Adverse Effects Of Cigarette Smoking Research Articles

Why Female Smokers Have Poorer Long-Term Health Outcomes than Male Smokers: The Role of Cigarette Smoking During Pregnancy.

Objectives: Women's health status is better than men but the opposite is true for female smokers who usually have poorer long-health outcomes than male smokers. The objectives of this study were to thoroughly reviewed and analyzed relevant literature and to propose a hypothesis that may explain this paradox phenomenon. Methods: We conducted a search of literature from three English databases (EMBASE, MEDLINE, and Google Scholar) from inception to 13 November 2023. A combination of key words and/or subject headings in English was applied, including relevant terms for cigarette smoking, sex/gender, pregnancy, and health indicators. We then performed analysis of the searched literature. Results: Based on this review/analysis of literature, we proposed a hypothesis that may explain this paradox phenomenon: female smokers have worse long-term health outcomes than male smokers because some of them smoke during pregnancy, and the adverse effects of cigarette smoking during pregnancy is much stronger than cigarette smoking during non-pregnancy periods. Conclusion: Approval of our pregnancy-amplification theory could provide additional evidence on the adverse effect on women's long-term health outcomes for cigarette smoking during pregnancy.

Repeated intratracheal instillation of whole-cigarette smoke condensate to assess lung damage in a rat model.

Cigarette smoke induces an inflammatory response in the lungs by recruiting inflammatory cells, leading to lung diseases such as lung cancer, chronic obstructive pulmonary disease, and pulmonary fibrosis. Existing inhalation exposure methods for assessing the adverse effects of cigarette smoke require expensive equipment and are labor-intensive. Therefore, we attempted to develop a novel method to assess these adverse effects using intratracheal instillation (ITI) of whole cigarette smoke condensate (WCSC). The WCSC (0, 5, 10, or 20 mg/mL) was administered by ITI once daily for 6 or 12 days using an automatic video instillator. Repeated WCSC ITI increased the lung weight, and monocyte chemoattractant protein-1 (MCP-1), neutrophil, and lymphocyte levels within bronchoalveolar lavage fluid compared to the control. In the histopathological analysis of the lung tissue, a mild inflammatory response was observed in the 6 and 12 days 20 mg/mL WCSC exposure groups. The genome-wide RNA-seq expression patterns revealed that inflammatory and immune response-related genes, such as the chemokine signaling pathway, Th1/Th2 cell differentiation, and cytokine-cytokine receptor interaction, were employed following WCSC exposure. In addition, MCP-1 was time-dependent and increased in the 10 mg/mL exposure group compared to the control group. These results suggested that the WCSC might induce the potential pulmonary inflammatory response. Furthermore, we proposed that ITI may be a rapid and effective method of evaluating the adverse effects of WCSC within a short exposure period (less than 2 weeks), and it can be used to evaluate cigarette inhalation toxicity studies as an alternative method.

The effect of hydroalcoholic extract of Cichorium intybus leaf on aryl hydrocarbon receptor expression in the testis of Wistar rats exposed to cigarette smoke.

Cigarette smoke (CS) contains compounds such as reactive oxygen species (ROS). Oxidative stress caused by excessive ROS eventually leads to germ cell apoptosis and male infertility. The leaves of Cichorium intybus (chicory) are rich in natural antioxidants, but their protective effects on the adverse effects of CS on testicular tissue have not been studied. 24 Wistar rats were classified into four groups: control, extract: treatment with chicory extract (200 mg/kg body weight/day) for 13 weeks, smoke: exposed to CS for 13 weeks, and smoke + extract: exposed to CS and treated with the C. intybus extract. Histological and biochemical analyses and apoptosis assay were done, and Ahr, and Cyp1a1 expression was determined. Treatment with C. intybus compensated for the reduction of Sertoli cells, spermatogonia, spermatocytes, and spermatids caused by CS. Chicory extract reduced free radicals and improved antioxidant status. The lowest and highest percentage of apoptotic cells was observed in the extract and smoke groups, respectively, while simultaneous treatment with C. intybus extract led to a significant reduction of apoptotic cells. The mean Ahr levels in the control, extract, smoke and smoke + extract groups were 1.00±0.57, 1.93±0.25, 5.98±0.42, and 0.62±0.22, respectively (p˂0.05). The mean levels of Cyp1a1 expression in the control, extract, smoke and smoke + extract groups were 1.00±0.31, 2.28±0.65, 5.55±0.40, and 0.21±0.23 (p˂0.05). The C. intybus extract probably affected Cyp1a1 expression by downregulation of Ahr. These led to a decrease in free radicals and apoptosis, and an improvement in antioxidant status.

