Sidestream Cigarette Smoke Research Articles

Development and application of the Ames test using a direct-exposure module: The assessment of mutagenicity of incense and sidestream cigarette smoke.

We had previously developed an improved Ames module to directly determine the mutagenicity of gaseous formaldehyde (HCHO) and toluene without liquid extraction. This study further evaluated the suitability and sensitivity of this module on whole and real polluted air samples. For this, two common brands of stick incense (A and B) and cigarettes (A and B) were harvested, and various types of incense smoke (IS) and sidestream cigarette smoke (SCS) samples were generated by lighting 3, 6, 12, 24, 30, or 36 incense sticks, and by lighting 1, 2, or 3 cigarettes, respectively, in an acrylic box. CO2 , CO, total volatile organic compound (TVOC), PM1.0, and HCHO concentrations in the air samples were determined, and all air samples did not partially fit the requirements of the air quality standards. The smoke samples were then directly exposed to TA100 for 10, 20, 30, or 60 min in our exposure module. Exposure to IS (brand A) for 30 to 60 min and exposure to IS (brand B) for 60 min led to statistically (p < 0.05) weak (below the twofold rule) but dose-dependent mutagenic activities either with or without metabolic activation. Furthermore, a short-term exposure (10-60 min) to SCS (brands A and B) displayed statistically significant (p < 0.05) direct-acting, indirect-acting, time- and dose-dependent mutagenic activities. Furthermore, our data also support that the liver S9 enzyme could enhance the mutagenic activities in most IS and SCS samples. This study confirmed that the modified Ames module can be applied to directly detect the mutagenic activities of real polluted air samples.

Embryonic Exposure to Cigarette Smoke Extract Impedes Skeletal Development and Evokes Craniofacial Defects in Zebrafish.

Exposure to cigarette smoke represents the largest source of preventable death and disease in the United States. This may be in part due to the nature of the delayed harmful effects as well as the lack of awareness of the scope of harm presented by these products. The presence of “light” versions further clouds the harmful effects of tobacco products. While active smoking in expectant mothers may be reduced by educational and outreach campaigns, exposure to secondhand smoke is often involuntary yet may harm the developing embryo. In this study, we show that the main component of secondhand smoke, sidestream cigarette smoke, from several brands, including harm-reduction versions, triggered unsuccessful hatching at 3 dpf and reduced overall survival at 6 dpf in developing zebrafish. At non-lethal concentrations, craniofacial defects with different severity based on the cigarette smoke extract were noted by 6 dpf. All tested products, including harm-reduction products, significantly impacted cartilage formation and/or bone mineralization in zebrafish embryos, independent of whether the bones/cartilage formed from the mesoderm or neural crest. Together, these results in a model system often used to detect embryonic malformations imply that exposure of a woman to secondhand smoke while pregnant may lead to mineralization issues in the skeleton of her newborn, ultimately adding a direct in utero association to the increased fracture risk observed in children of mothers exposed to cigarette smoke.

Malondialdehyde Level and Tissue Apoptosis Count as an Early-Detection Marker of Oral Potentially Malignant Disorders.

The malondialdehyde (MDA) level and TA count represent the progression of oral potentially malignant disorders (OPMD) to malignancy and thus may be used as an indicator of oral epithelial dysplasia (OED). This study aimed to determine the MDA level and tissue apoptosis (TA) count in oropharyngeal tissue of Wistar rats exposed to sidestream cigarette smoke. Wistar rats were divided into three groups: T4 group (4-week cigarette smoke exposure), T8 group (8-week cigarette smoke exposure), and control group, which was not exposed to cigarette smoke. The oropharyngeal tissue of the rats from each group was examined histopathologically to count the number of apoptotic cells, and then the blood serum was made to measure the MDA level. Bonferroni test was performed to see the differences in each group for MDA level. While the data from tissue apoptosis were analyzed using Mann-Whitney U test for the significance. All data were considered significant if p < 0.05. The MDA level and TA count increased as the duration of cigarette smoke exposure increased. In the T8 group, the MDA level and TA count were significantly higher compared with the T4 and control groups with a p-value < 0.05. Exposure to sidestream cigarette smoke increased the TA count and MDA level in the oropharyngeal tissue of Wistar rats. The TA count and MDA level may be used as markers of OPMD.

