Cigarette Smoke Inhalation Research Articles

The Interaction of Apical Periodontitis, Cigarette Smoke, and Alcohol Consumption on Liver Antioxidant Status in Rats

This study aimed to investigate the impact of alcohol (A), secondhand cigarette smoking (ShS), and their combined effect on liver antioxidant activity and hepatic damage in rats with induced apical periodontitis (AP). Thirty-five female Wistar rats were randomly allocated into five groups (n = 7): (1) control (rats without ShS, alcoholic diet, or AP), (2) control-AP (induced AP only), (3) ShS-AP (ShS exposure and induced AP), (4) A-AP (alcoholic diet and induced AP), and (5) A+ShS-AP (alcoholic diet, ShS exposure, and induced AP). Alcohol was administered through semi-voluntary intake, while ShS exposure involved the daily inhalation of cigarette smoke. The experimental period lasted 8 weeks, with AP induction occurring in the 4th week following molar pulp exposure. Liver samples were collected post-euthanasia for histomorphometric and antioxidant marker analyses. All AP-induced groups exhibited increased liver sinusoidal dilation compared to the control group (p < 0.05). AP significantly reduced total antioxidant capacity (FRAP) across all groups (p < 0.05). In AP-induced groups, FRAP levels were further decreased in ShS-AP and A+ShS-AP compared to control-AP (p < 0.05). AP also led to a decrease in the glutathione defense system (p < 0.05). Rats with alcohol exposure (A-AP and A+ShS-AP) showed reduced glutathione peroxidase activity (p < 0.05). Glutathione reductase activity was comparable in the control and control-AP groups (p > 0.05), but significantly decreased in the alcohol and ShS-exposed groups (p < 0.05). Apical periodontitis can relate to morphological changes in the liver’s sinusoidal spaces and impairment of liver’s antioxidant capacity of rats, particularly when combined with chronic alcohol consumption and exposure to cigarette smoke.

Effects of cigarette smoke inhalation on spatial memory in mice: the interplay between carbon monoxide and nicotine

Effects of cigarette smoke inhalation on spatial memory in mice: the interplay between carbon monoxide and nicotine

A 90-day subchronic exposure to heated tobacco product aerosol caused differences in intestinal inflammation and microbiome dysregulation in rats.

Smoking is one of the most important predisposing factors of intestinal inflammatory diseases. Heated tobacco product (HTP) is a novel tobacco category that is claimed to deliver reduced chemicals to human those reported in combustible cigarette smoke (CS). However, the effect of HTP on intestine is still unknown. In the framework of Organization for Economic Co-operation and Development guidelines 413 guidelines, Sprague-Dawley rats were exposed to HTP aerosol and CS for 13 weeks. The atmosphere was characterized and oxidative stress and inflammation of intestine were investigated after exposure. Furthermore, the faeces we performed with 16S sequencing and metabolomics analysis. HTP aerosol and CS led to obvious intestinal damage evidenced by increased intestinal pro-inflammatory cytokines and oxidative stress in male and female rats After HTP and CS exposure, the abundance that obviously changed were Lactobacillus and Turiciacter in male rats and Lactobacillus and Prevotella in female rats. HTP mainly induced the metabolism of amino acids and fatty acyls such as short-chain fatty acids and tryptophan, while CS involved into the main metabolism of bile acids, especially indole and derivatives. Although different metabolic pathways in the gut mediated by HTP and CS, both to inflammation and oxidative stress were ultimately induced. HTP aerosol and CS induced intestinal damage mediated by different gut microbiota and metabolites, while both lead to inflammation and oxidative stress. The concentration of various harmful components in heated tobacco product aerosol is reported lower than that of traditional cigarette smoke, however, its health risk impact on consumers remains to be studied. Our research findings indicate that heated tobacco product and cigarette smoke inhalation induced intestinal damage through different metabolic pathways mediated by gut microbiome, indicating the health risk of heated tobacco product in intestine.