Evaluation of Blood Pressure, Liver Function, and Hemoglobin Concentration Alterations in Cigarette Smokers on the West Coast of Libya

Background: Cigarette smoking is one of the 10 greatest contributors to global death and disease. Cigarette smoking is the most common type of tobacco use. In average, to date 47.5% of men and 10.3% of women are current smokers. Tobacco continues to be the second major cause of death in the world. It consists of many chemicals, including cytotoxic, carcinogenic and free radicals, therefore it affects many organs if not all. Objective: The aim of this study is to assess the extent of adverse effect of cigarette smoking on blood pressure, liver function, and hemoglobin concentration in male population on the West Coast of Libya. Methods: This study was conducted on (200) healthy male subjects, their ages ranged from 15 to 85 years. They were divided into four groups; 50 non-smokers as control group (age between 15-35 years), 50 smokers (age between 15-35 years), 50 non-smokers as control group (age between 36-84 years) and 50 smokers (age between 36-84 years). The blood was collected in EDTA tubes to test the Complete blood count (CBC) and in plain tubes for biochemical assay (activities of liver enzymes). The Blood pressure of subjects was measured directly after sample collection. Result: The blood pressure among the group of age 36-84y was significantly higher (P < 0.05) when compared between the smokers and the nonsmokers group, while among the group of age 15-35 was not significant. The results of liver enzymes activities among the group of age 36-84y showed that ALT and ALP were significantly high (P <0.05) in the smoker group when compared with the nonsmoker group, while serum AST was not significant (P>0.05). However, among the group of age between 15-35 years, the results showed that statistically significant differences (P<0.05) were observed in ALT and AST activities for the smoker group when compared with the nonsmoker group. Regarding RBCs count and hemoglobin concentration among both of groups (age between 15-35 & 36-84 years), the results showed that a significant difference in mean RBCs count and hemoglobin concentration were noted between the smokers and the nonsmokers. Conclusion: It can be concluded that exposure to cigarette smoking leads to an increase the blood pressure. Cigarette smoking can lead to an increase in liver enzymes activities, RBCs count and Hb concentration.

Long-Term Adverse Effects of Cigarette Smoking on the Incidence Risk of Metabolic Syndrome With a Dose-Response Relationship: Longitudinal Findings of the Korean Genome and Epidemiology Study Over 12 Years

ObjectiveTo investigate the association between the intensity and cumulative dose of cigarette smoking and incidence risk of metabolic syndrome (MetS) in a longitudinal prospective study over 12 years of follow-up. MethodsThis study included 3151 men aged 40 to 69 years from the Korean Genome and Epidemiology Study. MetS was defined as proposed by the Joint Interim Statement of the Circulation 2009 report. The hazard ratios (HRs) and 95% confidence intervals (95% CIs) for incidence risk of MetS were calculated from 2 separate perspectives: (1) number of cigarettes smoked per day (intensity) and (2) total number of cigarettes smoked over a person’s lifetime (cumulative dose) using multiple logistic regression analyses. ResultsIn comparison with never smokers, the HRs (95% CIs) were 0.97 (0.78-1.21) for former smokers and 1.50 (1.07-2.01) with 0 to 9 cigarettes per day, 1.66 (1.34-2.06) with 10 to 19 cigarettes per day, and 1.75 (1.34-2.29) with ≥20 cigarettes per day for current smokers after adjusting for confounding variables. Similar positive dose-response relationships were also observed when the cumulative dose of cigarette smoking was categorized into former and current smokers, with subcategories of <20 and >20 pack-years (PYs). The HRs (95% CIs) were 0.99 (0.77-1.23) for <20 PYs and 0.99 (0.77-1.28) for ≥20 PYs for former smokers and 1.63 (1.32-2.02) for <20 PYs and 1.67 (1.30-2.14) for ≥20 PYs for current smokers after adjusting for the same covariables. ConclusionCigarette smoking intensity and cumulative dose were both found to be positively associated with the incidence risk of MetS in men.