Gallic Acid-Containing Gelatin-Based Nonwoven Mat with Synergistic Photodegradation and Photoindication Function for Reducing Nicotine.

Cigarette smoking is a popular habit that has negative health consequences for populations. In this study, we developed a gallic acid-containing, gelatin-based nonwoven mat with photodegradation and photoindication functions. This could react with sidestream cigarette smoke and simultaneously inhibit the activity of the microbe growth in the air. The results of a fluorescence emission spectrum evidenced this photoindication function. Neither the nicotine nor gallic acid showed a redshift emission spectrum. However, the emission spectrum of the nonwoven mat exhibited the redshift and increased in intensity after absorbing the sidestream cigarette smoke. In this spectral evidence, the natural polymer played a key role in the photoindication function’s display because it could dissolve the nicotine of the sidestream cigarette smoke and cause it to react with the gelatin structure. The high performance liquid chromatography–mass spectroscopy results indicated that the gallic acid and ultraviolet (UV) light enhanced the absorption of nicotine and nicotine-like derivatives, which were dissolved by the Tween 80 of nonwoven mat. The liquid paraffin and Tween 80 could oxidize, dehydrogenate, and demethylate the nicotine that was absorbed by the gelatin nonwoven mat. In conclusion, the nonwoven mat developed in this study provided the functions to filter the nicotine of sidestream smoke and activate the photoindication property by absorbing 365-nm UV light.

Conditioned Media of Adipose-Derived Stem Cells Suppresses Sidestream Cigarette Smoke Extract Induced Cell Death and Epithelial-Mesenchymal Transition in Lung Epithelial Cells.

The role of the epithelial–mesenchymal transition (EMT) in lung epithelial cells is increasingly being recognized as a key stage in the development of COPD, fibrosis, and lung cancers, which are all highly associated with cigarette smoking and with exposure to second-hand smoke. Using the exposure of human lung cancer epithelial A549 cells and non-cancerous Beas-2B cells to sidestream cigarette smoke extract (CSE) as a model, we studied the protective effects of adipose-derived stem cell-conditioned medium (ADSC-CM) against CSE-induced cell death and EMT. CSE dose-dependently induced cell death, decreased epithelial markers, and increased the expression of mesenchymal markers. Upstream regulator analysis of differentially expressed genes after CSE exposure revealed similar pathways as those observed in typical EMT induced by TGF-β1. CSE-induced cell death was clearly attenuated by ADSC-CM but not by other control media, such as a pass-through fraction of ADSC-CM or A549-CM. ADSC-CM effectively inhibited CSE-induced EMT and was able to reverse the gradual loss of epithelial marker expression associated with TGF-β1 treatment. CSE or TGF-β1 enhanced the speed of A549 migration by 2- to 3-fold, and ADSC-CM was effective in blocking the cell migration induced by either agent. Future work will build on the results of this in vitro study by defining the molecular mechanisms through which ADSC-CM protects lung epithelial cells from EMT induced by toxicants in second-hand smoke.

A Laboratory Method to Measure Skin Surface Staining by Cigarette Smoke, Tobacco Heating Products and E-Cigarettes

Summary Exhaled or side-stream cigarette smoke (CS) may visually stain a consumer's skin over time. Tobacco heating products (THPs) and e-cigarettes (ECs) have reduced staining potential because they do not produce side-stream aerosols and their exhaled aerosols have significantly reduced levels of toxicants, particles and odour. Here we assess discolouration of porcine skin in vitro after exposure to particulate matter (PM) or aerosols from CS (3R4F), two THPs (glo and glo sens) and an EC (iSwitch Maxx). PM was prepared by capturing aerosols on Cambridge filter pads and eluting with dimethyl sulfoxide (DMSO). Abattoir-obtained porcine skin samples were incubated with PM or DMSO control at 37 °C between 0 and 6.0 h. For aerosol assessment, porcine skin samples were exposed to between 50 and 400 puffs of the products, or air control, using a smoking machine. Colour profiles and staining levels of each skin sample were measured at different timepoints and puff thresholds using a spectrophotometer. Staining increased with time and dose, the greatest changes being observed following exposure to aerosols and PM from CS. THP, EC and control values were significantly different from CS after 0.5 h exposure to PM or 50 puffs of aerosols. The minimal staining induced by THPs and EC was comparable to controls. These data suggest that THPs and ECs could offer hygiene benefits to consumers who switch from smoking cigarettes. Further studies are required to assess the longer-term effects of THPs and ECs on skin discoloration. [Contrib. Tob. Nicotine Res. 30 (2021) 158–166]

Effects of Chronic Secondhand Smoke (SHS) Exposure on Cognitive Performance and Metabolic Pathways in the Hippocampus of Wild-Type and Human Tau Mice.

