaminophenol Sulfate. International journal of toxicology1991, 10 (1), 53–65. [Google Scholar]
• Andersen F. A.Final reporton the safety assessment of 2,4-Diaminophenol and 2,4- DiaminophenolDihydrochloride. Journal of the American collegeof toxicology1994, 13 (5), 330–343. 10.3109/10915819409140610. [CrossRef] [Google Scholar]
• Addendum to the finalreport on the safety assessment of Hydroquinone. Journal of the American college of toxicology1994, 13 (3), 167–230. 10.3109/10915819409141000. [CrossRef] [Google Scholar]
• Andersen F. A.; Bergfeld W. F.; Belsito D. V.; Hill R. A.; Klaassen C. D.; Liebler D. C.; Marks J. G. Jr; Shank R. C.; Slaga T. J.; Snyder P. W.Final amendedsafety assessment ofhydroquinone as used in cosmetics. Int. J. Toxicol.2010, 29 (6), 274S–87S. 10.1177/1091581810385957. [PubMed] [CrossRef] [Google Scholar]
• Final Report on theSafety Assessment of t-Butyl Hydroquinone. Internationaljournal of toxicology1991, 10 (1), 1–7. 10.3109/10915819109078618. [CrossRef] [Google Scholar]
• Pang S. N. J.Finalreport on the safety assessment of toluene-2,5-diamine, toluene-2,5-diaminesulfate, and toluene-3,4-diamine. Journal ofthe American college of toxicology1992, 11 (4), 423–445. 10.3109/10915819209141883. [CrossRef] [Google Scholar]
• Burnett C. L.; Bergfeld W. F.; Belsito D. V.; Klaassen C. D.; Marks J. G. Jr; Shank R. C.; Slaga T. J.; Snyder P. W.; Alan Andersen F.Final amendedreport of the safety assessment of toluene-2,5-diamine,toluene-2,5-diamine sulfate, and toluene-3,4-diamine as used in cosmetics. International journal of toxicology2010, 29 (3_suppl), 61S–83S. 10.1177/1091581810361964. [PubMed] [CrossRef] [Google Scholar]
• Schettgen T.; Heinrich K.; Kraus T.; Gube M.Determination of 2,5-toluylenediamine(2,5-TDA) and aromatic amines in urine after personal applicationof hair dyes: kinetics and doses. Archives oftoxicology2011, 85 (2), 127–33. 10.1007/s00204-010-0563-3. [PubMed] [CrossRef] [Google Scholar]
• Final report on thesafety assessment of disperse Blue 7. Internationaljournal of toxicology2007, 26 (Suppl 2), 65–77. 10.1080/10915810701351210. [PubMed] [CrossRef] [Google Scholar]
• Final Report on theSafety Assessment of Disperse Violet. Internationaljournal of toxicology1991, 10 (1), 103–111. 10.3109/10915819109078618. [CrossRef] [Google Scholar]
• Andersen F. A.Final reporton the safety assessment of Disperse Yellow 3. Journal of the American college of toxicology1996, 15 (4), 311–319. 10.3109/10915819609008723. [CrossRef] [Google Scholar]
• Fiume M. Z.Final reporton the safety assessment of Acid Violet 43. International journal of toxicology2001, 20 (Suppl 3), 1–6. 10.1080/10915810152902547. [PubMed] [CrossRef] [Google Scholar]
• Final report on thesafety assessment of Basic Blue 99. Internationaljournal of toxicology2007, 26 (Suppl 2), 51–63. 10.1080/10915810701351202. [PubMed] [CrossRef] [Google Scholar]
• Andersen F. A.Final reporton the safety assessment of HC Blue No. 2. Journalof the American college of toxicology1994, 13 (5), 361–373. 10.3109/10915819409140612. [CrossRef] [Google Scholar]
• Final report on thesafety assessment of HC Yellow No. 5. Internationaljournal of toxicology2007, 26 (Suppl 2), 113–124. 10.1080/10915810701351244. [PubMed] [CrossRef] [Google Scholar]
• Final report on thesafety assessment of HC Red No. 7. Internationaljournal of toxicology2008, 27 (Suppl 1), 45–54. 10.1080/10915810802032438. [PubMed] [CrossRef] [Google Scholar]
• Chye S. M.; Tiong Y. L.; Yip W. K.; Koh R. Y.; Len Y. W.; Seow H. F.; Ng K. Y.; Ranjit D. A.; Chen S. C.Apoptosisinduced by para-phenylenediamine involves formation of ROS and activationof p38 and JNK in chang liver cells. Environmentaltoxicology2014, 29 (9), 981–990. 10.1002/tox.21828. [PubMed] [CrossRef] [Google Scholar]
• Abd-ElZaher M. A.; Fawzy I. A.; Ahmed H. M.; Abd-Allah A. M.; Gayyed M. F.Some toxicological health hazards associated with subchronicdermal exposure to paraphenylene-diamine (PPD): An experimental study. Egyptian journal of forensic sciences2012, 2 (3), 105–11. 10.1016/j.ejfs.2012.06.003. [CrossRef] [Google Scholar]
• Nohynek G. J.; duch*e D.; Garrigues A.; Meunier P. A.; Toutain H.; Leclaire J.Under the skin: Biotransformationof para-aminophenoland para-phenylenediamine in reconstructed human epidermis and humanhepatocytes. Toxicology letters2005, 158 (3), 196–212. 10.1016/j.toxlet.2005.03.014. [PubMed] [CrossRef] [Google Scholar]
• Aeby P.; Sieber T.; Beck H.; Gerberick G. F.; Goebel C.Skin sensitization to p-phenylenediamine: the divergingroles of oxidation and N-acetylation for dendritic cell activationand the immune response. Journal of investigativedermatology2009, 129 (1), 99–109. 10.1038/jid.2008.209. [PubMed] [CrossRef] [Google Scholar]
• Singh R. L.; Khanna S. K.; Shanker R.; Singh G. B.Acute and short-termtoxicity studies on p-aminodiphenylamine. Veterinaryand human toxicology1986, 28 (3), 219–223. [PubMed] [Google Scholar]
• SCCP . Opinion on N-Phenyl-p-phenylenediamine; European Commission: Brussels, 2006. https://ec.europa.eu/health/ph_risk/committees/04_sccp/docs/sccp_o_089.pdf (accessed).
