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PubMedDate not supplied

Tobacco-specific N-nitrosamines in the saliva of habitual male snuff dippers.

Saliva was collected every ten minutes from habitual male snuff dippers and analysed for tobacco-specific N-nitrosamines (TSNA). Detectable levels of at least two TSNA were found in all samples collected between 10 and 30 minutes after the snuff had been placed in the mouth. Total concentrations of TSNA up to 241 ng/g were found in the saliva. Trace levels of TSNA were still found in the saliva 20 minutes after the snuff had been removed.

Adult↗
PubMedDate not supplied

Influence of nitrate, ascorbic acid, and nitrate reductase microorganisms on N-nitrosamine formation during Korean-style soysauce fermentation.

Traditional Korean soysauce samples were collected from households in Chinju, Gyeongnam, Korea and analysed for volatile N-nitrosamines. Five of 24 samples contained NDMA (range = 1.6-10.4 micrograms/l) which was the only volatile N-nitroso compound found. Soysauce made from well water contained NDMA more often (4 of 6 samples) than soysauce made from tap water (1 of 18). This suggests that the water source is a determinate in the NDMA content of soysauce, probably due to a higher nitrate content of well water. The source of salt used did not clearly influence NDMA content. Soysauce was prepared in the laboratory using traditional methods but with 0 to 400 mg/l nitrate and in some cases made 6.5 to 65 mM in ascorbic acid and fermented for 120 days. The NDMA content of the samples was positively correlated with increasing nitrate concentration. Nitrate at 400 mg/l resulted in an NDMA content of 203 micrograms/l. Ascorbic acid substantially inhibited NDMA formation. All samples contained large numbers of nitrate reductase-containing organisms (greater than 1 x 10(7) CFU/ml).

Ascorbic Acid↗
PubMed2003

Tobacco-specific nitrosamines in tobacco from U.S. brand and non-U.S. brand cigarettes.

Tobacco-specific nitrosamines (TSNAs) are one of the major classes of carcinogens found in tobacco products. As part of collaborative efforts to reduce tobacco use and resulting disease, the U.S. Centers for Disease Control and Prevention (CDC) carried out a two-phase investigation into the worldwide variation of the levels of TSNAs in cigarette tobacco. In the first phase, representatives of the World Health Organization (WHO) purchased cigarettes; scientists from the CDC subsequently measured the levels of TSNAs in tobacco from 21 different countries. Although the data collected from this initial survey suggested that globally marketed U.S.-brand cigarettes typically had higher TSNA levels than locally popular non-U.S. cigarettes in many countries, the number of samples limited the statistical power of the study. To improve statistical power and to ensure adequate sampling, the CDC conducted a second survey of 14 countries. In addition to the United States, the CDC selected the world's 10 most populous countries and three additional countries, so that at least two countries from each of the six WHO regions were represented. For each country, the CDC compared 15 packs of Marlboro cigarettes, which is the world's most popular brand of cigarettes, with 15 packs of a locally popular non-U.S. brand in the study country. Marlboro cigarettes purchased in 11/13 foreign countries had significantly higher tobacco TSNA levels than the locally popular non-U.S. brands purchased in the same country. The findings suggest that TSNA levels in tobacco can be substantially reduced in some cigarettes.

Carcinogens↗
PubMed2005

Determination of carcinogenic tobacco-specific nitrosamines in mainstream smoke from U.S.-brand and non-U.S.-brand cigarettes from 14 countries.

Tobacco-specific nitrosamines (TSNAs) comprise one of the major classes of carcinogenic compounds in mainstream cigarette smoke. As part of collaborative efforts between the World Health Organization and the U.S. Centers for Disease Control and Prevention (CDC) to reduce tobacco use and resulting disease, the CDC examined carcinogenic TSNA levels from cigarettes obtained from selected countries around the world. Using a modern, high-throughput liquid chromatography/mass spectrometry/mass spectrometry method under stringent quality control protocols, we determined the carcinogenic TSNA levels in mainstream smoke from a globally marketed brand, Marlboro, and from local top-selling cigarette brands from 14 countries. The levels of carcinogenic TSNAs in mainstream smoke collected using a 35-ml puff volume, 60-s puff interval, and 2-s puff duration correlated well (R=0.79, p<.0001) with previously reported levels in the corresponding tobacco filler. Marlboro cigarettes purchased in 10 countries had significantly higher carcinogenic TSNA levels in mainstream smoke than did local-brand cigarettes from the same country. In only one country, Brazil, were the carcinogenic TSNA levels in mainstream smoke from Marlboro cigarettes significantly lower than in the locally popular brand. However, carcinogenic TSNA levels in mainstream smoke from Brazilian Marlboro cigarettes were usually lower than those in mainstream smoke from the Marlboros purchased in the other 13 countries, suggesting a reason for the difference. The wide range of mainstream smoke carcinogenic TSNA levels measured in the present study (8.7-312 ng/cigarette) suggest that manufacturers can lower the carcinogenic TSNA levels and that, for similar filter ventilation, carcinogenic TSNA levels in the tobacco filler of a cigarette are a useful indicator of the corresponding levels in mainstream smoke.