Hubungan Perilaku Merokok Konvensional terhadap Saturasi Oksigen pada Pasien General Anestesi di Ruang Intra Anestesi

Smoking that causes pathophysiological changes in almost all parts of the lower respiratory tract including lung organs, inhaled cigarette smoke contains harmful chemicals that can damage the immune system of the respiratory tract so that it can cause disorders of the respiratory tract. Some respiratory system disorders such as airway obstruction, or conditions that can result in airway obstruction, airway infections, and other disorders that can inhibit gas exchange. To determine the relationship of smoking behavior to oxygen saturation in general anesthesia patients in the Intra-Anesthesia Room of Level III Hospital Reksodiwiryo Padang. The type of research is quantitative, with a sample size of 34 respondents using purposive sampling technique. Univariate data analysis is presented in the form of a frequency distribution and bivariate analysis using the chi-square test, data processing using the IBM SPSS version 25.0 computer program. The most age is 26-35 years, which is 17 people (50,0%), the most education is high school, which is 16 people (47,1%), the most jobs are traders, which is 10 people (29,4%), the most conventional smoking behavior is heavy smokers, which is 13 people (38,2%), the most oxygen saturation is abnormal, which is 23 people (67,6%), and there is a relationship between smoking behavior and oxygen saturation in general anesthesia patients in the Intra-Anesthesia Room of Level III Hospital, Reksodiwiryo Padang (p = 0,014). The most age is 26-35 years, the most education is high school, the most jobs are traders, the most conventional smoking behavior is heavy smokers, the most oxygen saturation is abnormal and there is a relationship between smoking behavior to oxygen saturation in general anesthesia patients in the Intra-Anesthesia Room of Level III Hospital Reksodiwiryo Padang

Associations between urinary hydroxylated polycyclic aromatic hydrocarbon biomarker concentrations and measures of timing of delivery and infant size at birth

Preterm birth is a leading cause of neonatal mortality and presents significant public health concerns. Environmental chemical exposures during pregnancy may be partially to blame for disrupted delivery timing. Polycyclic aromatic hydrocarbons (PAHs) are products of incomplete combustion, exposure to which occurs via inhalation of cigarette smoke and automobile exhaust, and ingestion of charred meats. Exposure to PAHs in the US population is widespread, and pregnant women represent a susceptible population to adverse effects of PAHs. We aimed to investigate associations between gestational exposure to PAHs and birth outcomes, including timing of delivery and infant birth size. We utilized data from the PROTECT birth cohort where pregnant women provided spot urine samples at up to three study visits (median 16, 20, and 24 weeks gestation). Urine samples were assayed for eight hydroxylated PAH concentrations. Associations between PAHs and birth outcomes were calculated using linear/logistic regression models, with adjustment for maternal age, education, pre-pregnancy BMI, and daily exposure to environmental tobacco smoke. Models accounted for urine dilution using specific gravity. We also explored effect modification by infant sex. Interquartile range (IQR) increases in all averaged PAH exposures during the second trimester were associated with reduced gestational age at delivery and increased odds of overall PTB, although these associations were not statistically significant (p > 0.05). Most PAHs at the second study visit were most strongly associated with earlier delivery and increased odds of overall and spontaneous PTB, with visit 2 2-hydroxynapthalene (2-NAP) being significantly associated with increased odds of overall PTB (OR:1.55; 95 %CI: 1.05,2.29). Some PAHs resulted in earlier timing of delivery among only female fetuses, specifically 2-NAP on overall PTB (female OR:1.52 95 %CI: 1.02,2.27; male OR:0.78, 95 %CI: 0.53,1.15). Future work should more deeply investigate differential physiological impacts of PAH exposure between pregnancies with male and female fetuses, and on varying developmental processes occurring at different points through pregnancy.

The fate of an inhaled cigarette puff in the human respiratory tract

Objective Cigarette smoking can lead to a host of adverse health effects such as lung and heart disease. Increased lung cancer risk is associated with inhalation of carcinogens present in a puff of smoke. These carcinogenic compounds deposit in the lung at different sites and trigger a cascade of events leading to adverse outcomes. Understanding the site-specific deposition of various smoke constituents will inform the study of respiratory diseases from cigarette smoking. We previously developed a deposition model for inhalation of aerosol from electronic nicotine delivery systems. In this study, the model was modified to simulate inhalation of cigarette smoke consisting of soluble and insoluble tar, nicotine, and cigarette-specific constituents that are known or possible human carcinogens. Materials and Methods The deposition model was further modified to account for nicotine protonation and other cigarette-specific physics-based mechanisms that affect smoke deposition. Model predictions showed a total respiratory tract uptake in the lung for formaldehyde (99%), nicotine (80%), and benzo[a]pyrene (60%). Results The site of deposition and uptake depended primarily on the constituent’s saturation vapor pressure. High vapor pressure constituents such as formaldehyde were preferentially absorbed in the oral cavity and proximal lung regions, while low vapor pressure constituents such as benzo[a]pyrene were deposited in the deep lung regions. Model predictions of exhaled droplet size, droplet retention, nicotine retention, and uptake of aldehydes compared favorably with experimental data. Conclusion The deposition model can be integrated into exposure assessments and other studies that evaluate potential adverse health effects from cigarette smoking.