Adverse effects of cigarette smoking on exhaled breath carbon monoxide, blood carboxyhemoglobin, and hematological parameters amongst Sri Lankan adult tobacco smokers: A descriptive study

Adverse effects of cigarette smoking on exhaled breath carbon monoxide, blood carboxyhemoglobin, and hematological parameters amongst Sri Lankan adult tobacco smokers: A descriptive study

Smoking a Dangerous Addiction: A Systematic Review on an Underrated Risk Factor for Oral Diseases.

Despite growing knowledge of the adverse effects of cigarette smoking on general health, smoking is one of the most widely prevalent addictions around the world. Globally, about 1.1 billion smokers and over 8 million people die each year because of cigarette smoking. Smoking acts as a source for a variety of oral and systemic diseases. Various periodontal issues such as increased pocket depth, loss of alveolar bone, tooth mobility, oral lesions, ulcerations, halitosis, and stained teeth are more common among smokers. This systematic review was conducted according to the guidelines from PRISMA, and research articles were retrieved from the Web database sources on 31 May 2021. The quality of research articles was ensured by the type of evidence from combined schema incorporating as schema-13 evidence type description, Cochrane health promotion and public health field (CHPPHF), and the health gains notation framework-14 screening question for quality assessment of qualitative and quantitative studies. Smokers have been found to have bleeding on probing, periodontal pockets, and clinical attachment loss compared to nonsmokers. Oral and respiratory cancers are among the most lethal known diseases caused by cigarette smoking and other commonly occurring sequelae such as stained teeth, periodontal diseases, etc.

THE EFFICACY OF FLAVONOID IN RED MULBERRY ON REDUCING FREE RADICALS AND ALVEOLAR MACROPHAGES DUE TO CIGARETTE SMOKE EXPOSURE IN WISTAR RATS

Background. Free radicals in cigarette smoke will hurt health when they enter to the respiratory tract. An excessive increase of free radicals in the body will cause oxidative stress. Free radicals are generated physiologically by the body's metabolism and can neutralize antioxidants in the body. An imbalance number of free radicals will result in cell damage and death. It has characterized by an increase in malondialdehyde levels in the blood and alveolar macrophages in the lung tissue. Giving red mulberry (Morus rubra) as an intake of antioxidants from outside the body can prevent adverse effects of cigarette smoke. Objective. This study analyses flavonoids' impact on red mulberry in reducing free radicals due to exposure to cigarette smoke by lowering levels of malondialdehyde and alveolar macrophages. Method. This research is experimental with a post-test control group design using male Wistar rats (Rattus novergicus) as experimental animals. Treatment of experimental animals through red mulberry per oral and exposure to cigarette smoke had conducted for 30 days. The parameters used were levels of malondialdehyde and alveolar macrophages in the lung tissue. Results. The research showed an increase in free radicals in the group exposed to cigarette smoke. Increasing intake of red mulberry can further reduce malondialdehyde levels and the number of alveolar macrophages (p&lt;0.05). Conclusions. The antioxidants in red mulberry can reduce malondialdehyde levels in the blood and the number of alveolar macrophages in lung tissue due to exposure to cigarette smoke.

Mitochondrial Network and Biogenesis in Response to Short and Long-Term Exposure of Human BEAS-2B Cells to Aerosol Extracts from the Tobacco Heating System 2.2.

