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 multi-center 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 (95% 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; >or=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.
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 multi-center 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 (95% 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; >or=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.
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