Cigarette Smoking and Plasma Levels of Nicotine

Isaac, P.F.; Rand, M. J.

doi:10.1038/236308a0

Cited by 252 publications

(97 citation statements)

References 7 publications

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“…It should be noted that the pump, marketed as a 2-week infusion device, actually takes 17.5 days to be exhausted completely (information supplied by the manufacturer) and thus the nicotine infusion terminates during GD21. Maternal plasma nicotine levels achieved with this administration model resemble those seen in heavy smokers (25-60 ng/ml) as characterized previously (Isaac and Rand, 1972;Levin and Slotkin, 1998;Lichtensteiger et al, 1988;Murrin et al, 1985;Slotkin, 1992Slotkin, , 1998Slotkin, , 1999Slotkin, , 2004). This animal model also resembles the effects of maternal smoking in that fetal nicotine levels exceed those found in maternal plasma (Luck et al, 1985;Sarasin et al, 2003).…”

Section: Animals and Nicotine Infusionssupporting

confidence: 73%

Does Prenatal Nicotine Exposure Sensitize the Brain to Nicotine-Induced Neurotoxicity in Adolescence?

Abreu‐Villaça

Seidler

Slotkin

2004

Neuropsychopharmacol

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Offspring of women who smoke during pregnancy are themselves more likely to take up smoking in adolescence. We evaluated neurotoxicant effects of prenatal and adolescent nicotine exposure in developing rats to evaluate whether these contribute to a biological basis for this relationship. Rats were given nicotine or vehicle throughout pregnancy and the offspring then again received nicotine or vehicle during adolescence (postnatal days PN30-47.5); this regimen reproduces the plasma nicotine levels found in smokers. Indices of neural cell number (DNA concentration and content), cell size (protein/DNA ratio), and cell membrane surface area (membrane/total protein) were then evaluated in brain regions during adolescent nicotine administration (PN45) and up to 1 month post-treatment. By itself, prenatal nicotine administration produced cellular alterations that persisted into adolescence, characterized by net cell losses in the midbrain and to a lesser extent, in the cerebral cortex, with corresponding elevations in the membrane/total protein ratio. The hippocampus showed a unique response, with increased DNA content and regional enlargement. Adolescent nicotine treatment alone had similar, albeit smaller effects, but also showed sex-dependence, with effects on protein biomarkers preferential to females. When animals exposed to nicotine prenatally were then given nicotine in adolescence, the net outcome was worsened, largely representing summation of the two individual effects. Our results indicate that prenatal nicotine exposure alters parameters of cell development lasting into adolescence, where the effects add to those elicited directly by adolescent nicotine; neurotoxicant actions may thus contribute to the association between maternal smoking and subsequent smoking in the offspring.

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Section: Animals and Nicotine Infusionssupporting

confidence: 73%

Does Prenatal Nicotine Exposure Sensitize the Brain to Nicotine-Induced Neurotoxicity in Adolescence?

Abreu‐Villaça

Seidler

Slotkin

2004

Neuropsychopharmacol

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“…In the current study, we administered nicotine to pregnant Rhesus macaque monkeys throughout pregnancy until just before term, using continuous infusions of nicotine via osmotic minipumps, so as to avoid confounding effects of fluctuating drug levels and the associated incidence of fetal hypoxia/ischemia (Levin and Slotkin, 1998;Slotkin, 1992Slotkin, , 1999Slotkin, , 2004, carefully matching the dose rate so as to simulate the plasma levels of nicotine commonly associated with maternal smoking or with use of transdermal nicotine patches (Benowitz et al, 1990;Fredrickson et al, 1995;Isaac and Rand, 1972;Lichtensteiger et al, 1988;Luck et al, 1985;Murrin et al, 1987). Fetal brain regions, heart and lung were then examined for four families of biomarkers known to characterize neurodevelopmental deficits associated with nicotine exposure.…”

Section: Introductionmentioning

confidence: 99%

Effects of Prenatal Nicotine Exposure on Primate Brain Development and Attempted Amelioration with Supplemental Choline or Vitamin C: Neurotransmitter Receptors, Cell Signaling and Cell Development Biomarkers in Fetal Brain Regions of Rhesus Monkeys

Slotkin

Seidler

Qiao

et al. 2004

Neuropsychopharmacol

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Studies in developing rodents indicate that nicotine is a neuroteratogen that disrupts brain development by stimulating nicotinic acetylcholine receptors (nAChRs) that control neural cell replication and differentiation. We administered nicotine to pregnant Rhesus monkeys from gestational day 30 through 160 by continuous infusion, achieving maternal plasma levels comparable to those in smokers (30 ng/ml). Fetal brain regions and peripheral tissues were examined for nAChR subtypes, other neurotransmitter receptors, and indices of cell signaling and cell damage. Nicotine evoked nAChR upregulation, but with distinct regional disparities indicative of selective stimulatory responses. Similarly, indices of cell loss (reduced DNA), cell size and neuritic outgrowth (protein/DNA and membrane/total protein ratios) were distinct for each region and did not necessarily follow the rank order of nAChR upregulation, suggesting the involvement of additional mechanisms such as oxidative stress. We then attempted to offset the adverse effects of nicotine with standard dietary supplements known to interact with nicotine. By itself, choline elicited nicotine-like actions commensurate with its promotion of cholinergic neurotransmission. When given in combination with nicotine, choline protected some regions from damage but worsened nicotine's effects in other regions. Similarly, Vitamin C supplementation had mixed effects, increasing nAChR responses while providing protection from cell damage in the caudate, the brain region most susceptible to oxidative stress. Our results indicate that nicotine elicits neurodevelopmental damage that is highly selective for different brain regions, and that dietary supplements ordinarily thought to be neuroprotectant may actually worsen some of the adverse effects of nicotine on the fetal brain.

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“…Others have reported nicotine intakes per cigarette around 1000 µg or more, and found no correlation with the machine determined nicotine yield of the cigarette (Benowitz and Jacob, 1984;Feyerabend et al, 1985;Isaac and Rand, 1972).…”

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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Cigarette Smoking and Plasma Levels of Nicotine

Cited by 252 publications

References 7 publications

Does Prenatal Nicotine Exposure Sensitize the Brain to Nicotine-Induced Neurotoxicity in Adolescence?

Does Prenatal Nicotine Exposure Sensitize the Brain to Nicotine-Induced Neurotoxicity in Adolescence?

Effects of Prenatal Nicotine Exposure on Primate Brain Development and Attempted Amelioration with Supplemental Choline or Vitamin C: Neurotransmitter Receptors, Cell Signaling and Cell Development Biomarkers in Fetal Brain Regions of Rhesus Monkeys

Measurements of dermal uptake of nicotine directly from air and clothing

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