3.20 Nicotine and carbon monoxide poisoning

Acute nicotine poisoning can occur through:¹

• Ingestion of tobacco or other products containing nicotine (such as pesticides, nicotine replacement medications or e-cigarette liquids) or;
• Absorption of nicotine transdermally (through the skin), either from exposure to pesticides,² unprocessed tobacco leaves (see ‘green tobacco sickness’ below), or e-cigarette liquids (particularly in children).

Symptoms of mild nicotine poisoning may include nausea and vomiting, progressing with increased exposure to cholinergic syndrome, which includes diarrhoea, increased salivation, increased respira­tory secretions, and bradycardia (slow heart rate). Severe poisoning can lead to seizures and respiratory depression.³ Death may occur through respiratory failure.¹

Although highly toxic, death due to ingested tobacco is extremely rare due to the unpleasant flavour of tobacco, the vomit response and the rapid metabolism of  nicotine.¹ 

3.20.1 Ingestion and transdermal exposure

A US study analysed calls to poison control centres between 2001 and 2016. During this time period, over 120,000 calls were received relating to tobacco (and e-cigarette) exposure in children younger than 5 years of age. Most calls involved ingestion of cigarettes, followed by ingestion of chewing tobacco. Over 16% of the calls resulted in children needing medical attention.⁴

Reports of ingestion of nicotine-containing e-liquids (used in e-cigarettes) have increased since the availability of these products on the US market. A 2016 retrospective analysis of calls to the US poison control centres (for children under 6 years of age) found that over a three year period (2012–2015), the monthly number of calls related to e-cigarette exposure increased by nearly 1500%.⁵ Compared to children exposed to cigarettes, those exposed to e-cigarettes were over 5 times more likely to require admission to hospital, and around 2.5 times more likely to have a serious outcome. In Australia in June 2018, an infant died after ingesting liquid nicotine.⁶ See InDepth discussion of E-cigarettes (18B.4) for more information about nicotine poisoning in the context of e-cigarette use.

Although the rate of poisonings due to transdermal exposure to tobacco products and e-cigarette liquids is very low (compared to ingestion), studies have found transdermal exposure is most likely to occur with e-cigarettes and e-liquids.^{4, 5} For example, in one study, transdermal exposure was responsible for 12.1% of e-liquid poisoning events compared to 1% of cigarette-related events.⁴

Cases have also been reported in which children have ingested or had transdermal exposure to nicotine replacement therapy patches, causing symptoms of nicotine poisoning, and in more severe cases, requiring hospitalisation.⁷

Suicides resulting from nicotine poisoning have also been reported, including from direct ingestion of tobacco leaves or nicotine-containing solutions, and even transdermal exposure from homemade nicotine patches.^8-10

Nicotine is a scheduled poison in Australia, its distribution being controlled by state and territory drugs and poisons legislation, all of which refer to a nationally-accepted Standard for Uniform Scheduling of Drugs and Poisons devised by the Therapeutic Goods Administration of the Australian Government.¹¹ In an exemption considered by many public health interests to be anomalous, tobacco prepared and packed for smoking is excluded from the Standard. Nicotine preparations for human therapeutic use as an aid in withdrawal are also excluded. See Chapter 12 for further information.

3.20.2 Green tobacco sickness

Green tobacco sickness (GTS) affects individuals involved in tobacco farming, especially during the harvesting season.^{12, 13} GTS occurs when nicotine is absorbed through the skin and enters the bloodstream from direct contact with newly cut green tobacco leaves . It has also been suggested that high levels of airborne nicotine in tobacco farming facilities may contribute to GTS through inhalation.¹⁴

Sufferers commonly experience dizziness, nausea, headache and vomiting; less frequent symptoms include abdominal pain, shortness of breath, diarrhoea, altered heart rate and blood pressure, sweating and increased salivation.^{2, 12, 13}

Non-smokers are more likely to be affected by GTS than smokers (likely as a result of lower nicotine tolerance),^{2, 15, 16} which has in some cases led to tobacco growers encouraging workers to take up smoking.¹³  A study of tobacco farmers in Brazil found that other risk factors for GTS included certain tobacco farming activities (transporting bales, harvesting wet leaves) and performing tasks requiring significant physical exertion. A possible rationale for this is that nicotine absorption through the skin may be increased by sweating, a faster heart rate and vasodilation (when blood vessels dilate to increase blood flow).¹⁶

