Smoke-exposed Groups Research Articles

Comparative Assessment of Acute Pulmonary Effects Induced by Heat-Not-Burn Tobacco Aerosol Inhalation in a Murine Model

Tobacco smoking remains a major global health concern, causing preventable deaths and economic strain. Although new tobacco products such as heat-not-burn (HnB) are safer alternatives to traditional cigarettes, research on their associated risks remains limited. This study aimed to investigate the effects of HnB smoke exposure on the lungs compared to those of traditional cigarettes and the combined use of HnB and cigarettes using experiments with a mouse model. We quantitatively analyzed changes in the levels of 92 blood plasma proteins using the proximity extension assay method and observed significant changes in their levels in mice exposed to different smoke conditions; specifically, the levels of certain proteins, including Ccl20, Cxcl1, and Pdgfb, increased in the HnB smoke-exposed group, suggesting activation of nicotine pathways. Comparative analysis with traditional cigarette smoke-exposed mice further highlighted similarities and differences in their protein expression profiles. This study contributes to an improved understanding of the biological mechanisms underlying the harmful effects of alternative nicotine delivery systems and identifies potential biomarkers associated with the harmful effects of HnB smoke exposure. However, the precise impact of nicotine on the immune system may be influenced by various factors, necessitating further research.

Effect of cigarette smoke exposure and cessation on regional diffusion properties in rat intervertebral discs.

Cigarette smoking is a recognized risk factor for orthopedic disorders, particularly intervertebral disc (IVD) degenerative disease. However, the IVD pathophysiology, especially the spatial-temporal remodeling progression in the context of cigarette smoking, remains unclear. This study aimed to address this knowledge gap through a quantitative assessment of IVD structural composition and diffusion properties using a Sprague-Dawley rat model. Twenty-four rats were divided into control and smoke exposure cohorts, each with two sub-groups of six rats. One smoke exposure sub-group was sacrificed after 2 months of daily cigarette smoke exposure in a custom smoking apparatus, while the other was sacrificed after an additional 5 months of smoke cessation. The control groups were age-matched to the smoke exposure groups. A fluorescent recovery after photobleaching (FRAP) technique was used to determine solute diffusivities and multi-photon excitation (MPE) imaging was performed to characterize structural changes in the annulus fibrosus (AF), nucleus pulposus (NP), and cartilage endplate (CEP). A decrease in diffusivity was observed in the CEP and the AF (radial direction only) after 2 months of smoke exposure. MPE imaging showed aberrant CEP calcification and reduced AF radial collagen fiber bundle diameter, suggesting that the IVD exhibits regionally dependent structural remodeling due to smoke exposure. Furthermore, the smoke cessation group showed deteriorating alterations of structure and diffusivities in all three-disc regions, including the NP, indicating that five-month smoke cessation alone didn't reverse the progression of IVD degenerative remodeling during aging. This study advances the understanding of IVD pathophysiology in the context of cigarette smoke exposure and cessation, laying the groundwork for potential earlier diagnosis and optimized interventions.

Assessment of exposure and DNA damage from second-hand smoke using potential biomarker in urine: cigarettes and heated tobacco products

Second-hand smoke exposure is an established cause of several adverse health effects. Tobacco smoke exposure in the environment has been improved by the WHO Framework Convention on Tobacco Control. However, concerns have been raised regarding the health effects of heated tobacco products. Analysis of tobacco smoke biomarkers is critical for assessing the health effects of second-hand tobacco smoke exposure. In this study, nicotine metabolites (nicotine, cotinine, trans-3'-hydroxycotinine) and carcinogenic 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol were analysed in the urine of non-smokers with or without passive exposure to cigarettes and heated tobacco products. In addition, 7-methylguanine and 8-hydroxy-2'-deoxyguanosine were simultaneously measured as DNA damage markers. The results revealed higher levels of urinary nicotine metabolites and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol in participants exposed to second-hand tobacco smoke (both cigarettes and heated tobacco products) at home. In addition, the urinary levels of 7-methylguanine and 8-hydroxy-2'-deoxyguanosine tended to be higher in the second-hand tobacco smoke-exposed group. The urinary levels of nicotine metabolites and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol were high in workplaces with no protection against passive smoking. These biomarkers will be useful for evaluating passive exposure to tobacco products.