Revolutionizing respiratory health research: “commercially-available lung-on-a-chip and air-liquid interface systems”

Inhalation of ultrafine particles, aerosol contaminants, and cigarette smoke can induce respiratory diseases. As humans are constantly exposed to various exogenous substances, it is crucial to study their impacts on respiratory diseases and airway dysfunction. Recently, organ-on-a-chip technology has been applied in many research studies to understand disease mechanisms, drug screening, and drug testing. The combination of organ-on-a-chip technology and the air-liquid interface (ALI) culture method is emerging as a new platform for realistically mimicking the microenvironment and physiological motions of the human lungs. Breathing motion can be simulated through cyclic stretching, while blood flow can be replicated using channel flow within the chip. The ALI system is critical for mucociliary differentiation, pseudostratified morphology, and epithelial barrier function development. The combination of organ-on-a-chip technology and ALI systems allows the integration of cyclic stretch as a breathing motion and microfluidic channels as circulatory systems. The chip system can also integrate the lung epithelial cells, extracellular matrix, and microstructures, providing microenvironments such as fibroblast, collagen, and immune cells to the epithelial cells. This review discusses chip systems as effective tools for recapitulating human lung environments and how they are applied in biological studies against various pulmonary diseases such as infections or inflammation, fibrosis, and malignancy.

INTRODUCING THE EFFECTS OF SMOKING ON THE HEART AND BLOOD VESSELS TO REDUCE SMOKING BEHAVIOR AMONG STUDENTS

Smoking causes various diseases in our bodies, such as heart disease and blood vessel disorders, lung cancer, oral cavity cancer, laryngeal cancer, high blood pressure, impotence as well as pregnancy disorders and fetal defects. The dangers of smoking are not only aimed at smokers (active smokers) but also for non-smokers who inhale cigarette smoke around smokers (passive smokers) and in fact the effects received from passive smokers will be much more dangerous than active smokers. Because of the many negative impacts that arise for teenage smokers, it is necessary to provide knowledge and understanding to teenagers, especially Islamic boarding school children, regarding the dangers posed by smoking. The goal is to increase understanding by providing education to Students regarding the effects of smoking on the heart and blood vessels as an effort to reduce smoking behavior among students in PP. Al Hikam Bangkalan. The methods used in counseling are lectures and questions answer. Before counseling, participants were given a pre-test, then after counseling, participants were given a post-test. The results of the pre-test and post-test are assessed and then data processing and evaluation are carried out. Pre-test results and post-test regarding knowledge of the effects of smoking on the heart and blood vessels through a questionnaire, there was a direct increase in scores by students who took part in this activity. The percentage increase in average value was 9.7%. This significant increase in the average value indicates a change in the level of knowledge of the participants after attending the counseling session. Introducing the effects of smoking on the heart and blood vessels as an effort to reduce smoking behavior among students in PP. Al Hikam Bangkalan has increased knowledge and understanding of the dangers of smoking.

MiRNA-210 is involved in cigarette smoke extract-induced apoptosis of MLE-12 via the Shh signaling pathway.

