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American Journal of Epidemiology Advance Access originally published online on November 1, 2006
American Journal of Epidemiology 2007 165(1):63-71; doi:10.1093/aje/kwk002
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American Journal of Epidemiology Copyright © 2006 by the Johns Hopkins Bloomberg School of Public Health All rights reserved; printed in U.S.A.

ORIGINAL CONTRIBUTIONS

Personal Hair Dye Use and Risks of Glioma, Meningioma, and Acoustic Neuroma among Adults

Elizabeth C. Bluhm1,2, Shelia Hoar Zahm1, Howard A. Fine3, Peter M. Black4, Jay S. Loeffler5, William R. Shapiro6, Robert G. Selker7 and Peter D. Inskip1

1 Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD
2 Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, Bethesda, MD
3 Neuro-Oncology Branch, National Cancer Institute, Bethesda, MD
4 Department of Neurosurgery, Brigham and Women's Hospital, Boston, MA
5 Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA
6 Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ
7 Division of Neurosurgery, Western Pennsylvania Hospital, Pittsburgh, PA

Correspondence to Elizabeth C. Bluhm, Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Boulevard, MSC 7238, Rockville, MD 20892-7238 (e-mail: bluhme{at}mail.nih.gov).

Received for publication February 24, 2006. Accepted for publication May 26, 2006.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Previous studies have suggested an association of personal hair dye use with bladder and hematopoietic cancers. Risks for brain tumors are not well understood. The authors investigated associations between use of synthetic hair dyes and risk of brain tumors in a hospital-based case-control study. The study included adults newly diagnosed with glioma (n = 489), meningioma (n = 197), or acoustic neuroma (n = 96) between 1994 and 1998 at three urban US hospitals and 799 controls. Odds ratios were estimated and 95% confidence intervals were calculated using unconditional logistic regression. Detailed exposure histories were obtained by interview. There was no consistent pattern of elevated odds ratios for glioma, meningioma, or acoustic neuroma with use or prolonged use of permanent, semipermanent, temporary, or gradual hair dyes. Although use of permanent brown hair dye for 20 or more years was associated with glioma among women, the estimate was imprecise (odds ratio = 3.8, 95% confidence interval: 1.2, 12.5) and was based on just 13 exposed cases; thus, this could be a chance finding. Overall, there was little consistent evidence for an association of synthetic hair dye use with glioma, meningioma, or acoustic neuroma. However, prolonged use of dark-colored permanent dyes warrants further investigation given the high prevalence of hair dyeing.

glioma; hair dyes; meningioma; neuroma, acoustic

Abbreviations: CI, confidence interval; NAT, N-acetyltransferase; OR, odds ratio


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Hair dye is used widely in developed nations, both to change natural hair color and to cover gray hair (1). Components of hair dyes include aromatic amines, which have been found to be mutagenic in vitro (2) and carcinogenic in rodents (3, 4). Personal hair dye use has been modestly associated with cancers of the bladder (5, 6) and breast (7) and with non-Hodgkin's lymphoma (8–10), Hodgkin's lymphoma (8), multiple myeloma (8, 11), and leukemia (9); however, other case-control (12–21) and cohort (22–26) studies have not found associations with cancer. Risk appears to differ by dye permanence (5), color (8), cumulative lifetime number of uses (5, 6, 8), calendar time period of use (10), and polymorphisms in xenobiotic metabolizing genes (6). In a meta-analysis, Takkouche et al. (27) identified statistically significant elevated risks for hematopoietic cancers (including non-Hodgkin's lymphoma, lymphocytic leukemia, and multiple myeloma), ovarian cancer, and brain cancer among persons using hair dye.

In prior studies of personal hair dye use, investigators have reported a suggestive association with astrocytoma (28) and a significant association with brain tumors (29) (pooled odds ratio (OR) = 1.83, 95 percent confidence interval (CI): 1.16, 2.89 (27)). In a recent case-control study among Nebraska women, Heineman et al. (30) reported an association of permanent hair dye use with glioblastoma multiforme (OR = 3.5, 95 percent CI: 1.7, 7.3) that increased with duration of use (p = 0.001). Occupational studies of hairdressers have reported increased risks of bladder cancer (31, 32) and multiple myeloma (33, 34) but not glioma (35), meningioma (36), or acoustic neuroma (36). In 1993, the International Agency for Research on Cancer of the World Health Organization classified the exposures of hairdressers and barbers as probably carcinogenic (Group 2A) but concluded that evidence was insufficient to evaluate personal use of hair dye (Group 3) (32). The international SEARCH (Surveillance of Environmental Aspects Related to Cancer in Humans) study and other case-control studies have found no clear pattern of increased risks for brain tumors among children whose mothers used hair dye during pregnancy (37, 38).