Effect of Exposure to E-Cigarette Vapor and Cigarette Smoke on Seminiferous Tubules Diameter and Spermatozoa Quality of Mice (Mus musculus)

This study aims to compare the quality of spermatozoa (motility and viability) and the diameter ofseminiferous tubules of mice (Mus musculus) by exposing to cigarette smoke and electronic cigarette vapor.This study used 28 male mice divided into 7 groups. Treatment group C was exposed to air, group A1given 1 cigarette/day, group A2 given 2 cigarettes/day, group A3 given 3 cigarettes/day, group B1 given0.7 ml/day, group B2 given 1,3 ml/day, group B3 given 2 ml/day. The treatments were carried out for 36days. The result of this study showed significant difference (p<0.05) in spermatozoa motility percentagebetween C, A1, A2, A3, B3, but in B1 showed no significant difference (p>0,05) with B2. Spermatozoaviability percentage showed significant difference (p<0.05) between control and all treatment groups.Diameter of seminiferous tubules showed significant difference (p<0,05) between C, A1, A2, A3, B1, B3, butin B2 showed no significant difference (p>0.05) with A1 and A2. In conclusion, this study showed that bothcigarette smoke and e-cigarette vapor exposure can decrease the quality of spermatozoa and diameter ofseminiferous tubules. E-cigarette vapor exposure groups showed better quality of spermatozoa and greaterdiameter of seminiferous tubules compared to cigarette smoke exposure groups.

Effect of Conjugated Linoleic Acid (CLA) Supplementation on Expression of B-Cell Lymphoma-2 (Bcl-2) in the Bladder Epithelium of Wistar (Rattus norvegicus) Rats Exposed to Cigarette Smoke.

Bladder carcinoma is the 10th most common cancer in the world with an incidence about 3% of all cancers. The risk factor for smoking is found in 81% of all cases of bladder carcinoma. One of the protein groups associated with bladder urothelial carcinoma is B-Cell Lymphoma-2 (Bcl-2). Nicotine-derived nitrosamine ketone (NNK) contained in cigarette smoke would increase the proliferation of cancer cells through increased the expression of Bcl-2. The expression of Bcl-2 could be suppressed in the presence of Conjugated Linoleic Acid (CLA), a polyunsaturated fatty acid that has role in reducing the risk of cancer development which is reported in several studies, and then stimulate cell apoptosis. To determine the effect of CLA supplementation on Bcl-2 expression in the bladder of rats which is exposed to cigarette smoke. The study is an experimental study with true experimental posttest only control group design on Wistar rats. Sample was divided into 2 case groups: 0.5% of diet (125 mg) CLA supplementation in group A, 1% of diet (250 mg) CLA in group B; and 2 control groups: group without CLA supplementation (group C) as positive control and without cigarette smoke exposure (group D) as negative control. The study takes 60 days of exposure and then Bcl-2 expression on bladder epithelial was evaluated by immunohistochemistry staining. The results descriptively showed that rats in group C has an average Bcl-2 expression of 25.8±7.33%, while rats in group D has an average Bcl-2 expression 14.1±7.73% which means cigarette smoke exposure has been shown to increase the expression of Bcl-2 by 45.35% (p=0.019) in the bladder mucosa of experimental animals. Group B obtained an average Bcl-2 expression was 14.2±9.6% and has a significant difference when compared to group C, it shows that the addition of 1% CLA would reduce the expression of Bcl-2 by 44.96% (p=0.032). However, for group A, group with 0.5% diet of CLA supplementation did not showed decrease of Bcl-2 expression when compared to the group C (p=0.37). Conjugated Linoleic Acid (CLA) supplementation 1% of diet can reduce Bcl-2 expression in bladder epithelium of wistar rats (Rattus norvegicus) exposed to cigarette smoke.