The aim of the study is the regulatory effect of MicroRNA-210 (MiR-210) on cigarette smoke extract (CSE)-induced mouse lung epithelial type II cells (MLE-12) apoptosis and determine whether the MiR-210 is involved in cigarette smoke extract-induced apoptosis of MLE-12 via Shh signaling pathway. Expression of MiR-210 in CSE-induced MLE-12 was assessed by qRT-PCR. The emphysema mouse model and MiR-210 knockdown mice were each established by inhaling cigarette smoke or intratracheal lentiviral vector instillation. The Sonic hedgehog (Shh), Ptch1, Gli1, B-cell lymphoma-2 (Bcl-2), and Caspase 3 protein expressions were detected by Western blotting. mRNA expressions of MiR-210, Shh, Ptch1, and Gli1 were measured using quantitative real-time polymerase chain reaction (qRT-PCR). Apoptotic ratios in mice and CSE-induced HPVEC were assessed using TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assays and flow cytometry. Our results showed that MiR-210 mRNA levels were significantly down-regulated in the CSE-induced MLE 12. MLE 12 apoptosis with down-regulated Shh, Ptch1, Gli1, and Bcl-2 expression, increased Caspase 3 expression in the emphysema mouse model and CSE-induced MLE 12. Knockdown MiR-210 can facilitate cell apoptosis and emphysema via the Shh signaling pathway in mice. In vitro, MiR-210 can attenuate the apoptosis of CSE-exposed MLE 12. Moreover, MiR-210 regulated the Shh pathway and promoted its expression. MiRNA-210 is involved in cigarette smoke extract-induced apoptosis of MLE-12 via the Shh signaling pathway. The present study reveals that MiRNA-210 may be a key regulator of cellular apoptosis and could be explored as a potential therapeutic target in the future.

Abstract PO5-08-02: Endocrine Disruptors and Life STILe in Patients Carrying BRCA Pathogenic VAriants With Breast and/or Ovarian CAncer and Women Without Neoplasm: the STILVARCA study

Abstract Background. Pathogenetic variants (PVs) in the BRCA1/2 genes can be found in 20% of patients with breast (BC) or/and ovarian (OC) cancers. In subjects carrying PVs in these genes, the absence of repair of damage to the DNA double helix causes its accumulation favoring neoplasm development. Exposure to environmental pollutants (e.g. Cadmium (Cd), through contaminated food and drinking water, cigarette smoke, dust and fumes inhalation) may play a role in the development of BC and OC. Cd acts as an “endocrine disruptor” through its binding to the estrogen receptor, promoting cell proliferation and increase in mutation rate. Individual lifestyle habits may be associated with cancer onset and progression in these patients. Our aim was to evaluate the interference of environmental factors in the development of BC and/or OC in women carrying PVs in BRCA1/2 genes. Methods. We conducted an observational, multicentric, case-control, retrospective study of patients with PV in BRCA1/2 genes and with BC, OC, or both diagnosed from 2012 to 2020 (Group 1, G1), or without cancer (Group 2, G2). 89 patients (82.4%) developed BC, 17 (15.8%) OC, and 2 (1.8%) experienced both BC and OCs. We collect data about demographics, body mass index (BMI), occupation (divided in employed, educative professions/students, healthcare professions, unemployed/retired and other), type of BRCA mutation (mBRCA), smoking habits (SH), pack/year index, estroprogestinic (EP) use and duration, adherence to Mediterranean diet (with PREDIMED questionnaire) and physical activity (using IPAQ questionnaire). Fisher's exact test and Anova were used to compare patient’s features among the two group. A univariate and multivariable model were fitted to investigate the relationship between adherence to Mediterranean diet, physical activity, Cd exposure through smoking habits (SH), EP use, and cancer development. Results. We evaluated 208 patients, 108 (51.9%) in Group 1 and 100 (48.1%) in Group 2. Table 1 shows ed the features of enrolled patients. 128 (61.5%) had a mBRCA1, 80 (38.5%) a mBRCA2. Analysis of the two groups revealed significative differences in age (47.2 vs 35.6years in G1 and G2, respectively; p< .001), SH (38.9% in G1 and 20.0% in G2; p=.002), EP use (36.1% in G1 and 21.0% in G2; p=.021), and occupation (office workers develop cancer more easily, while professions associated with education/students have a lower possibility of developing cancer). No difference was found regarding pack/year index, EP intake duration, adherence to Mediterranean diet, and physical activity. At univariate analysis, predictive factors for cancer incidence were: SH (OR 2.545; 95% CI 1.363 – 4.752 - p=.003); EP use (OR 2.126; 95% CI 1.143 – 3.957 - p=.017); adherence to Mediterranean diet (OR 1.500; 95% CI 1.016 – 2.215 – p=.041). No relationship was found with BMI, occupation and physical activity. At multivariable analysis, SH (OR 2.606; 95% CI 1.370 – 4.959 - p=.004), EP use (2.340; 95% CI 1.224 – 4.474 - p=.010), and adherence to Mediterranean diet (OR 1.544; 95% CI 1-027 – 2.320 – p=.037) were predictive of cancer development. Conclusion. In this preliminary analysis, the risk of development of BC or/and OC in patients with BRCA mutation was influenced by SH, EP use, and adherence to Mediterranean diet. Many environmental factors seem to play a role in the carcinogenesis of mBRCA VP patients. Paths of lifestyle education are highly recommended in BRCAm-carrying women. Table 1. Characteristics of enrolled patients Citation Format: Antonio Franco, Alessandro Rossi, Daniela Andreina Terribile, Emanuela Lucci Cordisco, Ida Paris, Margherita Muratore, Elena Florio, Vanda Salutari, Francesco Pavese, Federica Francesca L'Erario, Antonella Palazzo, Enrico Di Guglielmo, Giulia Borghesiani, Ludovica Cardinali, Elisabetta Ferretti, Giovanni Terrana, Diana Giannarelli, Giovanni Scambia, Silvia Migliaccio, Alessandra Fabi. Endocrine Disruptors and Life STILe in Patients Carrying BRCA Pathogenic VAriants With Breast and/or Ovarian CAncer and Women Without Neoplasm: the STILVARCA study [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO5-08-02.