Adverse effects of cigarette smoke on health are widely known. Heating rather than combusting tobacco is one of strategies to reduce the formation of toxicants. The sensitive nature of mitochondrial dynamics makes the mitochondria an early indicator of cellular stress. For this reason, we studied the morphology and dynamics of the mitochondrial network in human bronchial epithelial cells (BEAS-2B) exposed to total particulate matter (TPM) generated from 3R4F reference cigarette smoke and from aerosol from a new candidate modified risk tobacco product, the Tobacco Heating System (THS 2.2). Cells were subjected to short (1 week) and chronic (12 weeks) exposure to a low (7.5 µg/mL) concentration of 3R4F TPM and low (7.5 µg/mL), medium (37.5 µg/mL), and high (150 µg/mL) concentrations of TPM from THS 2.2. Confocal microscopy was applied to assess cellular and mitochondrial morphology. Cytosolic Ca2+ levels, mitochondrial membrane potential and mitochondrial mass were measured with appropriate fluorescent probes on laser scanning cytometer. The levels of proteins regulating mitochondrial dynamics and biogenesis were determined by Western blot. In BEAS-2B cells exposed for one week to the low concentration of 3R4F TPM and the high concentration of THS 2.2 TPM we observed clear changes in cell morphology, mitochondrial network fragmentation, altered levels of mitochondrial fusion and fission proteins and decreased biogenesis markers. Also cellular proliferation was slowed down. Upon chronic exposure (12 weeks) many parameters were affected in the opposite way comparing to short exposure. We observed strong increase of NRF2 protein level, reorganization of mitochondrial network and activation of the mitochondrial biogenesis process. Comparison of the effects of TPMs from 3R4F and from THS 2.2 revealed, that similar extent of alterations in mitochondrial dynamics and biogenesis is observed at 7.5 µg/mL of 3R4F TPM and 150 µg/mL of THS 2.2 TPM. 7 days exposure to the investigated components of cigarette smoke evoke mitochondrial stress, while upon chronic, 12 weeks exposure the hallmarks of cellular adaptation to the stressor were visible. The results also suggest that mitochondrial stress signaling is involved in the process of cellular adaptation under conditions of chronic stress caused by 3R4F and high concentration of THS 2.2.

Cigarette Smoke Reduces the Efficacy of Cisplatin in Head and Neck Cancer Cells - Role of ABCG2.

We evaluated the influence of smoking on head and neck squamous cell carcinomas (HNSCC), which are in their majority tobacco-driven. Tobacco smoke is expected to influence the expression of ABCG2-transporters involved in multidrug resistance. The aim of the study was to evaluate the effect of cigarette smoke condensate (CSC) on ABCG2 expression on HNSCC cells, to demonstrate the adverse effects of cigarette smoke during anticancer treatment in vitro and to assess the prevalence of ABCG2 expression in HNSCC. HNSCC cell lines were treated with CSC and basal and induced ABCG2 expression was examined. The impact of CSC on cellular viability/proliferation during cytotoxic drug treatment was also evaluated. ABCG2 expression levels in HNSCC were correlated with the smoking history of patients. HNSCC cells showed low basal ABCG2 expression. CSC treatment resulted in a threefold increase in the expression of ABCG2 and in resistance to cisplatin. Tumor samples of never smokers showed significantly higher ABCG2 expression compared to ever smokers. ABCG2 expression correlated with pack years of cigarette consumption. Tobacco consumption is linked to an inducible and increased ABCG2 protein expression and has an impact on drug resistance.

Perception of knowledge toward surgery-Related adverse effects of cigarette smoking among Al-Ahsa population, Saudi Arabia

Perception of knowledge toward surgery-Related adverse effects of cigarette smoking among Al-Ahsa population, Saudi Arabia

Vaping, Smoking, and the Physical Fitness of Active Young Men

Adverse effects of cigarette smoking on physical performance are well studied. Because of the recent rise in popularity of vaping, it is important to evaluate its effect on fitness both independently and in conjunction with traditional cigarette use. This was a secondary analysis performed in 2018 on data collected from U.S. Army Soldiers during 2016. All metrics were self-reported via an electronic questionnaire. Personal characteristics of current ENDS users, smokers, and dual users were compared with a reference group that reported no history of use. Adjusting for age and physical training habits, an ANCOVA was used to compare Army physical fitness test results. A Fisher's exact test determined specific mean differences between groups. This study population consisted of 2,854 men aged 24.6 years on average. Differences in physical training and fitness were shown between the groups. Never users averaged the most total physical training, followed by ENDS users, smokers, and then dual users. Compared with never users on the fitness tests, ENDS users had an adjusted mean difference of +27 seconds on the 2-mile run, -4.56 push-ups, and -2.01 sit-ups; smokers averaged +8 seconds, -2.15 push-ups, and -1.44 sit-ups; and dual users averaged +32 seconds, -5.17 push-ups, and -3.88 sit-ups. Dual users had significantly (p<0.05) lower scores than current smokers and never users on all 3 fitness events. This study suggests that individuals who use e-cigarettes and tobacco cigarettes average a lower level of fitness than individuals who abstain.