Carcinogens↗
PubMed2005

Urinary tobacco-specific nitrosamines and 4-aminobiphenyl hemoglobin adducts measured in smokers of either regular or light cigarettes.

Cigarette brands may differ in their reported yields of "tar" as determined by the Federal Trade Commission smoking-machine method. Brands with relatively lower tar and nicotine yields often are described as light cigarettes. Smokers of light cigarettes generally maintain a nicotine intake comparable to that of smokers of regular cigarettes through compensatory smoking behaviors, but similar data have not been reported for carcinogen biomarkers. In the present study we measured serum cotinine concentrations (a marker of nicotine exposure), urinary levels of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL, a tobacco-specific nitrosamine [TSNA]), and hemoglobin adducts of 4-aminobiphenyl (4-ABP) in 150 smokers of either regular or light cigarettes. The TSNA and aromatic amines are known carcinogens in tobacco smoke. Multiple regression models were developed for each of the analytes and used to calculate adjusted geometric means. We found no significant differences in the levels of these biomarkers between customary users of light and regular cigarettes. Thus the concentrations of the carcinogen biomarkers NNAL and 4-ABP in the smokers who regularly smoked light cigarettes were essentially the same as those in the smokers who chose regular cigarettes.

Adult↗
PubMed2006

Tobacco-specific nitrosamines in new tobacco products.

New tobacco products, designed to attract consumers who are concerned about the health effects of tobacco, have been appearing on the market. Objective evaluation of these products requires, as a first step, data on their potentially toxic constituents. Tobacco-specific nitrosamines (TSNAs) are an important class of carcinogens in tobacco products, but virtually no data were available on their levels in these products. In the present study, we analyzed several new products-Ariva, Stonewall, Exalt, Revel, Smokey Mountain, and Quest-for TSNAs and compared their TSNA levels with those in nicotine replacement products and conventional smokeless tobacco and cigarette brands. TSNAs were not detected in Smokey Mountain, which is a tobacco-free snuff product. The lowest levels among the new products containing tobacco were in Ariva and Stonewall (0.26-0.28 microg/g wet weight of product). The highest levels in the new products were found in Exalt (3.3 microg/g tobacco), whereas Revel and Quest had intermediate amounts. Only trace amounts were found in nicotine replacement products, and conventional brands had levels consistent with those reported in the literature. These results demonstrate that TSNA levels in new tobacco products range from relatively low to comparable with those found in some conventional brands.

Carcinogenicity Tests↗
PubMed1989

Tobacco-specific nitrosamines in mainstream smoke of West German cigarettes--tar alone is not a sufficient index for the carcinogenic potential of cigarette smoke.

Fifty-five types of commercial cigarettes on the West German market were analyzed for tobacco-specific nitrosamines (TSNA) in mainstream smoke. The cigarettes included filter and nonfilter cigarettes with very high, high, medium, low and ultra-low tar and nicotine yields. The observed range for N'-nitrosonornicotine was from 5 to 625 ng/cigarette and for 4-(methylnitrosoamino)-1-(3-pyridyl)-1-butanone from not detected (less than 4 ng/cigarette) to 432 ng/cigarette. The highest TSNA values were obtained for nonfilter cigarettes made of dark tobaccos and the lowest values for nonfilter Oriental-type cigarettes. Relatively high TSNA yields were also observed in filter cigarettes with moderate and lower tar deliveries. The results demonstrated that there is no correlation between TSNA and tar deliveries in mainstrain smoke. The TSNA deliveries in mainstream smoke depended on the actual tobacco composition. According to these results the tar delivery, although crucial, is not a sufficient index for the biological activity and the carcinogenic potential of cigarette smoke.

