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In 2005, approximately 2.3% of U.S. adults used smokeless tobacco. Moist snuff leads all types of smokeless tobacco in revenues and marketing expenditures. The U.S. Surgeon General has concluded that smokeless tobacco use can lead to nicotine addiction. The National Toxicology Program of the National Institutes of Health has classified smokeless tobacco as a human carcinogen. Tobacco-specific nitrosamines (TSNAs) are potent carcinogens in smokeless tobacco products, and the pH of the product influences the content of un-ionized nicotine which is the form of nicotine most rapidly absorbed in the mouth. The Centers for Disease Control and Prevention analyzed 40 top-selling brands of moist snuff to measure nicotine, moisture, pH, un-ionized nicotine, and TSNAs, including 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL). The study findings indicate that moist snuff brands varied widely in content of rapidly absorbed, addictive un-ionized nicotine (500-fold range) and of carcinogenic TSNAs (18-fold range). Product characteristics such as packaging and moisture content appeared to be correlated with concentrations of un-ionized nicotine, and flavor characteristics of low-priced brands may correlate with TSNA concentrations. These findings warrant further study in light of (a) the marketing of smokeless tobacco for use in places where smoking is prohibited, (b) the promotion of smokeless tobacco as a harm-reduction product, and (c) the ever-expanding number of highly flavored smokeless varieties brought to the market.

A method for simultaneous determination of buprenorphine (BUP), norbuprenorphine (NBUP), methadone, 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP), cocaine, benzoylecgonine (BE), ecgonine methyl ester (EME), anhydroecgonine methyl ester (AEME), morphine, codeine, 6-acetylmorphine (6AM), heroin, 6-acetylcodeine (6AC), nicotine, cotinine, and trans -3′-hydroxycotinine (OH-cotinine) by liquid chromatography tandem mass spectrometry in oral fluid (OF) was developed and extensively validated. Acetonitrile (800 μL) and OF (250 μL) were added to a 96-well Isolute-PPT+protein precipitation plate. Reverse-phase separation was achieved in 16 min and quantification was performed by multiple reaction monitoring. The assay was linear from 0.5 or 1 to 500 μg/L. Intraday, interday, and total imprecision were less than 13% ( n  = 20), analytical recovery was 92–114% ( n  = 20), extraction efficiencies were more than 77% ( n  = 5), and process efficiencies were more than 45% ( n  = 5). Although ion suppression was detected for EME, cocaine, morphine, 6AC, and heroin (less than 56%) and enhancement was detected for BE and nicotine (less than 316%), deuterated internal standards compensated for these effects. The method was sensitive (limit of detection 0.2–0.8 μg/L) and specific (no interferences) except that 3-hydroxy-4-methoxyamphetamine interfered with AEME. No carryover was detected, and all analytes were stable for 24 h at 22 °C, for 72 h at 4 °C, and after three freeze–thaw cycles, except cocaine, 6AC, and heroin (22–97% loss). The method was applied to 41 OF specimens collected throughout pregnancy with a Salivette® OF collection device from an opioid-dependent BUP-maintained pregnant woman. BUP ranged from 0 to 7,400 μg/L, NBUP from 0 to 71 μg/L, methadone from 0 to 3 μg/L, nicotine from 32 to 5,020 μg/L, cotinine from 125 to 508 μg/L, OH-cotinine from 11 to 51 μg/L, cocaine from 0 to 419 μg/L, BE from 0 to 351 μg/L, EME from 0 to 286 μg/L, AEME from 0 to 7 μg/L, morphine from 0 to 22 μg/L, codeine from 0 to 1 μg/L, 6AM from 0 to 4 μg/L, and heroin from 0 to 2 μg/L. All specimens tested negative for EDDP and 6AC. This method permits a fast and simultaneous quantification of 16 drugs and metabolites in OF, with good selectivity and sensitivity.

Suicide by self-poisoning is rather common around the world. This paper presents an exceptional complex suicide in which nicotine was applied in the form of self-made patches soaked with an extraction from fine-cut tobacco. In addition, the 51-year-old suicide victim took a lethal dose of diphenhydramine. Toxicological analysis also revealed the presence of tetrazepam in subtherapeutic concentrations. The scene of death suggested an autoerotic accident at first, as the body was tied with tapes, cables and handcuffs. As a result of the entire investigations, the fatality had to be classified as a suicidal intoxication by nicotine and diphenhydramine.

