Smoking behaviour and increase in nicotine and carboxyhaemoglobin in venous blood

Abstract

The connection between smoking behaviour (number of puffs, puff volume, depth of inhalation, duration of inhalation) and the increase in both nicotine and carboxyhaemoglobin (COHb) in venous blood was investigated with methods developed especially for measurement of the puff volume, the depth of inhalation, and the duration of inhalation in 28 inhaling cigarette smokers. A significant correlation could be demonstrated between the smoking parameters and the nicotine and carboxyhaemoglobin increase. The weighting obtained shows that the number of puffs is the most important parameter affecting the increase in nicotine, whereas the depth of inhalation and the puff volume are of much less relevance. The duration of inhalation does not affect the nicotine level. A significant increase in nicotine cannot be attained in non-inhalative smoking of cigarettes with an acid mainstream smoke (n= 14). The increase in COHb is most affected by the puff volume, and slightly less by the number of puffs and the depth of inhalation. The duration of inhalation does not affect the COHb level.The morbidity and mortality from smoking is dose dependent. There is a correlation with the age of starting smoking and the duration of smoking [10,Abbreviations." C= compliance of the lung; Cst = static compliance of the lung; CO = carbon monoxide; COHb = carboxyhaemoglobin; Dco=diffusion of carbon monoxide in the lung; Hb = haemoglobin; PACO = alveolar partial pressure of carbon monoxide; PcCO = partial pressure of carbon monoxide in the pulmonary capillaries; P(A_olCO = difference in partial pressure between the alveolar cavity and the pulmonary capillaries; VC = vital capacity; lZco = amount of diffusion of carbon monoxide per unit of time 34], the number of cigarettes smoked per day [24,34,59], the tar and nicotine content of the cigarette [35], the number of puffs per cigarette, and the depth of inhalation [10,34,35]. Inhalation and depth of inhalation play a major role in the pathogenesis of most tobacco-related diseases [34,35]. Besides health education, the development of less hazardous cigarettes is called for. Filter-tipped cigarettes have been introduced and the tar/nicotine content of cigarettes has been reduced, but the lowering of nicotine content is of benefit only if the smoker does not satisfy his nicotine requirement by changing his smoking behaviour [8,33]. No precise data are yet available as to how the individual parameters of the smoking technique (number of puffs, puff volume, depth of inhalation, and duration of inhalation) affect the nicotine and COHb level [56].

Reconciling Human Smoking Behavior and Machine Smoking Patterns: Implications for Understanding Smoking Behavior and the Impact on Laboratory Studies

“…Published studies also are inconsistent for relating puff topography to various biomarkers such as CO and nicotine/cotinine levels, where different parameters affect these biomarkers differently (61,104,108-118). For example, puff number and to a lesser extent the puff volume and duration affect nicotine levels, while CO level are mostly influenced by puff volume and less by puff number (113). Zacny and coworkers reported that both nicotine and CO increase proportionally with an increase in puff volume (61).…”

A Link between Adolescent Nicotine Metabolism and Smoking Topography

“…Mechanisms for such relationships have been suggested (e.g., nicotine receptor activation, airway sensorial effect [29]) but remain speculative. Finally, the implications of our puff-duration findings are unclear, because in at least one study, puff duration did not affect nicotine concentrations [8]. …”

“…For example, adult slow nicotine metabolizers smoke fewer cigarettes daily and weekly [3–5] and have lower smoke exposure as measured by expired air carbon monoxide and plasma nicotine levels, than normal and fast metabolizers [4]. Consumption patterns, as well as smoking topography (i.e., how each cigarette is smoked), influence body nicotine and toxicant concentrations and have implications for tobacco addiction and health harm [6–8]. …”

Reduced exposure evaluation of an Electrically Heated Cigarette Smoking System. Part 1: Non-clinical and clinical insights

“…In addition, serum cotinine and plasma nicotine were also determined in some of the clinical evaluations (Benowitz, 1988). Carboxyhemoglobin (COHb) was selected as a biomarker of CO exposure based on its classical use for determination of tobacco smoke exposure (Rieben, 1992; Society for Research on Nicotine and Tobacco Subcommittee on Biochemical Verification, 2002; Scherer, 2006). Total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) plus its O-glucuronide conjugate 4-[(methylnitrosamino)-1-(3-pyridyl)but-1-yl]-b-O-D-glucosiduronic acid (NNAL-Gluc) was determined as a tobacco-specific biomarker of exposure to NNK (Hecht and Tricker, 1999).…”