Brain-derived neurotrophic factor gene variants and obesity in former smokers

ObjectiveFrom genome-wide association studies, brain-derived neurotrophic factor (BDNF) locus on chromosome 11 was the only SNP associated with both smoking and body mass index (BMI) in European, African and Asian population. This study aims to explore the unique genetic predisposition to obesity in former smokers by examining the effects of BDNF on BMI and waist circumference (WC).MethodsThe study design is case-control study with a cohort validation in supplementary. We included 15,072 ethnic Chinese participants in the Guangzhou Biobank Cohort Study (GBCS) with data of four BDNF SNPs related to both BMI and smoking behavior. We used baseline smoke exposure data in 2003–2007 and follow-up outcomes of general obesity (by BMI) and central obesity (WC) in 2008–2012. Odds ratios (ORs) and 95% confidence intervals (CIs) for general obesity and central obesity associated with these SNPs were derived from logistic regression.ResultsOf 15,072 participants (3169 men and 11,903 women), 1664 (11.0%) had general and 7868 (52.2%) had central obesity. In 1233 former smokers, the rs6265 GG, versus AA, genotype was associated with higher risks of general obesity (OR = 1.79, 95% CI = 1.06–3.01) and central obesity (OR = 2.08, 95% CI = 1.47–2.92) after adjustment. These associations were not significant in never or current smokers. In former heavy (≥20 cigarettes/day) smokers, the rs6265 GG genotype showed a higher odds for general obesity (OR = 2.15, 95% CI = 1.05–4.40), while no association was found in former light (1–9 cigarettes/day) smokers. Similar results were found for the association of rs6265 with central obesity and for the associations of other two BDNF SNPs (rs4923457 and rs11030104) with both general and central obesity.ConclusionsWe firstly identified the genetic predisposition (BDNF SNPs) to general and central obesity in former smokers, particularly in former heavy smokers. The different associations of the SNPs for general/central obesity in different smoke exposure groups may be related to the competitive performance of the sites and epigenetic modification, which needs further study.

Comparison of Oxidative Effects of Electronic Cigarette and Tobacco Smoke Exposure Performed Experimentally

Objective: Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. Method: We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (N = 8); the electronic cigarette group (N = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (N = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. Results: Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (p < 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (p < 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (p < 0.000). Conclusion: Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.

The role of glucose metabolism and insulin resistance in cardiac remodelling induced by cigarette smoke exposure.

The aim of this study is to evaluate whether the alterations in glucose metabolism and insulin resistance are mechanisms presented in cardiac remodelling induced by the toxicity of cigarette smoke. Male Wistar rats were assigned to the control group (C; n = 12) and the cigarette smoke‐exposed group (exposed to cigarette smoke over 2 months) (CS; n = 12). Transthoracic echocardiography, blood pressure assessment, serum biochemical analyses for catecholamines and cotinine, energy metabolism enzymes activities assay; HOMA index (homeostatic model assessment); immunohistochemistry; and Western blot for proteins involved in energy metabolism were performed. The CS group presented concentric hypertrophy, systolic and diastolic dysfunction, and higher oxidative stress. It was observed changes in energy metabolism, characterized by a higher HOMA index, lower concentration of GLUT4 (glucose transporter 4) and lower 3‐hydroxyl‐CoA dehydrogenase activity, suggesting the presence of insulin resistance. Yet, the cardiac glycogen was depleted, phosphofructokinase (PFK) and lactate dehydrogenase (LDH) increased, with normal pyruvate dehydrogenase (PDH) activity. The activity of citrate synthase, mitochondrial complexes and ATP synthase (adenosine triphosphate synthase) decreased and the expression of Sirtuin 1 (SIRT1) increased. In conclusion, exposure to cigarette smoke induces cardiac remodelling and dysfunction. The mitochondrial dysfunction and heart damage induced by cigarette smoke exposure are associated with insulin resistance and glucose metabolism changes.