The Relationship between Cigarette Smoke Exposure and Stunting among Children in the Working Area of the Pangkajene Health Center, Sidrap Regency in 2023

Background: The major health problem currently is the smoking habit which cannot be separated from society, because smoking is considered a common thing carried out among people. As a result of this habit, cigarette smoke exposure has a direct impact on the growth and development of the children by interfering the absorption of nutrients which will later disrupt their growth and development and can influence the incidence of stunting. Purpose: This study aimed to determine the relationship between cigarette smoke exposure and the incidence of stunting among children in the working area of ​​the Pangkajene Health Center, Sidrap Regency in 2023. Method: This study was conducted from May, 25th to June, 25th 2023. This study employed a quantitative study with a cross sectional approach. A total of 45 respondents was chosen as sample in this study, using purposive sampling technique. The data collection method in this study used a questionnaire and the relationship between cigarette smoke exposure and the incidence of stunting among toddlers. Results: Exposure to cigarette smoke has a direct impact on the growth and development of their children by interfering with the absorption of nutrients in children which will later interfere with their growth and development. Conclusion: Exposure to cigarette smoke is one of the important problems that causes stunting in children because the chemicals produced can have both direct and indirect effects on children. Therefore, education is needed regarding the importance of not smoking and the negative impacts resulting from inhaling cigarette smoke.

THE DEVELOPMENT OF AUTOMATIC CIGARETTE SMOKE DETECTION SYSTEM USING TA12-100 AND MQ-135 SENSORS

Indonesia is ranked 3rd with the highest number of active smokers in the world after India and China. Cigarettes contain more than 4000 chemical compounds that are harmful to active smokers and passive smokers. The large number of active smokers in Indonesia also has an impact on passive smokers where passive smokers also inhale cigarette smoke. The purpose of this research is to build an automatic cigarette smoke detector to support air hygiene control, protect passive smokers, and save electricity used. The stages in designing this research include analysis of product specifications, assembly, programming, and trials. This study was designed using Arduino UNO as the microcontroller, the MQ-135 sensor as a tool to detect cigarette smoke, the TA12-100 sensor to calculate electrical power consumption, the relay as an automatic switch, and the exhaust fan as a smoke neutralizer. The results of this study are that the MQ-135 sensor can detect cigarette smoke properly with the Relay as an automatic switch that functions to turn on the exhaust fan automatically. Based on the test results on the TA12-100 sensor, the consumption of electrical energy with an automatic mechanism is more efficient than the consumption of electrical energy in a manual way, with a difference of 0.0000385 kWH and Rp. 0.05205. Future research could focus on developing a more complex system for overall air cleanliness control, rather than just focusing on cigarette smoke detection.

Cigarette Smoke Extract Induces MUC5AC Expression Through the ROS/ IP3R/Ca2+ Pathway in Calu-3 Cells.

