Environmental Tobacco Smoke Components Research Articles

Nicotine Reduces Human Brain Microvascular Endothelial Cell Response to Escherichia coli K1 Infection by Inhibiting Autophagy.

Studies have shown that exposure to environmental tobacco smoke can increase the risk of bacterial meningitis, and nicotine is the core component of environmental tobacco smoke. Autophagy is an important way for host cells to eliminate invasive pathogens and resist infection. Escherichia coli K1 strain (E. coli K1) is the most common Gram-negative bacterial pathogen that causes neonatal meningitis. The mechanism of nicotine promoting E. coli K1 to invade human brain microvascular endothelial cells (HBMECs), the main component of the blood–brain barrier, is not clear yet. Our study found that the increase of HBMEC autophagy level during E. coli K1 infection could decrease the survival of intracellular bacteria, while nicotine exposure could inhibit the HBMEC autophagic response of E. coli K1 infection by activating the NF-kappa B and PI3K/Akt/mTOR pathway. We concluded that nicotine could inhibit HBMEC autophagy upon E. coli K1 infection and decrease the scavenging effect on E. coli K1, thus promoting the occurrence and development of neonatal meningitis.

Meconium samples used to assess infant exposure to the components of ETS during pregnancy.

The aim of the study was to use meconium samples to assess fetal exposure to compounds present in environmental tobacco smoke (ETS). In order to assess fetal exposure to toxic tobacco smoke compounds, samples of meconium from the offspring of women with different levels of tobacco smoke exposure, and the samples of saliva from the mothers were analyzed. Thiocyanate ion as a biomarker of tobacco smoke exposure, and other ions that are indices of such exposure were determined by means of ion chromatography. The results of ion chromatography analysis of the meconium and maternal saliva samples for the presence of cations and anions (including thiocyanate ion) indicate that the concentration level of specific ions depends on the intensity of environmental tobacco smoke exposure of pregnant women. Based on the results, it can be concluded that meconium samples can be used to determine the substances from tobacco smoke. The results confirm the effect of smoking during pregnancy on the presence and content of substances from tobacco smoke.

Cytotoxicity and mutagenicity of sidestream cigarette smoke particulate matter of different particle sizes.

Sidestream cigarette smoke, the major component of environmental tobacco smoke, is a complex and reactive aerosol. The particulate matter (PM) in sidestream smoke is one of the carriers of chemical constituents. However, particle size-dependent toxicological effects of PM are poorly understood. In this study, we evaluated the relationship between the PM size and in vitro cytotoxicity and mutagenicity of sidestream cigarette smoke. A NanoMoudi-II(™) 125A was used to collect PM samples ranging from 10 nm to 10 μm. The in vitro toxicity of PM was evaluated using a neutral red cytotoxicity assay and Salmonella mutagenicity assay. The results showed that the cytotoxicity and mutagenicity of PM larger than 1 μm was significantly lower than PM sized 10 nm-1 μm. Furthermore, there was a noticeable trend that the smaller the size of the PM of sidestream cigarette smoke, the greater the toxicity. This study suggests that the toxicity of PM in sidestream cigarette smoke is size-dependent.

Aberrant Cell and Basement Membrane Architecture Contribute to Sidestream Smoke-Induced Choroidal Endothelial Dysfunction

Environmental tobacco smoke (ETS) is widely regarded as a major modifiable risk factor for age-related macular degeneration (AMD). Yet, precisely how it exerts its pathologic effects is poorly understood. Since early-stage AMD is characterized by choroidal capillary loss, this study examined the effect of sidestream smoke (SS), the major component of ETS, on the viability of choroidal endothelial cells (EC), with an emphasis on the role of aberrant cell and basement membrane (BM) architecture in mediating SS-induced response. Chorioretinal ECs (RF/6A) were treated with SS, and cell viability and architecture were analyzed by colorimetric assay and actin cytoskeletal organization, respectively. The structure of RF/6A EC-secreted BM was examined by immunofluorescence for collagen IV and immunoblotting for lysyl oxidase (LOX), a collagen-crosslinking enzyme. Finally, fresh RF/6A ECs were cultured on decellularized SS-treated BM to evaluate its active role in EC dysfunction. The RF/6A EC viability decreased progressively with increasing SS dose, which correlated strongly with a significant decline in actin cytoskeleton-dependent EC spreading. Sidestream smoke also caused marked disruption of the RF/6A EC-secreted BM that was accompanied by suppression of LOX expression. Further, fresh, non-SS-treated RF/6A ECs exhibited a significant loss in viability and actin cytoskeletal organization when cultured on SS-treated corrupt BM. These findings indicate that aberrant physical cues in the form of EC and BM architecture likely have an important role in choriocapillaris dysfunction seen in SS-associated early AMD and implicate choroidal BM as a potential target for AMD management strategies.

