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N -nitrosonornicotine (NNN) and N -nitrosoanabasine (NAB) are both tobacco-specific nitrosamines bearing two heterocyclic amino groups, NAB bearing an extra -CH 2 - group (conferring a hexa- rather than penta-membered cycle) but with significantly decreased carcinogenicity. However, their activating enzymes and related mutagenicity remain unclear. In this study, the chemical-CYP interaction was analyzed by molecular docking, thus the binding energies and conformations of NNN for human CYP2A6, 2A13, 2B6, 2E1 and 3A4 appeared appropriate as a substrate, so did NAB for human CYP1B1, 2A6, 2A13 and 2E1. The micronucleus test in human hepatoma (HepG2) cells with each compound (62.5–1000 μM) exposing for 48 h (two-cell cycle) was negative, however, pretreatment with bisphenol AF (0.1–100 nM, CYPs inducer) and ethanol (0.2% v:v, CYP2E1 inducer) potentiated micronucleus formation by both compounds, while CITCO (1 μM, CYP2B6 inducer) selectively potentiated that by NNN. In C3A cells (endogenous CYPs enhanced over HepG2) both compounds induced micronucleus, which was abolished by 1-aminobenzotriazole (60 μM, CYPs inhibitor) while unaffected by 8-methoxypsoralen (1 μM, CYP2A inhibitor). Consistently, NNN and NAB induced micronucleus in V79-derived recombinant cell lines expressing human CYP2B6/2E1 and CYP1B1/2E1, respectively, while negative in those expressing other CYPs. By immunofluorescent assay both compounds selectively induced centromere-free micronucleus in C3A cells. In PIG-A assays in HepG2 cells NNN and NAB were weakly positive and simply negative, respectively; however, in C3A cells both compounds significantly induced gene mutations, NNN being slight more potent. Conclusively, both NNN and NAB are mutagenic and clastogenic, depending on metabolic activation by partially different CYP enzymes. [Display omitted] • Two tobacco-specific nitrosamines induced genotoxic effect in mammalian cells. • Genotoxicity of NNN was activated by human CYP2B6/2E1, and NAB by CYP1B1/2E1. • Pretreating HepG2 cells with bisphenol AF potentiated the effects of NNN and NAB. • The mode of chromosome damage by NNN and NAB were consistently pure clastogenesis. [ABSTRACT FROM AUTHOR]

A simple and sensitive method, using automated online in-tube solid-phase microextraction (SPME) coupled with liquid chromatography-tandem mass spectrometry (LC-MS/MS), was developed for the determination of four tobacco-specific nitrosamines (TSNAs) in mainstream and sidestream smoke of combustion cigarettes and heated tobacco products. These TSNAs were separated within 4 min on a Capcell Pak C18 MGⅢ column and detected in the positive ion mode by multiple reaction monitoring. The optimum in-tube SPME conditions were 30 draw/eject cycles of 40 μL of sample at a flow rate of 200 μL min−1 using a Supel-Q PLOT capillary column as an extraction device. The extracted TSNAs were easily desorbed from the column by passage of the mobile phase, with no carryover observed. This in-tube SPME LC–MS/MS method showed good linearity for four TSNAs in the 0.5–100 pg mL−1 ranges, with correlation coefficients above 0.9998 (n = 24), using stable isotope-labeled TSNAs as internal standards. The validation assays for limit of detection, limit of quantification, specificity, precision and accuracy of the analytes were consistent with the requirements recommended by the ICH guidelines. The validated method was utilized successfully to analyze four TSNAs in mainstream and sidestream smoke samples without any interference peaks. Overall recoveries of TSNAs spiked into smoke sample solutions were 97.3–104.6%. The developed method can automate the extraction, concentration and analysis of samples, and is sensitive and selective for TSNAs. This method was used to analyze TSNAs in mainstream and sidestream smoke samples of several commercially available combustion cigarettes and heated tobacco products. A simple and sensitive method for the determination of four tobacco-specific nitrosamines in mainstream and sidestream smokes of combustion cigarettes and heated tobacco products was developed by automated online in-tube solid-phase microextraction coupled with liquid chromatography-tandem mass spectrometry. Image 1 • Online in-tube solid-phase microextraction of tobacco-specific nitrosamines was optimized. • Tobacco-specific nitrosamines were simultaneously determined by in-tube SPME coupled with liquid chromatography–tandem mass spectrometry. • This method is automated, simple, rapid, selective, and sensitive. • This method was utilized successfully to analyze pg levels of tobacco-specific nitrosamines. • The method was applied to analysis of mainstream and sidestream smoke samples. [ABSTRACT FROM AUTHOR]

