Tobacco Combustion Research Articles

Current Evidence on Tobacco Harm Reduction in Pneumology: Interviews with Two Key Opinion Leaders

The negative impact of smoking on the lung is well documented. Cigarette smoke is the cause of 90% of cases of chronic obstructive pulmonary disease (COPD), which includes chronic bronchitis and emphysema. COPD is a progressive and debilitating condition with morbidity and mortality rates similar to myocardial infarction (MI) and stroke. Despite the widely recognised risks, millions of people continue to smoke, in some cases even after receiving a diagnosis of COPD and despite knowing that the habit will accelerate disease progression. While there is no doubt that smoking cessation is the most important health intervention for all cigarette smokers, it can be challenging. Nicotine addiction, social norms and culture, and the length of time it can take smokers to feel the adverse consequences of the habit all contribute to the high cessation failure rate. However, increasing clinical and epidemiological evidence indicates that for those who are unwilling or cannot stop smoking, harm reduction strategies can help reduce exposure to the harmful chemicals and carcinogens released during tobacco combustion. Electronic devices heat processed tobacco without combusting it to deliver an aerosol containing fewer toxic products or harmful and potentially harmful constituents (HPHC) than cigarette smoke. Clinical evidence to support their use is growing. In Japan, for example, a decrease in hospitalisations due to COPD exacerbation after the introduction of such heat-not-burn (HNB), or tobacco heating systems (THS), has been reported. In this article, Wolfgang Popp, Döbling Doctor’s Center, Privatklinik Döbling, Vienna, Austria, and Klara Szondy, Semmelweis University, Budapest, Hungary, discuss the impact of cigarette smoke on the lung, and how to support smoking cessation in those willing and able to quit smoking. They also explain when strategies that reduce the harmful effects of smoking may be useful, and outline the latest evidence supporting the use of HNB systems.

A Review of Properties of Bituminous Mix Containing Bitumen Modified with Cigarette Buds, Steel Slag, and Granite Powder

Researchers have been focusing on a potential and stable solution for the top-notch environmental issue of pollution by imperishable waste products such as Cigarette Buds (CB), Steel Slag (SS) and Granite Powder (GP). The recycling of cigarette buds is not possible due to throwing away in the random manner. Cigarette buds are harmful for the environment because it consists of cellulose acetate fibers, burnt tobacco and tar in addition to multiple toxic chemicals. Depending upon the geographic and environmental conditions, it takes a large amount of time to biodegrade this waste which eventually contaminate the environment if left unattended. Therefore, CB could be utilized as a potential replacement of bitumen. On the other hand, natural resources such as aggregates and fillers form the important constituents of bituminous mix. Due to the significant industrial development, waste deposits (SS and GP) have increased in recent years. SS is metallurgical and waste material of steel industry & GP is a waste material of granite polishing industry, when used as a partial replacement of natural aggregate and lime respectively gives satisfactory results. Therefore, partial replacement of these elements with SS and GP respectively, would be a great solution towards the reduction of environmental impacts of road construction. In this study, a detailed review of different properties of modified bitumen and resulting mix containing CB, SS and GP has been presented. The properties of bituminous mix considered for review are density, penetration, softening point, viscosity, Marshall test parameters, rutting, indirect tensile strength, and modulus of rupture.

Smoking-Associated Exposure of Human Primary Bronchial Epithelial Cells to Aldehydes: Impact on Molecular Mechanisms Controlling Mitochondrial Content and Function.

Chronic obstructive pulmonary disease (COPD) is a devastating lung disease primarily caused by exposure to cigarette smoke (CS). During the pyrolysis and combustion of tobacco, reactive aldehydes such as acetaldehyde, acrolein, and formaldehyde are formed, which are known to be involved in respiratory toxicity. Although CS-induced mitochondrial dysfunction has been implicated in the pathophysiology of COPD, the role of aldehydes therein is incompletely understood. To investigate this, we used a physiologically relevant in vitro exposure model of differentiated human primary bronchial epithelial cells (PBEC) exposed to CS (one cigarette) or a mixture of acetaldehyde, acrolein, and formaldehyde (at relevant concentrations of one cigarette) or air, in a continuous flow system using a puff-like exposure protocol. Exposure of PBEC to CS resulted in elevated IL-8 cytokine and mRNA levels, increased abundance of constituents associated with autophagy, decreased protein levels of molecules associated with the mitophagy machinery, and alterations in the abundance of regulators of mitochondrial biogenesis. Furthermore, decreased transcript levels of basal epithelial cell marker KRT5 were reported after CS exposure. Only parts of these changes were replicated in PBEC upon exposure to a combination of acetaldehyde, acrolein, and formaldehyde. More specifically, aldehydes decreased MAP1LC3A mRNA (autophagy) and BNIP3 protein (mitophagy) and increased ESRRA protein (mitochondrial biogenesis). These data suggest that other compounds in addition to aldehydes in CS contribute to CS-induced dysregulation of constituents controlling mitochondrial content and function in airway epithelial cells.