Background:Exposure to secondhand smoke (SHS) is a risk factor for developing sporadic forms of sporadic dementia. A human tau (htau) mouse model is available that exhibits age-dependent tau dysregulation, neurofibrillary tangles, neuronal loss, neuroinflammation, and oxidative stress starting at an early age (3–4 months) and in which tau dysregulation and neuronal loss correlate with synaptic dysfunction and cognitive decline.Objective:The goal of this study was to assess the effects of chronic SHS exposure (10 months’ exposure to ) on behavioral and cognitive function, metabolism, and neuropathology in mice.Methods:Wild-type (WT) and htau female and male mice were exposed to SHS (90% side stream, 10% main stream) using the SCIREQ® inExpose™ system or air control for 168 min per day, for 312 d, 7 d per week. The exposures continued during the days of behavioral and cognitive testing. In addition to behavioral and cognitive performance and neuropathology, the lungs of mice were examined for pathology and alterations in gene expression.Results:Mice exposed to chronic SHS exposure showed the following genotype-dependent responses: a) lower body weights in WT, but not htau, mice; b) less spontaneous alternation in WT, but not htau, mice in the Y maze; c) faster swim speeds of WT, but not htau, mice in the water maze; d) lower activity levels of WT and htau mice in the open field; e) lower expression of brain PHF1, TTCM1, , and HSP90 protein levels in WT male, but not female, mice; and f) more profound effects on hippocampal metabolic pathways in WT male than female mice and more profound effects in WT than htau mice.Discussion:The brain of WT mice, in particular WT male mice, might be especially susceptible to the effects of chronic SHS exposure. In WT males, independent pathways involving ascorbate, flavin adenine dinucleotide, or palmitoleic acid might contribute to the hippocampal injury following chronic SHS exposure. https://doi.org/10.1289/EHP8428

Application of a Fluorescent Probe for the Online Measurement of PM-Bound Reactive Oxygen Species in Chamber and Ambient Studies.

This manuscript details the application of a profluorescent nitroxide (PFN) for the online quantification of radical concentrations on particulate matter (PM) using an improved Particle Into Nitroxide Quencher (PINQ). A miniature flow-through fluorimeter developed specifically for use with the 9,10-bis(phenylethynyl)anthracene-nitroxide (BPEAnit) probe was integrated into the PINQ, along with automated gas phase corrections through periodic high efficiency particle arrestor (HEPA) filtering. The resulting instrument is capable of unattended sampling and was operated with a minimum time resolution of 2.5 min. Details of the fluorimeter design and examples of data processing are provided, and results from a chamber study of side-stream cigarette smoke and ambient monitoring campaign in Guangzhou, China are presented. Primary cigarette smoke was shown to have both short-lived (t1/2 = 27 min) and long-lived (t1/2 = indefinite) PM-bound reactive oxygen species (ROS) components which had previously only been observed in secondary organic aerosol (SOA).

Effects of sidestream tobacco smoke on P53 expressions in Rattus novergicus tongue epithelial mucosa