Environmental Tobacco Smoke Exposure Among Casino Dealers

This study quantified casino dealers' occupational exposure to environmental tobacco smoke (ETS). We measured casino dealers' exposure to ETS components by analyzing full-shift air and preshift and postshift urine samples. Casino dealers were exposed to nicotine, 4-vinyl pyridine, benzene, toluene, naphthalene, formaldehyde, acetaldehyde, solanesol, and respirable suspended particulates. Levels of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) in urine increased significantly during an 8-hour work shift both with and without adjustment for creatinine clearance. Creatinine-unadjusted cotinine significantly increased during the 8-hour shift, but creatinine-adjusted cotinine did not increase significantly. Casino dealers at the three casinos were exposed to airborne ETS components and absorbed an ETS-specific component into their bodies, as demonstrated by detectable levels of urinary NNAL. The casinos should ban smoking on their premises and offer employee smoking cessation programs.

VOC and Particulate Emissions from Commercial Cigarettes: Analysis of 2,5-DMF as an ETS Tracer

Emissions of particulate matter (PM) and a broad suite of target volatile organic compounds (VOCs) in total, main-stream (MS) and side-stream (SS) smoke emissions are measured for six types of commercial cigarettes. The suitability of 2,5-dimethyl furan (DMF) as a tracer for environmental tobacco smoke (ETS) is investigated using laboratory results and a field study of 47 residences. Over 30 VOCs were characterized in cigarette smoke, including several that have not been reported previously. "regular tar", "low tar", menthol, and nonmenthol cigarettes showed only minor differences in PM and VOC emissions. When total emissions are considered, PM emissions averaged 18 +/- 2 mg cigarette(-1) and VOC emissions averaged 3644 +/- 160 mg cigarette(-1). DMF appears to satisfy all requirements for a tracer, namely, uniqueness, detectability, similar emission factors across tobacco products (211 +/- 16 microg cigarette(-1)), consistent proportions to other ETS compounds, and behavior similar to other ETS components in relevant environments. On the basis of field study results, DMF more reliably indicated smoking status than occupant-completed questionnaires, and cigarette smoking was responsible for significant fractions of benzene (50%), styrene (49%), and other VOCs in the smoker's homes.

Smoke from traditional commercial, harm reduction and research brand cigarettes impairs oviductal functioning in hamsters (Mesocricetus auratus) in vitro

Cigarette smoke from 2R1 research brand cigarettes and specific toxicants in smoke inhibit oviductal functioning. Our purpose was to test the hypothesis that smoke from commercial cigarettes, including harm reduction cigarettes, inhibits oviductal functioning and to measure the concentration of previously identified toxicants in smoke from research and commercial cigarettes. Mainstream (MS) and sidestream (SS) smoke solutions from two research, six traditional commercial and three harm reduction brands were tested in vitro using an oviductal assay that measures ciliary beat frequency, oocyte retrieval rate and smooth muscle contraction. Generally, smoke from each brand of cigarette was inhibitory in the three oviductal bioassays. SS, the major component of environmental tobacco smoke, was usually more inhibitory than MS, the smoke inhaled by active smokers. Nine cigarette toxicants, previously shown to be highly inhibitory in the oviductal bioassays, were quantified in MS and SS. 4-Methylpyridine, which was inhibitory by itself in picomolar doses, was present in the highest concentration in MS and SS solutions from all brands tested. In general, toxicant concentrations were higher in SS than in MS solutions. These data show that commercial brands of cigarettes, including harm reduction cigarettes, contain toxicants that inhibit biological processes in the oviduct and could affect reproductive outcomes.