Interaction of health literacy and second-hand smoke exposure on psychopathological symptoms of middle school students

Objective: To explore the interaction of health literacy and second-hand smoke exposure on psychopathological symptoms of middle school students. Methods: From November 2015 to January 2016, 22 628 middle school students from Shenyang of Liaoning Province, Bengbu of Anhui Province, Xinxiang of Henan Province, Ulanqab of Inner Mongolia Autonomous Region, Chongqing Municipality, and Yangjiang of Guangdong Province were enrolled by using the multi-stage cluster convenience sampling method. A questionnaire was used to collect the data including demographic information, health literacy, second-hand smoke exposure, and psychopathological symptoms. A multivariate logistic regression model was used to analyze the interaction of health literacy and second-hand smoke exposure on psychopathological symptoms of middle school students. Results: The age of students was (15.36±1.79) years old, of which 10 990 were boys, accounting for 48.6% of total students. The detection rate of psychopathological symptoms was 29.1% (6 581/22 628). The detection rate of psychopathological symptoms in those who were exposed to second-hand smoke was 38.1% (2 401/6 304), which was higher than that in the non-second-hand smoke exposure group [25.6% (4 180/16 324)] (P<0.001). The OR (95%CI) of the interaction between medium and low levels of overall health literacy, low level of interpersonal dimension of health literacy and second-hand smoke exposure was 1.19 (1.15-1.24), 2.00 (1.92-2.10) and 1.59 (1.52-1.66), respectively. Conclusion: There was a positive interaction between middle and low levels of overall health literacy, low level of interpersonal dimension of health literacy and second-hand smoke exposure on psychopathological symptoms of middle school students.

NAT1 genetic variation increases asthma risk in children with secondhand smoke exposure

Objective We previously reported that children exposed to secondhand smoke (SHS) that carried variants in the NAT1 gene had over two-fold higher hair cotinine levels. Our objective was to determine if NAT1 polymorphisms confer increased risk for developing asthma in children exposed to SHS. Methods White participants in the Cincinnati Childhood Allergy and Air Pollution Study (n = 359) were genotyped for 10 NAT1 variants. Smoke exposure was defined by hair cotinine and parental report. Asthma was objectively assessed by spirometry and methacholine challenge. Findings were replicated in the Genomic Control Cohort (n = 638). Results Significant associations between 5 NAT1 variants and asthma were observed in the CCAAPS exposed group compared to none in the unexposed group. There was a significant interaction between NAT1 rs13253389 and rs4921581 with smoke exposure (p = 0.02, p = 0.01) and hair cotinine level (p = 0.048, p = 0.042). Children wildtype for rs4921581 had increasing asthma risk with increasing hair cotinine level, whereas those carrying the NAT1 minor allele had an increased risk of asthma regardless of cotinine level. In the GCC, 13 NAT1 variants were associated with asthma in the smoke-exposed group, compared to 0 in the unexposed group, demonstrating gene-level replication. Conclusions Variation in the NAT1 gene modifies asthma risk in children exposed to secondhand-smoke. To our knowledge, this is the first report of a gene-environment interaction between NAT1 variants, smoke exposure, cotinine levels, and pediatric asthma. NAT1 genotype may have clinical utility as a biomarker of increased asthma risk in children exposed to smoke.

Inhalation exposure to cigarette smoke induces endothelial nitric oxide synthase uncoupling and enhances vascular collagen deposition in streptozotocin-induced diabetic rats

Smoking is an acknowledged risk factor for vascular disorders, and vascular complication is a main outcome of diabetes. Hence, we investigated the impact of cigarette smoke on blood vessels in diabetes, postulating that smoking might aggravate diabetic vascular impairment. Sprague–Dawley rats were divided into four groups: control, cigarette smoke-exposed, diabetic, and cigarette smoke-exposed diabetic groups. Streptozotocin-induced diabetic rats were exposed to cigarette smoke by inhalation at total particulate matter concentration of 200 μg/L for 4 h/day, 5 day/week for a total of 4 weeks. Diabetes caused structural change of aorta, but additional cigarette smoke exposure did not induce further alteration. Collagen, a marker for fibrosis, was increased in media of diabetic aorta, and this increase was augmented by cigarette smoke. Cigarette smoke induced endothelial nitric oxide synthase (eNOS) uncoupling in the diabetic group. Malondialdehyde was increased and glutathione was decreased in blood from diabetes, but these effects were not exaggerated by cigarette smoke. Cigarette smoke caused NADPH oxidase (NOX) 2 expression in diabetic aorta and enhanced diabetes-induced NOX4 expression in aorta. Taken together, cigarette smoke exposure can aggravate vascular fibrosis and induce eNOS uncoupling in diabetes under experimental condition, suggesting that smoking might exacerbate diabetic vascular impairments.