Background: Smoking, both active and passive, has been widely recognised as toxic to the human body, since it induces several forms of cancer, including that affecting the oral cavity. Benzopyrene, the carcinogen contained in tobacco smoke, can even lead tocarcinogenesis which potentially affects the regulation of cell apoptosis in both active and passive smokers. Purpose: This study aims to investigate the carcinogenic effects of cigarette smoke on apoptosis of rat tongue mucosae through p53 expression. To determine the risk of malignant transformation through tumor suppressor genes in the apoptotic pathway. Methods: Rattus norvegicus subjects were divided into four groups, namely Treatment Group 1 exposed to sidestream cigarette smoke for four weeks (P1), Treatment Group 2 exposed to sidestream cigarette smoke for eight weeks (P2), Control Group not exposed to sidestream cigarette smoke for four weeks (K2), and Control Group (K) not exposed to sidestream cigarette smoke for eight weeks (K2). The exposure process was conducted using a smoking pump and alternating exposure. Four micron-thick sections of formalin were subsequently fixed together with paraffin embedded biopsy material from tongue mucosa of Rattus norvegicus. The tissue sections from the treatment groups were then analyzed immunohistochemically to compare the expressions of p53 and Bcl-2 proteins with those of the control groups. Results: The T-test results indicated statistically significant differences in the expressions of p53 between the 4-week control group (K1) and the 4-week treatment group (P1) (p=0.01, p&lt;0.05) as well as between the 8-week control group (K2) and the 8-week treatment group (P2) (p=0.03, p&lt;0.05). Conclusion: Exposure to cigarette smoke can induce changes in tumor suppressor genes and also affect the regulation of cell apoptosis, thus changing cell structure and leading to malignancy.

Hyperplasia of Wistar rat tongue mucosa due to exposure to cigarette side-stream smoke

Background: Hyperplasia, a condition whereby an excessive number of cells are produced due to their uncontrolled division, represents a common symptom of carcinogenesis. Cancer is a physical manifestation of cell malignancy resulting from abnormal proliferation. Globally, oral cancer currently constitutes the sixth largest lethal form of the condition. The most common etiology of oral cancer is tobacco of which cigarettes are the most popular related product. The health risks associated with cigarette smoke not only affect active smokers but also individuals who ingest it passively. Sidestream smoke comes from the lighted end of a burning tobacco product such as a cigarette, pipe or cigar and contains nicotine and many harmful cancer-causing chemicals. Inhaling sidestream smoke increases the risk of lung and other types of cancer. Purpose: The purpose of this study was to understand how sidestream cigarette smoke initiates precancerous changes, in this case hyperplasia, in the oral mucosa epithelium of Wistar rats. Methods: The subjects were divided into three groups, a 4-week treatment group (P1), an 8-week treatment group (P2), and a control group (K), each consisting of ten subjects. The subjects were exposed to a daily two-cigarette dose of smoke. The experiment used a post-test only control group design. All samples were sacrificed during the fourth and eighth weeks. Haematoxylin-eosin staining was performed on the tongues of the Wistar rats to establish the presence of hyperplasia. Data was analyzed using a one-way ANOVA test. Results: After the Wistar rats had been exposed to cigarette smoke, an increased degree of epithelial cell proliferation (hyperplasia) showed a significant difference with a p-value &lt;0.05 during the eighth week. Conclusion: Exposure to cigarette sidestream smoke induces increased epithelial cell proliferation (hyperplasia) in Wistar rats.

A sensitive method for the determination of tobacco-specific nitrosamines in mainstream and sidestream smokes of combustion cigarettes and heated tobacco products by online in-tube solid-phase microextraction coupled with liquid chromatography-tandem mass spectrometry

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.

Molecular characterization of aldehydes and ketones in particle phase of mainstream and sidestream cigarette smoke.

Aldehydes and ketones (AKs) in cigarette smoke are risk to humans and environment. Due to the complexity of itself and the interference of the smoke tar matrix, the aldehydes and ketones in particle phase (AKPs) of mainstream smoke (MSS) and sidestream smoke (SSS) have not been well investigated. In this study, the AKPs of MSS and SSS were derivatized into polar products by reaction with Girard T reagent. The derivatives were isolated rapidly by column chromatography and analysed by Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR MS). Fifteen species of aldehydes and ketones were detected by positive ion electrospray ionization (ESI) FT-ICR MS: O1–6, N1O1–4, N2O1–3 and N3O2–3. The total number of AKPs obtained by ESI FT-ICR MS in MSS and SSS is about 1100 and 970, respectively. After hydrolysis, the original AKPs were obtained and 63 carbonyls were identified and quantified by gas chromatography–mass spectrometry (GCMS). The nitrogen-containing and high-oxygen AKPs were further characterized by Orbitrap mass spectrometry. Structures of compounds with high relative abundance in the mass spectrum were speculated (e.g. a series of degradants of cembrenediol) by comparison with the results of GCMS.