Filtration↗
PubMed1989

Induction of sister chromatid exchanges by tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in human and hamster cells.

4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a nicotine derived N-nitrosamine, is a carcinogen that induces tumors in mice, rats and hamsters. To assess the ability of NNK to interact with the cellular DNA as an essential step in carcinogenesis, the induction of sister chromatid exchange (SCE) was examined in cultured normal human lymphocytes (HL) and Chinese hamster V79 cells. SCE formation is a sensitive indicator of carcinogen-DNA interaction that correlates with the induction of mutation and neoplastic cell transformation. HL and V79 cells were treated for 2 h with 20, 50, 100 and 200 micrograms/ml of NNK with and without application of metabolic activation S-9 mixture, and subsequently incubated for two rounds of replication in the presence of 5-bromodeoxyuridine required for SCE visualization. In V79 cells NNK produced a dose-dependent increase in SCE only with metabolic activation. In HL NNK induced a small but statistically significant increase in SCE with or without metabolic activation. These data provide the first evidence that NNK and/or its metabolic derivatives are able to induce DNA damage leading to SCE formation both in hamster and human cells. The differences in response between the two cell types suggests the existence of a difference in susceptibility associated with NNK metabolism and its interaction with cellular DNA.

Animals↗
PubMed1989

Influence of smoking parameters on the delivery of tobacco-specific nitrosamines in cigarette smoke--a contribution to relative risk evaluation.

The influence of the smoking parameters (puff profile, puff duration, puff volume, puff frequency) on the delivery of tobacco-specific nitrosamines (TSNAs) in mainstream smoke was investigated for six different cigarette brands, including filter cigarettes with very low to medium smoke yields and non-filter cigarettes with high and very high smoke yields. The puff profile did not influence the TSNA yields. The puff duration also had no remarkable influence on the TSNA delivery with the exception of a non-filter cigarette made of dark tobaccos. The puff volume and the puff frequency significantly influenced the TSNA yields. Increasing puff volume and frequency resulted in increasing TSNA values. The total volume drawn through a cigarette was calculated. The dependency of the TSNA delivery on the total volume was almost linear at least up to a total volume of approximately 500 ml/cigarette. The TSNA yield was the same for the same total volume no matter whether the total volume was due to a changing puff volume or a changing puff frequency. The total volume drawn through a cigarette is the main responsible factor for the TSNA delivery in mainstream smoke. Total volume data from smokers of low- and medium-tar cigarettes are used to calculate TSNA intake. The different smoking behaviour observed for smokers of low-tar and low-nicotine cigarettes as compared to standard smoking conditions is discussed with respect to the TSNA dependency on smoke parameters.

Humans↗
PubMed1989

Preformed tobacco-specific nitrosamines in tobacco--role of nitrate and influence of tobacco type.

Fifty-five types of commercial cigarettes on the open market in the FRG and several samples of pure tobacco types were analyzed for preformed tobacco-specific nitrosamines (TSNA) and nitrate in the tobacco. For the cigarette tobaccos the observed range for N'-nitrosonornicotine (NNN) was 50-5316 ng/cigarette and for 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) from not detected (less than 50 ng/cigarette) to 1120 ng/cigarette. Nitrate levels ranged from 0.6 to 14.4 mg/cigarette. The highest TSNA values were obtained for cigarettes made of dark tobaccos and the lowest for Oriental type cigarettes. The results demonstrated that there is a correlation between TSNA and nitrate levels. The tobacco type is another important influencing factor, especially for NNK. In Virginia tobaccos unexpectedly high NNK values were observed. For the samples of the pure tobacco types, NNN levels ranged from 20 to 8850 p.p.b. and NNK levels from not detected (less than 50 p.p.b.) to 1400 p.p.b. The observed range for nitrate was from traces (less than 0.005%) to 4.1%. Pure Oriental tobaccos which are low in nitrate showed the lowest TSNA concentrations. In the high nitrate Burley tobaccos the highest TSNA concentrations could be determined. Virginia tobaccos which show a low nitrate content are low in NNN but rather high NNK concentrations were found. The results from these pure tobacco types demonstrate that the nitrate content of the tobacco has a great influence on the TSNA level. However, Virginia tobaccos show higher NNK concentrations than expected according to their low nitrate content.