Distinction among different hair coloring products in epidemiologic studies is potentially important given the distinct chemical properties of dyes. Permanent (oxidative) dye precursors are mixed with hydrogen peroxide and chemical couplers such as resourcinol (1,3-dihydroxybenzene) to generate a colored oxidation product within the hair shaft (39). Semipermanent and temporary dyes directly deposit color on the outer cuticle or surface of each hair and wash out after one to several dozen shampooings (32, 39). Gradual (progressive) dyes undergo a very slow oxidation reaction between component metal salts (lead, silver, or bismuth) and hair keratin sulfur and are intended for daily application (39). The color produced by each dye is determined by the proportional composition of chemicals, in addition to hair texture, color, and application technique, including pretreatment.

In this study, we investigated associations between personal use of permanent, semipermanent, temporary, and gradual synthetic hair dyes and the risks of glioma, meningioma, and acoustic neuroma in adults. We used detailed information about hair dye exposures collected within a broader case-control study of the relation between environmental exposures, genetic susceptibility, and risk of adult brain tumors.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
Data collection
The overall study design has been described previously (40, 41). Briefly, adult cases were identified through active daily surveillance of patients seen at three urban US hospitals (in Boston, Massachusetts, Pittsburgh, Pennsylvania, and Phoenix, Arizona) between 1994 and 1998 who were within 8 weeks of histologic confirmation of intracranial glioma, meningioma, or acoustic neuroma. Magnetic resonance imaging diagnosis of acoustic neuroma was allowed. (There were four such patients.) Hospital-based controls with a noncancer diagnosis were frequency-matched (1:1) to the total case series by age (within 10-year strata), sex, race/ethnicity (non-Hispanic White, Hispanic White, Black, or other/unknown), hospital, and distance from residence to the hospital. Of the eligible subjects, 92 percent (n = 782) of cases and 86 percent (n = 799) of controls agreed to participate. The study protocol was approved by the institutional review board of each participating hospital and the National Cancer Institute, and each subject or his/her proxy provided written consent.

A trained research nurse administered a computer-assisted questionnaire at the subject's bedside or in a suitable hospital location, ascertaining demographic information, medical history, and information about exposures of interest in brain tumor etiology, including ever use of a hair dye or hair coloring product; ever use of any permanent, semipermanent, and/or temporary dye; ever use of a product that changed hair color gradually; number of uses per week, month, or year; usual color used; year or age at which use started; and year or age at which use stopped. Specific colors were classified as black, brown, red, blond, or other. Any subject who had used more than one color was assigned the darker color. Peroxide and other bleaching products, which deplete color from the hair shaft, were excluded from analyses. Duration of use and total lifetime number of uses were calculated from self-reported start and stop dates and frequency.

A proxy interview was conducted for any patient unable to respond. A proxy respondent answered the hair dye section of the questionnaire for 18 percent of glioma cases, 8 percent of meningioma cases, 3 percent of acoustic neuroma cases, and 3 percent of controls. The proxy was usually a spouse (47 percent), parent (21 percent), or child (12 percent).