Pharmacokinetic and Pharmacodynamic Characterization of Tetrahydrocannabinol-Induced Cannabinoid Dependence After Chronic Passive Cannabis Smoke Exposure in Rats.

Introduction: Cannabis is the most widely used illicit drug in the US, and cannabis use among young adults continues to rise. Previous studies have shown that chronic administration of delta 9-tetrahydrocannabinol (THC), the main psychoactive component of cannabis, induces dependence in animal models. Because smoking is the most frequent route of THC self-administration, it is critical to investigate the effects of cannabis smoke inhalation. The goal of the current study was to develop a rat model to characterize the pharmacokinetics (PKs) of THC after cannabis smoke inhalation, and to determine if chronic cannabis smoke inhalation leads to the development of cannabis dependence. Materials and Methods: For the PK study, male Wistar rats were administered THC intravenously (1 mg/kg) or exposed to smoke from 5 or 10 sequentially smoked cannabis cigarettes (5.3% THC) in an automated smoking machine. Plasma samples were collected from 10 min to 10 hours post smoke exposure (or intravenous administration) and analyzed using liquid chromatography-mass spectrometry to characterize the PK of THC. A three-compartment PK model was used to characterize the PKs. In a separate study, three groups of male Wistar rats were trained in an intracranial self-stimulation (ICSS) procedure, and exposed to smoke from burning 5 or 10 cannabis cigarettes (or clean air control conditions), 5 days/week for 4 weeks. Discussion and Conclusions: Across exposure days, the change from baseline in ICSS thresholds for cannabis smoke-exposed groups was significantly lower and response latencies were significantly faster in the cannabis smoke-exposed groups compared to controls, suggesting that chronic cannabis smoke exposure has rewarding properties. Acute administration of the CB1 receptor antagonist rimonabant (0.3, 1.0, 3.0 mg/kg) induced a dose-dependent increase in ICSS thresholds in the smoke-exposed rats, suggestive of dependence and withdrawal. Finally, an effect compartment PK-pharmacodynamic model was used to describe the relationship between THC concentrations and changes in ICSS thresholds after cannabis smoke exposure.

The effect of cigarette smoke on the shear bond strength of metallic and ceramic orthodontic brackets: An in vitro study

The bond strength between enamel and the bracket base is influenced by exposure to the oral environment. The aim of the current study was to determine the effect of cigarette smoke on the shear bond strength (SBS) of bonded metallic and ceramic orthodontic brackets. a sample of 60 sound extracted premolars were divided into four groups (n=15 each) as follows: group (A): ceramic brackets without smoke exposure, (B): metallic brackets without smoke exposure, (C): ceramic brackets with smoke exposure, (D): metallic brackets with smoke exposure. Smoking exposure was simulated using the British American Tobacco's exposure chamber manufactured by Curbridge Engineering (Hampshire, UK). Metallic and ceramic brackets were bonded to the enamel using conventional acid etching technique. SBS (MPa) was tested using the universal Instron testing machine at a constant cross head speed of 1mm/min until failure. Kolmogorov-Smirnov test was used to test the normality of the measurements. One-way analysis of variance (ANOVA) was used to compare the means of SBSs between the four groups, Post-hoc with least significance difference was used to perform a pairwise comparison between means. Statistical significance was set at P<0.05. The highest SBS corresponded to the ceramic type brackets bonded to a non-smoking sample (15.7±9.5) while the lowest levels of SBS was related to metallic type brackets bonded to smoke exposed sample (2.8±0.7) and the difference was statistically significant (P<0.05). Cigarette smoke consumption has significant effects on the SBS of orthodontic brackets. SBS levels were significantly lower in the smoke exposure groups and the lowest values corresponded to the cigarette smoke exposed metallic brackets.