Emissions, puffing topography, mouth level exposure and consumption among Japanese users of tobacco heated products

<p><strong>Background:</strong> Tobacco heating products (THPs), which heat rather than burn tobacco, have been demonstrated by a number of studies to produce an aerosol with substantially lower levels of toxicants and reduced cytotoxicity relative to cigarette smoke. As they evolve in design and function, however, it is important to verify that variant THPs maintain sufficient equivalence to the original product if we are to leverage existing foundational datasets. Recent studies suggest that a bridging approach, in which a variant is shown to be comparable to the original product on which a large foundational dataset has been generated, might be used to ensure that the same product-related claims apply.</p><p><strong>Methods:</strong> In this study, emissions and consumer behaviour were assessed for two variants of glo<sup>TM</sup> THPs: an extensively tested glo<sup>TM</sup> type 1 (glo 2.0), and glo<sup>TM</sup> type 3 (glo hyper) in base and boost modes. Emissions testing was conducted by measuring the percentage reduction of TobReg9 toxicants, relative to a 1R6F reference cigarette.</p><p><strong>Results:</strong> Consumer behaviour, including puffing topography, average daily consumption (ADC) and mouth level exposure (MLE) to NFDPM and nicotine was measured among 63 regular glo<sup>TM</sup> users in Tokyo, Japan. Emissions testing showed a substantial reduction in TobReg9 toxicants compared to the reference cigarette (95.5-97.3%), whilst there were no substantial differences in the ADC, puffing behaviour or MLE among the three THPs.</p><p><strong>Conclusions</strong>: Emissions analysis based on TobReg9 toxicants and consumer behaviour data provide evidence that the glo<sup>TM</sup> type 3 is comparable to glo<sup>TM</sup> type 1, indicating the possibility of using a bridging approach for the analysis of variant THPs based on use behaviour alone.</p>

Immunological Insights into Cigarette Smoking-Induced Cardiovascular Disease Risk.

Smoking is one of the most prominent addictions of the modern world, and one of the leading preventable causes of death worldwide. Although the number of tobacco smokers is believed to be at a historic low, electronic cigarette use has been on a dramatic rise over the past decades. Used as a replacement for cigarette smoking, electronic cigarettes were thought to reduce the negative effects of burning tobacco. Nonetheless, the delivery of nicotine by electronic cigarettes, the most prominent component of cigarette smoke (CS) is still delivering the same negative outcomes, albeit to a lesser extent than CS. Smoking has been shown to affect both the structural and functional aspects of major organs, including the lungs and vasculature. Although the deleterious effects of smoking on these organs individually is well-known, it is likely that the adverse effects of smoking on these organs will have long-lasting effects on the cardiovascular system. In addition, smoking has been shown to play an independent role in the homeostasis of the immune system, leading to major sequela. Both the adaptive and the innate immune system have been explored regarding CS and have been demonstrated to be altered in a way that promotes inflammatory signals, leading to an increase in autoimmune diseases, inflammatory diseases, and cancer. Although the mechanism of action of CS has not been fully understood, disease pathways have been explored in both branches of the immune system. The pathophysiologically altered immune system during smoking and its correlation with cardiovascular diseases is not fully understood. Here we highlight some of the important pathological mechanisms that involve cigarette smoking and its many components on cardiovascular disease and the immune systems in order to have a better understanding of the mechanisms at play.