Effects of cigarette smoke components on myocardial differentiation of mouse embryonic stem cells.

The heart is the first organ formed in the developing fetus, and abnormal development of the heart is a major cause of fetal death. The adverse effects of cigarette smoke on the heart have been well established, but it is not well understood how cigarette smoke components regulate signaling molecules and cardiac specific functions during the early differentiation stage of the embryonic heart. In this study, we identified changes in the size of mouse embryoid bodies (mEBs) in response to treatment with cigarette smoke extract (CSE) via regulation of HDAC2, p53, p21, and cyclin D1 protein expression, which are cardiac differentiation and cell-cycle markers, respectively. In addition, exposure of mouse embryonic stem cells (mESCs) to cigarette smoke components inhibited myocardial differentiation and development through the expression of HDAC1, HDAC2, GATA4, NKX2-5, TBX5, HAND1, and Troponin I. Long-term exposure studies showed that CSE and nicotine may delay the development of mouse cardiomyocytes from mESCs and inhibit the contractibility, which is a fundamental function of the heart. Taken together, these findings suggest that cigarette smoke components, including nicotine, may affect abnormal myocardial differentiation and development.

Smoking in pregnancy: pathophysiology of harm and current evidence for monitoring and cessation

Key content Smoking in pregnancy is a risk factor for miscarriage, stillbirth, placental abruption, preterm birth, low birthweight and neonatal morbidity and mortality. The adverse effects of cigarette smoke are primarily driven by carbon monoxide, tar and nicotine. Psychosocial interventions are effective in helping women to quit smoking during pregnancy. There is weak evidence that nicotine replacement therapy (NRT) with behavioural support can improve cessation rates in pregnancy. Electronic cigarettes are more popular among smokers, but evidence of their safety and effectiveness in pregnancy are lacking. Learning objectives To understand the pathophysiology of harm from cigarette smoking. To describe the role of exhaled carbon monoxide testing among pregnant women. To review the evidence on the safety and use of NRT and electronic cigarettes as methods of cessation.

6. SMOKING AND SCHIZOPHRENIA: STILL A BURNING PROBLEM

The prevalence of tobacco use in schizophrenia is 3x that of the general population and the disparity is growing. Persons with schizophrenia die on average 10-15 years earlier than those in the general population and smoking is the largest preventable cause of this premature mortality. Understanding the association between smoking and schizophrenia is a high priority as is the development of more effective smoking cessation strategies for this population. In this symposium, we examine epidemiological aspects of smoking and schizophrenia. We also examine novel smoking cessation interventions that have been recently developed for persons with schizophrenia. While we typically consider the effects of cigarette smoking in persons with schizophrenia, there is new evidence that smoking may play a causal role in the development of psychosis. In the first presentation, Dr. Robin Murray presents data showing that daily tobacco use is associated with an increased risk of psychotic illness and also that smoking is associated with an earlier age at onset of psychotic illness. Data were drawn from a systematic review of the literature including studies with an overall sample of almost 300,000 persons and from two case control studies of persons with a first episode of psychosis. Tobacco smoking was significantly more common in the patient groups even after adjusting for cannabis use. Plausible biological explanations add weight to the causal hypothesis. In the second presentation, Dr. Faith Dickerson turns to the adverse effects of cigarette smoking in schizophrenia. Data are drawn from two cohorts looking at the cross sectional association between tobacco use and cognitive functioning and suicide attempts; a third and longitudinal cohort examined the association between smoking at baseline and subsequent natural cause morality. Smoking was significantly and inversely associated with total cognitive score and also with a history of suicide attempts. In the third cohort, smoking at baseline was the strongest predictor of subsequent natural cause mortality in a multivariate model including other demographic and clinical variables. These data contradict the notion that smoking is “self medication” for persons with schizophrenia. In the third presentation, Dr. Mary Brunette describes the results of a randomized trial with schizophrenia smokers comparing two brief web-based motivational interventions for smoking cessation adapted for people with cognitive impairments. Nearly 40% of the sample reported quit attempts at the 6-month follow-up though only 4% had verified abstinence. Brief web-based treatments can motivate schizophrenia smokers to use cessation treatments. In the final presentation, Dr. Gail Daumit describes an ongoing trial testing an 18-month intervention delivered in community mental health centers to smokers with serious mental illness who are interested in quitting. The intervention involves group and individual smoking cessation and weight management counseling, smoking cessation pharmacotherapy, and exercise. The intervention aims to promote smoking abstinence, improved physical activity, and weight control. Baseline results will be presented.The discussion will be led by Dr. Eden Evins, a leading expert in smoking cessation treatments for persons with schizophrenia.

