6.2Pharmacokinetics

Last updated: January 2018

Suggested citation: Christensen, D. 6.2 Pharmacokinetics. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2018. Available from http://www.tobaccoinaustralia.org.au/chapter-6-addiction/6-2-pharmacokinetics

Burning tobacco releases nicotine, the primary addictive substance in cigarettes.1 Nicotine, and other compounds, are suspended in smoke ‘tars’ that are quickly absorbed in the lungs, mouth, nose, skin, stomach, and intestines.1 Research in the 1990s established that the average cigarette contained approximately 10 milligrams (mg) of nicotine2 (no estimates of the nicotine content of cigarettes currently sold in Australia could be located). Nicotine blood concentrations vary depending on the amount of smoke inhaled, genetic and demographic factors, and health issues.3 During the course of a day a typical daily smoker absorbs 20 to 40 mgs of nicotine to maintain an estimated 15 mg steady state blood concentration to avoid withdrawal symptoms or cravings.1  

When nicotine is absorbed from the lungs it is carried directly to the heart, and then to the brain.4 Once in the bloodstream, nicotine is distributed widely throughout the body including to the liver, kidneys, spleen, and lungs. Among pregnant women who smoke, nicotine crosses the placental barrier and reaches the foetus, while among those breastfeeding, nicotine is passed to the baby via breast milk.5, 6

When tobacco is smoked, nicotine reaches peak blood level concentration within five minutes.7 Nicotine half-life is estimated to be 90 to 150 minutes,4 although this duration is also mediated by the individual’s pattern of tobacco use and biological differences.8 The majority of nicotine is metabolised in the liver primarily, at the first stage, by the enzyme CYP-2A6 to produce the primary metabolite (by-product of metabolism) cotinine. Nicotine and its metabolite cotinine are excreted by the kidneys depending on the pH of the urine, flow rate, tobacco use, reabsorption rate, drug use, genetics, and renal function.8

 

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References

1. Advocat C, Comaty J, and Julien R, Julien’s primer of drug action.  13th ed New York: Worth Publishers; 2014. Available from: http://www.ncbi.nlm.nih.gov/nlmcatalog/101666863.

2. Kozlowski LT, Mehta NY, Sweeney CT, Schwartz SS, Vogler GP, et al. Filter ventilation and nicotine content of tobacco in cigarettes from Canada, the United Kingdom, and the United States. Tobacco Control, 1998; 7(4):369–75. Available from: https://www.ncbi.nlm.nih.gov/pubmed/10093170

3. Benowitz NL. Pharmacology of nicotine: Addiction, smoking-induced disease, and therapeutics. Annual Review of Pharmacology and Toxicology, 2009; 49:57–71. Available from: https://www.ncbi.nlm.nih.gov/pubmed/18834313

4. Benowitz N. Clinical pharmacology of nicotine: Implications for understanding, preventing, and teaching tobacco addiction. Clinical Pharmacology & Therapeutics, 2008; 83:531–41. Available from: https://www.ncbi.nlm.nih.gov/pubmed/18305452

5. Dahlstrom A, Lundell B, Curvall M, and Thapper L. Nicotine and cotinine concentrations in the nursing mother and her infant. Acta Paediatrica Scandinavica, 1990; 79(2):142–7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/2321475

6. Dempsey DA and Benowitz NL. Risks and benefits of nicotine to aid smoking cessation in pregnancy. Drug Safety, 2001; 24(4):277–322. Available from: https://www.ncbi.nlm.nih.gov/pubmed/11330657

7. Baraona LK, Lovelace D, Daniels JL, and McDaniel L. Tobacco harms, nicotine pharmacology, and pharmacologic tobacco cessation interventions for women. Journal of Midwifery & Women's Health, 2017; 62(3):253–69. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28556464

8. Benowitz NL, Hukkanen J, and Jacob P, 3rd. Nicotine chemistry, metabolism, kinetics and biomarkers. Handbook of Experimental Pharmacology, 2009; 192(192):29–60. Available from: https://www.ncbi.nlm.nih.gov/pubmed/19184645

 

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