Absorption and metabolism of nicotine from cigarettes.

Armitage, A. K.; Dollery, C. T.; George, C. F.; Houseman, T H; Lewis, Paul; Turner, David M.

doi:10.1136/bmj.4.5992.313

Cited by 273 publications

(150 citation statements)

References 8 publications

(3 reference statements)

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“…To examine the relevance of rodent nicotine exposure to the human condition, we analyzed plasma levels of nicotine in mice treated with the 7 mg/kg/ day dose and found an average of 29.9 ± 15.5 ng/ml, a result that is similar to the average maximum arterial blood concentration of human chronic smokers (range B20-40 ng/ml) (Armitage et al, 1975;Matta et al, 2007;O'Dell et al, 2006).…”

Section: Dopamine and Nicotine Motivationmentioning

confidence: 93%

“…The use of a variety of time points in our measurements of somatic withdrawal symptoms allowed us to find the most appropriate time for withdrawal motivation studies in both mice and rats. Although the dose used in mice (7 mg/kg/ day) and rats (3.15 mg/kg/day) exceeds the amount of nicotine smoked by the heaviest smokers of high-yield cigarettes (Armitage et al, 1975;Epping-Jordan et al, 1998), it is important to consider that rats and mice have much higher metabolic and drug clearance rates (Matta et al, 2007) than humans. Furthermore, plasma levels of nicotine measured presently were similar to those observed in humans and measured in previous rodent studies (Guillem et al, 2005;O'Dell et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

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Dopaminergic Signaling Mediates the Motivational Response Underlying the Opponent Process to Chronic but Not Acute Nicotine

Grieder

Sellings

Vargas‐Perez

et al. 2009

Neuropsychopharmacol

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The mesolimbic dopamine (DA) system is implicated in the processing of the positive reinforcing effect of all drugs of abuse, including nicotine. It has been suggested that the dopaminergic system is also involved in the aversive motivational response to drug withdrawal, particularly for opiates, however, the role for dopaminergic signaling in the processing of the negative motivational properties of nicotine withdrawal is largely unknown. We hypothesized that signaling at dopaminergic receptors mediates chronic nicotine withdrawal aversions and that dopaminergic signaling would differentially mediate acute vs dependent nicotine motivation. We report that nicotine-dependent rats and mice showed conditioned place aversions to an environment paired with abstinence from chronic nicotine that were blocked by the DA receptor antagonist a-flupenthixol (a-flu) and in DA D 2 receptor knockout mice. Conversely, a-flu pretreatment had no effect on preferences for an environment paired with abstinence from acute nicotine. Taken together, these results suggest that dopaminergic signaling is necessary for the opponent motivational response to nicotine in dependent, but not non-dependent, rodents. Further, signaling at the DA D 2 receptor is critical in mediating withdrawal aversions in nicotine-dependent animals. We suggest that the alleviation of nicotine withdrawal primarily may be driving nicotine motivation in dependent animals. Neuropsychopharmacology (2010) 35, 943-954;

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Section: Dopamine and Nicotine Motivationmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Dopaminergic Signaling Mediates the Motivational Response Underlying the Opponent Process to Chronic but Not Acute Nicotine

Grieder

Sellings

Vargas‐Perez

et al. 2009

Neuropsychopharmacol

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show abstract

“…A typical adult male breathes ~ 0.7 m 3 /h (US EPA, 2011), and the average nicotine concentration in the chamber was 420 µg/m 3 . Armitage (1975) reports that for smokers 80-90% of nicotine in the inhaled air is absorbed (bioavailable), while for "nonsmokers" the value is 30-66%. Iwase (1991) reports nicotine absorption of 60-80% for non-smoking women.…”

Section: Inhalation Compared To Dermal Uptakementioning

confidence: 99%

“…This estimated equivalency is based on multiple studies. Using cigarettes containing 14 C-labeled nicotine, Armitage et al (1975) reported that the dose for a regular cigarette smoker would be about 25% of the nicotine in a cigarette, while that of a "non-smoker" would be only about 10%.…”

Section: Accepted Articlementioning

confidence: 99%

Measurements of dermal uptake of nicotine directly from air and clothing

et al. 2016

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In this preliminary study, we have investigated whether dermal uptake of nicotine directly from air or indirectly from clothing can be a meaningful exposure pathway. Two participants wearing only shorts and a third participant wearing clean cotton clothes were exposed to environmental tobacco smoke (ETS), generated by mechanically “smoking” cigarettes, for three hours in a chamber while breathing clean air from head-enveloping hoods. The average nicotine concentration (420 μg/m3) was comparable to the highest levels reported for smoking sections of pubs. Urine samples were collected immediately before exposure and 60 hour post-exposure for bare-skinned participants. For the clothed participant, post-exposure urine samples were collected for 24 hour. This participant then entered the chamber for another three-hour exposure wearing a hood and clothes, including a shirt that had been exposed for five days to elevated nicotine levels. The urine samples were analyzed for nicotine and two metabolites—cotinine and 3OH-cotinine. Peak urinary cotinine and 3OH-cotinine concentrations for the bare-skinned participants were comparable to levels measured among non-smokers in hospitality environments before smoking bans. The amount of dermally absorbed nicotine for each bare-skinned participant was conservatively estimated at 570 μg, but may have been larger. For the participant wearing clean clothes, uptake was ~20 μg, and while wearing a shirt previously exposed to nicotine, uptake was ~80 μg. This study demonstrates meaningful dermal uptake of nicotine directly from air or from nicotine-exposed clothes. The findings are especially relevant for children in homes with smoking or vaping

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“…The half -life of nicotine in the body was assumed to be a triangular distribution with a minimum value of 1 h, a most likely value of 2 h, and a maximum value of 4 h (Benowitz et al, 1982;Feyerabend et al, 1985;Robinson et al, 1992;Zevin et al, 1997 ). The fraction of nicotine absorbed was assumed to be uniformly distributed between 0.6 and 0.8 ( Armitage et al, 1975;Russell and Feyerabend, 1978;Benowitz and Jacob, 1987;Iwase et al, 1991;Molander et al, 1996 ).…”

Section: Estimation Of Gas Phase Nicotine Dosementioning

confidence: 99%

Doses and lung burdens of environmental tobacco smoke constituents in nonsmoking workplaces

Me²,

et al. 2000

J Expo Sci Environ Epidemiol

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Absorption and metabolism of nicotine from cigarettes.

Cited by 273 publications

References 8 publications

Dopaminergic Signaling Mediates the Motivational Response Underlying the Opponent Process to Chronic but Not Acute Nicotine

Dopaminergic Signaling Mediates the Motivational Response Underlying the Opponent Process to Chronic but Not Acute Nicotine

Measurements of dermal uptake of nicotine directly from air and clothing

Doses and lung burdens of environmental tobacco smoke constituents in nonsmoking workplaces

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