Effects of Smoking on the Prevalence of Allergic Disorders in Russian Adolescents: A Retrospective Cross-sectional Study.

IntroductionSmoking is one of the leading causes of death. Smoking also decreases lung efficiency and impairs lung function in children of all ages. Second-hand tobacco smoking increases both the frequency and severity of childhood asthma. However, the role of active tobacco smoking in the manifestation of asthma remains inconclusive. The aim of this article was to describe the current understanding of the prevalence and adverse effects of cigarette smoking and to determine whether there is an association between smoking and the manifestation and progression of asthma among adolescents and high school students in Russia.ObjectivesThis study aimed to determine the true prevalence of bronchial asthma (BA), allergic rhinitis (AR), and atopic dermatitis (AD) in the population of adolescents in the Russian Federation. In the GA2LEN (Global Allergy and Asthma European Network) study, we analyzed participant responses to confirm a connection between smoking and asthma exacerbation or development. This study examined the association between parental smoking and childhood atopic disorders. We sought to determine the effects of exposure to environmental tobacco smoke and childhood cigarette smoking on asthma symptoms among high school and college students in Moscow, Russia. We analyzed the reactions to the present tobacco control policy and evaluated the significance of the success of the policy. A number of methods were used, including questionnaires, surveys, and statistical analysis software.ResultsOur research indicates a moderate decrease in smoking prevalence among Russian teenagers. From the data and results of our study, 25.3% of the respondents said that they have ever smoked for as long as a year. Among the participants who had ever smoked, most of them started smoking at the age of 16 years while the state-reported average age for a new smoker is 11.4. Fifty percent of the respondents who had shortness of breath had been woken by an attack once a week in the last three months. Only 21.1% of the people with asthma were taking medicines for it. According to our calculations, there is no significant association between smoking status and the prevalence of asthma, hay fever, and sinusitis. More respondents (34.2%) had fathers who regularly smoked during their childhood than mothers who regularly smoked during their childhood or before the children were born (7.9%). There is a statistically significant association between a mother smoking during childhood or before the birth of a child and that child being hospitalized before the age of two years for lung disease.ConclusionThe fact that the smoking rates among study participants are relatively low is quite encouraging and anti-smoking campaigns should be intensified to drive the rates lower. The data analyzed do not provide sufficient evidence to show that there is any causative association between smoking status and the development of asthma, hay fever, or sinusitis. Since there is no clear association between smoking status and the development of asthma, hay fever, or allergic sinusitis, it is imperative to say that smoking cessation will have very little effect on allergy prevalence as per the data analyzed. From the conducted analysis, it is evident that there is a clear link between second-hand smoke and asthma in children. According to our results, children whose mothers smoked are especially vulnerable to asthma and other respiratory disorders.

Comparison of monoamine oxidase inhibition by cigarettes and modified risk tobacco products.