A comparative study on the physicochemical properties of tobacco ash from lit bright cigarettes with different cut tobacco fillers

The physicochemical properties of tobacco ash under different combustion pyrolysis simulation conditions and in different areas of lit cigarettes rolling from various cut tobacco fillers were investigated using optical image, cigarette ash integrity (CAI), chromatic aberration (CA), scanning electron microscope (SEM), energy dispersive X-ray spectrometer (EDS), fourier transform infrared spectrometer (FTIR) and microscale combustion calorimeter (MCC), respectively. The study of ash appearance showed that lit cigarettes rolling from expanded cut stem (ECS) and reconstituted tobacco (RT) had lighter grey for the outer cigarette paper ash and darker color for the inner cut tobacco ash than those rolling from flue-cured tobacco (FCT) and expanded cut tobacco (ECT), respectively. Further study of CA and combustion rate indicated cigarette with ECS showed a highest burning rate and ΔL, followed in order by RT, ECT and FCT. SEM results displayed that various tobacco’s microstructures were still preserved at 450 °C, but fully broken at 750 °C and in the ash area of lit cigarettes, and then replaced by thin surface set with many particles for FCT, many connected lines coated with tiny particles for ECT, surface embedded with many rods for ECS and particle-containing surface for RT at 900 °C. EDX results illustrated that the above newly formed microstructures at 900 °C are mainly composed of O, C, Ca, Mg, K Cl, S and P, with a small amount of Fe, Al, Si, Mn and Co, of which some elements like K, S, P and Cl showed a migration into the gas phase. It can also obtained from EDX results that ECS left maximum C/O, K and Cl in the burning cone and tobacco ash area, followed in order by RT, FCT and ECT. FTIR study showed that carbonates have been produced substantially in the combustion cone for ECS, but just generated a little for FCT, ECT and RT. MCC analysis demonstrated that RT’s coke had the lowest thermal stability, while ECS’s coke began to release heat at lower temperature and ended at higher temperature in comparison with FCT and ECT. The correlation analysis showed that the ash appearance of burning cigarettes can be enhanced via a rise of K/Cl, K/S and K/(Cl+S) and a reduction of nicotine and ratio of sugar to nicotine.

Xenobiotics Delivered by Electronic Nicotine Delivery Systems: Potential Cellular and Molecular Mechanisms on the Pathogenesis of Chronic Kidney Disease.

Chronic kidney disease (CKD) is characterized as sustained damage to the renal parenchyma, leading to impaired renal functions and gradually progressing to end-stage renal disease (ESRD). Diabetes mellitus (DM) and arterial hypertension (AH) are underlying diseases of CKD. Genetic background, lifestyle, and xenobiotic exposures can favor CKD onset and trigger its underlying diseases. Cigarette smoking (CS) is a known modified risk factor for CKD. Compounds from tobacco combustion act through multi-mediated mechanisms that impair renal function. Electronic nicotine delivery systems (ENDS) consumption, such as e-cigarettes and heated tobacco devices, is growing worldwide. ENDS release mainly nicotine, humectants, and flavorings, which generate several byproducts when heated, including volatile organic compounds and ultrafine particles. The toxicity assessment of these products is emerging in human and experimental studies, but data are yet incipient to achieve truthful conclusions about their safety. To build up the knowledge about the effect of currently employed ENDS on the pathogenesis of CKD, cellular and molecular mechanisms of ENDS xenobiotic on DM, AH, and kidney functions were reviewed. Unraveling the toxic mechanisms of action and endpoints of ENDS exposures will contribute to the risk assessment and implementation of proper health and regulatory interventions.

E-Cigarettes Reexamined: Product Toxicity.

The introduction of e-cigarettes, or electronic nicotine delivery systems (ENDS), has been accompanied by controversy regarding their safety and effectiveness as a cessation aid and by an explosion in their use by youth. Their use does not involve the combustion of tobacco and the creation of harmful combustion products; they have been seen as a "harm reduction" tool that may be of assistance in promoting smoking cessation. Recognition that ENDS can deliver an array of chemicals and materials with known adverse consequences has spurred more careful examination of these products. Nicotine, nitrosamines, carbonyl compounds, heavy metals, free radicals, reactive oxygen species, particulate matter, and "emerging chemicals of concern" are among the constituents of the heated chemical aerosol that is inhaled when ENDS are used. They raise concerns for cardiovascular and respiratory health that merit the attention of clinicians and regulatory agencies. Frequently cited concerns include evidence of disordered respiratory function, altered hemodynamics, endothelial dysfunction, vascular reactivity, and enhanced thrombogenesis. The absence of evidence of the consequences of their long-term use is of additional concern. Their effectiveness as cessation aids and beneficial impact on health outcomes continue to be examined. It is important to ensure that their production and availability are thoughtfully regulated to optimise their safety and permit their use as harm reduction devices and potentially as smoking-cessation aids. It is equally vital to effectively prevent them from becoming ubiquitous consumer products with the potential to rapidly induce nicotine addiction among large numbers of youth. Clinicians should understand the nature of these products and the implications of their use.