Nicotine, a lipid-soluble alkaloid obtained from the dried leaves of Nicotiana, is most frequently encountered in tobacco products for smoking, chewing or sniffing as well as in a limited number of pesticides. Though nicotine is one of the most toxic drugs of abuse, it has rarely led to fatalities. Sudden death can be caused by cardiovascular arrest, respiratory muscle paralysis and/or central respiratory failure. A 42-year-old man was found dead by his wife. He was lying on the floor, next to a box containing many empty bottles of beer and vodka. Some labeled chemical bottles found at the scene contained various substances, including nicotine and brucine. Gross examination of the organs at autopsy revealed no specific findings. The toxicological examination failed to disclose any lethal toxic agents other than a high concentration of nicotine and its primary metabolite cotinine in femoral venous blood (2.2 μg/mL). Blood alcohol was determined to be 2.1 g/L in femoral venous blood. Only a paucity of fatal cases of nicotine poisoning has been reported in the literature so far.

Tobacco is one of the most easily accessible and commonly abused drugs world-wide. Nicotine, one of its principal constituents, can cause serious or fatal overdoses. Whilst the deliberate ingestion of this substance appears to be relatively rare, often the important signs of its consumption are not recognised, sometimes with fatal results. Here we describe two cases of intentional fatal ingestion of nicotine. The nicotine was extracted from tobacco using instructions available on the Internet. The first case involved a male aged 19 who died in 2008. The post-mortem blood and urine levels of nicotine were 5.5 mg/l and >80 mg/l respectively; the blood level is in line with the generally recognised fatal level of >5 mg/l. The levels of nicotine's main metabolite, cotinine, for this case were 2.5 mg/l and 7.9 mg/l for blood and urine respectively. A comparative case in 1999 involved a 32 year-old male. The level of post-mortem nicotine in his blood was 1.0 mg/l. These are believed to be the first UK suicides by nicotine using instructions from the Internet reported in the literature. Information that nicotine was the agent responsible only became apparent some time after death. There may be more deaths due to this cause that go unrecognised because quantification of nicotine and cotinine levels is not often conducted, due to the wide prevalence of smoking. It is important that all evidence at the scene of a sudden and unexplained death is carefully evaluated, including potential clues on PCs and lap-tops.

Hydrophobic silica nanopowder has been used as an effective latent fingermark development agent and subsequently as an enhancement agent in the surface-assisted laser desorption/ionisation-time of flight (SALDI-TOF) mass spectrometry for analysis of fingermark components. The technique has been used in the detection of nicotine and cotinine in the fingermarks of smokers. In order to have confidence in concluding that the nicotine in such samples is indicative of cigarette usage, it is necessary to establish that contamination by environmental contact or from hand to hand contact with smokers or from passive smoking does not lead to false identification of non-smokers as smokers. To investigate this possibility, the background level of nicotine in fingermark material from a number of commonly used places was determined. In addition, a series of experiments was carried out to assess the extent to which nicotine can be transferred through handshakes and finger transfer as well as touching of door handles. The rate of loss of nicotine from latent fingermarks was also assessed over a 24-h period under ambient laboratory conditions. Finally, a laboratory-based model system was evaluated to ascertain the possible transport of nicotine in cigarette smoke from a source to adjacent areas to simulate cross-contamination of a non-smoker by passive exposure. It was observed that person-to-person transfer from a smoker to a non-smoker can occur following handshakes but at low levels and that passive cross-contamination from contact with surfaces is possible under simulated conditions. However, levels of nicotine in the wider environment were found to be too low for detection using this technique which may reflect the half-life of nicotine in latent fingermarks which was about 11 h. Likewise, transfer via smoke is possible to objects within about 0.1 m of the cigarette but it is unlikely that significant secondary nicotine contamination will occur on the faces and hands of adjacent non-smokers.