Chromatography, Gas↗
PubMed1989

Effects of urinary potassium and sodium ion concentrations and pH on N-butyl-N-(4-hydroxybutyl)nitrosamine-induced urinary bladder carcinogenesis in rats.

The promoting activities of low and high sodium or potassium ion concentrations, under conditions of neutral as well as elevated urinary pH, in urinary bladder carcinogenesis, were investigated in rats treated with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN). Male Wistar rats were given 0.05% BBN in their drinking water for 4 weeks and then treated for 32 weeks with either control diet (group 1) or this diet supplemented with equimolar amounts of the following minerals: 2.34% NaCl (group 2), 2.98% KCl (group 3), 3.36% NaHCO3 (group 4), 1.68% NaHCO3 + 2% KHCO3 (group 5), or 4% KHCO3 (group 6). The alkalizing salts NaHCO3 and KHCO3 induced comparable increases in urinary pH and elevated urinary sodium or potassium ion concentrations respectively. The combination of NaHCO3 + KHCO3 similarly caused an elevation of the urinary pH and less increased sodium and potassium ion concentrations. In the groups fed NaHCO3 and KHCO3 either alone or in combination, the incidences of papillary/nodular hyperplasia, papillomas and carcinomas in the urinary bladder had increased as compared to controls. NaCl and KCl also induced high urinary sodium or potassium ion concentrations without alteration of urinary pH. This was accompanied by increased incidences of simple hyperplasia, papillary/nodular hyperplasia, and/or papillomas but no carcinomas. The present results indicate that the potassium ion is as potent as the sodium ion in promoting urinary bladder carcinogenesis under conditions of elevated urinary pH, and that both the sodium and potassium ions may exert weak promoting activity under conditions of neutral urinary pH.

Animals↗
PubMed1990

Effect of nicotine and tobacco-specific nitrosamines on the metabolism of N'-nitrosonornicotine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone by rat oral tissue.

The effect of N'-nitrosoanatabine (NAT) and nicotine on the metabolism of N'-nitrosonornicotine (NNN) and 4-(methyl-nitrosamino)-1-(3- pyridyl)-1-butanone (NNK) by cultured rat oral tissue was investigated. The effect of NNN on NNK metabolism and the effect of NNK on NNN metabolism was also determined. NNK inhibited NNN metabolism more than NNN inhibited NNK metabolism. NAT inhibited the metabolism of NNK but not of NNN. Nicotine, which is present at greater than 500 times the levels of NNN and NNK in smokeless tobacco, inhibited the metabolism of both nitrosamines. Inhibition of 1 microM NNN metabolism was greater than that of 1 microM NNK when the concentration of nicotine was 1, 10 or 100 microM. Nicotine at 100 microM inhibited the formation of all metabolites of NNN by 85-92%. These results suggest that NNN and nicotine may be metabolized by a common enzyme.

Animals↗
PubMed1991

Relationships between serum thyroid stimulating hormone levels and development of thyroid tumors in rats treated with N-bis-(2-hydroxypropyl)nitrosamine.

Relationships between serum thyroid stimulating hormone (TSH) levels, carcinogen dose and development of thyroid tumors were studied in Wistar rats of both sexes treated with N-bis-(2-hydroxypropyl)nitrosamine (DHPN). DHPN (210 mg/100 g body wt) was injected i.p. weekly. Wistar rats were used, divided into five groups of males (M1-M5) and five groups of females (F1-F5). M1 and F1 received one injection of DHPN, M2 and F2 two injections of DHPN, M3 and F3 three injections of DHPN, M4 and F4 four injections, and M5 and F5 as control rats received saline vehicle. The resultant incidences of total thyroid tumors were 4% in group M1, 24% in M2, 80% in M3, 76% in M4, 0% in F1, 4% in F2, 20% in F3, 17% in F4 and 0% in M5 and F5. Thus dose dependence for DHPN carcinogenesis was found in both sexes for up to at least three injections of DHPN and in all cases males proved more susceptible than females. Similar results were gained for carcinomas treated separately. A sex difference in DHPN induction of thyroid tumor was thus shown for Wistar rats opposite to that reported to exist in humans. However, no clear relationship between dose of DHPN or incidence of thyroid tumors and serum TSH concentration was evident at the end of the experiment (week 30).