There are no widely accepted clinical guidelines for the diagnosis of GTS. It has been suggested that measuring cotinine levels (cotinine is the main metabolite of nicotine) in urine and other bodily fluids may aid in the diagnosis of GTS. However, it is unclear what threshold level must be reached to make a positive diagnosis.^{2, 17}

Treatment of GTS is supportive, with rest, rehydration and treatment of specific symptoms as required (for example, anti-nausea medications).² New possible targeted treatments for GTS have been proposed, including mecamylamine (a blood pressure medication, which blocks nicotine at the nicotinic acetylcholine receptors), varenicline and cystine (both of which are smoking cessation pharmacotherapies) and even a ‘nicotine vaccine’.² However, more research is required.  Recent reports have suggested that nicotine may not be the sole cause of GTS. This is because sufferers do not appear to build tolerance to GTS symptoms and the average duration of GTS (2.4) days does not align with the fast metabolism of nicotine.²

The incidence of GTS is reduced by provision of appropriate protective clothing and other workplace safety measures (such as mechanical harvesting to prevent direct contact with tobacco leaves).^{2, 13}

An international review reported that 8–89% of tobacco harvesters may be affected by GTS in the course of a season, this wide variation probably being due to differences between study methodologies as well as a range of working conditions.¹³ There are an estimated 33 million tobacco farm workers in the world, a substantial proportion living in developing countries. Long-term health outcomes for individuals exposed to nicotine transdermally for extended periods of time are not known.¹³ See also Section 10.14 for a discussion of ethical issues related to tobacco farming.

3.20.3 Carbon monoxide poisoning

Carbon monoxide (CO) is a clear gas that has no odour. CO binds to red blood cells and displaces oxygen (creating carboxyhaemoglobin) which impairs oxygen delivery throughout the body. Common symptoms of CO poisoning include headache, dizziness, fatigue, nausea and vomiting, altered mental state, chest pain and shortness of breath, and loss of consciousness, and even death.¹⁸ Common sources of CO poisoning include faulty gas heaters and cookers, barbeques, outdoor heaters and exhausts from cars, boats and generators.¹⁹  Poisoning can occur when these sources are used in poorly-ventilated areas. While it is well-established that carboxyhaemoglobin levels are elevated in chronic smokers compared to non-smokers,²⁰ a number of cases of acute CO poisoning have also been reported in individuals using tobacco products, including waterpipes.^21-23 In these cases, poisoning was due to heavy tobacco use over a short period of time.

Relevant news and research

For recent news items and research on this topic, click here.(Last updated May 2021)

References for Section 3.20

1. US Department of Health and Human Services. The Health Consequences of Smoking: Nicotine Addiction. A report of the Surgeon General. Rockville, Maryland: US Department of Health and Human Services, Public Health Service, Centers for Disease Control, Center for Health Promotion and Education, Office on Smoking and Health, 1988. Available from: https://profiles.nlm.nih.gov/spotlight/nn/catalog/nlm:nlmuid-101584932X423-doc.

2. McMahon LR. Green tobacco sickness: mecamylamine, varenicline, and nicotine vaccine as clinical research tools and potential therapeutics. Expert Rev Clin Pharmacol, 2019:1-7. Available from: https://ww.ncbi.nlm.nih.gov/pubmed/30650314

3. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: https://www.cdc.gov/tobacco/data_statistics/sgr/50th-anniversary/index.htm.

4. Wang B and Rostron B. Tobacco-related Poison Events Involving Young Children in the US, 2001-2016. Tob Regul Sci, 2017; 3(4):525-35. Available from: http://www.ncbi.nlm.nih.gov/pubmed/30338270

5. Kamboj A, Spiller HA, Casavant MJ, Chounthirath T, and Smith GA. Pediatric Exposure to E-Cigarettes, Nicotine, and Tobacco Products in the United States. Pediatrics, 2016; 137(6). Available from: http://www.ncbi.nlm.nih.gov/pubmed/27244861