Chronic obstructive pulmonary disease (COPD) is caused by exposure to noxious external particles, air pollution, and the inhalation of cigarette smoke. Airway mucus hypersecretion particularly mucin5AC (MUC5AC), is a crucial pathological feature of COPD and is associated with its initiation and progression. In this study, we aimed to investigate the effects of cigarette smoke extract (CSE) on MUC5AC expression, particularly the mechanisms by which reactive oxygen species (ROS) induce MUC5AC expression. The effects of CSE on the expression of MUC5AC and mucin5B (MUC5B) were investigated in vitro in Calu-3 cells. MUC5AC and MUC5B expression levels were measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), immunofluorescence staining, and enzyme-linked immunosorbent assay (ELISA). Total cellular levels of ROS and Ca2+ were determined using DCFH-DA and Fluo-4 AM. Subsequently, the expression levels of IP3R, IRE1α, p-IRE1α and XBP1s were measured by Western blotting. Gene silencing was achieved by using small-interfering RNAs. Our findings revealed that exposure to CSE increased MUC5AC levels and upregulated ROS, IP3R/Ca2+ and unfolded protein response (UPR)-associated factors. In addition, knockdown of IP3R using siRNA decreased CSE-induced Ca2+ production, UPR-associated factors, and MUC5AC expression. Furthermore, 10 mM N-acetyl-l-cysteine (NAC) treatment suppressed the effects of CSE, including ROS generation, IP3R/ Ca2+, UPR activation, and MUC5AC overexpression. Our results suggest that ROS regulates CSE-induced UPR and MUC5AC overexpression through IP3R/ Ca2+ signaling. Additionally, we identified NAC as a promising therapeutic agent for mitigating CSE-induced MUC5AC overexpression.

The Effect of Training Male Smokers About the Effects of Secondhand Smoke in Pregnant Wives on Their Self-Efficacy.

Contact with second-hand cigarette smoke includes inhalation of cigarette smoke caused by the burning of the cigarette itself and inhalation of smoke exhaled by the smoker. Wife's pregnancy can be a motivating factor to change the behavior of men who smoke. Therefore, this study was conducted in order to determine the effect of training male smokers on the effects of secondhand smoke during pregnancy on their self-efficacy. The present study is an interventional type of pre-test and post-test. In this phase, random sampling was done from health centers in Isfahan, the participants were 140 smoking spouses of pregnant women, who referred to health centers to receive pregnancy care, and were divided into two intervention and control groups. The data collection tool was a researcher-made questionnaire on men's self-efficacy regarding second-hand cigarette smoke. The validity of the questionnaire was confirmed based on the opinion of the expert panel with content validity ratio (CVR)=0.87 and content validity index (CVI)=0.88, and its reliability was confirmed with Cronbach's alpha=0.97. All data were analyzed with SPSS18 software and Chi-score, Fisher, t-test. There was no significant difference between the comparison of demographic variables in the intervention and control groups (p>0.05). The results of the paired t-test to compare before and after the training showed that the average score of self-efficacy (p<0.001) in the intervention group had increased significantly after the training, and according to the independent t-test, the average score of self-efficacy After training, it was more in the intervention group than the control group (p<0.05). Men's self-efficacy regarding second-hand smoke increased after training, so the current training package is effective in training and can be suggested for future studies.

Effects of cigarette smoke inhalation on the immune-inflammatory profile of experimental apical periodontitis in rats.

To evaluate the effects of cigarette smoke inhalation on the immune-inflammatory profile of experimental apical periodontitis in rats. In total, 32 male Wistar rats were divided into four groups (n = 8): AP-induced apical periodontitis; S-cigarette smoke inhalation; APS-induced AP and cigarette smoke inhalation; and C (control)-neither AP nor cigarette smoke inhalation. To induce cigarette smoke inhalation, the animals were kept in a chamber filled with tobacco smoke for 8 min thrice a day for 50 days. AP was induced 20 days after inhalation initiation by exposing their coronary pulp to their oral environment for 30 days. After animals were euthanized, their right hemimaxillae were removed for histopathological, semi-quantitative and immunohistochemical (F4/80, CD206 and iNOS) analyses. Quantitative data showed a moderate number of inflammatory infiltrates in AP and an intense number in APS (p < .05). Comparing F4/80+ cells showed no statistically significant differences among groups, but we found more CD206+ cells in AP than in C and S (p > .05). INOS+ immunostaining showed a significant increase in AP and APS, when compared with C and S (p < .05). APS had more iNOS+ cells than AP (p < .05). Cigarette smoke inhalation worsened AP, leading to a predominantly pro- inflammatory profile in our experimental model.