Introduction Insurance agencies might request laboratories to differentiate whether a deceased has been a smoker or not to decide about refunding of his nonsmoker rate. In this context, the question on a solid proof of tobacco alkaloids and major metabolites in tissues came up. Currently, an appropriate assay is still lacking to analyze tissue distribution in smokers or nonsmokers. Nicotine (NIC), nornicotine (NNIC), anatabine (ATB), anabasine (ABS), and myosmine (MYO) are naturally occurring alkaloids of the tobacco plant; most important phase I metabolites of NIC are cotinine (COT), norcotinine (NCOT), trans -3′-hydroxycotinine (HCOT), nicotine- N′ -oxide (NNO), and cotinine- N -oxide (CNO). An analytical assay for their determination was developed and applied to five randomly selected autopsy cases. Methods Homogenates using 500 mg aliquots of tissue samples were analyzed by liquid chromatography/tandem mass spectrometry following solid phase extraction. The method was validated according to current international guidelines. Results NIC, COT, NCOT, ABS, ATB, and HCOT could be detected in all tissues under investigation. Highest NIC concentrations were observed in the lungs, whereas highest COT concentrations have been found in the liver. MYO was not detectable in any of the tissues under investigation. Conclusions The assay is able to adequately separate isobaric analyte pairs such as NIC/ABS/NCOT and HCOT/CNO thus being suitable for the determination of tobacco alkaloids and their phase I metabolites from tissue. More autopsy cases as well as corresponding body fluids and hair samples will be investigated to differentiate smokers from nonsmokers.

Both plasma and saliva cotinine levels have been reported in surveys of smoking behavior, and it is of interest to know how closely these two measures correspond. Plasma and saliva specimens were gathered from a sample of 605 respondents in the 1998 Health Survey for England and assayed for cotinine by a well-proven gas chromatographic method. Plasma and saliva cotinine concentrations were highly correlated (r=.99). On average, concentrations in saliva were 25% higher than in plasma, and this ratio applied both at the low levels attributable to passive smoking and across the range of active smoking values. The ratio was somewhat lower in younger people than in older people and also varied significantly by body mass index but did not differ by gender. Calculation of the limits of agreement revealed substantial uncertainty in the predicted plasma value corresponding to a given saliva cotinine, and vice versa. For comparisons across subjects, the mean plasma cotinine level corresponding to a mean saliva cotinine level can be estimated with confidence, but at the level of the individual, considerable predictive uncertainty remains.

We assessed the effects of prenatal exposure to environmental tobacco smoke on fetal growth and length of gestation. The study population consisted of 389 nonsmoking women who were selected from a population-based study in southeast Finland on the basis of questionnaire information after delivery (response rate 94%). The final exposure assessment was based on nicotine concentration of maternal hair sampled after the delivery, which measures exposure during the past 2 months (i.e., the third trimester). The exposure categories were defined a priori as high (nicotine concentration ≥ 4.00 μg/g; n = 52), medium (0.75 to < 4.00 μg/g; n = 186), and low as the reference category (< 0.75 μg/g; n = 151). In logistic regression analysis, controlling for confounding, the risk of preterm delivery (< 37 weeks) was higher in the high [adjusted odds ratio (OR) = 6.12; 95% confidence interval (CI), 1.31-28.7] and medium exposure categories (adjusted OR = 1.30; 95% CI, 0.30-5.58) compared with the reference category, and there was a 1.22 (95% CI, 1.07-1.39) increase in adjusted OR with a 1 μg/g increase in hair nicotine concentration. The corresponding adjusted OR was 1.06 (95% CI, 0.96-1.17) for low birth weight and 1.04 (95% CI, 0.92-1.19) for small-for-gestational-age.

Study objective: The aim of this study was to compare the two biomarkers of exposure to environmental tobacco smoke (ETS); urine cotinine and hair nicotine, using questionnaires as the standard. Design: A cross sectional study of children consecutively admitted to hospital for lower respiratory illnesses during the period of the study. Settings: Three regional hospitals in the larger Wellington area, New Zealand. Participants: Children aged 3–27 months and admitted to the above hospitals during August 1997 to October 1998. A total of 322 children provided 297 hair samples and 158 urine samples. Main results: Hair nicotine levels were better able to discriminate the groups of children according to their household's smoking habits at home (no smokers, smoke only outside the home, smoke inside the house) than urine cotinine (Kruskall-Wallis; χ2=142.14, and χ2=49.5, respectively (p<0.0001)). Furthermore, hair nicotine levels were more strongly correlated with number of smokers in the house, and the number of cigarettes smoked by parents and other members of the child's households. Hair nicotine was better related to the questionnaire variables of smoking in a multivariate regression model (r2=0.55) than urine cotinine (r2=0.31). Conclusions: In this group of young children, hair nicotine was a more precise biomarker of exposure to ETS than urine cotinine levels, using questionnaire reports as the reference. Both biomarkers indicate that smoking outside the house limits ETS exposure of children but does not eliminate it.