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N-acetyltransferase 1 polymorphism increases cotinine levels in Caucasian children exposed to secondhand smoke: the CCAAPS birth cohort

G. Lemasters,G. K. Khurana Hershey,U. Sivaprasad,Lisa J. Martin,Valentina Pilipenko,M. Ericksen,J. Burkle,M. Lindsey,D. Bernstein,J. Lockey,J. Gareri,A. Lubetsky,G. Koren,J. B. Biagini Myers

Published 2014 in The Pharmacogenomics Journal

ABSTRACT

Cotinine is a proxy for secondhand smoke (SHS) exposure. Genetic variation along nicotine and cotinine metabolic pathways may alter the internal cotinine dose, leading to misinterpretations of exposure-health outcome associations. Caucasian children with available SHS exposure and hair cotinine data were genotyped for metabolism-related genes. SHS-exposed children had 2.4-fold higher hair cotinine (0.14±0.22 ng mg−1) than unexposed children (0.06±0.05 ng mg−1, P<0.001). SHS-exposed children carrying the NAT1 minor allele had twofold higher hair cotinine (0.18 ng mg−1 for heterozygotes and 0.17 ng mg−1 for homozygotes) compared with major allele homozygotes (0.09 ng mg−1, P=0.0009), even after adjustment for SHS dose. These findings support that NAT1 has a role in the metabolic pathway of nicotine/cotinine and/or their metabolites. The increased cotinine levels observed for those carrying the minor allele may lead to SHS exposure misclassification in studies utilizing cotinine as a biomarker. Additional studies are required to identify functional single-nucleotide polymorphism(s) (SNP(s)) in NAT1 and elucidate the biological consequences of the mutation(s).

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