Evaluation of the impact of waterpipe tobacco smoke exposure on the activity and expression of rat hepatic CYP450: a pharmacokinetic study

Waterpipe smoke contains many toxic constituents that can alter drug pharmacokinetics. This study assessed the effect of waterpipe smoke exposure on the activity and expression of CYP450 enzymes in rats. Animals (n = 10/group) were exposed to either waterpipe smoke or side-stream cigarette smoke for 1 h/day (6 days/week) for 31 days, or fresh air (control). An intragastric cocktail solution containing three probe drugs, phenacetin, chlorzoxazone and testosterone was administered to assess the activity of CYP1A2, CYP2E1 and CYP3A, respectively. Serum concentrations were determined using LC-MS/MS and the pharmacokinetic parameters were calculated. The mRNA expression of hepatic enzymes was also quantified. Waterpipe and cigarette smoke exposure did not significantly alter the pharmacokinetics of phenacetin, chlorzoxazone and testosterone. For example, the clearance and drug exposure values were comparable among groups for all probe drugs. Additionally, there was no significant effect of waterpipe and cigarette smoke on mRNA expression of hepatic CYP1A2, CYP2E1 and CYP3A2. The results demonstrate that waterpipe smoke exposure had no effect on the functional expression of three key CYP450 isoforms in rats. Future research is required with longer exposure periods to waterpipe smoke. Such work serves to enhance current understanding of effect of waterpipe smoke exposure on pharmacokinetics.

Determination of Hydrogen Cyanide in Cigarette Smoke by Continuous Flow Analysis Method Using Safer Chemistry

Summary A new safe and sensitive method to determine hydrogen cyanide (HCN) in cigarette smoke using continuous flow analyser (CFA) has been developed and validated. The use of highly toxic potassium cyanide (KCN) as a standard necessitates the development of a safer method for the determination of HCN in cigarette smoke. In this described method KCN is replaced by less toxic potassium tetracyanozincate (Lethal Dose LD50 oral is 7.49 mg/kg for KCN and 2000 mg/kg for potassium tetracyanozincate). Furthermore, the new method uses isonicotinic acid-barbituric acid (coupling reagent) instead of pyridine-pyrazolone as a reagent for the determination of HCN, and hence eliminates the use of pyridine. In this method HCN is trapped on both the Cambridge Filter Pad, then extracted with aqueous sodium hydroxide solution, and in an impinger containing the same solution. The solution thus extracted is oxidised to cyanogen chloride by Chloramine-T and treated with coupling reagent, the resulting stable chromophore was measured colorimetrically at 600 nm. The regression equation was linear in the range of 1 to 25 μg/mL for cyanide with a correlation coefficient (R2) &gt; 0.9998. The limit of detection (LOD) was 0.76 μg/cig and the overall relative standard deviation (RSD) of the method was less than 10%. Excellent recoveries of cyanide were obtained in the range from 92% to 112% and the HCN yields from the Kentucky Reference Cigarette 3R4F obtained from the newly developed method are in good agreement with those from the conventional KCN method. The proposed method is robust, reliable, selective and safer than any of the existing methods for determination of hydrogen cyanide in mainstream as well as in sidestream cigarette smoke.

Selective Uptake of Third-Hand Tobacco Smoke Components to Inorganic and Organic Aerosol Particles.

Third-hand smoke (THS) is an emerging route of exposure to tobacco smoke in the indoor environment. Few studies have investigated the chemical behavior of THS, although initial findings suggest that semivolatile components of THS can partition to indoor aerosol. By exposing single-component particles to THS in an environmental chamber, this study demonstrates a pronounced dependence of THS uptake on aerosol composition. First, it was found that primarily reduced nitrogen compounds (that produced C xH yN z+ ion signal) in THS partitioned strongly to acidic ammoniated sulfate particles, whereas overall THS uptake to more pH-neutral sodium sulfate particles was minimal. Second, THS uptake to pure hydrocarbon particles (squalane) was even greater than to ammoniated sulfate particles with the uptake arising from mainly C xH y compounds. The greater uptake of THS to squalane was mostly driven by the dominant fraction of C xH y compounds in the side stream cigarette smoke aerosol, the composition of which is likely to be broadly similar to THS in these experiments. Third, oxygenated organic particles (sucrose) and solid ammonium sulfate particles showed minimal uptake. These results indicate that particulate THS inhalation exposure will be strongly dependent on the chemical nature of the particles present in the indoor environment.

