Abstract:Cotinine, whatever the collection method and analysed by EIA kits, shows good differentiation between smokers and non-smokers. Salivary samples have the advantage of being non-invasive, although collection methodology is important, as cotinine levels may vary.
“…Accordingly, future studies on the biological bases of ethanol and nicotine interactions are necessary and the use of other strains and species may provide valuable data. Though nicotine concentration may seem high in the drinking solution, nicotine absorption from the buccal cavity yields cotinine plasma levels (Klein et al, 2003(Klein et al, , 2004Sparks and Pauly, 1999) comparable to those found in adolescent smokers (Binnie et al, 2004;Caraballo et al, 2004;Wood et al, 2004). As for ethanol, according to previous studies in adolescent rodents, even the moderate doses used in the present study result in blood levels well above the legal driving limit (Silveri and Spear, 2000).…”
Smoking and consumption of alcoholic beverages are frequently associated during adolescence. This association could be explained by the cumulative behavioral effects of nicotine and ethanol, particularly those related to anxiety levels. However, despite epidemiological findings, there have been few animal studies of the basic neurobiology of the combined exposure in the adolescent brain. In the present work we assessed, through the use of the elevated plus maze, the short-and long-term anxiety effects of nicotine (NIC) and/or ethanol (ETOH) exposure during adolescence (from the 30th to the 45th postnatal day) in four groups of male and female C57BL/6 mice: (1) Concomitant NIC (nicotine free-base solution (50 mg/ml) in 2% saccharin to drink) and ETOH (ethanol solution (25%, 2 g/kg) i.p. injected every other day) exposure; (2) NIC exposure; (3) ETOH exposure; (4) Vehicle. C57BL/6 mice were selected, in spite of the fact that they present slower ethanol metabolism, because they readily consume nicotine in the concentration used in the present study. During exposure (45th postnatal day: PN45), our results indicated that ethanol was anxiolytic in adolescent mice and that nicotine reverted this effect. Short-term drug withdrawal (PN50) elicited sex-dependent effects: exposure to nicotine and/or ethanol was anxiogenic only for females. Although neither nicotine nor ethanol effects persisted up to 1 month postexposure (PN75), the coadministration elicited an anxiogenic response. In spite of the fact that generalizations based on the results from a single strain of mice are prone to shortcomings, our results suggest that the deficient response to the anxiolytic effects of ethanol in adolescents co-exposed to nicotine may drive higher ethanol consumption. Additionally, increased anxiety during long-term smoking and drinking withdrawal may facilitate relapse to drug use.
“…Accordingly, future studies on the biological bases of ethanol and nicotine interactions are necessary and the use of other strains and species may provide valuable data. Though nicotine concentration may seem high in the drinking solution, nicotine absorption from the buccal cavity yields cotinine plasma levels (Klein et al, 2003(Klein et al, , 2004Sparks and Pauly, 1999) comparable to those found in adolescent smokers (Binnie et al, 2004;Caraballo et al, 2004;Wood et al, 2004). As for ethanol, according to previous studies in adolescent rodents, even the moderate doses used in the present study result in blood levels well above the legal driving limit (Silveri and Spear, 2000).…”
Smoking and consumption of alcoholic beverages are frequently associated during adolescence. This association could be explained by the cumulative behavioral effects of nicotine and ethanol, particularly those related to anxiety levels. However, despite epidemiological findings, there have been few animal studies of the basic neurobiology of the combined exposure in the adolescent brain. In the present work we assessed, through the use of the elevated plus maze, the short-and long-term anxiety effects of nicotine (NIC) and/or ethanol (ETOH) exposure during adolescence (from the 30th to the 45th postnatal day) in four groups of male and female C57BL/6 mice: (1) Concomitant NIC (nicotine free-base solution (50 mg/ml) in 2% saccharin to drink) and ETOH (ethanol solution (25%, 2 g/kg) i.p. injected every other day) exposure; (2) NIC exposure; (3) ETOH exposure; (4) Vehicle. C57BL/6 mice were selected, in spite of the fact that they present slower ethanol metabolism, because they readily consume nicotine in the concentration used in the present study. During exposure (45th postnatal day: PN45), our results indicated that ethanol was anxiolytic in adolescent mice and that nicotine reverted this effect. Short-term drug withdrawal (PN50) elicited sex-dependent effects: exposure to nicotine and/or ethanol was anxiogenic only for females. Although neither nicotine nor ethanol effects persisted up to 1 month postexposure (PN75), the coadministration elicited an anxiogenic response. In spite of the fact that generalizations based on the results from a single strain of mice are prone to shortcomings, our results suggest that the deficient response to the anxiolytic effects of ethanol in adolescents co-exposed to nicotine may drive higher ethanol consumption. Additionally, increased anxiety during long-term smoking and drinking withdrawal may facilitate relapse to drug use.
“…First, cigarette smoking and cessation-related measures were self-reported without validation by biochemical testing, and might be subject to social desirability bias. However, selfreported smoking status correlates with serum cotinine levels (10). Second, because NHIS does not include institutionalized populations and persons in the military, results are not generalizable to these groups.…”
“…Other methods that could more accurately estimate smoking exposure are expired carbon monoxide levels and cotinine measurements in body fluids such as saliva, serum and urine (Dolcini et al 2003). The relationships between self-reported smoking data and cotinine levels in some body fluids have been shown to be highly correlated (Binnie et al 2004). …”
Background & Aim: Tobacco smoking exerts a harmful effect on the periodontal tissues manifested by periodontal pockets, attachment loss and periodontal bone loss. Current evidences on the effects of tobacco on periodontal health mainly concern cigarette smoking. In view of the increasing popularity of water pipe smoking in Arabian countries and reports confirming that water pipe smoking has health effects similar to those of cigarette smoking, there is a need for a better understanding of the potential harm of this smoking habit. The present thesis was carried out in order to explore whether water pipe smoking is associated with periodontal health in a manner similar to cigarette smoking.
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