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Smokers urine

R.M. Characterization of the glucuronide conjugate of cotinine A previously unidentified major metabolite of nicotine in smokers urine. Chem Res Toxicol 5 280,... [Pg.252]

Carmella et al. (15A05) identified 4-(Af-methylnitrosamino)-l-(3-pyridinyl)-l-butanol (NNAL) and its glucuronide in the urine of cigarette smokers, thus providing the first evidence for metabolites of TSNAs in human urine. No NNK was detected. Results with smokers urine were consistent with those found previously with monkeys urine. [Pg.704]

A number of LC tandem MS methods have been reported for OPAHs in environmental samples and biological fluids. Ramsauer et al. [48] and Andreoli et al. [49] describe LC—ESI—MS/MS methods for the determination of PAH metabolites in human urine. Andreoli et al. specifically targeted naphthalene metabolites for study for occupationally exposed workers, while Ramsauer et al. studied a broader range of hydroxylated PAHs in urine from smokers and nonsmokers. Levels of hydroxyl PAHs in smokers urine were also measured by Jacob, Wilson, and Benowitz [50] by LC—APCl—MS/MS however, this method utilized a derivitization step with pentafluorobenzyl bromide to increase sensitivity. LC—APCl—MS/ MS was employed by Fan et al. [51] to determine 1-hydroxypyrene and 3-hydroxybenzo[fl]pyrene in urine. [Pg.346]

SRM 3674 Organic Contaminants in Fortified Non-Smokers Urine (in preparation) ... [Pg.374]

For applications in the diagnostics and biomarker area, 8-oxo-7,8-dihydro-2,-deoxyguanosine (8-oxoGuo) was measured as an oxidation stress biomarker in urine samples from smokers and non-smokers (Hu et al. 2006). When 100, uL of samples (10 times dilution) were used, a detection limit of 5.7 pg/mL (2.0 fmol) was achieved. The cycle time was 10 min per sample. The application was used for clinical scale. A similar approach was used for the detection of N7-methylguanine, another carcinogen exposure biomarker in human urine (Chao et al. 2005). [Pg.282]

Several studies provided data on blood and urine concentrations of cyanide and thiocyanate following occupational exposures at low concentrations. These values are generally similar to those of smokers who have not been occupationally exposed to HCN. Whole-blood cyanide concentrations during... [Pg.275]

A common metabolite found in the urine and plasma of patients treated with gold drugs is [Au(CN)2], an ion which readily enters cells and can inhibit the oxidative burst of white blood cells. It may therefore be an active metabolite of gold drugs. It also exhibits anticancer and anti-HIV activity. The high Au contents of red blood cells of smokers receiving gold therapy has been attributed to the inhalation of HCN in smoke (420). [Pg.254]

The urine of people who are heavy smokers contains mutagenic chemicals, chemicals that cause mutations in biological cells. Bioanalytical laboratories can analyze urine samples for these chemicals, but the samples must be cleaned up first prior to extraction with methylene chloride. The procedure for this cleanup utilizes an open column chromatography. Columns several inches tall and about an inch wide are prepared by packing them with an adsorbing resin that has been treated with methyl alcohol. The urine samples are passed through these columns as part of the sample preparation scheme. [Pg.319]

Following chronic occupational exposure to 0.19-0.75 ppm hydrogen cyanide, 24-hour urinary levels of thiocyanate were 6.23 (smokers) and 5.4 pg/mL (nonsmokers) in exposed workers as compared with 3.2 (smokers) and 2.15 pg/mL (nonsmokers) in the controls (Chandra et al. 1980). This study demonstrates that tobacco smoking contributes to higher thiocyanate levels excreted in the urine. No studies were located regarding excretion of cyanide in animals after inhalation exposure to cyanide. [Pg.79]

Levels of cyanide and its metabolite thiocyanate in blood serum and plasma, urine, and saliva have been used as indicators of cyanide exposure in humans, particularly in workers at risk of occupational exposures, in smokers or nonsmokers exposed to sidestream or environmental tobacco smoke, in populations exposed to high dietary levels of cyanide, and in other populations with potentially high exposures (see Section 5.6). The correlation between increased cyanide exposure and urinary thiocyanate levels was demonstrated in workers exposed to 6.4-10.3 ppm cyanide in air (El Ghawabi et al. 1975). In another study, blood cyanide concentrations were found to vary from 0.54 to 28.4 pg/100 mL in workers exposed to approximately 0.2-0.8 ppm cyanide in air, and from 0.0 to 14.0 pg/100 mL in control workers... [Pg.181]

Djuric D, Raicevic P, Konstantinovic I. 1962. Excretion of thiocyanates in urine of smokers. Arch. Environ. Health 5 12-15. [Pg.244]

Tuomi T, Johnsson T, Reijula K. 1999. Analysis of nicotine, 3-hydroxycotinine, cotenine, and caffeine in urine of passive smokers by HPLC-tandem mass spectrometry. Clin Chem 45 2164. [Pg.176]

Although on average about 70-80% of nicotine is metabolized via the cotinine pathway in humans, only 10-15% of nicotine absorbed by smokers appears in the urine as unchanged cotinine (Benowitz et al. 1994). Six primary metabolites of cotinine have been reported in humans 3 -hydroxycotinine (McKennis et al. 1963 Neurath et al. 1987), 5 -hydroxycotinine (also called allohydroxycotinine) (Neurath 1994), which exists in tautomeric equilibrium with the open chain derivative... [Pg.36]

In vitro stndies have shown that there are distinct transport systems for both baso-lateral and apical uptake of nicotine (Takami et al. 1998). Nicotine has been shown to be actively transported by kidney cells, most likely by the organic ion transporter OCT2 (Zevin et al. 1998 Urakami et al. 1998). Cimetidine decreases renal clearance of nicotine by 47% in nonsmoking volunteers (Bendayan et al. 1990). This is consistent with the inhibition of basolateral uptake by cimetidine detected in vitro. Mecamylamine reduces renal clearance of nicotine in smokers dosed with intra-venons nicotine when urine is alkalinized, but not when nrine is acidified (Zevin et al. 2000). [Pg.47]

The primary alkaloid in tobacco is nicotine, but tobacco also contains small amounts of minor alkaloids such as anabasine, anatabine, myosmine, and others. The minor alkaloids are absorbed systemically and can be measured in the urine of smokers and users of smokeless tobacco (Jacob et al. 1999). The measurement of minor alkaloids is a way to quantitate tobacco use when a person is also taking in pure nicotine from a nicotine medication or a nontobacco nicotine delivery system. This method has been used to assess tobacco abstinence in clinical trials of smoking cessation with treatment by nicotine medications (Jacob et al. 2002). [Pg.53]

Neurath GB (1994) Aspects of the oxidative metabolism of nicotine. Clin Investig 72(3) 190-195 Neurath GB, Dunger M, Orth D, Pein FG (1987) Trans-3 -hydroxycotinine as a main metabolite in urine of smokers. Int Arch Occup Environ Health 59(2) 199-201 Neurath GB, Orth D, Pein FG (1991) Detection of nomicotine in human urine after infusion of nicotine. In Adlkofer F, Thurau K (eds) Effects of nicotine on biological systems. Birkhauser Verlag, Basel, pp 45 9... [Pg.58]

Yamasaki, E. and Ames, B. N. The Concentration of Mutagens from Urine with the Nonpolar Resin XAD-2 Cigarette Smokers have Mutagenic Urine , Proc. Natl. Acad. Sci. U.S.A. (1977) 74, 3555. [Pg.12]


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