• Hagiwara A.; Miyata E.; Tamano S.; Shibata M.-A.; Sugiura S.; Inoue M.; Hirose M.Non-Carcinogenicityof 2,2′-[(4-Aminophenyl)imino]bisethanolSulfate in a Long-term Feeding Study Fischer 344 Rats. Food and chemical toxicology1996, 34 (6), 537–546. 10.1016/0278-6915(96)00010-5. [PubMed] [CrossRef] [Google Scholar]
• SCCP . Opinion on toluene-2,5-diamineand its sulfate; European Commission: Brussels, 2012. https://op.europa.eu/en/publication-detail/-/publication/68467996-7b0d-4bce-bf8f-cbd38adbd91d (accessed).
• Zhou S.; Li R.; Zhang Z.; Gu M.; Zhu H.; Fang J.; Ji Z.; Xu X.; Tang L.Analysis of mutagenic componentsof oxidative hair dyes with the Ames test. Human& experimental toxicology2021, 40 (11), 1921–1937. 10.1177/09603271211013433. [PubMed] [CrossRef] [Google Scholar]
• Montgomery R.; Wilkinson M.Allergic contacturticaria secondary to hair dye use. Contactdermatitis2017, 77 (4), 257–9. 10.1111/cod.12811. [PubMed] [CrossRef] [Google Scholar]
• Søsted H.; Menné T.Allergy to 3-nitro-p-hydroxyethylaminophenol and 4-amino-3-nitrophenolin a hair dye. Contact dermatitis2005, 52 (6), 317–9. 10.1111/j.0105-1873.2005.00583.x. [PubMed] [CrossRef] [Google Scholar]
• Washio K.; Ijuin K.; f*ckunaga A.; Nagai H.; Nishigori C.Contact anaphylaxiscaused by Basic Blue 99 in hair dye. Contactdermatitis2017, 77 (2), 122–3. 10.1111/cod.12740. [PubMed] [CrossRef] [Google Scholar]
• Ellis R. A.; Wilkinson S. M.Contact dermatitis to 4-amino-2-hydroxytoluene in hairdye. Contact dermatitis2009, 60 (2), 118–9. 10.1111/j.1600-0536.2008.01491.x. [PubMed] [CrossRef] [Google Scholar]
• Søsted H.; Agner T.; Andersen K. E.; Menné T.55 Cases ofallergic reactions to hair dye: A descriptive, consumer complaint-basedstudy. Contact dermatitis2002, 47 (5), 299–303. 10.1034/j.1600-0536.2002.470508.x. [PubMed] [CrossRef] [Google Scholar]
• King T.; Sabroe R.; Holden C.Allergic contactdermatitis causedby 1-naphthol, a red coupler, in a purple permanent oxidative hairdye. Contact dermatitis2018, 79 (2), 99–100. 10.1111/cod.12997. [PubMed] [CrossRef] [Google Scholar]
• Gregoriou S.; Mastraftsi S.; Hatzidimitriou E.; Tsimpidakis A.; Nicolaidou E.; Stratigos A.; Katsarou A.; Rigopoulos D.Occupationaland non-occupational allergic contact dermatitis to hair dyes in Greece.A 10-year retrospective study. Contact dermatitis2020, 83 (4), 277–85. 10.1111/cod.13598. [PubMed] [CrossRef] [Google Scholar]
• Towle K. M.; Hwang R. Y.; Fung E. S.; Hollins D. M.; Monnot A. D.Hair dyeand risk of skin sensitization induction: a product survey and quantitativerisk assessment for para-phenylenediamine (PPD). Cutaneous and ocular toxicology2020, 39 (4), 311–6. 10.1080/15569527.2020.1802740. [PubMed] [CrossRef] [Google Scholar]
• Goebel C.; Troutman J.; Hennen J.; Rothe H.; Schlatter H.; Gerberick G. F.; Blömeke B.Introduction of a methoxymethyl sidechain into p-phenylenediamine attenuates its sensitizing potency andreduces the risk of allergy induction. Toxicologyand applied pharmacology2014, 274 (3), 480–7. 10.1016/j.taap.2013.11.016. [PubMed] [CrossRef] [Google Scholar]
• Belhadjali H.; Akkari H.; Youssef M.; Mohamed M.; Zili J.Bullous allergiccontact dermatitis to pure henna in a 3-year-old girl. Pediatric dermatology2011, 28 (5), 580–1. 10.1111/j.1525-1470.2010.01201.x. [PubMed] [CrossRef] [Google Scholar]
• Lestringant G. G.; Bener A.; Frossard P. M.Cutaneousreactions to henna andassociated additives. British journal of dermatology1999, 141 (3), 598–600. 10.1046/j.1365-2133.1999.03086.x. [PubMed] [CrossRef] [Google Scholar]
• Swan B. C.; Tam M. M.; Higgins C. L.; Nixon R. L.Allergic contactdermatitis to substitute hair dyes in a patient allergic to para-phenylenediamine:Pure henna, black tea and indigo powder. Australasianjournal of dermatology2016, 57 (3), 219–21. 10.1111/ajd.12454. [PubMed] [CrossRef] [Google Scholar]
• Lorenz P.; Heinrich M.; Garcia-Käufer M.; Grunewald F.; Messerschmidt S.; Herrick A.; Gruber K.; Beckmann C.; Knoedler M.; Huber R.; Steinborn C.; Stintzing F. C.; Gründemann C.Constituents from oak bark (Quercusrobur L.) inhibit degranulation and allergic mediator release frombasophils and mast cells in vitro. Journal ofethnopharmacology2016, 194, 642–50. 10.1016/j.jep.2016.10.027. [PubMed] [CrossRef] [Google Scholar]
• Lind M. L.; Johnsson S.; Lidén C.; Meding B.; Boman A.Hairdressers’skin exposure to hair dyes during different hair dyeing tasks. Contact dermatitis2017, 77 (5), 303–10. 10.1111/cod.12833. [PubMed] [CrossRef] [Google Scholar]
• Gube M.; Heinrich K.; Dewes P.; Brand P.; Kraus T.; Schettgen T.Internal exposureof hairdressers to permanent hairdyes: a biomonitoring study using urinary aromatic diamines as biomarkersof exposure. International archives of occupationaland environmental health2011, 84 (3), 287–92. 10.1007/s00420-010-0539-x. [PubMed] [CrossRef] [Google Scholar]
• Takkouche B.; Regueira-Méndez C.; Montes-Martínez A.Risk of canceramong hairdressers and related workers: a meta-analysis. International journal of epidemiology2009, 38 (6), 1512–31. 10.1093/ije/dyp283. [PubMed] [CrossRef] [Google Scholar]