Statistical analysis
Unconditional logistic regression was used to estimate odds ratios and calculate 95 percent likelihood-based confidence intervals for associations of each type of brain tumor with use of hair dyes, using SAS software, version 8.2 (SAS Institute, Inc., Cary, North Carolina). The reference category for all analyses consisted of subjects who had never used hair dye. Within the glioma cases, we also separately analyzed glioblastoma multiforme (International Classification of Diseases for Oncology, Second Edition (42), code 9440; hereafter referred to as glioblastoma). Variables evaluated for potential confounding included education, income, marital status, religion, and hair graying (coded as ever graying versus never graying or as graying at age <20, 20–29, or 30–39 years versus age 40 years or older, including those who attained ages ≥40 years without graying). Adjustments for graying and income had a negligible effect on risk estimates and were not included in the final models. Reported results were adjusted for matching factors, marital status at the time of interview, and educational attainment, except where otherwise indicated. Age at diagnosis was coded by decade. We also entered age as a continuous variable, but this had little effect on odds ratios. We evaluated possible effect modification by age at diagnosis and hospital site and also analyzed the influence of altered mental status among patients with glioma. Odds ratios are reported where there were three or more exposed cases. Two-sided p values based on likelihood ratio tests were calculated.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
Characteristics of cases and controls
The study enrolled 489 cases with glioma, 197 cases with meningioma, 96 cases with acoustic neuroma, and 799 controls. The most common reasons for hospital admission among controls were injury (n = 197), circulatory disease (n = 179), and musculoskeletal disorder (n = 172). A majority of subjects with meningioma and acoustic neuroma were female, whereas more subjects with glioma, particularly high-grade glioma, were male. Among cases with glioma, 232 were diagnosed with glioblastoma multiforme. Mean ages at diagnosis and interview were 52 years for glioma, 55 years for meningioma, and 51 years for acoustic neuroma. The mean age at interview for controls was 50 years. Non-Hispanic Whites comprised more than 82 percent of controls and each group of brain tumor cases. Compared with controls, patients with glioma were more likely to be college-educated; glioma and meningioma patients were more likely to be married and Jewish. The largest proportion of all cases was recruited in Arizona (53 percent) (table 1). Men were not included in detailed analyses of hair dye use because data for men were generally too sparse to support such analyses.


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  		TABLE 1 Demographic characteristics of brain tumor patients and controls in a hospital-based case-control study, United States, 1994–1998

 
Exposure to hair dyes and risk of brain tumors
Seventy-nine percent of female controls and 16 percent of male controls reported ever having used hair dye (table 2). No statistically significant association was observed between ever use of hair dye—or ever use of permanent, semipermanent, temporary, or gradual hair dye—and diagnosis of glioma, meningioma, or acoustic neuroma (table 2). Among women, use of permanent dyes was associated with odds ratios of 1.0 for glioma (95 percent CI: 0.6, 1.6), 0.8 (95 percent CI: 0.4, 1.7) for glioblastoma, 0.8 (95 percent CI: 0.5, 1.4) for meningioma, and 0.9 (95 percent CI: 0.4, 2.1) for acoustic neuroma. Increasing duration of use, frequency of use, cumulative lifetime use, younger age at starting use, and color of permanent dye used were not significantly associated with any type of brain tumor (table 3). No significant associations were seen among subjects who used permanent dyes exclusively (data not shown).


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  		TABLE 2 Odds ratios for brain tumors among men and women according to use of specific types of synthetic hair dye, United States, 1994–1998

 

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  		TABLE 3 Odds ratios for brain tumors among women according to duration and frequency of hair dye use and color of permanent hair dye, United States, 1994–1998

 
No characteristic of semipermanent dye or temporary dye use was associated with glioma, meningioma, or acoustic neuroma (data not shown). Gradual hair dye was used by only 37 men and 26 women, yielding odds ratios for glioma of 0.6 (95 percent CI: 0.3, 1.3) in men and 2.0 (95 percent CI: 0.6, 6.3) in women (table 2).

Long-term (≥20 years) use of brown permanent dye was associated with elevated but imprecise risks of glioma (OR = 3.8, 95 percent CI: 1.2, 12.5) and acoustic neuroma (OR = 14.9, 95 percent CI: 2.1, 170), based on small numbers of exposed cases and controls (table 4). The odds ratio for glioblastoma among long-term brown dye users was 2.3 (95 percent CI: 0.5, 10.7). Fewer subjects used red permanent dyes; among short- to medium-duration (1–19 years) users of red dyes, there were elevated risks of glioma (OR = 3.3, 95 percent CI: 1.0, 10.8) and acoustic neuroma (OR = 18.4, 95 percent CI: 2.1, 234), but the risks were extremely imprecise. The odds ratios for long-term users were sensitive to cutpoints of exposure categories. For example, there were eight glioma cases and 10 controls with ≥25 years of use of brown permanent dye (OR = 2.6, 95 percent CI: 0.7, 10.4). With continuous coding of years of use, there were weak or marginally significant trends for the relations between duration of use of brown permanent dye and glioma (p-trend = 0.05) and acoustic neuroma (p-trend = 0.24) (data not shown). Associations were similar for high- and low-grade glioma, among glioma cases with or without a change in mental status, and after exclusion of proxy responders (data not shown). For example, in analyses limited to self-respondents, ever use of permanent hair dye was associated with an odds ratio for glioma of 0.9 (95 percent CI: 0.6, 1.5) and an odds ratio for glioblastoma of 0.7 (95 percent CI: 0.3, 1.4). Likewise, among self-respondents with long-term use of brown permanent hair dye, the odds ratio for glioma was 6.4 (95 percent CI: 1.8, 27) and the odds ratio for glioblastoma was 2.9 (95 percent CI: 0.6, 16.7).