Adenoma↗
PubMed1991

Effect of phenethyl isothiocyanate on the metabolism of the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone by cultured rat lung tissue.

The effect of phenethyl isothiocyanate (PEITC), a dietary inhibitor of carcinogenesis, on the metabolism of the tobacco specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) by cultured rat peripheral lung tissues was investigated. Initially, the metabolism of NNK by the tissues was studied by incubating the lung explants in medium containing 1 and 10 microM [5-3H]NNK for 3, 6, 12, and 24 h. NNK metabolites were analyzed and quantified by HPLC and expressed as nmol/mg DNA. NNK was metabolized by three pathways; alpha-carbon hydroxylation, pyridine N-oxidation and carbonyl reduction. The principal metabolic pathway involved the conversion of NNK to the pyridine N-oxidized metabolites: 4-(methylnitrosamino)-1-(3-pyridyl-N-oxide)-1-butanone (NNK-N-oxide) and 4-(methylnitrosamino)-1-(3-pyridyl-N-oxide)-1-butanol (NNAL-N-oxide). When combined, NNK-N-oxide and NNAL-N-oxide constituted approximately 70% of the total metabolites in the medium at 24 h. To determine the effects of PEITC on the metabolism of NNK, lung explants were either treated with both 10 microM [5-3H]NNK and PEITC (10, 50, and 100 microM) for 24 h, or they were pre-treated with these same concentrations of PEITC for 16 h and then co-treated with both PEITC and 10 microM [5-3H]NNK for 24 h. In both treatment series, PEITC inhibited the alpha-carbon hydroxylation and pyridine N-oxidation of NNK and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), which is produced from NNK by carbonyl reduction. In general, the inhibition of NNK metabolism was greater when the explants were pre-treated with PEITC. These results suggest that PEITC is an effective inhibitor of the conversion of NNK to metabolites that elicit DNA damage. Our results are in agreement with previously published data in which PEITC was shown to inhibit NNK metabolism and tumorigenesis in the rat lung.

Animals↗
PubMed1991

Unusually high levels of carcinogenic tobacco-specific nitrosamines in Sudan snuff (toombak).

The aim of these studies was to determine the levels of carcinogenic tobacco specific nitrosamines (TSNA) in Sudanese oral snuff (toombak) as recent retrospective epidemiological studies suggested an association between the use of toombak and subsequent development of oral cancer. We have analyzed the TSNA levels in 20 samples of Sudanese toombak, of four different quality levels, collected from five different vendors. Using GC coupled with thermal energy analysis, four TSNA were quantified in snuff extracts: N'-nitrosonornicotine (NNN), N'-nitrosoanatabine (NAT), N'-nitrosoanabasine (NAB) and 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Unusually high levels of these TSNA (mean; range, mg/g snuff, dry wt) were detected; NNN (1.13; 0.50-3.08); NAT (0.08; 0.02-0.29); NAB (0.22; 0.02-2.37); and NNK (2.31; 0.62-7.87). Previously, the highest levels of NNN and NNK reported in any snuff were 0.154 and 0.014 mg/g dry wt respectively. In comparison, the levels in Sudanese toombak were up to 20 and 560 times higher respectively. As the public health implications of these findings are significant, attempts should be made to reduce exposure to TSNA in oral snuff users in Sudan.

Carcinogens↗
PubMed1991

A tobacco smoke-derived nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, is activated by multiple human cytochrome P450s including the polymorphic human cytochrome P4502D6.