• Hueber-Becker F.; Nohynek G. J.; Dufour E. K.; Meuling W. J.; de Bie A. T.; Toutain H.; Bolt H. M.Occupationalexposure of hairdressersto [14C]-para-phenylenediamine-containing oxidative hair dyes: a massbalance study. Food and chemical toxicology2007, 45 (1), 160–9. 10.1016/j.fct.2006.08.002. [PubMed] [CrossRef] [Google Scholar]
• Hueber-Becker F.; Nohynek G. J.; Meuling W. J.; Benech-Kieffer F.; Toutain H.Human systemic exposure to a [14C]-para-phenylenediamine-containingoxidative hair dye and correlation with in vitro percutaneous absorptionin human or pig skin. Food and chemical toxicology2004, 42 (8), 1227–36. 10.1016/j.fct.2004.02.020. [PubMed] [CrossRef] [Google Scholar]
• Goebel C.; Diepgen T. L.; Blömeke B.; Gaspari A. A.; Schnuch A.; Fuchs A.; Schlotmann K.; Krasteva M.; Kimber I.Skin sensitizationquantitative risk assessment for occupational exposure of hairdressersto hair dye ingredients. Regulatory toxicologyand pharmacology2018, 95, 124–32. 10.1016/j.yrtph.2018.03.006. [PubMed] [CrossRef] [Google Scholar]
• Kirchhof M. G.; Dutz J. P.The immunopathology of cutaneouslupus erythematosus. Rheumatic diseases clinicsof north America2014, 40 (3), 455–74. 10.1016/j.rdc.2014.04.006. [PubMed] [CrossRef] [Google Scholar]
• VanAerde E.; Kerre S.; Goossens A.Discoid lupus triggeredby allergic contact dermatitis caused by a hair dye. Contact dermatitis2016, 74 (1), 61–4. 10.1111/cod.12496. [PubMed] [CrossRef] [Google Scholar]
• Sanchez-Guerrero J.; Karlson E. W.; Colditz G. A.; Hunter D. J.; Speizer F. E.; Liang M. H.Hair dye use andthe risk of developing systemic lupuserythematosus: A cohort study. Arthritis andrheumatism1996, 39 (4), 657–62. 10.1002/art.1780390418. [PubMed] [CrossRef] [Google Scholar]
• Petri M.; Allbritton J.Hair product use in systemic lupus erythematosus. Acase-control study. Arthritis and rheumatism1992, 35 (6), 625–9. 10.1002/art.1780350605. [PubMed] [CrossRef] [Google Scholar]
• Jiménez-Alonso J.; Sabio J. M.; Pérez-Alvarez F.; Reche I.; Hidalgo C.; Jáimez L.Hair dye treatment use and clinicalcourse in patients with systemic lupus erythematosus and cutaneouslupus. Lupus2002, 11 (7), 430–434. 10.1191/0961203302lu231oa. [PubMed] [CrossRef] [Google Scholar]
• Ngwanya R. M.; Spengane Z.; Khumalo N.Angioedema,an unusual reaction tohair dye. pan african medical journal2018, 30, 103. 10.11604/pamj.2018.30.103.12061. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Isik S. M. D.; Caglayan-Sozmen S. M. D.; Anal O. M. D.; Karaman O. M. D.; Uzuner N. M. D.Severe Neck andFace Edema in an Adolescent-DelayedHypersensitivity Reaction to Hair Dye. Pediatricemergency care2017, 33 (6), 422–3. 10.1097/PEC.0000000000000898. [PubMed] [CrossRef] [Google Scholar]
• vanGenderen M. E.; Carels G.; Lonnee E. R.; Dees A.Severe facialswelling in a pregnant woman after using hair dye. BMJ. case reports2014, 2014, bcr2013202562. 10.1136/bcr-2013-202562. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Ishida W.; Makino T.; Shimizu T.Severe Hair Loss of the Scalp dueto a Hair Dye Containing para-phenylenediamine. ISRN dermatology2011, 2011, 947284. 10.5402/2011/947284. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Seo J. A.; Bae I. H.; Jang W. H.; Kim J. H.; Bak S. Y.; Han S. H.; Park Y. H.; Lim K. M.Hydrogen peroxideand monoethanolamine are the key causative ingredients for hair dye-induceddermatitis and hair loss. Journal of dermatologicalscience2012, 66 (1), 12–9. 10.1016/j.jdermsci.2011.12.015. [PubMed] [CrossRef] [Google Scholar]
• Dulon M.; Peters C.; Wendeler D.; Nienhaus A.Trends in occupationalairway diseases in german hairdressers: Frequency and causes. American journal of industrial medicine2011, 54 (6), 486–93. 10.1002/ajim.20947. [PubMed] [CrossRef] [Google Scholar]
• Moscato G.; Pignatti P.; Yacoub M. R.; Romano C.; Spezia S.; Perfetti L.Occupational asthmaand occupational rhinitis in hairdressers. Chest2005, 128 (5), 3590–8. 10.1378/chest.128.5.3590. [PubMed] [CrossRef] [Google Scholar]
• Helaskoski E.; Suojalehto H.; Virtanen H.; Airaksinen L.; Kuuliala O.; Aalto-Korte K.; Pesonen M.Occupational asthma,rhinitis, and contact urticaria caused by oxidative hair dyes in hairdressers. Annals of allergy, asthma & immunology2014, 112 (1), 46–52. 10.1016/j.anai.2013.10.002. [PubMed] [CrossRef] [Google Scholar]
• Hollund B. E.; Moen B. E.; Lygre S. H.; Florvaag E.; Omenaas E.Prevalenceof airway symptoms among hairdressers in Bergen, Norway. Occupational and environmental medicine2001, 58 (12), 780–5. 10.1136/oem.58.12.780. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Chrispal A.; Begum A.; Ramya I.; Zachariah A.Hair dye poisoning--anemerging problem in the tropics: an experience from a tertiary carehospital in South India. Tropical doctor2010, 40 (2), 100–3. 10.1258/td.2010.090367. [PubMed] [CrossRef] [Google Scholar]
• Senthilkumaran S.; Ram J.; Menezes R. G.; Sweni S.; Thirumalaikolundusubramanian P.Pneumothoraxin hair dye poisoning: An unrecognized danger. Lung India2011, 28 (4), 323–4. 10.4103/0970-2113.85753. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Elevli M.; Civilibal M.; Ersoy O.; Demirkol D.; Gedik A. H.Paraphenylenediamine hair dye poisoning: an uncommon cause of rhabdomyolysis. Indian journal of pediatrics2014, 81 (7), 709–11. 10.1007/s12098-013-1074-z. [PubMed] [CrossRef] [Google Scholar]