The adverse effects of cigarette smoking are well documented, and the two main strategies for reducing smoking prevalence are prevention of smoking initiation and promotion of smoking cessation. More recently, a third and complementary avenue, tobacco harm reduction has emerged, which is aimed to reduce the burden of smoking-related diseases. This has been enabled by the development of novel products such as electronic cigarettes (e-cigarettes) and heated tobacco products, designed to deliver nicotine with significantly reduced levels of the toxicants that are emitted by cigarettes. Several potential modified risk tobacco products (pMRTP) have been reported to emit significantly less toxicants than cigarettes and significantly reduce toxicant exposure in smokers who switch completely to such products. These are two prerequisites for pMRTPs to reduce harm and the risk of smoking-related disease. However, concerns remain regarding the addictive nature of these products. Smoking addiction is a complex phenomenon involving multiple pharmacological and non-pharmacological factors. Although the main pharmacological substance associated with smoking addiction is nicotine, accumulating evidence suggests that nicotine mostly acts as a primary reinforcer and that other factors are involved in establishing smoking addiction. Inhibition of monoamine oxidases (MAO)-mammalian flavoenzymes with a central role in neurotransmitter metabolism-has also been suggested to be involved in this process. Therefore, we aimed to comparatively investigate the ability of several types of pMRTPs and cigarette smoke (3R4F) to inhibit MAO activity. The results showed that the heated tobacco product Tobacco Heating System (THS) 2.2 and the MESH 1.1 e-cigarette possessed no MAO inhibitory activity while 3R4F significantly inhibits the levels of MAO activity (3R4F MAO-A and B; > 2 μM nicotine). Snus products have similar inhibition profiles as 3R4F but for larger nicotine concentrations (snus MAO-A; ∼68-fold, snus MAO-B; ∼23-fold higher compared to 3R4F). These observations were confirmed by analytical datasets of potential MAO inhibitors emitted by these products. In conclusion, we have demonstrated that specific pMRTPs, namely THS 2.2 and MESH 1.1, have a significantly lower MAO-inhibitory activity than 3R4F. These findings provide a basis for further investigation of the role of MAO inhibitors in cigarette addiction as well as the implications of the findings for abuse liability of pMRTPs in comparison with cigarettes.

Cigarette Smoke and E-Cigarette Vapor Dysregulate Osteoblast Interaction With Titanium Dental Implant Surface.

The purpose of this study was to determine the possible deleterious effects of e-cigarette vapor on osteoblast interaction with dental implant material. Osteoblasts were cultured onto Ti6Al4V titanium implant disks and were then exposed or not to whole cigarette smoke (CS), as well as to nicotine-rich (NR) or nicotine-free (NF) e-vapor for 15 or 30 minutes once a day for 1, 2, or 3 days, after which time various analyses were performed. Osteoblast growth on the titanium implant disks was found to be significantly ( P < .001) reduced following exposure to CS and to the NR and NF e-vapors. Osteoblast attachment to the dental implant material was also dysregulated by CS and the NR and NF e-vapors through a decreased production of adhesion proteins such as F-actin. The effects of CS and e-cigarette vapor on osteoblast growth and attachment were confirmed by reduced alkaline phosphatase (ALP) activity and tissue mineralization. The adverse effects of CS and the NR and NF e-vapors on osteoblast interaction with dental implant material also involved the caspase-3 pathway, as the caspase-3 protein level increased following exposure of the osteoblasts to CS or e-vapor. It should be noted that the adverse effects of CS on osteoblast growth, attachment, ALP, and mineralized degradation were greater than those of the NR and NF e-vapors, although the latter did downregulate osteoblast interaction with the dental implant material. Overall results suggest the need to consider e-cigarettes as a possible contributor to dental implant failure and/or complications.

Friday, September 28, 2018 4:05 PM–5:05 PM abstracts: basic science of spinal fusion: 234. Phytochemicals combat the detrimental effects of cigarette smoke on osteogenic differentiation