Vardenafil alleviates cigarette smoke-induced chronic obstructive pulmonary disease by activating autophagy via the AMPK/mTOR signalling pathway: an in vitro and in vivo study.

Chronic obstructive pulmonary disease (COPD) has always attracted global attention with its high prevalence, incidence rate, and mortality. Exposure to cigarette smoke is one of main causes of COPD. Therefore, it is still necessary to study its pathogenesis and find new therapeutic strategies for early COPD prevention and treatment. Vardenafil, a type 5 phosphodiesterase (PDE5) inhibitor, is known to have an efficient therapy in some cardiovascular, pulmonary, and vascular diseases, which is an important mechanism for COPD. However, it still loss relevant research on whether vardenafil is effective in COPD and its mechanism. In this study, the cigarette smoke inhalation was performed to establish cigarette smoke-induced COPD model using C57BL/6 mice and 16HBE cells were treated with cigarette smoke extract (CSE). Mice were treated with vardenafil for 30 d. Then condition of lung injury was evaluated using histological analysis. The content of cytokines and the number of inflammatory cells in lung tissues or bronchoalveolar lavage fluid were measured. Additionally, western blot analysis was employed to evaluate the activation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR)-mediated autophagy in vitro. The results showed that vardenafil abolished CSE's effect by activating autophagy via the AMPK/mTOR signalling pathway in vitro. Vardenafil attenuated cigarette smoke-induced lung injury and inflammation response by activating autophagy via the AMPK/mTOR signalling pathway in vivo. These results provide valuable insights into the molecular mechanisms underlying vardenafil's beneficial effects in cigarette smoke-induced COPD treatment. In conclusion, vardenafil alleviates cigarette smoke-induced experimental COPD by activating autophagy via the AMPK/mTOR signalling pathway.

Modulation of cigarette smoke induced alterations by aqueous Ocimum sanctum leaf extract in pulmonary tissue of rodents

Smoking has been associated with an increased risk of asthma, lung cancer, cardiovascular diseases, chronic bronchitis, and a massive amount of oxidative stress. The present study was undertaken to determine the modulatory effects of Holi Basil/Tulsi, (Ocimum sanctum) leaf extract on cigarette smoke-induced pulmonary damage in mice. Cigarette smoke (CS) inhalation increased the levels of pulmonary lipid peroxidation, and reactive oxygen species and decreased the levels of glutathione. Histoarchitectural alterations and enhanced tissue lactate dehydrogenase (LDH) activity in pulmonary tissue was distinctly indicative of damage. Enhanced mucin production was also observed through mucicarmine and Alcian Blue-Periodic Acid Schiff (PAS) staining. Increased expression of MUC5AC was also observed. Alterations in the lung were also evident through FTIR studies. Administration of Ocimum sanctum leaf extract (80 mg/kg b.w) to CS exposed mice ameliorated these alterations to a greater extent. These findings are suggestive of the fact that Ocimum sanctum leaf extract effectively modulated CS-induced deleterious effects on pulmonary tissue.

Testicular tissue response following a 90-day subchronic exposure to HTP aerosols and cigarette smoke in rats.

Researches have shown that chronic inhalation of cigarette smoke (CS) disrupts male reproductive system, but it is unclear about the mechanisms behind reproductive damages by tobacco toxicants in male rats. This study was designed to explore the effects of heated tobacco products (HTP) aerosols and CS exposure on the testicular health of rats. Experiments were performed on male SD rats exposed to filtered air, HTP aerosols at 10 μg/L, 23 μg/L, and 50 μg/L nicotine-equivalent contents, and also CS at 23 μg/L nicotine-equivalent content for 90 days in five exposure groups (coded as sham, HTP_10, HTP_23, HTP_50 and Cig_23). The expression of serum testosterone, testicular tissue inflammatory cytokines (IL-1β, IL-6, IL-10, TNF-α), reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA), NLRP3 inflammasome-related mRNAs and proteins (NLRP3, ASC, and Caspase-1), the degree of pyroptosis and histopathology were investigated. The results demonstrated that HTP_50 and Cig_23 caused varying degrees of oxidative damage to rat testis, resulting in a decrease of sperm quantity and serum testosterone contents, an increase in the deformity rate, expression levels of proinflammatory cytokines, and NLRP3 inflammasome-related mRNA, and an increase in the NLRP3, ASC, and Caspase-1-immunopositive cells, pyroptosis cell indices, and histopathological damage in the testes of rats. Responses from the HTP_10 and HTP_23 groups were less than those found in the above two exposure groups. These findings indicate that HTP_50 and Cig_23 induced oxidative stress in rat testes, induced inflammation and pyroptosis through the ROS/NLRP3/Caspase-1 pathway, and destroyed the integrity of thetesticular tissue structure.