• Ram R.; Swarnalatha G.; Prasad N.; Dakshinamurty K. V.Paraphenylenediamine ingestion: an uncommon cause of acute renal failure. Journal of postgraduate medicine2007, 53 (3), 181–2. 10.4103/0022-3859.33860. [PubMed] [CrossRef] [Google Scholar]
• SandeepReddy Y.; Abbdul Nabi S.; Apparao C.; Srilatha C.; Manjusha Y.; Sri Ram Naveen P.; Krishna Kishore C.; Sridhar A.; Siva Kumar V.Hair Dye Related Acute Kidney Injury- A Clinical and Experimental Study. Renal failure2012, 34 (7), 880–4. 10.3109/0886022X.2012.687346. [PubMed] [CrossRef] [Google Scholar]
• Lewington A. J.; Cerdá J.; Mehta R. L.Raising awareness of acute kidneyinjury: a global perspective of a silent killer. Kidney international2013, 84 (3), 457–67. 10.1038/ki.2013.153. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Manjunatha B.; Han L.; Kundapur R. R.; Liu K.; Lee S. J.Herbul black henna(hair dye) causes cardiovascular defects in zebrafish (Danio rerio)embryo model. Environmental science and pollutionresearch international2020, 27 (12), 14150–9. 10.1007/s11356-020-07762-z. [PubMed] [CrossRef] [Google Scholar]
• Manjunatha B.; Wei-bing P.; Ke-chun L.; Marigoudar S. R.; Xi-qiang C.; Xi-min W.; Xue W.The effectsof henna(hair dye) on the embryonic development of zebrafish (Danio rerio). Environmental science and pollution research international2014, 21 (17), 10361–7. 10.1007/s11356-014-2968-7. [PubMed] [CrossRef] [Google Scholar]
• Harder T.; Roepke K.; Diller N.; Stechling Y.; Dudenhausen J. W.; Plagemann A.Birth weight, early weight gain,and subsequent risk of type 1 diabetes: systematic review and meta-analysis. American journal of epidemiology2009, 169 (12), 1428–36. 10.1093/aje/kwp065. [PubMed] [CrossRef] [Google Scholar]
• Jiang C.; Hou Q.; Huang Y.; Ye J.; Qin X.; Zhang Y.; Meng W.; Wang Q.; Jiang Y.; Zhang H.; Li M.; Mo Z.; Yang X.The effect of pre-pregnancy hairdye exposure on infant birth weight: a nested case-control study. BMC pregnancy and childbirth2018, 18 (1), 144. 10.1186/s12884-018-1782-5. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Lynch B. S.; Delzell E. S.; Bechtel D. H.Toxicology reviewand risk assessmentof resorcinol: thyroid effects. Regulatory toxicologyand pharmacology2002, 36 (2), 198–210. 10.1006/rtph.2002.1585. [PubMed] [CrossRef] [Google Scholar]
• Aminian O.; Saburi A.; Mohseni H.; Akbari H.; Chavoshi F.; Akbari H.Occupational risk of bladder cancer among Iranian maleworkers. Urology annals2014, 6 (2), 135–8. 10.4103/0974-7796.130643. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Yu M. C.; Skipper P. L.; Tannenbaum S. R.; Chan K. K.; Ross R. K.Arylamineexposures and bladder cancer risk. Mutationresearch2002, 506–507, 21–8. 10.1016/S0027-5107(02)00148-3. [PubMed] [CrossRef] [Google Scholar]
• Farzaneh F.; Mehrparvar A. H.; Lotfi M. H.Occupations andthe Risk of BladderCancer in Yazd Province: A Case-Control Study. international journal of occupational and environmental medicine2017, 8 (4), 191–8. 10.15171/ijoem.2017.1085. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Platzek T.Risk fromexposure to arylamines from consumer products and hair dyes. Frontiers in bioscience (Elite Ed)2010, 2 (3), 1169–1183. 10.2741/e177. [PubMed] [CrossRef] [Google Scholar]
• Harling M.; Schablon A.; Schedlbauer G.; Dulon M.; Nienhaus A.Bladder canceramong hairdressers: a meta-analysis. Occupationaland environmental medicine2010, 67 (5), 351–8. 10.1136/oem.2009.050195. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Golka K.; Heitmann P.; Gieseler F.; Hodzic J.; Masche N.; Bolt H. M.; Geller F.Elevated bladdercancer risk dueto colorants--a statewide case-control study in North Rhine-Westphalia,Germany. Journal of toxicology and environmentalhealth Part A2008, 71 (13–14), 851–5. 10.1080/15287390801985869. [PubMed] [CrossRef] [Google Scholar]
• Gubéran E.; Raymond L.; Sweetnam P. M.Increased risk formale bladder canceramong a cohort of male and female hairdressers from Geneva. International journal of epidemiology1985, 14 (4), 549–54. 10.1093/ije/14.4.549. [PubMed] [CrossRef] [Google Scholar]
• Alderson M.Cancer mortalityin male hairdressers. Journal of epidemiologyand community health1980, 34 (3), 182–5. 10.1136/jech.34.3.182. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Matsumoto M.; Suzuki M.; Kano H.; Aiso S.; Yamazaki K.; f*ckushima S.Carcinogenicity of ortho-phenylenediamine dihydrochloridein rats and mice by two-year drinking water treatment. Archives of toxicology2012, 86 (5), 791–804. 10.1007/s00204-012-0800-z. [PubMed] [CrossRef] [Google Scholar]
• Bioassayof 4-chloro-o-phenylenediamine for possible carcinogenicity. U. S., Natl. Cancer Inst., Carcinog. Tech. Rep. Ser.1978, 63, 1–115. [PubMed] [Google Scholar]
• Murata M.; Nishimura T.; Chen F.; Kawanishi S.OxidativeDNA damage induced by hair dye components ortho-phenylenediaminesand the enhancement by superoxide dismutase. Mutation research2006, 607 (2), 184–91. 10.1016/j.mrgentox.2006.04.014. [PubMed] [CrossRef] [Google Scholar]
