Journal
CLINICAL PHARMACOLOGY & THERAPEUTICS
Volume 94, Issue 3, Pages 400-406Publisher
WILEY
DOI: 10.1038/clpt.2013.114
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Funding
- State of California Tobacco Related-Disease Research Program [15RT-0229]
- US Public Health Service from the National Institute on Drug Abuse [DA020830, DA02277, DA12393]
- University Endowed Chair in Addiction
- Canadian Institutes of Health Research Centre for Addiction and Mental Health [TMH-109787]
- Centre for Addiction and Mental Health foundation
- Canada Foundation for Innovation [20289, 16014]
- Ontario Ministry of Research and Innovation
- National Institutes of Health/National Center for Research Resources University of California, San Francisco Clinical and Translational Science Institute [UL1 R024131]
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The formation of cotinine, the main proximate metabolite and a biomarker of nicotine exposure, is mediated primarily by cytochrome P450 (CYP)2A6. Our aim was to determine whether higher cotinine levels in young children exposed to secondhand smoke (SHS) are a result of age-related differences in pharmacokinetics. Forty-nine participants, aged 2-84 months, received oral deuterium-labeled cotinine, with daily urine samples for up to 10 days for cotinine half-life measurement. DNA from saliva was used for CYP2A6 genotyping. The estimate of half-life using a mixed-effect model was 17.9 h (95% confidence interval: 16.5, 19.3), similar to that reported in adults. There was no statistically significant effect of sex, race, age, or weight. Children with normal-activity CYP2A6*1/*1 genotypes had a shorter half-life than those with one or two reduced-activity variant alleles. Our data suggest that higher cotinine levels in SHS-exposed young children as compared with adults are due to greater SHS exposure rather than to different cotinine pharmacokinetics.
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