Document Detail

The possible role of ammonia toxicity on the exposure, deposition, retention, and the bioavailability of nicotine during smoking.
MedLine Citation:
PMID:  18450355     Owner:  NLM     Status:  MEDLINE    
A complete and rigorous review is presented of the possible effect(s) of ammonia on the exposure, deposition and retention of nicotine during smoking and the bioavailability of nicotine to the smoker. There are no toxicological data in humans regarding ammonia exposure within the context of tobacco smoke. Extrapolation from occupational exposure of ammonia to smoking in humans suggests minimal, non-toxicological effects, if any. No direct study has examined the effect of the ammonia on the total rate or amount of nicotine reaching the arterial bloodstream or brains of smokers. Machine-smoking methods have been reported which accurately quantify >99% of the nicotine in mainstream (MS) smoke for a wide variety of commercial and test cigarettes, including a series of experimental cigarettes having a range in MS smoke ammonia yields using the US Federal Trade Commission (FTC) protocol. However, the actual exposure of nicotine to smokers depends on their own smoking behavior. The nicotine ring system is relatively thermally stable. Protonated nicotine forms nicotine which evaporates before the nicotine ring system decomposes. The experimental data indicate that neither nicotine transfer from tobacco to MS smoke nor nicotine bioavailability to the smoker increases with an increase in any of the following properties: tobacco soluble ammonia, MS smoke ammonia, "tobacco pH" or "smoke pH" at levels found in commercial cigarettes. Gas phase nicotine deposits primarily in the mouth and upper respiratory tract. To the extent that ammonia increases the deposition of nicotine in the buccal cavity and upper respiratory tract during smoking, the total rate and amount of nicotine into the arterial bloodstream and to the central nervous system will decrease. Charged nicotine analogues are actively transported in a number of tissues. This active transport system appears to be insensitive to pH and the form of nicotine in the biological milieu, suggesting that protonated nicotine may be a substrate for active transport. Neither "smoke pH" of commercial cigarettes nor "smoke pHeff" nor the fraction of non-protonated nicotine in tobacco smoke particulate matter are useful, practical smoke parameters for providing understanding or predictability of nicotine bioavailability to smokers. Greater than 95% of both ammonia and nicotine are in the gas phase of environmental tobacco, and both are likely to deposit in the buccal cavity and upper respiratory tract following exposure.
Jeffrey I Seeman; Richard A Carchman
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Publication Detail:
Type:  Journal Article; Review     Date:  2008-03-04
Journal Detail:
Title:  Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association     Volume:  46     ISSN:  0278-6915     ISO Abbreviation:  Food Chem. Toxicol.     Publication Date:  2008 Jun 
Date Detail:
Created Date:  2008-05-09     Completed Date:  2008-07-10     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8207483     Medline TA:  Food Chem Toxicol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1863-81     Citation Subset:  IM    
SaddlePoint Frontiers, 12001 Bollingbrook Place, Richmond, VA 23236-3218, United States.
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MeSH Terms
Ammonia / analysis,  toxicity*
Hydrogen-Ion Concentration
Nicotine / pharmacokinetics*
Nicotinic Agonists / pharmacokinetics*
Risk Assessment
Smoke / analysis
Smoking / metabolism*
Tobacco / chemistry
Tobacco Smoke Pollution / adverse effects,  analysis
Reg. No./Substance:
0/Nicotinic Agonists; 0/Smoke; 0/Tobacco Smoke Pollution; 54-11-5/Nicotine; 7664-41-7/Ammonia

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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