• The established method overcame the deficiencies of matrix interference that reference methods encountered. • The established method is particularly good at quantifying TSNAs in low-TSNAs products. • Only water and dichloromethane were used for TSNAs extraction and purification. • The selection of water and dichloromethane for sample extraction and purification was clearly illustrated. A method for determining tobacco-specific nitrosamines (TSNAs) in tobacco and cigarette smoke using liquid chromatography-tandem mass spectrometry was established. The established method amended the deficiencies that exist in current mainstream methods. In this method, TSNAs in tobacco and cigarette smoke were extracted by water. The aqueous extract was then extracted by dichloromethane, and the extract could be analyzed by liquid chromatography-tandem mass spectrometry after a solvent replacement. This method was used to analyze flue-cured tobacco samples, and the response of the target compounds was about 10 times higher than that of the ammonium acetate extraction method. When analyzing cigarette smoke samples, the response strength and chromatographic peak purity of the target compounds were also significantly improved. The proposed method exhibited good linearities for both tobacco and cigarette smoke samples (r 2 > 0.99). The limits of detection (LODs) for tobacco and cigarette smoke samples were 0.2–1.0 ng/g and 0.1–0.3 ng/cigarette, respectively. Additionally, this method exhibited desirable accuracy and precision. The TSNAs recovery values from tobacco and cigarette smoke samples ranged from 95.7 % to 107.7 % with inter- and intra-day relative standard deviations (RSDs) of less than 7.4 %. This method is simple, effective, and has wide adaptability. It is a useful upgrade to the existing methods for analyzing TSNAs in tobacco and cigarette smoke. [ABSTRACT FROM AUTHOR]

Highlights • Novel trapping technique and high throughput method for NNN and NNK determination. • Accurate quantification of NNN and NNK in indoor air in ng/m3- pg/m3 range. • Validation with accuracy profiles to assess matrix effects on quantifications. • Evaluation of the impact on indoor air of THS 2.2, e-cigarettes and cigarettes. Abstract A sensitive and accurate method for the quantification of 1′-Demethyl-1′-nitrosonicotine (NNN) and 4-(methylnitrosamino)-1-(3-Pyridyl)-1-butanone (NNK) in indoor air was developed and validated. To this aim, a novel approach for the collection of two tobacco-specific nitrosamines, using silica sorbent cartridges followed by simplified sample preparation and isotope dilution liquid chromatography/electrospray ionization tandem mass spectrometry, was applied. This procedure led to a substantial improvement in terms of sensitivity and sample throughput as compared with methods using conventional trapping. For the validation, a matrix-based approach using an accuracy profile procedure was selected. The evaluated matrices were background air samples, environmental aerosols of a heat-not-burn tobacco product (Tobacco Heating System [THS] 2.2, commercialized under the brand IQOS ®), a rechargeable electronic cigarette (Solaris ®), and the environmental tobacco smoke (ETS) of a conventional cigarette (Marlboro Gold ®). The method showed excellent recoveries, sensitivity, and precision. The limits of detection of the method for NNN and NNK were 0.0108 ng/m3 and 0.0136 ng/m3, respectively. The calibration range of the instrument spanned 0.2–60 ng/mL. The calculated lower working range limit (LWRL) of the method for NNN was 0.126 ng/m3, and the LWRL for NNK was 0.195 ng/m3. The method was applied to evaluate surrogate environmental aerosols generated using smoking machines. This model is reliable but gives a large overestimation of the possible impact of THS 2.2 and e-cigarettes on indoor air, because the retention of NNN and NNK in the body of the consumers is not taken into account. As a consequence, the values reported do not reflect a real-life setting. The contents of the two target compounds in the surrogate environmental aerosols were 0.0830 ± 0.0153 ng/m3 of NNN and 0.0653 ± 0.0138 ng/m3 of NNK for THS 2.2, 0.0561 ± 0.0296 ng/m3 of NNN for e-cigarettes, and 0.816 ± 0.109 ng/m3 of NNN and 4.13 ± 1.04 ng/m3 NNK for cigarettes. These values correspond to 10% of the measured ETS concentration for NNN in environmental aerosols of THS 2.2 and 7% for those of e-cigarettes. For NNK, the value for the environmental aerosol of THS 2.2 was 2% of the ETS value. [ABSTRACT FROM AUTHOR]

