cotinine levels, thus a change in consumption does not explain the association we note with the reduced function UGT2B10 variant and higher cotinine levels. A more likely explanation for our findings is a reduction in cotinine metabolism, through decreased cotinine glucuronidation, which is consistent with the association noted between the reduced function UGT2B10 variant and increased cotinine levels. Indeed, a recent GWAS conducted by Patel and colleagues17 concluded that genetic variation within UGT2B10 contributes significantly to nicotine and cotinine glucuronidation but not to nicotine dose.