The tobacco industry's worldwide ETS consultants project: European and Asian components

The tobacco industry has formed regional environmental tobacco smoke (ETS) consultants programs in order to generate controversy on the issue of secondhand smoke (SHS) in Europe, Asia and Latin America. Only those countries in which the industry foresaw SHS restrictions were included. This paper describes the European and Asian components of the tobacco industry's worldwide ETS consultants program. A systematic search was carried out of tobacco industry documents available on the Internet between October 2002 and February 2004. Beginning in 1987, Philip Morris assembled an international ETS consultants program in collaboration with other tobacco companies based on their market shares in different regions of the world. The law firm Covington & Burling contacted and hired consultants with a wide range of expertise, usually affiliated with an academic institution, in order to avoid direct contact with the industry. The objective of the program was to influence policy makers, media and the public by providing, through their consultants, 'accurate' (pro-industry) information concerning smoking regulations in public places and workplaces, indoor air quality and ventilation standards, and scientific claims regarding SHS. Consultants also conducted research related to SHS and organized and attended regional and international symposiums related to SHS without acknowledging industry funding. Despite evidence that the issue of smoke-free environments was close to emerging within the general public throughout the world in the late 1980s, the tobacco industry used its well-organized network of consultants to avoid SHS regulations in most of the world.

Characterization of trace organic compounds associated with aged and diluted sidestream tobacco smoke in a controlled atmosphere—volatile organic compounds and polycyclic aromatic hydrocarbons

Abstract In this study, a wide range of volatile organic constituents of aged and diluted sidestream tobacco smoke (ADSS) were determined in a controlled atmosphere, where ADSS is the sole source of target compounds. The ADSS was generated in a 30 m3 environmental test chamber using a variety of cigarettes, including the Kentucky 1R4F reference cigarette and eight commercial brands, and a total of 24 experimental runs were conducted. Target analytes were divided into three groups, i.e. vapor and particulate phase markers for environmental tobacco smoke (ETS), volatile organic compounds (VOC) including carbonyls, and polycyclic aromatic hydrocarbons (PAH). The VOC samples were collected on triple sorbent traps, and then analyzed by thermal desorption coupled with gas chromatography/mass spectrometry (GC/MS), while the carbonyl compounds were sampled on DNPH cartridges, being analyzed by HPLC. ETS particles in the chamber were collected by high volume sampling, and then used for the determination of PAHs by GC/MS. Among more than 30 target VOCs, acetaldehyde appeared to be the most abundant compound, followed by 2-methyl-1,3-butadiene, and formaldehyde. The results from the chamber study were further used to generate characterized ratios of selected VOCs to 3-ethenyl pyridine (3-EP), a vapor phase ETS marker. The ratios appeared to be in generally good agreement with published values in the literature. This suggests that the characteristic ratios may be useful for quantifying the impact of ETS on the VOC concentrations in ‘real world’ indoor environments, which are affected by a complex mixture of components from multiple sources. The yields of ETS markers from this study are all slightly lower than those estimated by other studies, while VOC yields are in reasonable agreement in many cases with values in the literature. Among 16 target PAHs, chrysene appeared to be most abundant, followed by benzo(a)anthracene (BaA) and benzo(a)pyrene (BaP). The average contents of BaP and BaA in ADSS particles for the commercial brands were 12.8 and 21.5 μg g−1, respectively. These values are all approximately 1.5–3 times higher than those determined previously by other studies. The average yields of BaP per cigarette were estimated to be 209 and 215 ng for the reference and commercial cigarettes, respectively. Comparison of the PAH data from this study with literature values was complicated by a lack of consistency in cigarette smoke generating methodology among other studies. These data on the cigarette yields of ETS components may provide useful information to studies on the mathematical modeling of indoor air quality regarding tobacco smoke as a source of interest, or to studies on the assessment of human exposure to ETS.

Supplementation of French Maritime Pine Bark Extract (Pycnogenol®) Prevents Lung Injury and Lipid Peroxidation in Nude Mice Exposed to Side-Stream Cigarette Smoke (SSCS)

Side-stream cigarette smoke (SSCS) is a major component of environmental tobacco smoke. The purpose of this study was to investigate the development of lung injury and lipid peroxidation in the lung and liver of immunodeficient (Nude) mice exposed to acute SSCS (a total 5 hours of exposure). The effects of French maritime bark extract (Pycnogenol^®) supplementation of the mice were also determined. SSCS increased pulmonary resistance and lipid peroxidation in these mice. Pycnogenol^® supplementation increased vitamin E levels in lung and liver. In addition, Pycnogenol^® attenuated SSCS-mediated lung injury and lipid peroxidation. It appears that the enhanced resistance against SSCS-induced lung injury and lipid peroxidation may be primarily due to the antioxidant property of Pycnogenol^® in supplemented mice.