The Aboriginal population of Central Australia use endemic Nicotiana species to make a smokeless tobacco product known usually as pituri or mingkulpa. Nicotiana leaves are masticated with wood ash into a ‘quid’ that is chewed/sucked for absorption of nicotine. In addition to nicotine, smokeless tobacco products contain a spectrum of biologically active compounds that may contribute to effects on health. The objective of this study was to quantify nicotine, and related alkaloids and tobacco specific nitrosamines (TSNAs), in Nicotiana leaves used in pituri, and compare in vitro toxicity of pure nicotine with Nicotiana leaf extract at the same concentration of nicotine. An aqueous extract of dry leaves of Nicotiana gossei and a reference smokeless tobacco (CORESTA CRP2) were quantified for major pyridine alkaloids and TSNAs using HPLC-UV and LC–MS/MS. A range of extract concentrations and corresponding concentrations of nicotine standard were tested using an MTS assay to measure human lung epithelium cell (A549) survival. Cells treated for 24 h with the maximum concentration of 1.5 mg/ml of nicotine resulted in 77% viability. In contrast, extracts from N. gossei leaves and CRP2 containing a similar concentration of nicotine (1.3 mg/ml) resulted in remarkably lower viability of 1.5 and 6%, respectively. Comparison of cytotoxicity of pure nicotine with that of the extracts revealed that nicotine was not the source of their cytotoxicity. Other biologically active compounds such as the known carcinogens NNK and NNN, derived from nicotine and nornicotine and found to be present in the smokeless tobacco extracts, may be responsible. [ABSTRACT FROM AUTHOR]

Rapé, a diverse group of smokeless tobacco products indigenous to South America, is generally used as a nasal snuff and contains substantial amount of plant material with or without tobacco. Previously uncharacterized, rapé contains addictive and harmful chemicals that may have public health implications for users. Here we report % moisture, pH, and the levels of total nicotine, un-ionized nicotine, flavor-related compounds, tobacco-specific N-nitrosamines (TSNAs) and polycyclic aromatic hydrocarbons (PAHs) for manufactured and hand-made rapé. Most rapé products were mildly acidic (pH 5.17–6.23) with total nicotine ranging from 6.32 to 47.6 milligram per gram of sample (mg/g). Calculated un-ionized nicotine ranged from 0.03 to 18.5 mg/g with the highest values associated with hand-made rapés (pH 9.75–10.2), which contain alkaline ashes. In tobacco-containing rapés, minor alkaloid levels and Fourier transform infrared spectra were used to confirm the presence of Nicotiana rustica , a high nicotine tobacco species. There was a wide concentration range of TSNAs and PAHs among the rapés analyzed. Several TSNAs and PAHs identified in the products are known or probable carcinogens according to the International Agency for Research on Cancer. Milligram quantities of some non-tobacco constituents, such as camphor, coumarin, and eugenol, warrant additional evaluation. [ABSTRACT FROM AUTHOR]

• A FASI-sweeping-AFMC stacking capillary electrophoresis was established successfully. • A chemometric experimental design is performed to optimize the separation of five tobacco-specific nitrosamines (TSNAs). • Sensitivity enhancing factors up to 1722 folds and limits of detection down to 0.125 ng/mL are achieved. • Level changes of five TSNAs in commercial cigarette products were provided by using our approach. Tobacco-specific nitrosamines (TSNAs) as carcinogens endanger our health and life from cigarette products. However, the safe range of TSNAs levels in commercial cigarette products has not yet been established. For the purpose of safety and supervision, a three-step stacking approach including field amplified sample injection (FASI), sweeping, and analyte focusing by micelle collapse (AFMC), was developed for the simultaneous determination of five TSNAs levels in cigarette products. This approach also involved aspects of chemometric experimental design, including fractional factorial design and central composite design. After the multilevel optimization of the experimental design, the five TSNAs were well separated. The LOD (S/ N = 3) values of the N´-nitrosonornicotine (NNN), N´-nitrosoanatabine (NAT), N´-nitrosoanabasine (NAB), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in the FASI-sweeping-AFMC CE approach were 1.000 ng/mL, 0.500 ng/mL, 0.125 ng/mL, 1.000 ng/mL, and 0.500 ng/mL respectively. The results of relative standard deviation (RSD) and relative error (RE) were all less than 3.35%, demonstrating good precision and accuracy. Finally, this novel approach was further applied to monitor three commercial cigarette products, and a range of 250.1–336.6 ng/g for NNN, 481.6–526.7 ng/g for NAT, 82.2–247.6 ng/g for NAB, 167.7–473.7 ng/g for NNAL, and 39.4–246.7 ng/g for NNK could be observed among these. Based on these results, the novel CE stacking strategy was successfully applied for the analysis of five TSNAs levels in cigarette products and could serve as a tool for assays of quality control of nitrosamines. [ABSTRACT FROM AUTHOR]