• Turesky R. J.; Freeman J. P.; Holland R. D.; Nestorick D. M.; Miller D. W.; Ratnasinghe D. L.; Kadlubar F. F.Identification ofaminobiphenyl derivatives in commercial hair dyes. Chemical research in toxicology2003, 16 (9), 1162–73. 10.1021/tx030029r. [PubMed] [CrossRef] [Google Scholar]
• Airoldi L.; Orsi F.; Magagnotti C.; Coda R.; Randone D.; Casetta G.; Peluso M.; Hautefeuille A.; Malaveille C.; Vineis P.Determinants of 4-aminobiphenyl-DNAadducts in bladder cancer biopsies. Carcinogenesis2002, 23 (5), 861–6. 10.1093/carcin/23.5.861. [PubMed] [CrossRef] [Google Scholar]
• Gago-Dominguez M.; Castelao J. E.; Yuan J. M.; Yu M. C.; Ross R. K.Use ofpermanent hair dyes and bladder-cancer risk. International journal of cancer2001, 91 (4), 575–9. 10.1002/1097-0215(200002)9999:9999<::AID-IJC1092>3.0.CO;2-S. [PubMed] [CrossRef] [Google Scholar]
• Kogevinas M.; Fernandez F.; Garcia-Closas M.; Tardon A.; Garcia-Closas R.; Serra C.; Carrato A.; Castano-Vinyals G.; Yeager M.; Chanock S. J.; Lloreta J.; Rothman N.; Real F. X.; Dosemeci M.; Malats N.; Silverman D.Hair dye useis not associated with risk for bladder cancer: evidence from a case-controlstudy in Spain. European journal of cancer2006, 42 (10), 1448–54. 10.1016/j.ejca.2006.02.009. [PubMed] [CrossRef] [Google Scholar]
• Thun M. J.; Altekruse S. F.; Namboodiri M. M.; Calle E. E.; Myers D. G.; Heath C. W. Jr.Hair dye use and risk of fatal cancersin U.S. women. Journal of the national cancerinstitute1994, 86 (3), 210–5. 10.1093/jnci/86.3.210. [PubMed] [CrossRef] [Google Scholar]
• Henley S. J.; Thun M. J.Use of permanent hair dyes and bladder-cancer risk. International journal of cancer2001, 94 (6), 903–6. 10.1002/ijc.1547. [PubMed] [CrossRef] [Google Scholar]
• Hartge P.; Hoover R.; Altman R.; Austin D. F.; Cantor K. P.; Child M. A.; Key C. R.; Mason T. J.; Marrett L. D.; Myers M. H.; Narayana A. S.; Silverman D. T.; Sullivan J. W.; Swanson G. M.; Thomas D. B.; West D. W.Use ofhair dyes and risk of bladder cancer. Cancerresearch1982, 42 (11), 4784–4787. [PubMed] [Google Scholar]
• Andrew A. S.; Schned A. R.; Heaney J. A.; Karagas M. R.Bladder cancer riskand personal hair dye use. International journalof cancer2004, 109 (4), 581–6. 10.1002/ijc.11729. [PubMed] [CrossRef] [Google Scholar]
• Turati F.; Pelucchi C.; Galeone C.; Decarli A.; La Vecchia C.Personal hairdye use and bladder cancer: a meta-analysis. Annals of epidemiology2014, 24 (2), 151–9. 10.1016/j.annepidem.2013.11.003. [PubMed] [CrossRef] [Google Scholar]
• Ros M. M.; Gago-Dominguez M.; Aben K. K.; Bueno-de-Mesquita H.B.; Kampman E.; Vermeulen S. H.; Kiemeney L. A.Personal hair dyeuse and the risk of bladder cancer: a case-control study from TheNetherlands. Cancer causes control2012, 23 (7), 1139–48. 10.1007/s10552-012-9982-1. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Lin J.; Dinney C. P.; Grossman H. B.; Wu X.Personal permanenthair dye use is not associated with bladder cancer risk: evidencefrom a case-control study. Cancer epidemiologybiomarkers & prevention2006, 15 (9), 1746–9. 10.1158/1055-9965.EPI-06-0156. [PubMed] [CrossRef] [Google Scholar]
• Kelsh M. A.; Alexander D. D.; Kalmes R. M.; Buffler P. A.Personaluse of hair dyes and risk of bladder cancer: a meta-analysis of epidemiologicdata. Cancer causes control2008, 19 (6), 549–58. 10.1007/s10552-008-9123-z. [PubMed] [CrossRef] [Google Scholar]
• Huncharek M.; Kupelnick B.Personal useof hair dyes and therisk of bladder cancer: results of a meta-analysis. Public health reports (Washington, DC: 1974)2005, 120 (1), 31–8. 10.1177/003335490512000107. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Koutros S.; Silverman D. T.; Baris D.; Zahm S. H.; Morton L. M.; Colt J. S.; Hein D. W.; Moore L. E.; Johnson A.; Schwenn M.; Cherala S.; Schned A.; Doll M. A.; Rothman N.; Karagas M. R.Hair dye use andrisk of bladder cancer in the New England bladder cancer study. International journal of cancer2011, 129 (12), 2894–904. 10.1002/ijc.26245. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Gago-Dominguez M.; Bell D. A.; Watson M. A.; Yuan J. M.; Castelao J. E.; Hein D. W.; Chan K. K.; Coetzee G. A.; Ross R. K.; Yu M. C.Permanent hair dyesand bladder cancer:risk modification by cytochrome P4501A2 and N-acetyltransferases 1and 2. Carcinogenesis2003, 24 (3), 483–9. 10.1093/carcin/24.3.483. [PubMed] [CrossRef] [Google Scholar]
• Czene K.; Tiikkaja S.; Hemminki K.Cancer risksin hairdressers:assessment of carcinogenicity of hair dyes and gels. International journal of cancer2003, 105 (1), 108–12. 10.1002/ijc.11040. [PubMed] [CrossRef] [Google Scholar]
• Bolt H. M.; Golka K.The debate on carcinogenicityofpermanent hair dyes: new insights. Criticalreviews in toxicology2007, 37 (6), 521–36. 10.1080/10408440701385671. [PubMed] [CrossRef] [Google Scholar]
• Siegel R. L.; Miller K. D.; Jemal A.Cancer statistics,2019. CA-A cancer journal for clinicians2019, 69 (1), 7–34. 10.3322/caac.21551. [PubMed] [CrossRef] [Google Scholar]
• American Cancer SocietyCancer Facts & Figures; American CancerSociety: Atlanta,GA, 2019. https://www.cancer.org/content/dam/cancer-org/research/cancer-facts-and-statistics/annual-cancer-facts-and-figures/2019/cancer-facts-and-figures-2019.pdf (accessed).