Gas-phase organics in environmental tobacco smoke: 2. Exposure-relevant emission factors and indirect exposures from habitual smoking

Abstract Sorption of emitted gas-phase organic compounds onto material surfaces affects environmental tobacco smoke (ETS) composition and exposures indoors. We have introduced a new metric, the exposure relevant emission factor (EREF) that accounts for sorptive uptake and reemission to give the mass of individual ETS constituents available for exposure over a day in which smoking occurs. This paper describes month-long experiments to investigate sorption effects on EREFs and potential ETS exposures under habitual smoking conditions. Cigarettes were smoked in a 50-m3 furnished room over a 3-h period 6–7 days per week, with continuous ventilation at 0.3, 0.6, or 2.1 h−1. Organic gas concentrations were measured every few days over 4-h “smoking”, 10-h “post-smoking” and 10-h “background” periods. Concentration patterns of volatile ETS components including 1,3-butadiene, benzene and acrolein were similar to those calculated for a theoretical non-sorbing tracer, indicating limited sorption. Concentrations of ETS tracers, e.g. 3-ethenylpyridine (3-EP) and nicotine, and lower volatility toxic air contaminants including phenol, cresols, and naphthalene increased as experiments progressed, indicating mass accumulation on surfaces and higher desorption rates. Daily patterns stabilized after week 2, yielding a steady daily cycle of ETS concentrations associated with habitual smoking. EREFs for sorbing compounds were higher under steady cycle versus single-day smoking conditions by ∼50% for 3-EP, and by 2–3 times for nicotine, phenol, cresols, naphthalene, and methylnaphthalenes. Our results provide relevant information about potential indirect exposures from residual ETS (non-smoker enters room shortly after smoker finishes) and from reemission, and their importance relative to direct exposures (non-smoker present during smoking). Under the conditions examined, indirect exposures accounted for a larger fraction of total potential exposures for sorbing versus non-sorbing compounds, and at lower versus higher ventilation rates. Increasing ventilation can reduce indirect exposures to very low levels for non-sorbing ETS components, but indirect routes accounted for ∼50% of potential nicotine exposures during non-smoking periods at all ventilation rates.

Lung tumors in A/J mice exposed to environmental tobacco smoke: estimated potency and implied human risk.

Directly inhaled tobacco smoke is a recognized human lung carcinogen, and epidemiological studies suggest relative risks of about 1.2-1.4 for nonsmoking spouses of smokers typically exposed to environmental tobacco smoke (ETS). While many individual ETS components have been shown experimentally to induce lung tumors, ETS itself was only recently shown to induce lung tumors in a series of studies in which strain A/J mice were exposed to well-defined ETS atmospheres. Data from these studies indicate that ETS exposure clearly can increase combined malignant and benign lung tumors in multiple experiments involving male and female A/J mice, and thus provide convincing evidence that ETS is a positive mouse carcinogen. Tumorigenic potencies estimated from these A/J mouse bioassay data predict a corresponding range of increased human risk (0.2-0.5%) that overlaps that implied by case-control studies showing increased lung cancer risks in lifelong nonsmokers married to smokers. In A/J mice exposed to a significantly tumorigenic ETS concentration, lung tumors were found to be significantly smaller than those in corresponding control mice, and mice so exposed for 9 months had significantly fewer tumors/animal than mice exposed for 5 months followed by 4 months in filtered ETS-free air. These findings support hypotheses that ETS does not promote growth of spontaneous neoplastic foci in A/J mice, and that ETS-induced lung-tumor risk in A/J mice occurs predominantly by genotoxic effects that can be suppressed by reduced cell proliferation associated with chronic, high-level ETS exposure. The results obtained add to evidence that A/J mouse lung tumors induced by ETS provide a relevant biological model of ETS-induced human lung tumors.

Environmental tobacco smoke in an unrestricted smoking workplace: area and personal exposure monitoring.