Characteristics of Organophosphate Ester Formation during Smoking

This study examines the occurrence of organophosphate esters (OPEs) in cigarettes and sidestream cigarette smoke and to see the OPE formation characteristics during smoking. All seven OPEs in both gas and particulate phases were measured in sidestream cigarette smoke for four brands of cigarettes. Tributyl phosphate (TBP), tris(2-butoxyethyl) phosphate (TBEP), tris(2-chloroethyl) phosphate (TCEP), and triphenyl phosphate (TPP) were found frequently. Median total OPE increases in the air samples during smoking were 56.2 ng per cigarette for gas-phase OPEs and 2360 ng per cigarette for particulate-phase OPEs. TBP and TCEP could be absorbed to particles in air more readily than alkans as seen from the correlation line between gas&amp;ndash;particle partition coefficients (Kp) and the subcooled liquid vapor pressures (PL&amp;ordm;) for alkans. Furthermore, TBP was determined in the cigarettes. Median total OPE decreases in the cigarette samples during smoking were 1200 ng per cigarette. The combustion reaction increased TBP and TBEP levels in cigarettes, and particulate-phase TBEP in air appeared to influence the production of TBP, TCEP, and TPP. TBP and TBEP in cigarettes likely affect the production of TBP, TBEP, TCEP, and TPP in air during smoking.

Thirdhand Smoke at Philip Morris.

Thirdhand cigarette smoke is the fraction of cigarette smoke that remains in the environment long after a cigarette is extinguished. The Truth Tobacco Industry Documents collection at the University of California San Francisco was searched for information on thirdhand smoke. In 1991, scientists at Philip Morris Inc conducted some of the first studies on thirdhand cigarette smoke. For 110 days, 8 hours a day, they ran sidestream cigarette smoke through a 30 m3 room that contained carpet, curtain, and textured wallpaper. The room was ventilated with clean air every night. By comparing the chemicals in the air during the 8-hour smoking period and during the clean air ventilation period, they showed that some smoke chemicals persist in the air 12 hours after smoking. By extracting the nicotine and nitrosamines from samples of the carpet, curtain, and wallpaper, they found that high concentrations of nicotine and the carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) persisted in the room for more than 50 days; that surface chemistry affected nitrosamine concentrations; and that the concentration of NNK in the room, 110 days after the last cigarette was extinguished, could exceed the mass of NNK that entered the room as smoke. These data, from a controlled environment where the total number of cigarettes smoked is known, provide further evidence that cigarette smoke chemicals remain in the environment for months after smoking, that they reemit back into the air, and that they react to form new toxins and carcinogens. Smoke-free policies are the best method to reduce exposure to thirdhand smoke. This unpublished, original research from Philip Morris Inc demonstrates that majority of the nicotine and tobacco-specific nitrosamines in the secondhand smoke from each cigarette smoked indoors remains on indoor surfaces for months after the cigarette is extinguished. It also demonstrates that elevated concentrations of nicotine, ammonia, formaldehyde, and the gas-phase nitrosamine, N-nitrosopyrrolidine, can be found in the air for more than 12 hours after smoking; that surface chemistry affects nitrosamine formation and persistence; and that the amount of the carcinogenic nitrosamine NNK that persists months after smoking ends can exceed the amount that actually came out of the cigarettes.

Direct-acting DNA ethylating agents associated with tobacco use primarily originate from the tobacco itself, not combustion

Unburnt tobacco and tobacco smoke contain a variety of carcinogens, exposure to which are causally associated with the incidence of several human cancers. Herein, we used isotope-dilution LC–MS/MS for the quantification of alkylated purines in DNA, following in vitro exposure to aqueous extracts of tobacco itself, and tobacco smoke. Our results demonstrated the presence of direct-acting ethylating agent(s) in unburnt tobacco, which 4.0–6.3 times exceeded that in the particulate phase of sidestream cigarette smoke and 6.8–8.9 times exceeded that in mainstream smoke. Interestingly, particulate phase of sidestream cigarette smoke exhibited higher ethylating potency than that in mainstream smoke. This finding refutes the previous assumptions that the ethylating agent(s) associated with smoking, are derived from cigarette smoke. Indeed, our data show that combustion of tobacco actually decreases the ethylating potency of tobacco. Although the identity of this agent(s) remains unknown, our data suggest that it is highly hydrophilic, and hence likely to be easily extracted by saliva. This would allow intimate contact with the tissues of the oropharyngeal cavity. Taken together, these results have profound implications for tobacco use, in particular for tobacco chewers and passive smokers, whose exposure to ethylating agent(s) is greater than previously thought.