6. Haggan M. Baby died after drinking imported nicotine. Australian Journal of Pharmacy 2019. Available from: https://ajp.com.au/news/baby-died-after-drinking-imported-nicotine/

7. Woolf A, Burkhart K, Caraccio T, and Litovitz T. Childhood poisoning involving transdermal nicotine patches. Pediatrics, 1997; 99:e4. Available from: http://pediatrics.aappublications.org/cgi/content/abstract/99/5/e4

8. Yamamoto H, Takayasu T, Ishida Y, Nosaka M, Hata S, et al. A case of complex suicide due to acute nicotine intoxication caused by cigarette ingestion. International Journal of Legal Medicine, 2019. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31836934

9. Lardi C, Vogt S, Pollak S, and Thierauf A. Complex suicide with homemade nicotine patches. Forensic Science International, 2014; 236:e14-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/24439154

10. Solarino B, Rosenbaum F, Riesselmann B, Buschmann C, and Tsokos M. Death due to ingestion of nicotine-containing solution: case report and review of the literature. Forensic Science International, 2010; 195((1–3)):e19–22. Available from: https://www.ncbi.nlm.nih.gov/pubmed/19954906

11. Therapeutic Goods Administration. Scheduling delegate's interim decisions and invitation for further comment: ACCS/ACMS November 2016, 2.1 Nicotine. 2017. Available from: https://www.tga.gov.au/book-page/21-nicotine.

12. McBride JS, Altman DG, Klein M, and White W. Green tobacco sickness. Tobacco Control, 1998; 7:294-8. Available from: http://tobaccocontrol.bmj.com/cgi/reprint/7/3/294

13. Schmitt NM, Schmitt J, Kouimintzis DJ, and Wilhem K. Health risks in tobacco farm workers - a review of the literature Journal of Public Health, 2007; 15(4):255-64. Available from: https://link.springer.com/article/10.1007/s10389-007-0122-4

14. Yoo SJ, Park SJ, Kim BS, Lee K, Lim HS, et al. Airborne nicotine concentrations in the workplaces of tobacco farmers. J Prev Med Public Health, 2014; 47(3):144-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/24921017

15. Arcury TA, Quandt SA, and Preisser JS. Predictors of incidence and prevalence of green tobacco sickness among Latino farmworkers in North Carolina, USA. Journal of Epidemiology and Community Health, 2001; 55:818-24. Available from: http://jech.bmj.com/cgi/reprint/55/11/818

16. Fassa AG, Faria NMX, Meucci RD, Fiori NS, Miranda VI, et al. Green tobacco sickness among tobacco farmers in southern Brazil American Journal of Industrial Medicine, 2014; 57:726-35. Available from: https://pubmed.ncbi.nlm.nih.gov/24526387/

17. Fassa AG, Meucci RD, Fiori NS, Carrett MLV, and Faria NMX. Urinary cotinine in tobacco farmers in Southern Brazil. Revista de Saude Publica, 2018; 52:70. Available from: http://www.ncbi.nlm.nih.gov/pubmed/30066808

18. Rose JJ, Wang L, Xu Q, McTiernan CF, Shiva S, et al. Carbon monoxide poisoning: Pathogenesis, management, and future directions of therapy. American Journal of Respiratory and Critical Care Medicine, 2017; 195(5):596-606. Available from: https://pubmed.ncbi.nlm.nih.gov/27753502/

19. National Center for Environmental Health. Carbon Monoxide (CO) Poisoning Prevention 2020. Available from: https://www.cdc.gov/nceh/features/copoisoning/index.html.

20. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General, Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html.

21. Sen S, Peltz C, Beard J, and Zeno B. Recurrent carbon monoxide poisoning from cigarette smoking The American Journal of the Medical Sciences, 2010; 340(5):427-8 Available from: https://www.sciencedirect.com/science/article/abs/pii/S0002962915314634?via%3Dihub

22. Neilsen BK, Aloi J, and Sharma A. Acute Carbon Monoxide Poisoning Secondary to Cigarette Smoking in a 40-Year-Old Man: A Case Report. American Journal on Addictions, 2019. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31348564

23. La Fauci G, Weiser G, Steiner IP, and Shavit I. Carbon monoxide poisoning in narghile (water pipe) tobacco smokers. CJEM, 2012; 14(1):57-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22417961