ASSESSMENT OF INDOOR SECOND-HAND CIGARETTE SMOKE ON THE RESPIRATORY MECHANICS AND PREVENTIVE BENEFITS OF EUCALYPTOL: A MURINE MODEL

Second-hand smokers, in various settings such as recreational areas, schools, workplaces, homes and other enclosed public spaces also experience the detrimental effects of exposure to cigarette smoke (CS). Out of the 8 million deaths attributed to smoking, 1.2 million are a result of non-smokers being exposed to second-hand smoke. As a preventive strategy to these damages, Eucalyptol has been shown to be effective in the treatment of lung lesions caused by smoking. This study aimed to assess the effects of indoor second-hand cigarette smoke on respiratory mechanics and lung tissue, in addition to investigating the potential benefit of Eucalyptol against lung damage caused by this type of aggression. The experiments were conducted for 14 days with 40 BALB/c mice, divided into 5 groups: a control group, two groups nebulized with saline solution, divided into active and passive (second-hand) exposure to CS, two groups pre-treated with eucalyptol (10 mg/mL by nebulization) divided into active and passive exposure to CS. Lung mechanics data were collected on a flexiVent® small animal mechanical ventilator. In addition, ex vivo analysis of lung tissue micromechanics, morphometric analyzes and qualitative analyzes of lung tissue were performed. The results showed that 14 days of second-hand exposure generated significant tissue damage, causing infiltration of inflammatory cells and altering respiratory mechanics. However, pre-treatment with eucalyptol was able to prevent all changes caused by CS in both exposure protocols. We conclude that indoor second-hand smoke is capable of causing damage similar to active tobacco consumption and that Eucalyptol can be used as a preventive or nutritional resource against the changes caused by the inhalation of cigarette smoke.

Designing, implementing and evaluating an educational program regarding the effects of second-hand smoke in pregnancy on the knowledge, attitude and performance of male smokers

IntroductionContact with second-hand cigarette smoke includes inhalation of cigarette smoke caused by the burning of the cigarette itself and inhalation of smoke exhaled by the smoker. Wife's pregnancy can be a motivating factor to change the behavior of men who smoke. Therefore, this study was conducted with the aim of designing, implementing and evaluating an educational program regarding the effects of second-hand smoke in pregnancy on the knowledge, attitude and performance of male smokers.MethodologyThe present study is an interventional type of pre-test and post-test. In this phase, sampling from health centers in Isfahan was done randomly between March and July 2019, the participants were 140 smoking spouses of pregnant women, who visited health centers to receive pregnancy care, and were divided into two intervention groups and control were divided. The data collection tool was a researcher-made questionnaire on men's awareness, attitude and performance regarding second-hand smoke. All data were analyzed with SPSS18 software and Chi-score, Fisher, t-test.ResultsThe average age of the participants was 34 years. There was no significant difference between the comparison of demographic variables in the intervention and control groups (p > 0.05). The results of the paired t-test for comparing before and after the training showed that the average score of the emotional dimension of attitude in the two groups of intervention (p < 0.001) and control (p < 0.001), awareness (p < 0.001) and behavior (p < 0.001) was significantly increased in the intervention group after the training, and according to the independent t-test, the average score of the items mentioned after the training in the intervention group was higher than the control group (p < 0.05). Regarding perceived sensitivity (p = 0.066) and perceived severity (p = 0.065), no significant difference was observed.ConclusionThe awareness, emotional aspect of men's attitude and behavior regarding secondhand smoke increased, but the perceived sensitivity and severity in this regard was not significant despite the increase, so the current training package is effective in training, but considering more training sessions It is necessary with more concrete training with model or training videos in order to improve the sensitivity and perceived intensity of men.Trial registration: Registration of this randomized control trial has been completed with the Iranian Registry of Clinical Trials, IRCT20180722040555N1.