Spectrophotometric determination of ammonia levels in tobacco fillers of and sidestream smoke from different cigarette brands in Japan

BackgroundThe ammonia contained in tobacco fillers and mainstream and sidestream cigarette smoke accelerates nicotine dependence in cigarette smokers. Ammonia has been included in the non-exhaustive priority list of 39 tobacco components and emissions of cigarette published by the World Health Organization (WHO) Study Group on Tobacco Product Regulation. The development of a simple ammonia detection method will contribute to the establishment of tobacco product regulation under tobacco control policies and allow surveys to be conducted, even by laboratories with small research budgets.MethodsWe developed a simple colorimetric method based on the salicylate-chlorine reaction and absorption spectrometry with two reagents (sodium nitroprusside and sodium dichloroisocyanurate). To compare this method to conventional ion chromatography, we analyzed the ammonia levels in tobacco fillers extracted from 35 Japanese commercially marketed cigarette brands manufactured by four tobacco companies (Japan Tobacco (JT) Inc., British American Tobacco (BAT), Philip Morris Japan, and Natural American Spirit). We also analyzed the ammonia levels in the sidestream smoke from cigarettes of the brands that were found to contain high or low tobacco filler ammonia levels.ResultsThe ammonia levels in the reference cigarette (3R4F) measured by our method and ion chromatography were similar and comparable to previously reported levels. The ammonia levels in tobacco fillers extracted from 35 cigarette brands ranged from 0.25 to 1.58 mg/g. The mean ammonia level of JT cigarette brands was significantly higher (0.83 ± 0.28 mg/g) than that of Natural American Spirit cigarette brands (0.30 ± 0.08 mg/g) and lower than those in the other two cigarette brands (1.11 ± 0.19 mg/g for BAT and 1.24 ± 0.15 mg/g for Philip Morris) (p < 0.001 by Bonferroni test). The ammonia levels in the sidestream smoke of CABIN, Marlboro Black Menthol, American Spirit Light, and Seven Stars were 5.89 ± 0.28, 5.23 ± 0.12, 6.92 ± 0.56, and 4.14 ± 0.19 mg/cigarette, respectively. The ammonia levels were higher in sidestream smoke than in tobacco filler.ConclusionsOur simple colorimetric could be used to analyze ammonia in tobacco fillers and sidestream smoke. There were significant differences between the ammonia levels of the 35 commercially marketed cigarette brands in Japan manufactured by four tobacco manufacturers. Over 90% of the ammonia in sidestream smoke was in gaseous phase.

Exploring Conditions for Ultrafine Particle Formation from Oxidation of Cigarette Smoke in Indoor Environments.

Cigarette smoke is an important source of particles and gases in the indoor environment. In this work, aging of side-stream cigarette smoke was studied in an environmental chamber via exposure to ozone (O3), hydroxyl radicals (OH) and indoor fluorescent lights. Aerosol mass concentrations increased by 13-18% upon exposure to 15 ppb O3 and by 8-42% upon exposure to 0.45 ppt OH. Ultrafine particle (UFP) formation was observed during all ozone experiments, regardless of the primary smoke aerosol concentration (185-1950 μg m-3). During OH oxidation, however, UFP formed only when the primary particle concentration was relatively low (<130 μg m-3) and the OH concentration was high (∼1.1 × 107 molecules cm-3). Online aerosol composition measurements show that oxygen- and nitrogen- containing species were formed during oxidation. Gas phase oxidation of NO to NO2 occurred during fluorescent light exposure, but neither primary particle growth nor UFP formation were observed. Overall, exposure of cigarette smoke to ozone will likely lead to UFP formation in indoor environments. On the other hand, UPF formation via OH oxidation will only occur when OH concentrations are high (∼107 molecules cm-3), and is therefore less likely to have an impact on indoor aerosol associated with cigarette smoke.