Protective effect of aerobic exercise on the vocal folds against cigarette smoke exposure.

Laryngeal pathologies due to cigarette smoking vary among individuals, whereas some smokers remain disease free. These differences can be explained by multiple factors among individuals. In this context, an animal study was designed to determine if there is any protective effect of aerobic exercise against the detrimental effects of cigarette smoke on laryngeal tissues. A total of 24 male Wistar albino rats were divided into three groups of eight animals each: control (no smoke exposure), smoking (smoke exposure), and exercise (smoke exposure and exercise) groups. Histopathological (light and electron microscopy) and immunohistochemical (GSTA1, CYP1A1, CYP2E1) evaluations of the vocal folds were performed at the end of experimental period. Exercise group revealed statistically significant decrease in edema (p = 0.03) and inflammatory cell infiltration (p = 0.02) compared to smoking group. In electron microscopic evaluation; cytoplasmic vacuoles were also present in exercise group, but were smaller than smoking group. Edema and swollen mitochondria were also less prominent in exercise group. Condensed chromatin material in the periphery of nucleus was observed only in few cells in exercise group, and observed in more cells in smoking group. GSTA1 expression was higher (p = 0.047) and CYP1A1 expression was lower (p = 0.01) in exercise group than smoking group. Our results indicate that aerobic exercise has a protective role on the larynx against the damaging effect of cigarette smoke. Smokers who exercise regularly may be at a lower risk of cigarette smoke-related laryngeal diseases, as compared with those who do not exercise.

The Genetic Background of Mice Influences the Effects of Cigarette Smoke on Onset and Severity of Experimental Autoimmune Encephalomyelitis.

Multiple sclerosis (MS) is the most common inflammatory disorder of the central nervous system (CNS) in young adults leading to severe disability. Besides genetic traits, environmental factors contribute to MS pathogenesis. Cigarette smoking increases the risk of MS in an HLA-dependent fashion, but the underlying mechanisms remain unknown. Here, we explored the effect of cigarette smoke exposure on spontaneous and induced models of experimental autoimmune encephalomyelitis (EAE) by evaluating clinical disease and, when relevant, blood leukocytes and histopathology. In the relapsing-remitting (RR) transgenic model in SJL/J mice, we observed very low incidence in both smoke-exposed and control groups. In the optico-spinal encephalomyelitis (OSE) double transgenic model in C57BL/6 mice, the early onset of EAE prevented a meaningful evaluation of the effects of cigarette smoke. In EAE models induced by immunization, daily exposure to cigarette smoke caused a delayed onset of EAE followed by a protracted disease course in SJL/J mice. In contrast, cigarette smoke exposure ameliorated the EAE clinical score in C57BL/6J mice. Our exploratory studies therefore show that genetic background influences the effects of cigarette smoke on autoimmune neuroinflammation. Importantly, our findings expose the challenge of identifying an animal model for studying the influence of cigarette smoke in MS.

Prevalence of tandoor smoke exposure in female patients with asthma: A cross-sectional study from the east of Turkey