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  		TABLE 4 Odds ratios for selected brain tumors among women by duration of use of permanent hair dye and usual color of dye, United States, 1994–1998

 
We found no increase in risk of any brain tumor with hair dye use prior to 1980 in men or women (among women using permanent dye, odds ratios were 0.7 (95 percent CI: 0.4, 1.3) for glioma, 0.7 (95 percent CI: 0.4, 1.4) for meningioma, and 1.6 (95 percent CI: 0.7, 4.1) for acoustic neuroma). Exclusion of use within 10 or 20 years prior to diagnosis for cases or prior to interview for controls did not meaningfully change our results (data not shown). Sequential exclusion of each major control diagnostic group did not appreciably change our results. Results stratified by hospital site or by age at diagnosis (<52.5 years or ≥52.5 years (the mean age at diagnosis for all cases)) yielded no meaningful difference in odds ratios.

Subjects who reported their hair graying at a younger age had a lower risk of glioma than subjects who grayed at ages ≥40 years, a trend more pronounced in men (p-trend = 0.03) than in women (p-trend = 0.28) (data not shown). A similar trend was observed for glioblastoma (p-trend = 0.03 for men and women combined). The trends were robust to continuous and quadratic recoding of age at diagnosis, exclusion of proxy respondents, and sequential exclusion of major diagnostic groups in the control series. Adjusting the main effects of hair dye exposures for hair graying (never, before age 40, or at or after age 40) generally had little effect, but it increased the odds ratio for glioma in long-term brown permanent dye users from 3.8 to 4.9 (95 percent CI: 1.5, 19).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
To our knowledge, this is the largest and most detailed study to date of the relation between personal hair dye exposure and adult brain tumors. We did not find consistent evidence of an association of hair dye use with glioma, meningioma, or acoustic neuroma; however, we did observe a more than threefold significantly elevated odds ratio for glioma in women with ≥20 years of use of brown permanent hair dye. We did not find a significantly elevated odds ratio for glioblastoma in women with this exposure, unlike Heineman et al. (30), who found stronger associations with glioblastoma than with other gliomas.

Our generally negative findings differ from those of the three prior studies of personal hair dye and adult brain tumors (28–30). A smaller Swedish case-control study of astrocytoma was based on 78 cases and lacked detailed exposure information (28). A larger case-control study of 215 glioma cases from Ontario, Canada, did not distinguish between hair dye and hair spray and was further limited by reliance on a high proportion of proxy responses (73 percent) (29). Heineman et al. (30) assessed hair dye use in detail but also required proxy interviews for a large proportion of cases (79 percent), owing to the delay (mean = 2.5 years) between diagnosis and interview. By contrast, we were able to directly question subjects by conducting detailed in-hospital interviews shortly after diagnosis.

Concern about potential carcinogens in hair dyes has largely focused on the aromatic amine precursors of oxidative (permanent) dyes (39). Following a 1975 report of in vitro mutagenesis by Ames et al. (2), an independent expert review process (the Cosmetic Ingredient Review) was implemented by the Cosmetic, Toiletry and Fragrance Association in 1976 (39). Some dye components were removed from commercial products in the United States in the late 1970s (1, 13, 27, 32, 38). We did not find any increased risk of glioma or other tumors among women who had used permanent dyes before 1980, unlike Heineman et al. (30). However, our study's statistical power to detect such effects was low, particularly for acoustic neuroma.