TAPaC—tobacco-associated particulate matter emissions inside a car cabin: establishment of a new measuring platform

BackgroundParticulate matter (PM) emission caused by tobacco combustion leads to severe health burdens worldwide. Second-hand smoke exposure is extraordinarily high in enclosed spaces (e.g., indoor rooms, car cabins) and poses a particular threat to the health of vulnerable individuals (e.g., children, elderly, etc.). This study aimed to establish a new measuring platform and investigate PM emissions under four different ventilation conditions inside a car cabin without exposing any person to harmful tobacco smoke.MethodsPM concentrations were measured during the smoking of 3R4F reference cigarettes in a Mitsubishi Space Runner (interior volume 3.709 m3). The cigarettes were smoked with a machine, eliminating exposure of the researchers. Cigarettes were extinguished 4.5 min after ignition, and PM measurements continued until 10 min after ignition.ResultsHigh mean PM concentrations were measured for cigarettes without ventilation after 4.5 min (PM10: 1150 µg/m3, PM2.5: 1132 µg/m3, PM1: 861.6 µg/m3) and after 10 min (PM10: 1608 µg/m3, PM2.5: 1583 µg/m3, PM1: 1133 µg/m3). 3R4F smoked under conditions with turned on ventilation resulted in reduction of PM compared to those smoked without ventilation after 4.5 min (PM10:-47.5 to -58.4%, PM2.5:-47.2 to -58%, PM1:-39.6 to -50.2%) and after 10 min (PM10:-70.8 to -74.4%, PM2.5:-70.6 to -74.3%, PM1:-64.0 to -68.0%). Cigarettes smoked without ventilation generated high PM peaks at 4.5 min (PM10: 2207 µg/m3, PM2.5: 2166 µg/m3, PM1: 1421 µg/m3) and at 10 min (PM10: 1989 µg/m3, PM2.5: 1959 µg/m3, PM1: 1375 µg/m3). PM peaks of cigarettes smoked under different ventilation modes varied at 4.5 min (PM10: 630-845 µg/m3, PM2.5: 625-836 µg/m3, PM1: 543 - 693 µg/m3) and 10 min (PM10: 124 - 130 µg/m3, PM2.5: 124 - 129 µg/m3, PM1: 118 - 124 µg/m3).ConclusionThe new measuring platform provides a safer way for researchers to investigate PM emissions of cigarettes. These data are comparable to published research and show that smoking in a parked vehicle with the windows closed generates harmful PM emissions even when the vehicle ventilation is in operation. Future studies should be carried out using the new measuring platform investigating PM exposure and PM distribution of in-vehicle smoking under a wide range of conditions.

The Effect of Sisha on Respiratory Health

Smoking sisha is considered a more socially acceptable activity in Middle East. The prevalence of sisha smokers varies among adolescent in the Middle East. Smoking sisha involves burning tobacco with a certain aroma, commonly referred to as molasses, and burning it using coal. Some people consider sisha a safer alternative to cigarettes, but some of evidence show the harmful and detrimental respiratory health effects associated with the use of sisha.

Electronic Cigarettes: Facts and Myths

E-cigarettes are devices designed to deliver nicotine to users without burning tobacco. These are being marketed globally as a healthier substitute to the conventional cigarettes and as smoking quitting aids. The use of these devices has increased recently in developed countries with approximately 1.3 million users reported in the United Kingdom in 2013. Perception of these products as a safe alternative, appealing advertisements, and lax regulatory policies have helped gain popularity among the public. Despite all these claims, a debate is on-going because of insufficient scientific data regarding safety and efficacy of e-cigarettes as well as awareness of the potential health hazards. To solve the dilemma, more scientific studies in this field are required. Prompt regulatory response with strict vigilance on marketing and advertising may be desirable in the interest of users and public at large.

