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. Author manuscript; available in PMC: 2010 Oct 13.
Published in final edited form as: Handb Exp Pharmacol. 2009;(192):29–60. doi: 10.1007/978-3-540-69248-5_2

Table 2.

Biomarkers of tobacco exposure

Biomarker Precursor Specimen t½ Tobacco specific Other sources
Nicotine* Nicotine Blood, urine, saliva, hair 1–2 h Yes Nicotine replacement products
Cotinine* Nicotine Blood, urine, saliva, hair 16–18 h Yes Nicotine replacement products
Anatabine* Anatabine Urine 10–16 h Yes None
NNAL, NNAL-glucuronides NNK (TSNA) Blood, urine 6 week Yes None
Exhaled CO Carbon monoxide Exhaled air 2–6 h No Traffic, body formation
Carboxyhemoglobin carbon monoxide Blood 4–6 h No Traffic, body formation
1-Hydroxypyrene and other polycyclic aromatic hydrocarbon (PAH) metabolites PAHs Urine 20 h No Traffic, grilled meat, occupation, biomass combustion in homes
Mercopturic acid metabolites 1,3-Butadiene Urine No Traffic, combustion products
Mercopturic acid metabolites Acrolein Urine No Traffic, combustion products
Acetonitrile Acetonitrile Urine, blood, exhaled air 32 h No None
S-Phenyl-mercapturic acid Benzene Urine 9 h No Traffic, combustion products
Thiocyanate Hydrogen cyanide Serum, saliva, urine 7–14 days No Diet

NNAL 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol; NNAL-gluc 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol glucuronide; NNK 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone; TSNA tobacco-specific nitrosamines; PAH polycylcic aromatic hydrocarbons

In studies of smoking cessation, anatabine is recommended as nicotine replacement therapies will lead to the presence of nicotine and cotinine without any tobacco exposure