Abstract
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 dyeuse among 1321 cases and 1057 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; ≥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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1759-1764 |
| Number of pages | 6 |
| Journal | Carcinogenesis |
| Volume | 28 |
| Issue number | 8 |
| DOIs | |
| State | Published - Aug 2007 |
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ASJC Scopus subject areas
- Cancer Research
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Hair dye use, genetic variation in N-acetyltransferase 1 (NAT1) and 2 (NAT2), and risk of non-Hodgkin lymphoma. / Morton, Lindsay M.; Bernstein, Leslie; Wang, Sophia S.; Hein, David W.; Rothman, Nathaniel; Colt, Joanne S.; Davis, Scott; Cerhan, James R; Severson, Richard K.; Welch, Robert; Hartge, Patricia; Zahm, Shelia Hoar.
In: Carcinogenesis, Vol. 28, No. 8, 08.2007, p. 1759-1764.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Hair dye use, genetic variation in N-acetyltransferase 1 (NAT1) and 2 (NAT2), and risk of non-Hodgkin lymphoma
AU - Morton, Lindsay M.
AU - Bernstein, Leslie
AU - Wang, Sophia S.
AU - Hein, David W.
AU - Rothman, Nathaniel
AU - Colt, Joanne S.
AU - Davis, Scott
AU - Cerhan, James R
AU - Severson, Richard K.
AU - Welch, Robert
AU - Hartge, Patricia
AU - Zahm, Shelia Hoar
PY - 2007/8
Y1 - 2007/8
N2 - 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 dyeuse among 1321 cases and 1057 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; ≥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.
AB - 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 dyeuse among 1321 cases and 1057 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; ≥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.
UR - http://www.scopus.com/inward/record.url?scp=34548071866&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34548071866&partnerID=8YFLogxK
U2 - 10.1093/carcin/bgm121
DO - 10.1093/carcin/bgm121
M3 - Article
C2 - 17522066
AN - SCOPUS:34548071866
VL - 28
SP - 1759
EP - 1764
JO - Carcinogenesis
JF - Carcinogenesis
SN - 0143-3334
IS - 8
ER -