• Boice J. D. Jr.; Doody M. M.; Mandel J. S.BreastCancer Among Radiologic Technologists. JAMA1995, 274 (5), 394–401. 10.1001/jama.274.5.394. [PubMed] [CrossRef] [Google Scholar]
• Koenig K. L.; Pasternack B. S.; Shore R. E.; Strax P.Hair dye useand breast cancer: a case-control study among screening participants. American journal of epidemiology1991, 133 (10), 985–95. 10.1093/oxfordjournals.aje.a115818. [PubMed] [CrossRef] [Google Scholar]
• Zheng T.; Holford T. R.; Mayne S. T.; Owens P. H.; Boyle P.; Zhang B.; Zhang Y. W.; Zahm S. H.Use ofhair colouring products and breast cancer risk: a case-control studyin Connecticut. European journal of cancer (Oxford,England: 1990)2002, 38 (12), 1647–52. 10.1016/S0959-8049(02)00138-7. [PubMed] [CrossRef] [Google Scholar]
• Nasca P. C.; Baptiste M. S.; Field N. A.; Metzger B. B.; DeMartino R.An epidemiologic case-control studyof breast cancerand exposure to hair dyes. Annals of epidemiology1992, 2 (5), 577–86. 10.1016/1047-2797(92)90002-8. [PubMed] [CrossRef] [Google Scholar]
• Cook L. S.; Malone K. E.; Daling J. R.; Voigt L. F.; Weiss N. S.Hair productuse and the risk of breast cancer in youngwomen. Cancer causes control1999, 10 (6), 551–9. 10.1023/A:1008903126798. [PubMed] [CrossRef] [Google Scholar]
• Heikkinen S.; Pitkäniemi J.; Sarkeala T.; Malila N.; Koskenvuo M.Does hairdye use increase the risk of breast cancer?A population-based case-control study of finnish women. PloS one2015, 10 (8), e0135190. 10.1371/journal.pone.0135190. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Petro-Nustas W.; Norton M. E.; al-Masarweh I.Risk factorsfor breast cancer in Jordanian women. Journalof nursing scholarship2002, 34 (1), 19–25. 10.1111/j.1547-5069.2002.00019.x. [PubMed] [CrossRef] [Google Scholar]
• Nasca P. C.; Lawrence C. E.; Greenwald P.; Chorost S.; Arbuckle J. T.; Paulson A.Relationship of hairdye use, benign breast disease, and breast cancer. Journal of the national cancer institute1980, 64 (1), 23–28. [PubMed] [Google Scholar]
• Eberle C. E.; Sandler D. P.; Taylor K. W.; White A. J.Hair dyeand chemical straightener use and breast cancer risk in a large USpopulation of black and white women. Internationaljournal of cancer2020, 147 (2), 383–391. 10.1002/ijc.32738. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Xu S.; Wang H.; Liu Y.; Zhang C.; Xu Y.; Tian F.; Mei L.Hair chemicals may increase breastcancer risk: A meta-analysis of 210319 subjects from 14 studies. PLoS one2021, 16 (2), e0243792. 10.1371/journal.pone.0243792. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Kelsey J. L.; Gammon M. D.; John E. M.Reproductive factorsand breast cancer. Epidemiologic reviews1993, 15 (1), 36–47. 10.1093/oxfordjournals.epirev.a036115. [PubMed] [CrossRef] [Google Scholar]
• Hsieh C.-C.; Trichopoulos D.; Katsouyanni K.; Yuasa S.Age at menarche, ageat menopause, height and obesity as risk factorsfor breast cancer: associations and interactions in an internationalcase-control study. International journal ofcancer1990, 46 (5), 796–800. 10.1002/ijc.2910460508. [PubMed] [CrossRef] [Google Scholar]
• MacMahon B.; Trichopoulos D.; Brown J.; Andersen A. P.; Aoki K.; Cole P.; deWaard F.; Kauraniemi T.; Morgan R. W.; Purde M.; Ravnihar B.; Stromby N.; Westlund K.; Woo N. C.Age at menarche, probability of ovulationand breast cancer risk. International journalof cancer1982, 29 (1), 13–16. 10.1002/ijc.2910290104. [PubMed] [CrossRef] [Google Scholar]
• Apter D.; Vihko R.Early menarche, a risk factor forbreast cancer, indicates early onset of ovulatory cycles. journal of clinical endocrinology & metabolism1983, 57 (1), 82–6. 10.1210/jcem-57-1-82. [PubMed] [CrossRef] [Google Scholar]
• Macmahon B.; Trichopoulos D.; Brown J.; Andersen A. P.; Cole P.; Dewaard F.; Kauraniemi T.; Polychronopoulou A.; Ravnihar B.; Stormby N.; Westlund K.Age at menarche,urine estrogens and breast cancer risk. Internationaljournal of cancer1982, 30 (4), 427–431. 10.1002/ijc.2910300408. [PubMed] [CrossRef] [Google Scholar]
• Apter D.; Reinilä M.; Vihko R.Some endocrine characteristicsof early menarche, a risk factor for breast cancer, are preservedinto adulthood. International journal of cancer1989, 44 (5), 783–7. 10.1002/ijc.2910440506. [PubMed] [CrossRef] [Google Scholar]
• Stiel L.; Adkins-Jackson P. B.; Clark P.; Mitchell E.; Montgomery S.A review ofhair product use on breast cancer riskin African American women. Cancer medicine2016, 5 (3), 597–604. 10.1002/cam4.613. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Calaf G.M.; Ponce-Cusi R.; Aguayo F.; Munoz J. P.; Bleak T. C.Endocrine disruptorsfrom the environment affectingbreast cancer. Oncology letters2020, 20 (1), 19–32. 10.3892/ol.2020.11566. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Main K. M.; Mortensen G. K.; Kaleva M. M.; Boisen K. A.; Damgaard I. N.; Chellakooty M.; Schmidt I. M.; Suomi A. M.; Virtanen H. E.; Petersen D. V.; Andersson A. M.; Toppari J.; Skakkebaek N. E.Human breastmilk contamination withphthalates and alterations of endogenous reproductive hormones ininfants three months of age. Environ. HealthPerspect.2006, 114 (2), 270–6. 10.1289/ehp.8075. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• McDonald J. A.; Tehranifar P.; Flom J. D.; Terry M. B.; James-Todd T.Hair productuse, age at menarche and mammographicbreast density in multiethnic urban women. Environmentalhealth2018, 17 (1), 1. 