Highlights: [•] The pyridine alkaloids of tobacco have been the subject of intensive investigation. [•] Nature and function of tobacco alkaloid biosynthetic pathway genes are reviewed. [•] Model for the transcriptional regulation of nicotine biosynthesis is described. [•] Rationales for altering the alkaloid composition of tobacco are discussed. [Copyright &y& Elsevier]

Highlights: [•] The new analysis method of TSNAs in replacement liquids by LC–MS/MS. [•] First article for the identification and quantification of TSNAs in replacement liquids. [•] The TSNA analytical data in 105 replacement liquids of E-cigarettes. [Copyright &y& Elsevier]

Abstract: In recent years the number of waterpipe smokers has increased substantially worldwide. Here we report on the concentrations of tobacco-specific nitrosamines (TSNAs) and polycyclic aromatic hydrocarbons (PAHs) in waterpipe smoke and the analysis of selected biomarkers indicative for the body burden in waterpipe users. We further identify high amounts of unburned humectants (glycerol and propylene glycol) in the waterpipe smoke as main part of the so-called “tar” fraction. These results give cause for serious concern. For standardization we applied a machine smoking protocol. Smoke was collected on glass fiber filters and analyzed for nicotine, water, humectants, TSNAs, and PAHs. In addition, we determined carbon monoxide and found high amounts in the smoke being causative for high levels of carboxyhemoglobin (COHb) in the blood of smokers. In comparison to the reference cigarette 3R4F, the nicotine contents were 10-times higher, but TSNA levels were found lower in waterpipe smoke. This finding explained the low levels of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol detected in the urine of waterpipe smokers. Finally, the levels of benzo[a]pyrene were three times higher in waterpipe smoke compared to the reference cigarette. Altogether, the data presented in this study point to the health hazards associated with the consumption of waterpipes. [Copyright &y& Elsevier]

[Display omitted] • Airborne particulate matter (PM) is contaminated with the tobacco specific nitrosamine NNK. • The atmospheric stability of NNK in comparison to airborne nicotine is reported. • NNK is detected in PM in various geographic locations. • NNK shows a seasonal variation. • The load of NNK in PM 10 is quantified. The most important tobacco-specific nitrosamine found in cigarette smoke and formed in ageing smoke after cigarettes are extinguished is 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). It is formed from nitrosation of nicotine, under particular conditions both in indoor and outdoor environments. NNK has been classified as a potent lung carcinogen which is expected to be found primarily in the particle-phase and to be stable in particulate matter. In this study tests have been carried out to show that a bisulfate-treated filter is more efficient than an untreated filter to collect both nicotine and NNK, and that the latter is stable in outdoor particulate matter. To characterize NNK in the outdoor environment, airborne samples were collected from 11 cities in USA, UK, Hong Kong and Malta with characteristics varying from low to high population densities and from urban to suburban to rural, and with desert characteristics and distinct climates. It has been shown that airborne particle + gas phase nicotine and particle-phase NNK behave in a linearly correlated manner. A seasonal analysis was carried out on a subset of data available from five sites in California, where the load of NNK in PM 10 is driven by long range transport of the air masses passing over densely populated cities. In the winter season, the load of NNK in PM is higher than in summer in a statistically significant manner. The contamination of PM with NNK shows variability, but is observed at all sites. This paper highlights the potential risk of chronic exposure to NNK in particulate matter by the inhalation pathway. [ABSTRACT FROM AUTHOR]