Although our findings were largely negative for permanent hair dyes, we did observe an increased risk associated with long-term use of brown dye. Darker shades or tones of oxidative hair dyes contain a higher concentration of p-phenylenediamine and other intermediates and couplers than do lighter shades of dye (39, 43). Epidemiologic studies that have investigated dye color have suggested a risk associated with darker permanent or semipermanent hair colors, including red, brown/brunette, and black (8) or brown/brunette (44). It remains unclear by what biologic mechanism putative neurocarcinogens in hair dyes might affect regions of the brain believed to be protected by the blood-brain barrier in healthy adults (45). The tight endothelial cell junctions comprising the blood-brain barrier restrict the passage of many agents into the neuroglia (45). Investigations of occupational exposures to neurotoxins and carcinogens in humans have failed to consistently identify mechanisms of transport into the tissue of the brain or chemical exposures associated with risk of tumors of the brain (46, 47). However, proposed mechanisms for the disruption of the blood-brain barrier include acute arterial hypertension (45), molecular effects of autacoids (45) or inflammatory cytokines (48), and age-related immune system dysregulation (49).

We assessed hair graying as a potential confounder of the association between hair dye exposure and cancer risk, since early onset of hair graying may promote early use of dark hair dye (1, 8). However, we found a lower risk of glioma among subjects who reported early graying, with a statistically significant trend among men. Hair graying may reflect hormonal or other age-related biologic processes that are not yet understood (50–52). Adjusting our results for hair graying did not meaningfully change any odds ratio estimates for hair dye use.

This study benefited from a large size, high participation rates, a high proportion of self-responders versus proxy responders, and detailed information related to hair dye exposure. Early identification and recruitment of hospitalized cases enabled prompt interviewing of cases. The computer-based questionnaire algorithm minimized inconsistent reporting of exposures.

Study limitations include the possibility of increased odds ratios due to chance given the large number of comparisons. There was also potential for recall bias or random misclassification of self-reported hair dye exposure. Recall errors are likely to have been small for ever use versus never use and for usual color, but they may have been greater for reported ages at starting and stopping use and frequency of use. Provision of proxy assistance to the most mentally impaired brain cancer patients introduces the potential for differential exposure misclassification by an interviewee unfamiliar with the subject's personal hair care routines. However, we did not find evidence to support a hypothesis of underreporting by cases with cognitive impairment or high-grade versus low-grade glioma. In addition, there was no meaningful change in estimates analyzing self-respondents only. Some exposure misclassification may have resulted from individual differences in scalp surface area, average hair length, hair thickness (number of hairs per cm2), mean hair diameter, duration of dye treatment process, and rinsing technique, affecting the volume of dye used per application and thus, to some degree, the opportunity for cutaneous absorption and systemic exposure (39). Another design consideration is the appropriateness of using hospital-based controls to represent the exposure characteristics of the general population. However, it is not apparent that our controls had a different prevalence of hair dye use than other populations (53), and odds ratio estimates were little affected by exclusion of major diagnostic subgroups of controls.

The concern about hair dyes is based to a large degree on the high prevalence of use of these products (46–77 percent among women in the United States) (53). Despite the overall lack of evidence for an association between hair dye exposure and brain tumors in our study, a question for future research is whether a subset of the population is at risk based on genetic differences in xenobiotic metabolizing capacity. In a Los Angeles, California, case-control study, risk of bladder cancer associated with hair dye exposure was limited to persons with the slow phenotype of the enzyme N-acetyltransferase (NAT) 2. The association with hair dye was stronger among persons with the cytochrome P-450 1A2 slow acetylator phenotype and persons lacking the rapid acetylator NAT1*10 allele (6, 54). Because scalp skin is the major route of absorption of hair dyes, it has been hypothesized that the epidermal NAT1 enzyme is responsible for aromatic amine metabolism to potentially carcinogenic intermediates (39).

In this large case-control study of brain tumors, we did not find consistent evidence for an association of hair dye use with glioma, meningioma, or acoustic neuroma. Overall, there was little evidence for an association of permanent, semipermanent, temporary, or gradual hair dye use with these brain tumors; however, prolonged use of dark permanent colors, particularly brown, warrants further investigation given the high prevalence of hair dye use.


   ACKNOWLEDGMENTS
 
This research was supported by the Intramural Research Program of the National Institutes of Health (National Cancer Institute, Division of Cancer Epidemiology and Genetics).

The authors thank Henry Chen of Information Management Services, Inc. (Silver Spring, Maryland) for programming support.

Conflict of interest: none declared.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

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