10.1186/s12940-017-0345-y. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Llanos A. A. M.; Rabkin A.; Bandera E. V.; Zirpoli G.; Gonzalez B. D.; Xing C. Y.; Qin B.; Lin Y.; Hong C. C.; Demissie K.; Ambrosone C. B.Hair productuse and breast cancer risk among African American and White women. Carcinogenesis2017, 38 (9), 883–92. 10.1093/carcin/bgx060. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• White A. J.; Gregoire A. M.; Taylor K. W.; Eberle C.; Gaston S.; O’Brien K. M.; Jackson C. L.; Sandler D. P.Adolescentuse of hair dyes, straighteners and perms in relation to breast cancerrisk. International journal of cancer2021, 148 (9), 2255–63. 10.1002/ijc.33413. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Gwinn M.R.; Whipkey D. L.; Tennant L. B.; Weston A.Gene expressionprofiling of di-n-butyl phthalate in normal human mammary epithelialcells. Journal of environmental pathology, toxicologyand oncology2007, 26 (1), 51–61. 10.1615/JEnvironPatholToxicolOncol.v26.i1.60. [PubMed] [CrossRef] [Google Scholar]
• Lv L.; Lin G.; Lin G.; Gao X.; Wu C.; Dai J.; Yang Y.; Zou H.; Sun H.; Gu M.; Chen X.; Fu H.; Bao L.Case-controlstudyof risk factors of myelodysplastic syndromes according to World HealthOrganization classification in a Chinese population. American journal of hematology2011, 86 (2), 163–9. 10.1002/ajh.21941. [PubMed] [CrossRef] [Google Scholar]
• Nagata C.; Shimizu H.; Hirashima K.; Kakish*ta E.; Fujimura K.; Niho Y.; Karasawa M.; Oguma S.; Yoshida Y.; Mizoguchi H.Hair dye useand occupational exposure to organic solvents as risk factors formyelodysplastic syndrome. Leukemia research1999, 23 (1), 57–62. 10.1016/S0145-2126(98)00135-0. [PubMed] [CrossRef] [Google Scholar]
• Grodstein F.; Hennekens C. H.; Colditz G. A.; Hunter D. J.; Stampfer M. J.A prospectivestudy of permanent hair dye use and hematopoieticcancer. Journal of the national cancer institute1994, 86 (19), 1466–70. 10.1093/jnci/86.19.1466. [PubMed] [CrossRef] [Google Scholar]
• Mele A.; Stazi M. A.; Pulsoni A.; Visani G.; Monarca B.; Castelli G.; Rocchi L.; Avvisati G.; Mandelli F.Epidemiologyof acute promyelocytic leukemia. Haematologica1995, 80 (5), 405–408. [PubMed] [Google Scholar]
• Miligi L.; Seniori Costantini A.; Crosignani P.; Fontana A.; Masala G.; Nanni O.; Ramazzotti V.; Rodella S.; Stagnaro E.; Tumino R.; Viganò C.; Vindigni C.; Vineis P.Occupational, environmental,andlife-style factors associated with the risk of hematolymphopoieticmalignancies in women. American journal of industrialmedicine1999, 36 (1), 60–69. 10.1002/(SICI)1097-0274(199907)36:1<60::AID-AJIM9>3.0.CO;2-Z. [PubMed] [CrossRef] [Google Scholar]
• Benavente Y.; Garcia N.; Domingo-Domenech E.; Alvaro T.; Font R.; Zhang Y.; de Sanjose S.Regular useof hair dyes and risk of lymphoma in Spain. International journal of epidemiology2005, 34 (5), 1118–22. 10.1093/ije/dyi109. [PubMed] [CrossRef] [Google Scholar]
• Herrinton L. J.; Weiss N. S.; Koepsell T. D.; Daling J. R.; Taylor J. W.; Lyon J. L.; Swanson G. M.; Greenberg R. S.Exposureto hair-coloring products and the risk of multiple myeloma. American journal of public health1994, 84 (7), 1142–4. 10.2105/AJPH.84.7.1142. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Koutros S.; Baris D.; Bell E.; Zheng T.; Zhang Y.; Holford T. R.; Leaderer B. P.; Landgren O.; Zahm S. H.Use of hair colouring products andrisk of multiplemyeloma among US women. Occupational and environmentalmedicine2009, 66 (1), 68–70. 10.1136/oem.2008.041053. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Tavani A.; Negri E.; Franceschi S.; Talalmini R.; Serraino D.; La Vecchia C.Hair dye useand risk of lymphoid neoplasms and soft tissue sarcomas. International journal of cancer2005, 113 (4), 629–631. 10.1002/ijc.20565. [PubMed] [CrossRef] [Google Scholar]
• Rauscher G. H.; Shore D.; Sandler D. P.Hair dyeuse andrisk of adult acute leukemia. American journalof epidemiology2004, 160 (1), 19–25. 10.1093/aje/kwh166. [PubMed] [CrossRef] [Google Scholar]
• Parodi S.; Santi I.; Marani E.; Casella C.; Puppo A.; Garrone E.; Fontana V.; Stagnaro E.Lifestylefactors and risk of leukemia and non-Hodgkin’s lymphoma: acase-control study. Cancer causes control2016, 27 (3), 367–75. 10.1007/s10552-016-0713-x. [PubMed] [CrossRef] [Google Scholar]
• Towle K. M.; Grespin M. E.; Monnot A. D.Personal use ofhair dyes and risk of leukemia: a systematic literature review andmeta-analysis. Cancer medicine2017, 6 (10), 2471–86. 10.1002/cam4.1162. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Morton L.M.; Wang S. S.; Devesa S. S.; Hartge P.; Weisenburger D. D.; Linet M. S.Lymphoma incidence patterns by WHOsubtype in the United States, 1992–2001. Blood2006, 107 (1), 265–76. 10.1182/blood-2005-06-2508. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Wong O.; Harris F.; Wang Y.; Fu H.A hospital-basedcase-control study of non-Hodgkin lymphoid neoplasms in Shanghai:Analysis of personal characteristics, lifestyle, and environmentalrisk factors by subtypes of the WHO classification. Journal of occupational and environmental medicine2010, 52 (1), 39–53. 10.1097/JOM.0b013e3181c5c399. [PubMed] [CrossRef] [Google Scholar]