Aim: The aim of this study was to evaluate the use of cow dung cake (cdc) for heating, cooking and baking in female patients (pts) with asthma.Material and Methods: This cross-sectional study was conducted between January 2016 and 2018. The study included 522 female pts with asthma. Pts were divided into three groups based on using cdc (for heating, cooking and baking). Secondly, the pts who used cdc in tandoor for baking were evaluated and these pts were divided into three groups based on exposure to tandoor smoke [a) currently using, b) previously used, c) never used]. Age, BMI, comorbidity, the place where pts live, educational status, occupation, smoking status, pulmonary functions and complete blood counts of all pts were evaluated. All statistical calculations were performed with SPSS 23.0.Results: 219 (42%) of all pts were using the cdc, 165 (31.7%) pts were using tandoor, 106 (20.4%) pts had previously used tandoor. The pts who exposed to tandoor smoke previously were significantly older and these pts had higher BMIs. The incidence of comorbidities, the place where pts live, occupation and educational status were significantly different between tandoor smoke exposure groups. The pts who were currently using tandoor for baking lived in villages. In all three groups, most of the women were housewives and most of them who were exposed to tandoor smoke were illiterate. Hemoglobin levels of the pts who were exposed to tandoor smoke were higher. The pts who were currently using tandoor for baking had significantly lower MPV and pulmonary function tests such as FEV1, FVC, PEF and FEF 25% levels. Conclusion: The women with asthma who exposed to tandoor smoke are older, overweight, rural housewife people and they have comorbidities. The pulmonary functions and hemoglobin of them may be affected by exposure to tandoor smoke.

Association of Electronic Cigarette Vaping and Cigarette Smoking With Decreased Random Flap Viability in Rats.

Smoking is a known risk to wound healing, but whether electronic cigarettes present the same risk remains unknown. To evaluate the rate of flap necrosis in the e-cigarette vapor-exposed group and the unexposed control and to detect a difference in the rate of flap necrosis between the traditional cigarette smoke-exposed group and the unexposed control. From March 10, 2018, to May 4, 2018, a cohort study was conducted on 45 male Sprague-Dawley rats at Boston University School of Medicine. Each rat weighed approximately 100 g at the beginning of the study and was randomized to 1 of 3 groups: negative control (n = 15), experimental (exposed to e-cigarette vapor; n = 15), and positive control (exposed to traditional cigarette smoke; n = 15). Rats in the experimental and positive control groups were exposed to electronic cigarette vapor and traditional cigarette smoke in a smoking chamber for 30 minutes twice a day for 30 consecutive days. Levels of serum cotinine were monitored and maintained between 150 ng/mL and 200 ng/mL. After 30 days, random pattern dorsal skin flaps were raised. Percentage of flap necrosis for each group. All 45 rats survived the surgical procedure and postoperative recovery, and all rats thrived and gained weight over the course of the study. The highest rate of flap necrosis was found in the positive control cohort, with a mean (SD) of 68.7% (8.6%), followed by the experimental cohort, with a mean (SD) of 65.9% (11.8%); the negative control cohort had the least amount of flap necrosis, with a mean (SD) of 50.8% (9.4%). The percentage of flap necrosis in the negative control rats (95% CI, 46.0-55.6; P < .001) was substantially lower than that for both the positive control rats (95% CI, 64.3-73.0; P < .001) and the experimental rats (95% CI, 59.9-71.8; P < .001). No statistically significant difference in flap necrosis was noted between the rats in the experimental cohort and the rats in the positive control cohort (95% CI, 59.9-71.8 vs 95% CI, 64.3-73.0; P = .46). Smoking and vaping appear to be equally detrimental to wound healing and to be associated with a statistically significant increase in flap necrosis compared with the unexposed group. The results suggest that vaping should not be seen as a better alternative to cigarette smoking in the context of wound healing. NA.

PROTECTIVE EFFECT OF CHLORELLA VULGARIS ON DNA DAMAGE, OXIDATIVE STRESS, AND LUNG MORPHOLOGICAL CHANGES IN CIGARETTE SMOKE-EXPOSED RATS