BACKGROUND CONTEXT Cigarette smoking has been shown to inhibit bone healing and increase the risk of pseudarthrosis after spinal fusion. We previously reported that activation of the Aryl Hydrocarbon Receptor (Ahr) by dioxin, a prototype activator of the Ahr, inhibits bone regeneration and spine fusion in rat model. We also reported that the dioxin-mediated inhibition of osteogenic differentiation is mitigated by co-treatment with Ahr antagonists in vitro. PURPOSE Since dozens of dioxin-like Ahr ligands are present in cigarette smoke, we are investigating the downstream mechanisms of cigarette smoke action on osteogenic differentiation to identify potential therapeutic options to mitigate the effects of cigarette smoke on bone. METHODS Particulate phase extract (PPE) was prepared by passing CSE through a 0.1μm PTFE filter and eluting in the DMSO to yield a final concentration of 40mg/mL. Primary rat bone marrow stromal cells (BMSC) were purchased from Cell Biologics (Chicago, IL) and cultured under basal standard or osteogenic media. BMSC were subsequently exposed to either the vehicle control (DMSO) or dioxin or PPE. Some cells received co-treatment with Ahr antagonists, including: a-naphthoflavone (ANF, a synthetic antagonist); resveratrol (Res, a stilbenoid found in grapes and present in red wine), and 3,3’-diindolylmethane (DIM, a breakdown product of the indole-3-carbinol, which is present in cruciferous vegetables). EROD assays were used to evaluate Ahr-mediated CYP1 family induction, and ALP and mineralization assays were used to quantify effects on osteogenic differentiation. Cell proliferation assays and Wnt signaling assays were also performed. RESULTS PPE-treated cells showed increased activity of CYP1A subfamily proteins, demonstrating Ahr activation. PPE treatment inhibited ALP activity, an effect which was at least partially mitigated by co-treatment with each of the Ahr antagonists. A similar response was seen in and mineralization and cell proliferation assays. RNA expression studies showed that PPE down-regulated numerous pro-osteogenic genes, such as ALP, RunX2, OCN, and Phex, whereas co-treatment with Ahr antagonists prevented PPE-mediated inhibition of those RNA. Interestingly, PPE decreased the ratio of active:inactive β-Catenin, an effect which was recapitulated by treatment with dioxin (TCDD). CONCLUSIONS Cigarette smokers are a historically difficult patient population for spine surgeons to treat due to increased rates of pseudarthrosis and complications following spinal fusion procedures. Our results suggest that Ahr hyper-activation may play an important role in the adverse effects of cigarette smoke on bone healing—potentially by perturbation of canonical Wnt signaling—and that Ahr antagonists may be protective in combating cigarette smoke-mediated inhibition of bone regeneration and healing.

Hookah smoking is strongly associated with diabetes mellitus, metabolic syndrome and obesity: a population-based study

ObjectivesThe adverse effects of cigarette smoking have been widely studied before, whilst the effects of hookah smoking has received less attention, although it is a common habit in the Middle East. Here we have investigated the effects of cigarette and hookah smoking on biochemical characteristics in a representative population sample derived from the Mashhad stroke and heart atherosclerotic disorder (MASHAD) cohort study, from Northeastern Iran.Study designA total of 9840 subjects from the MASHAD population study were allocated to five groups; non-smokers (6742), ex-smokers (976), cigarette smokers (864), hookah smokers (1067), concomitant cigarette and hookah smokers (41).MethodsBaseline characteristics were recorded in a questionnaire. Biochemical characteristics were measured by routine methods. Data were analyzed using SPSS software and p < 0.05 was considered significant.ResultsAfter adjustment for age and sex; the presence of CVD, obesity, metabolic syndrome, DM and dyslipidemia were significantly (p < 0.001) related to smoking status. After multivariate analysis, HDL (p < 0.001), WBC (p < 0.001), MCV (p < 0.05), PLT (p < 0.01) and RDW (p < 0.001), and the presence of CVD (p < 0.01), obesity (p < 0.001), metabolic syndrome (p < 0.05) and DM (p < 0.01) remained significant between cigarette smokers and non-smokers. Between hookah smokers and non-smokers; uric acid (p < 0.001), PLT (p < 0.05) and RDW (p < 0.05), and the presence of obesity (p < 0.01), metabolic syndrome (p < 0.001), diabetes (p < 0.01) and dyslipidemia (p < 0.01) remained significant after logistic regression.ConclusionThere was a positive association between hookah smoking and metabolic syndrome, diabetes, obesity and dyslipidemia which was not established in cigarette smoking.