The objective of this investigation was to determine the extent of areal and day-to-day variability of stationary environmental tobacco smoke (ETS) concentrations in a single large facility where smoking was both prevalent and unrestricted, and to determine the degree of daily variation in the personal exposure levels of ETS constituents in the same facility. The subject facility was a relatively new four-story office building with an approximate volume of 1.3 million ft3. The exchange of outside air in the building was determined to be between 0.6 and 0.7 air changes per hour. Eighty-seven area samples (excluding background) were collected at 29 locations over the course of 6 days of sampling. Locations included offices and cubicles occupied by smokers and nonsmokers, common areas, and the computer and mail rooms. Twenty-four nonsmoking subjects wore personal sampling systems to collect breathing zone air samples on each of 3 days in succession. This generated a total of seventy-two 8-h time-weighted average (TWA) personal exposure samples. In all samples, respirable suspended particulate matter, ultraviolet light-absorbing and fluorescing particulate matter, solanesol, nicotine, and 3-ethenyl pyridine were determined. With the exception of a few locations, tobacco-specific airborne constituents were determined in all samples. Not surprisingly, areas with the highest ETS constituent concentrations were offices and cubicles of smokers. Median and 95th percentile concentrations for all area samples, excluding background, were determined to be 1.5 and 8.7 microg/m3 for nicotine, and 8.2 and 59 microg/m3 for ETS-specific particles (as solanesol-related particulate matter, Sol-PM), respectively. Personal exposure concentrations of ETS components were similar to those levels found in the area samples (median nicotine and Sol-PM concentrations were 1.24 and 7.1 microg/m3, respectively), but the range of concentrations was somewhat smaller. For example, the 95th percentile 8-h TWA nicotine and ETS-specific particle (as Sol-PM) concentrations were 3.58 and 21.9 microg/m3, respectively. Intrasubject variation of daily concentrations ranged from 20% to 60%, depending on the component. Self-reported proximity to smokers was supported by higher ETS concentrations determined from the personal monitors, but only to a modest extent. Although smoking was completely unrestricted inside the main office areas of the facility, ETS levels, either areal or from personal exposure measurements, were lower than those estimated by Occupational Safety and Health Administration to be present in such facilities.

Performance Evaluation of Simultaneous Monitoring of Personal Exposure to Environmental Tobacco Smoke and Volatile Organic Compounds

The objective of this study was to develop and demonstrate a methodology to determine human exposure to a variety of indoor air contaminants by personal monitoring. Target analytes included respirable suspended particulates, components of environmental tobacco smoke (ETS) and a wide range of volatile organic compounds (VOCs). A total of 60 non-smoking, non-occupational residents at homes in metropolitan Taegu, Korea, were recruited for this study. The subjects were classified into two groups, i.e. subjects living in homes with smokers and without smokers. Seasonal air samples were collected using three-channel personal samplers for each subject in two phases over a 24-hour period, i.e. awake time and sleeping time separately. Performance of sampling and analytical methods used for the simultaneous measurements of ETS and VOCs were evaluated with respect to sensitivity, repeatability and field application.

Performance Evaluation of Simultaneous Monitoring of Personal Exposure to Environmental Tobacco Smoke and Volatile Organic Compounds

The objective of this study was to develop and demon strate a methodology to determine human exposure to a variety of indoor air contaminants by personal monitor ing. Target analytes included respirable suspended par ticulates, components of environmental tobacco smoke (ETS) and a wide range of volatile organic compounds (VOCs). A total of 60 non-smoking, non-occupational res idents at homes in metropolitan Taegu, Korea, were recruited for this study. The subjects were classified into two groups, i.e. subjects living in homes with smokers and without smokers. Seasonal air samples were col lected using three-channel personal samplers for each subject in two phases over a 24-hour period, i.e. awake time and sleeping time separately. Performance of sam pling and analytical methods used for the simultaneous measurements of ETS and VOCs were evaluated with respect to sensitivity, repeatability and field application.

1,N(2)-propanodeoxyguanosine adduct formation in aortic DNA following inhalation of acrolein.

Recent reports indicate that many of the cytotoxic and health-threatening components of environmental tobacco smoke (ETS) reside in the vapor phase of the smoke. We have reported previously that inhalation of 1,3-butadiene, a prominent vapor phase component of ETS, accelerates arteriosclerotic plaque development in cockerels. In this study we asked whether inhaled acrolein, a reactive aldehyde that is also a prominent vapor-phase component of ETS, damages artery-wall DNA and accelerates plaque development. Cockerels inhaled 0, 1, or 10 ppm acrolein mixed with HEPA-filtered air for 6 hr. Half were killed immediately (day 1 group) for detection of the stable, premutagenic 1,N(2)-propanodeoxyguanosine acrolein adduct (AdG3) in aortic DNA via a (32)P-postlabeling/HPLC method, and half were killed after 10 days (day 10 group) for indirect assessment of adduct repair. In the day 1 group, acrolein-DNA adducts were 5 times higher in the 1 and 10 ppm groups than in HEPA-filtered air controls. However, in the day 10 group, adduct levels in the 1 and 10 ppm acrolein groups were reduced to the control adduct level. For the plaque studies, cockerels inhaled 1 ppm acrolein (6 hr/day, 8 weeks), mixed with the same HEPA-filtered air inhaled by controls. Plaque development was measured blind by computerized morphometry. Unlike butadiene inhalation, acrolein inhalation did not accelerate plaque development. Thus, even though repeated exposure to acrolein alone has no effect on plaque size under the exposure conditions described here, a single, brief inhalation exposure to acrolein elicits repairable DNA damage to the artery wall. These results suggest that frequent exposure to ETS may lead to persistent artery-wall DNA damage and thus provide sites on which other ETS plaque accelerants can act.

