Carcinogenesis Advance Access published online on May 23, 2007
Carcinogenesis, doi:10.1093/carcin/bgm121
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Published by Oxford University Press 2007.
Hair dye use, genetic variation in N-acetyltransferase 1 (NAT1) and 2 (NAT2), and risk of non-Hodgkin lymphoma
1 Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Rockville, MD
2 Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA
3 Department of Pharmacology and Toxicology and James Graham Brown Cancer Center, University of Louisville, School of Medicine, Louisville, KY
4 Fred Hutchinson Cancer Research Center and University of Washington, Seattle, WA
5 Mayo Clinic, College of Medicine, Rochester, MN
6 Department of Family Medicine and Karmanos Cancer Institute, Wayne State University, Detroit, MI
7 Core Genotyping Facility, Advanced Technology Center, National Cancer Institute, NIH, DHHS, Gaithersburg, MD
* To whom correspondence should be addressed: Lindsay M. Morton, Ph.D., Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, 6120 Executive Boulevard, EPS 5100, Rockville, MD 20892-7234, Ph: +301-435-3972; FAX:+402-0916; Email: mortonli{at}mail.nih.gov.
Background. Several previous studies have found non-Hodgkin lymphoma (NHL) risk to be associated with hair dye use, particularly use of permanent, dark colors and use before 1980, when hair dye formulations changed.
Methods. We examined NHL risk in relation to reported hair dye use among 1,321 cases and 1,057 controls from a US population-based multicenter study. DNA was extracted from blood or buccal cells to identify genetic variation in N acetyltransferase 1 (NAT1) and 2 (NAT2), which encode enzymes that metabolize aromatic amine compounds found in hair dyes.
Results. Among women, 509 cases and 413 controls reported hair dye use (odds ratio [OR]=1.2,95% confidence interval [CI]=0.9,1.6). Risk estimates were higher for use before 1980 than for use in 1980 or later, particularly for use of permanent, intense tone (black, dark brown, dark blonde) products (<1980: OR=1.6,95%CI 0.9,2.7; 
1980: OR=0.6,95%CI 0.4,1.1). Risk estimates were increased for women who used permanent, intense tone products before 1980 if they had the rapid/intermediate NAT2 phenotype (OR=3.3, 95%CI 1.3,8.6) or the NAT1*10 allele (OR=2.5,95%CI 0.9,7.6), but not if they were slow NAT2 acetylators (OR=1.5,95%CI 0.6,3.6) or had no copies of the NAT1*10 allele (OR=1.5,95%CI 0.7,3.3). NHL risk was not increased among women who began hair dye use after 1980 or among men.
Conclusion. Our results support previous research demonstrating elevated NHL risk among women who used dark color or intense tone permanent hair dyes before 1980. We present the first evidence suggesting that this risk may differ by genetic variation in NAT1 and NAT2.
Received March 13, 2007; revised May 11, 2007; accepted May 12, 2007.
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