A randomised, open-label, cross-over clinical study to evaluate the pharmacokinetic, pharmacodynamic and safety and tolerability profiles of tobacco-free oral nicotine pouches relative to cigarettes

RationaleTobacco harm reduction (THR) involves encouraging adult smokers who would otherwise continue to smoke to transition to less harmful forms of nicotine delivery. These products must offer adult smokers reduced exposure to chemicals associated with tobacco combustion, satisfactory blood plasma nicotine levels and serve as an acceptable alternative. The most recent THR innovation is tobacco-free oral nicotine pouches.ObjectivesThis study aimed to compare pharmacokinetic, pharmacodynamic and safety and tolerability profiles of two nicotine pouch variants (ZoneX #2 (5.8 mg nicotine/pouch); ZoneX #3 (10.1 mg nicotine/pouch)) with cigarette to assess the pouches’ THR potential.MethodsThis was a controlled use, randomised, open-label, cross-over clinical study with 24 healthy adult traditional tobacco users. Pharmacokinetic (plasma nicotine levels; up to 8 h post-use), pharmacodynamic (urge to smoke, product liking; up to 4 h post-use) and short-term safety and tolerability profiles were assessed.ResultsDistinct nicotine pouch pharmacokinetic profiles indicated nicotine absorption via the oral mucosa. Plasma nicotine levels were lower, and time to peak slower, for the nicotine pouches compared to cigarette (Cmax cigarette: 11.6 ng/ml vs. #2: 5.2 ng/ml, p < 0.0001; #3: 7.9 ng/ml, p < 0.0003) (Tmax cigarette: 8.6 min vs. #2: 26 min; #3: 22 min). All products effectively reduced subjects’ urge to smoke and presented favourable product liking scores; nicotine pouches were also well tolerated following short-term use (no serious adverse events).ConclusionsOverall, the assessed ZoneX nicotine pouches may offer an acceptable alternative for adult smokers to achieve satisfactory levels of nicotine delivery and, based on the pharmacokinetic parameters and under the study conditions, likely have a lower abuse liability and addictive potential for current adult smokers compared to continued cigarette smoking.Clinical trial identifier: NCT04891406 (clinicaltrials.gov).

NNK from tobacco smoking enhances pancreatic cancer cell stemness and chemoresistance by creating a β2AR-Akt feedback loop that activates autophagy.

Low responsiveness to chemotherapy is an important cause of poor prognosis in pancreatic cancer. Smoking is a high‐risk factor for pancreatic cancer and cancer resistance to gemcitabine; however, the underlying mechanisms remain unclear. 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK) is the main metabolite of tobacco burning and has been shown to be associated with cancer development and chemoresistance. However, in pancreatic cancer, its mechanism remains poorly understood. In this study, we found that NNK promoted stemness and gemcitabine resistance in pancreatic cancer cell lines. Moreover, NNK increased autophagy and elevated the expression levels of the autophagy‐related markers autophagy‐related gene 5 (ATG5), autophagy‐related gene 7 (ATG7), and Beclin1. Furthermore, the results showed that NNK‐promoted stemness and gemcitabine resistance was partially dependent on the role of NNK in cell autophagy, which is mediated by the β2‐adrenergic receptor (β2AR)‐Akt axis. Finally, we proved that NNK intervention could not only activate β2AR, but also increase its expression, making β2AR and Akt form a feedback loop. Overall, these findings show that the NNK‐induced β2AR‐Akt feedback loop promotes stemness and gemcitabine resistance in pancreatic cancer cells.

Novel Method for Investigating the Correlation of Sensory Contribution and Cigarette Mainstream Smoke

The quality of tobacco products is directly related to the sensory contributions of related compounds in the mainstream smoke during tobacco combustion. Currently, there is no clear and perfect quantitative calculation method for tobacco quality assessment and prediction. In this paper, samples of Qujing K326 and Dali Hongda were used as raw materials to simulate an actual tobacco smoke release environment. The mainstream smoke products were captured, separated and analyzed by gas chromatography-mass spectrometry (GC-MS). The relative percentage of each compound in mainstream tobacco smoke was obtained. Therefore, through relevant quantitative calculation, this study quantified the sensory contributions of compounds through flue gas separation. Finally, the evaluation quality of tobacco samples could be predicted accurately by neural network model. The methods used in this paper can provide important technical support for tobacco quality control.