Objective: The aim of this study was to determine the protective effect of Chlorella vulgaris (ChV), antioxidant-rich unicellular green alga, and in cigarette smoke-exposed rats.Methods: Male Sprague Dawley rats were divided into 4 groups: Control Group (C), ChV group (300 mg/kg body weight), cigarette smoke-exposed (S) group, and S group treated with ChV (S+ChV). Blood samples were drawn from the orbital sinus on days 0, 15, and 30 for the determination of DNA damage by Comet assay and plasma malondialdehyde (MDA) using high-performance liquid chromatography. Rats were killed on day 30, and lung tissue samples were taken for the evaluation of airspace enlargement and number of inflammatory cells.Results: Increased DNA damage (1004.8 au + 329.2, day 15; 1102.7 + 197.8, day 30) and high MDA levels (10.66 + 0.27, day 15; 10.29 + 0.9 day 30) were found in cigarette smoke-exposed rats on days 15 and 30 but were reduced significantly (p&lt;0.05) when treated with ChV (DNA: 482.6 + 223.3, day15; 423.5 + 74.6, day 30 and MDA: 6.1 + 0.6, day15; 6.6 + 2.5, day 30) for both days. Hematoxylin and eosin staining showed that cigarette smoke-exposed rats had high frequency of airspace enlargement and number of inflammatory cells which were reduced when treated with ChV.Conclusion: ChV has a protective role in cigarette smoke-exposed rats by reducing oxidative DNA damage, MDA levels, lung cells inflammation, and airspace enlargement.

The effect of emphysema induced by tobacco smoke exposure and different rearing ways on the atherosclerosis formation

Objective To explore the relationship and its mechanism of emphysema induced by different ways of rearing and tobacco smoke exposure with the atherosclerosis formation. Methods Forty-eight SD rats were randomly divided into 6 groups (n=8, each): a normal diet + tobacco smoke exposure (TSE) group, a fat-rich diet + TSE group, a limit intake + TSE group, a normal diet group, a fat-rich diet group, and a limit intake group for 24 weeks.Lee's index, serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), adiponectin (APN) levels, mean linear intercept (MLI), mean alveoli number (MAN), the aortic pathology change, vascular endothelial growth factor (VEGF) of aorta, and bone morphogenetic protein-2 (BMP-2) level were collected. Results Tobacco smoke exposure, fat-rich diet, and limit intake increased the severity of emphysema.The microscopic features of aorta showed an early atherosclerosis in the tobacco smoke exposure groups, but no atherosclerosis in the non-smoking groups.Interactions between tobacco smoke exposure and different ways of rearing on serum APN level (F=10.68, P<0.05) were found.In the tobacco smoke exposure groups, Pearson correlation analysis showed positive correlations of aortic VEGF and BMP-2 levels with MLI, serum TNF-α and IL-6 levels (r=0.431, 0.471, 0, 448, 0.449, 0.428, 0.447, all P<0.05), and an negative correlation with MAN (r=-0.411, -0.442, P<0.05). Conclusions Both tobacco smoke exposure and different ways of rearing can influence the formation of emphysema.There is a positive correlation between the severities of emphysema and atherosclerosis, and systemic inflammation may be involved. Key words: Tobacco smoke pollution; Pulmonary emphysema; Atherosclerosis; Feeding methods

Free Desmosine is a Sensitive Marker of Smoke-Induced Emphysema.

While the elastin-specific crosslinks, desmosine and isodesmosine (DID), are increased in blood, urine, and sputum of patients with clinically documented pulmonary emphysema, the usefulness of DID in detecting early lung injury remains untested. To this end, our laboratory has measured DID in a hamster model of smoke-induced emphysema, involving only minimal alveolar wall damage. Animals were either treated with cigarette smoke for 2h/day, 5 days/week, or exposed only to room air (controls) for a period of 3months. DID levels in bronchoalveolar lavage fluid (BALF) and whole lungs were determined at monthly intervals, using liquid chromatography and tandem mass spectrometry. Lung surface area was also determined, as a measure of airspace enlargement. The portion of BALF DID not bound to peptides (free DID) was significantly higher in smoke-exposed animals at 2months (9.2 vs 4.4pg/mg protein; p < 0.05), whereas total BALF DID showed no significant increases over the course of the study, and total lung DID remained unchanged. There was a mild, but significant, loss of lung surface area in the smoke-exposed group at 2months (28.8% vs 25.2%, p < 0.05), which showed no further progression, consistent with the return of free DID to control levels at 3months. These findings support the hypothesis that free DID are sensitive indicators of smoke-induced lung injury. Measurement of free DID in smokers with minimally decreased lung mass may help determine the utility of this parameter as a test for incipient pulmonary emphysema.