• Zahm S. H.; Weisenburger D. D.; Babbitt P. A.; Saal R. C.; Vaught J. B.; Blair A.Use of hair coloring products andthe risk of lymphoma, multiple myeloma, and chronic lymphocytic leukemia. American journal of public health1992, 82 (7), 990–7. 10.2105/AJPH.82.7.990. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Zhang Y.; Hughes K. J.; Zahm S. H.; Zhang Y.; Holford T. R.; Dai L.; Bai Y.; Han X.; Qin Q.; Lan Q.; Rothman N.; Zhu Y.; Leaderer B.; Zheng T.Genetic Variations in XenobioticMetabolic Pathway Genes, PersonalHair Dye Use, and Risk of Non-Hodgkin Lymphoma. American journal of epidemiology2009, 170 (10), 1222–30. 10.1093/aje/kwp263. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Zhang Y.; Holford T. R.; Leaderer B.; Boyle P.; Zahm S. H.; Flynn S.; Tallini G.; Owens P. H.; Zheng T.Hair-coloring product use and riskof non-Hodgkin’s lymphoma:a population-based case-control study in Connecticut. American journal of epidemiology2004, 159 (2), 148–54. 10.1093/aje/kwh033. [PubMed] [CrossRef] [Google Scholar]
• Zhang Y.; Sanjose S. D.; Bracci P. M.; Morton L. M.; Wang R.; Brennan P.; Hartge P.; Boffetta P.; Becker N.; Maynadie M.; Foretova L.; Cocco P.; Staines A.; Holford T.; Holly E. A.; Nieters A.; Benavente Y.; Bernstein L.; Zahm S. H.; Zheng T.Personal useof hair dye and the risk of certain subtypes of non-Hodgkin lymphoma. American journal of epidemiology2008, 167 (11), 1321–31. 10.1093/aje/kwn058. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Guo H.; Bassig B. A.; Lan Q.; Zhu Y.; Zhang Y.; Holford T. R.; Leaderer B.; Boyle P.; Qin Q.; Zhu C.; Li N.; Rothman N.; Zheng T.Polymorphismsin DNArepair genes, hair dye use, and the risk of non-Hodgkin lymphoma. Cancer causes control2014, 25 (10), 1261–70. 10.1007/s10552-014-0423-1. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Cantor K. P.; Blair A.; Everett G.; VanLier S.; Burmeister L.; Dick F. R.; Gibson R. W.; Schuman L.Hair dye useand risk of leukemia and lymphoma. Americanjournal of public health1988, 78 (5), 570–1. 10.2105/AJPH.78.5.570. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• McCall E. E.; Olshan A. F.; Daniels J. L.Maternalhair dyeuse and risk of neuroblastoma in offspring. Cancer causes control2005, 16 (6), 743–8. 10.1007/s10552-005-1229-y. [PubMed] [CrossRef] [Google Scholar]
• IARC/WHO . Cancer Incidence,Mortality and Prevalence Worldwide in 2008, 2008. http://globocan.iarc.fr (accessed).
• Couto A. C.; Ferreira J. D.; Rosa A. C. S.; Pombo-de-Oliveira M. S.; Koifman S.Brazilian CollaborativeStudy G. Pregnancy, maternalexposure to hair dyes and hair straightening cosmetics, and earlyage leukemia. Chemico-biological interactions2013, 205 (1), 46–52. 10.1016/j.cbi.2013.05.012. [PubMed] [CrossRef] [Google Scholar]
• Gao Z.; Wang R.; Qin Z. X.; Dong A.; Liu C. B.Protectiveeffect of breastfeeding against childhood leukemia in Zhejiang Province,P. R. China: a retrospective case-control study. Libran J. Med.2018, 13 (1), 1508273. 10.1080/19932820.2018.1508273. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Parodi S.; Merlo D. F.; Ranucci A.; Miligi L.; Benvenuti A.; Rondelli R.; Magnani C.; Haupt R.Risk of neuroblastoma,maternal characteristics and perinatal exposures: The SETIL study. Cancer epidemiology2014, 38 (6), 686–694. 10.1016/j.canep.2014.09.007. [PubMed] [CrossRef] [Google Scholar]
• Holly E. A.; Bracci P. M.; Hong M. K.; Mueller B. A.; Preston-Martin S.West Coast study of childhood braintumours and maternaluse of hair-colouring products. Paediatric andperinatal epidemiology2002, 16 (3), 226–35. 10.1046/j.1365-3016.2002.00420.x. [PubMed] [CrossRef] [Google Scholar]
• Ghazarian A. A.; Kelly S. P.; Altekruse S. F.; Rosenberg P. S.; McGlynn K. A.Future of testicular germ cell tumorincidence in the United States: Forecast through 2026. Cancer2017, 123 (12), 2320–8. 10.1002/cncr.30597. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• McGlynn K. A.; Cook M. B.Etiologic factors in testicular germ-celltumors. Future oncology2009, 5 (9), 1389–402. 10.2217/fon.09.116. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Ghazarian A. A.; Trabert B.; Robien K.; Graubard B. I.; McGlynn K. A.Maternal use of personal care productsduring pregnancyand risk of testicular germ cell tumors in sons. Environmental research2018, 164, 109–13. 10.1016/j.envres.2018.02.017. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
• Chen Z.; Robison L.; Giller R.; Krailo M.; Davis M.; Davies S.; Shu X. O.Environmental exposureto residential pesticides, chemicals, dusts, fumes, and metals, andrisk of childhood germ cell tumors. Internationaljournal of hygiene and environmental health2006, 209 (1), 31–40. 10.1016/j.ijheh.2005.08.001. [PubMed] [CrossRef] [Google Scholar]
• Garsa A. A.; Badiyan S. N.; DeWees T.; Simpson J. R.; Huang J.; Drzymala R. E.; Barani I. J.; Dowling J. L.; Rich K. M.; Chicoine M. R.; Kim A. H.; Leuthardt E. C.; Robinson C. G.Predictors of individual tumor localcontrol afterstereotactic radiosurgery for non-small cell lung cancer brain metastases. International journal of radiation oncology, biology, physics2014, 90 (2), 407–13. 10.1016/j.ijrobp.2014.05.047. [PubMed] [CrossRef] [Google Scholar]
• American Cancer Society . Hair Dyesand Cancer Risk; American CancerSociety: Atlanta, GA. https://www.cancer.org/cancer/cancer-causes/hair-dyes.html (accessed).
• IARC . IARCmonographs onthe evaluation of carcinogenic risks to humans; Some Aromatic Amines,Organic Dyes, and Related Exposures; IARC: Lyon, France, 2010;Vol. 99, pp 1–658. [PMC free article] [PubMed]