A review of the characteristic properties of selected tobacco chemicals and their associated etiological risks.

Despite the quantum of research findings on tobacco epidemic, a review on the formation characteristics of nicotine, aldehydes and phenols, and their associated etiological risks is still limited in literature. Accordingly, knowledge on the chemical properties and free radical formation during tobacco burning is an important subject towards unravelling the relationship between smoking behaviour and disease. This review investigates how scientific efforts have been advanced towards understanding the release of molecular products from the thermal degradation of tobacco, and harm reduction strategies among cigarette smokers in general. The mechanistic characteristics of nicotine and selected aldehydes are critically examined in this review. For the purpose of this work, articles published during the period 2004-2021 and archived in PubMed, Google Scholar, Medley, Cochrane, and Web of Science were used. The articles were selected based on the health impacts of cigarette smoking, tobacco burning kinetics, tobacco cessation and tobacco as a precursor for emerging diseases such as Covid-19. The toxicity of cigarette smoke is directly correlated with its chemical composition derived from the pyrolysis of tobacco stem and leaves. Most of the harmful toxic substances are generated by pyrolysis during smoking and depends on pyrolysis conditions. Detailed studies have been conducted on the kinetics of nicotine by use of robust theoretical models in order to determine the rate constants of reactions in nicotine and those of nicotine dissociation via C-C and C-N scission, yielding pyridinyl and methyl radicals, respectively. Research has suggested that acetaldehyde enhances the effect of nicotine, which in turn reinforces addiction characteristics whereas acrolein and crotonaldehyde are ciliatoxic, and can inhibit lung clearance. On the other hand, phenol affects liver enzymes, lungs, kidneys, and the cardiovascular system while m-cresol attacks the nervous system. The characteristics of chemical release during tobacco burning are very important in the tobacco industry and the cigarette smoking community. Understanding individual chemical formation from cigarette smoking will provide the necessary information needed to formulate sound tobacco reform policies from a chemical standpoint. Nonetheless, intense research is needed in this field in order to prescribe possible measures to deter cigarette smoking addiction and ameliorate the grave miseries bedevilling the tobacco smoking community.

Using Wool Keratin Derived Metallo-Nanozymes as a Robust Antioxidant Catalyst to Scavenge Reactive Oxygen Species Generated by Smoking.

Self-assembled nanostructures based on biomolecules (e.g., proteins and amino acids) and metal ions have promising applications in mimicking the nanostructure, properties, and functions of natural enzymes. Herein, a metal ion-mediated self-assembly method for constructing catalytically active Cu-wool-keratin (CuWK) two-dimensional nanozymes is presented. Specifically, by introducing copper ions as abiological cofactors, WK can serve as a protein scaffold to design and create Cu catalytic sites. The optimized hybrids with Cu-WK coordination framework exhibit significant superoxide dismutases-like activity, catalase-like activity, and hydroxyl radical scavenging ability. These combined antioxidant activities make CuWK a robust nanozyme to effectively remove various reactive oxygen species (ROS). In this work, the as-prepared CuWK as a new additive can be integrated into a cigarette filter system to effectively remove the produced ROS from the burning of tobacco. More importantly, the CuWK nanozymes as a critical element can be further utilized to construct a recycling cigarette holder. Therefore, the present work shows that nanozymes with advanced catalytic capabilities can be constructed by self-assembly of metal ions and proteins, thus facilitating the rational design and discovery of this kind of artificial metalloenzymes.

Characteristics, Source Contributions, and Source-Specific Health Risks of PM2.5-Bound Polycyclic Aromatic Hydrocarbons for Senior Citizens during the Heating Season in Tianjin, China.