Abstract: 4-Hydroxy-l-(3-pyridyl)-l-butanone (HPB)-releasing adducts are formed by metabolic activation of N′-nitrosonornicotine and 4-(methylnitrosamino)-l-(3-pyridyl)-l-butanone and have been proposed as specific biomarkers for exposure to tobacco smoke. However, in several studies hemoglobin adducts releasing HPB were on average less than threefold higher in smokers compared to nonsmokers. Using an improved analytical method we have recently found a sevenfold difference in DNA adduct levels in the lung from smoking and nonsmoking lung cancer patients. In the present study we extended the determination of HPB-releasing DNA adducts by gas chromatography–negative ion chemical ionization-mass spectrometry (GC–NICI-MS) to samples of peripheral lung, lower esophagus and cardia from tumor-free sudden death victims (primarily road traffic accidents, suicide and sudden cardiac arrest). The donors were classified as either current smokers or nonsmokers based on cotinine in either blood or urine (cut-off values for active smoking: >15ng cotinine/ml blood or >100ng cotinine/ml urine). Contrary to our expectation, DNA adduct levels (fmol HPB/mg DNA) in lung tissue from tumor-free smokers (N =32, 92±148) were not significantly different from values in nonsmokers (N =56, 61±66). The values in tumor-free smokers were on average more than fourfold lower compared to smoking lung cancer patients in our previous study. Adduct levels in the mucosa of esophagus (N =82; 133±160) and cardia (N =30; 108±102) of sudden death victims did not show any difference according to the current smoking status. HPB-releasing DNA adduct levels in cardia and esophagus were significantly correlated (N =29; Spearman r =0.609; p <0.001). In contrast, adduct levels in lung did not correlate with either esophagus (77 cases) or cardia (28 cases). Further studies are necessary to elucidate the discrepancies in lung DNA adduct levels in smokers with or without lung cancer and to identify obvious additional sources other than tobacco for these adducts. [Copyright &y& Elsevier]

Abstract: An improved analytical method was developed for the analysis of 4-hydroxy-1-(3-pyridyl)-1-butanone (HPB)-releasing DNA adducts in lung samples of patients undergoing surgery for lung cancer. HPB-releasing adducts can be formed by metabolic activation of the tobacco-specific nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and N′-nitrosonornicotine, and have been reported to play an important role in tobacco carcinogenesis. [2,2,3,3-D4]HPB (D4-HPB) was used as an internal standard, and HPB released by acid hydrolysis of DNA was determined by gas chromatography/mass spectrometry in the negative ion chemical ionisation mode. The method is sensitive with a limit of detection of 5.9fmol HPB and a limit of quantification of 15.2fmol HBP/mg DNA. The recovery of HPB was 82±17% and the background response was 10.1±1.8fmol HPB/sample. The concentration of HPB-releasing lung DNA adducts was significantly higher (p <0.0001) in 21 self-reported smokers compared to in 11 self-reported nonsmokers (404±258fmol versus 59±56fmol HPB/mg DNA, respectively). HPB-releasing hemoglobin adduct concentrations were only marginally higher in a subset of 12 smokers compared to in 7 nonsmokers (63±53fmol versus 42±34fmol HPB/g hemoglobin; p =0.36). No correlation was found between HPB-releasing adducts in DNA and hemoglobin (p =0.074). [Copyright &y& Elsevier]