Biomarkers of environmental tobacco smoke exposure.

Biomarkers are desirable for quantitating human exposure to environmental tobacco smoke (ETS) and for predicting potential health risks for exposed individuals. A number of biomarkers of ETS have been proposed. At present cotinine, measured in blood, saliva, or urine, appears to be the most specific and the most sensitive biomarker. In nonsmokers with significant exposure to ETS, cotinine levels in the body are derived primarily from tobacco smoke, can be measured with extremely high sensitivity, and reflect exposure to a variety of types of cigarettes independent of machine-determined yield. Under conditions of sustained exposure to ETS (i.e., over hours or days), cotinine levels reflect exposure to other components of ETS. Supporting the validity of cotinine as a biomarker, cotinine levels have been positively correlated to the risks of some ETS-related health complications in children who are not cigarette smokers.

Vitamin E supplementation prevents lung dysfunction and lipid peroxidation in nude mice exposed to side-stream cigarette smoke

Sidestream cigarette smoke (SSCS) is a major component of environmental tobacco smoke. The purpose of this study was to investigate development of lung injury and lipid peroxidation in the lung and liver of immunodeficient (Nude) mice exposed to a small amount of SSCS (a total 5 hours of exposure). The effects of vitamin E supplementation of the mice were also determined. SSCS increased pulmonary resistance and lipid peroxidation in these mice. Dietary vitamin E supplementation increased vitamin E levels in lung and liver. In addition, vitamin E attenuated SSCS-mediated pulmonary injury and lipid peroxidation. It appears that the enhanced resistance against SSCS-induced lung injury and lipid peroxidation may be primarily due to the increased antioxidant property of vitamin E in vitamin E-supplemented mice.

Studies of Environmental Tobacco Smoke Generated by Different Cigarettes

ABSTRACT A method was developed to reproducibly measure environmental tobacco smoke (ETS) components generated by different cigarettes. Measurements were carried out in an unventilated, controlled environment chamber. True ETS (the aged and diluted combination of exhaled mainstream plus sidestream smoke) was generated by human smokers. To reliably quantitate components normally present at trace levels, the comparisons were carried out at elevated ETS concentrations—greater than 40 times those typically encountered in “real-world” settings. The method was applied to four commercially available cigarettes and a cigarette prototype that primarily heats tobacco. Forty-three properties and components of the gas and particulate phases of ETS generated by the different cigarettes were measured. Good precision of measurement was obtained both within and between tests. Statistically significant differences in the concentration of ETS components were observed among the different commercial cigarettes and between the commercial and prototype cigarettes. Most ETS components from the prototype cigarette were reduced by >90% when compared to the commercial cigarettes. The method was used to determine the effect of cigarette design changes on the generation of ETS.

Composition of environmental tobacco smoke (ETS) from international cigarettes Part II: Nine country follow-up

The environmental tobacco smoke (ETS) generated by cigarettes from nine countries was examined to determine selected component yields and ETS marker ratios. The countries tested included: Argentina, Australia, Brazil, Canada, China, England, Japan, Korea, and the United States. Six leading brand styles from each country were smoked in an environmental test chamber. Concentrations of the gas phase ETS components CO, NO, NO 2, nicotine, 3-ethenylpyridine, myosmine, and total volatile organic compounds (TVOC) were measured. Particle mass concentrations were also measured along with the particulate phase markers ultraviolet particulate matter (UVPM), fluorescent particulate matter (FPM), and solanesol. The variation in the ETS generated by cigarettes from these nine countries was greater than observed in a previous test. Ratios of gravimetrically determined respirable suspended particles (RSP) to the surrogate standard concentrations for UVPM and FPM averaged 7.2 and 42, respectively. The average ratio of RSP to solanesol was determined to be 38. ETS component yields were relatively consistent among the countries tested and averaged 14, 59, 41, 1.3, and 0.4 mg/cig. for RSP, CO, TVOC, NO, and NO 2, respectively.