Polycyclic aromatic hydrocarbons (PAHs) have carcinogenic impacts on human health. However, limited studies are available on the characteristics, sources, and source-specific health risks of PM2.5-bound PAHs based on personal exposure data, and comparisons of the contributions of indoor and outdoor sources are also lacking. We recruited 101 senior citizens in the winter of 2011 for personal PM2.5 sample collection. Fourteen PAHs were analyzed, potential sources were apportioned using positive matrix factorization (PMF), and inhalational carcinogenic risks of each source were estimated. Six emission sources were identified, including coal combustion, gasoline emission, diesel emission, biomass burning, cooking, and environmental tobacco smoking (ETS). The contribution to carcinogenic risk of each source occurred in the following sequence: biomass burning > diesel emission > gasoline emission > ETS > coal combustion > cooking. Moreover, the contributions of biomass burning, diesel emission, ETS, and indoor sources (sum of cooking and ETS) to PAH-induced carcinogenic risk were higher than those to the PAH mass concentration, suggesting severe carcinogenic risk per unit contribution. This study revealed the contribution of indoor and outdoor sources to mass concentration and carcinogenic risk of PM2.5-bound PAHs, which could act as a guide to mitigate the exposure level and risk of PM2.5-bound PAHs.

Abstract WP226: Secondhand Smoking And Odds Of Stroke Among Non-smoking Indigenous Africans From Ghana And Nigeria: A Matched Case-control Study

Introduction: Second-hand smoking (SHS) is an emerging phenomenon in cardiovascular disease (CVD) epidemiology, but whether SHS is associated with stroke is not clearly understood. We assessed the association between SHS and stroke risk in a cohort of West Africans in the Stroke Investigative Research and Educational Network (SIREN) study. Hypothesis: SHS is not associated with stroke among indigenous West Africans from Ghana and Nigeria. Methods: 3131 stroke cases who had never smoked matched (for age and sex) with 3131 healthy smoke-free controls were identified in the multi-centre SIREN study in Ghana and Nigeria. Information on SHS was obtained through the collection of data on regular exposure to exhaled smoke or burning tobacco in an indoor environment. We assessed the relationship between SHS and stroke by estimating the odds ratio (OR) and 95% confidence interval (CI) using conditional logistic regression, adjusting for relevant covariates at P &lt;0.05 in a two-sided test. Results: The mean age of the participants was 58.8±14.1years (males, 48.0%). History of exposure to SHS was present in 20.2% of the overall sample. The multivariable-adjusted OR for the association between SHS and all stroke events was 1.12 (0.93, 1.34), P = 0.210. When the association was stratified by stroke type, the multivariable-adjusted OR were 1.42 (1.03, 1.98) P = 0.033 for haemorrhagic stroke and 1.01 (0.80, 1.26) P = 0.935 for ischaemic stroke. Conclusion(s): SHS was independently associated with higher odds of haemorrhagic stroke, but not ischaemic stroke in this cohort of indigenous West Africans. Intervention(s) to reduce SHS might help lower the burden of stroke in this population, pending longitudinal studies to evaluate the causal effect of SHS on stroke.

Heavy Metals in Waterpipe Smoke and the Related Health Risks - A Review

Excessive intake of heavy metals has harmful effects on health and waterpipe smoking could be one of the intake routes. Regarding the growing trend of waterpipe smoking in the world, in this study the heavy metal exposure related to waterpipe smoke and the health risks were surveyed in the published literature. Science Direct, Google Scholar and PubMed databases were searched using the keywords of heavy metals, hookah, shisheh and waterpipe. The results showed high concentrations of heavy metals in waterpipe smoke, tobacco, and charcoal. Also, high levels of heavy metals are reported in blood and toenails of the waterpipe cafes’ employees and for the smokers. The expected cancer risk for Cd, Cr, Ni, and as was higher than 1×10-6, and non-cancer risk for Cr was greater than 1. Burning of tobacco and charcoal is source of heavy metals in waterpipe smoke

Smoking and Endothelial Dysfunction: An Integrated - Medical and Molecular Review

Cigarette smoke is a complex mixture of about 7,000 different toxic substances, many of which are generated during the burning of the tobacco leaf, some in the gas phase and others in the particulate matter. The gas phase represents approximately 60% of the smoke from the burning of tobacco, 99% of this phase is composed of nitrogen, oxygen, carbon dioxide, carbon monoxide, hydrogen, argon, and methane. Atherosclerosis associated with smoking is not necessarily an effect of nicotine, but probably the joint action of the various constituents of cigarette smoke. ROS from the gas phase of tobacco contributes to the onset and progression of atherosclerosis. Bupropion and varenicline are used for smoking cessation despite the side effects; however, we are still far from effective treatment to assist the definitive discontinuation of the habit of smoking. This review discusses the main mechanisms associated with vascular damage from the smoking.