We have developed a human B-lymphoblastoid cell line, designated 2D6/Hol, which stably expresses human cytochrome P450 CYP2D6 cDNA. This cell line exhibits bufuralol 1'-hydroxylase activity and immunologically detectable CYP2D6 protein. The specific activity of (+)-bufuralol 1'-hydroxylase in microsomes from 2D6/Hol cells was comparable to that observed in human liver microsomes. This cell line was used to examine the mutagenicity activation of three tobacco smoke-derived nitrosamines, N-nitrosonornicotine (NNN), 1-(N-methyl-N-nitrosamino)-1-(3-pyridinyl)-4-butanal) (NNA) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), by CYP2D6. Exposure of 2D6/Hol cells to NNK concentrations of 30-90 micrograms/ml induced a concentration-dependent decrease in relative survival and increase in mutant fraction at the hypoxanthine guanine phosphoribosyl transferase (hprt) locus. In contrast, NNK was non-mutagenic and non-cytotoxic to control cells at exposure concentrations up to 150 micrograms/ml. NNK mutagenicity in 2D6/Hol cells was compared to the responses observed in isogenic cell lines expressing human CYP1A2 (1A2/Hol), human CYP2A3 (2A3/Hol) and human CYP2E1 (2E1/Hol). These three additional human cytochrome P450-expressing cell lines were also found to be sensitive to NNK-induced mutagenicity and cytotoxicity. We found no evidence for CYP2D6-mediated activation of NNN or NNA. NNN was non-cytotoxic and non-mutagenic to both control and 2D6/Hol cells. NNA was equally cytotoxic and mutagenic to control cells and 2D6/Hol cells. The activation of NNA to a mutagen may have been carried out by P450 native to the AHH-1 TK +/- cell line. The 2D6/Hol cell line, in conjunction with the control cell line and other isogenic cell lines expressing other human cytochrome P450 cDNAs provides a useful system for the examination of the role of the polymorphic CYP2D6 in human procarcinogen activation and drug metabolism.

Biotransformation↗
PubMed1991

L-arginine-dependent formation of N-nitrosamines by the cytosol of macrophages activated with lipopolysaccharide and interferon-gamma.

The cytosol fraction of J774-1 murine macrophages activated with lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) was found to nitrosate a wide range of secondary and tertiary amines. The reaction was dependent on L-arginine and NADPH. The optimal pH for nitrosation was 7.2-7.3. Nitrosation was inhibited by arginine derivatives such as NG-monomethyl-L-arginine and NG-nitro-L-arginine, well-known inhibitors of nitric oxide (NO) synthase. These results indicate that nitrosation is mediated by NO synthase, which catalyzes formation of NO and L-citrulline from L-arginine. Nitrosamine formation also required oxygen and was inversely correlated with the basicity of nitrosatable amines. The nitrosation was inhibited by oxyhemoglobin, an NO trapping agent, and enhanced by superoxide dismutase, which stabilizes NO. LPS + IFN-gamma induced approximately 500-600 times greater nitrosation activity than that of non-activated macrophages. Macrophages treated with LPS alone exhibited 3-4 times greater nitrosation activity than untreated macrophages, whereas macrophages treated with IFN-gamma alone did not show enhanced nitrosation activity. A combination of the cytosols from macrophages treated with LPS alone and IFN-gamma alone did not nitrosate morpholine as rapidly as the cytosol of macrophages treated with both compounds together. The activity for forming L-citrulline and nitrite/nitrate from L-arginine was markedly induced by treatment with either LPS alone or LPS + IFN-gamma but not with IFN-gamma. Those results suggest that some other factor(s) in addition to NO synthase is involved for efficient nitrosation by the macrophage cytosol. This factor(s) was not induced in macrophages by either LPS- or IFN-gamma alone, but was induced only in the presence of the two compounds.

Amino Acid Oxidoreductases↗
PubMed1992

Analysis of tobacco-specific N-nitrosamines in indoor air.

A method was developed and applied for the assessment of tobacco-specific N-nitrosamines (TSNA) in indoor air polluted with tobacco smoke. Air samples were collected on Cambridge filters treated with 0.01 M potassium bisulfate, extracted with dichloromethane and enriched by column chromatography. The fraction containing the TSNA was concentrated and placed on a thermal desorption cartridge packed with Tenax GR. The sample was thermally desorbed and analyzed by capillary GC using a thermal energy analyzer. When the method was applied in a test laboratory in which one, two and four cigarettes were smoked during 30 min, linearity was observed. Field studies included sampling in bars, restaurants and trains. The concentration of N'-nitrosonornicotine (NNN) ranged from not detected to 23 pg/l, that of N'-nitrosoanatabine ranged from not detected to 9 pg/l, while 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) was detected in concentrations ranging from 1 to 29 pg/l. This means an exposure to NNN and NNK of 0.1-0.3 cigarette equivalents. Thus, non-smokers can be exposed to highly carcinogenic TSNA.

Air Pollution, Indoor↗