Abstract: N′-Nitrosonornicotine (NNN) was the first tobacco-specific nitrosamine (TSNA) identified as carcinogen in tobacco smoke, but no data exist on in vivo interactions between NNN and other tobacco alkaloids, TSNA or phenethyl isothiocyanate (PEITC) which have been demonstrated in various studies on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Acute effects on NNN metabolism were tested in male Fischer F344 rats injected s.c. with 30nmol/kg body weight (bw) [5-3H]NNN either alone or simultaneously with 15μmol/kg bw nicotine, nornicotine, anatabine, or anabasine, 150μmol/kg bw cotinine, 3μmol/kg bw myosmine, or 300nmol/kg bw of either N′-nitrosoanatabine or N′-nitrosoanabasine. Another group of rats was fed a diet supplemented with PEITC at 1μmol/g diet starting 24h before NNN treatment. Within 24h more than 80% and about 10% of the radioactivity was excreted with urine and feces, respectively. Urinary metabolites were separated by reversed-phase radio-HPLC and identified by co-chromatography with UV standards. In two sets of experiments with control rats treated with NNN only, 4-hydroxy-4-(3-pyridyl)butanoic acid (hydroxy acid, 44.4/44.8%), 4-oxo-4-(3-pyridyl)butanoic acid (keto acid, 32.4/31.5%), NNN-N-oxide (5.0/3.8%), 4-(3-pyridyl)butane-1,4-diol (diol, 1.1/1.0%) and norcotinine (2.3/1.0%) were consistently detected besides unmetabolised NNN (4.7/3.3%). Co-treatment with nicotine, cotinine, nornicotine and PEITC shifted the contribution of the two major metabolites significantly in favor of hydroxy acid (108–113% of control) as compared to keto acid (86–90% of control). The same treatments also increased norcotinine (135–170% of control). These changes are consistent with a decreased metabolic activation of NNN. In subacute studies rats received NNN in drinking water for 4 weeks at a daily dose of 30nmol/kg bw with or without nornicotine at 15μmol/kg bw or myosmine at 3μmol/kg bw. On the last day of the experiment all rats received [5-3H]NNN at 30nmol/kg bw with a contaminated apple bite followed by collection of urine and feces for 18h. Most of the radioactivity, 87–96% of the dose, was recovered in urine and only minor amounts have been excreted in feces or persisted in blood. In urine of the NNN-control group keto acid (32.2%) and unmetabolised NNN (3.9%) were present in identical amounts as in the acute experiment whereas hydroxy acid (41.4% of total radioactivity in urine, 93% of acute NNN control) was reduced in expense of the minor NNN metabolites. Co-administration of nornicotine resulted in a small but significant rise of keto acid (107% of control) and a significant decrease in NNN-N-oxide (76% of control). After co-treatment with myosmine the increase of keto acid (104% of control) was even less but still significant whereas NNN-N-oxide and diol were significantly reduced to 72% and 79% of control, respectively. Our experiments with rats indicate significant mutual effects of some of the major tobacco alkaloids and most relevant TSNA. Further studies on the impact on smokers and the inhibitory effects of isothiocyanates are needed for a final risk assessment. [Copyright &y& Elsevier]

The chemical-analytical profile of two US brands of oral moist snuff was determined. These two brands were bought in five geographical locations (NY, MA, CO, CA and KY in the US). They were mixed thoroughly to yield representative samples. Brand A had a pH of 5.84 and nicotine content of 0.42%, while brand B had a pH of 7.99 and nicotine content of 2.73%. At pH 5.84, only 1% of the nicotine is present as a free base while 59% of nicotine is present in unprotonated form at pH 7.99. It is the unprotonated form of nicotine that is most readily absorbed through the mucous membrane in the oral cavity. Snuff A contained also significantly lower levels of moisture, nitrate, nitrite and tobacco-specific nitrosamines than snuff B. The University of Kentucky reference snuff 1S3 was analyzed as an external control sample. These two snuff brands are currently being assayed with rats in a short-term and in long-term bioassays to test the concept that the tobacco-specific N-nitrosamines are major contributors to the carcinogenic activity of oral snuff. [ABSTRACT FROM AUTHOR]

Third-hand smoke (THS) is composed of surface-deposited remnants resulting from tabacco-smoking. Because THS components have properties of remaining on, re-emitting from and reacting on and with surfaces, in-situ analysis of the components on different surfaces is both in high demand and challenging. The aim of this study is to establish desorption corona beam ionization (DCBI)-MS/MS as an analytical tool for THS research. To this end, an in-situ DCBI-MS/MS approach was developed for the quantitative analysis of typical THS environmental markers, i.e. nicotine and cotinine on different surfaces such as fruits, cotton clothing, glass, and toys etc. The limits of detection of nicotine and cotinine were both 1.4 μg m-2. Low-temperature DCBI-MS/MS was applied to the direct detection of THS on fingers without any skin damage. Smoking-related biomarkers analyses in urine were accomplished, with a 10 s DCBI analysis time. The on-surface tobacco-specific nitrosamines (TSNAs), such as 1-(N-methyl-N-nitrosamino)-1-(3-pyridinyl)-4-butanal) (NNA), 4-(methylnitrosamino)-1-(3-pyridinyl)-1-butanone (NNK), and N-nitroso nornicotine (NNN) were in-situ successfully detected in dust samples. Image 1 • Quantitative and in-situ detection of third-hand smoke (THS) on different surfaces. • Low-temperature Desorption Corona Beam Ionization (DCBI) on bio-surfaces such as fingers and arm skin for in-situ detection of third-hand smoke. • High-throughput analysis of THS biomarkers in human urine. • Direct and in-situ monitoring of tobacco-specific nitrosamines(TSNAs)in dust samples. [ABSTRACT FROM AUTHOR]