Maternal consumption of caffeine and second-hand tobacco smoke as risk factors for the development of oral clefts.

OBJECTIVE: The aim of this case-control study was to investigate environmental factors, such as caffeine, folic acid, nutritional iron supplementation, multivitamin complexes, alcohol, and tobacco (second-hand smoking), which have been described as risk factors for the development of oral clefts. METHODS: This case-control study employed convenience sampling and included 409 mothers: 132 with children with oral clefts (cases) and 277 with children without oral clefts (controls). The age range of the children in both groups was 0 to 2 years. A questionnaire was administered to each mother to inquire about their habits and food consumption during the first trimester of pregnancy. RESULTS: Folic acid supplementation was observed in 116 (87.8%) of the case group (p < 0.001) and 271 (97.8%) of the control group. Regarding the use of ferrous sulfate, 114 (86.3%) of the case group and 271 (97.8%) of the control group reported using it. In the case group, 84 (63.6%) mothers reported being exposed to second-hand smoke, and 5 (3.7%) reported alcohol consumption (p = 0.797). In terms of caffeine consumption, 127 mothers (95.4%) in the case group consumed it (p = 0.13), while 247 (88.8%) reported consumption in the control group. CONCLUSIONS: The results suggest a direct relationship between secondhand smoke, alcohol consumption, and the lack of maternal supplementation with oral clefts.

Euglena gracilis Extract Protects From Tobacco Smoke Carcinogen-Induced Lung Cancer by Altering Gut Microbiota Metabolome.

Extracts from Euglena gracilis have been shown to prevent cancer growth in mouse models. However, the molecular mechanism of this anti-cancer activity has not been determined nor has the effect of Euglena extracts on tobacco smoke carcinogen-induced carcinogenesis. Here, we investigate the hypothesis that this anti-cancer activity is a result of changes in the intestinal microbiota induced by oral administration of the extract. We found that a Euglena gracilis water extract prevents lung tumorigenesis induced by a tobacco smoke-specific carcinogen (NNK) in mice treated either 2 weeks before or 10 weeks after NNK injection. Both of these treatment regimens are associated with significant increases in 27 microbiota metabolites found in the mouse feces, including large increases in triethanolamine, salicylate, desaminotyrosine, N-acetylserine, glycolate, and aspartate. Increases in the short-chain fatty acids (SCFAs) including acetate, propionate and butyrate are also observed. We also detected a significant attenuation of lung carcinoma cell growth through the induction of cell cycle arrest and apoptosis caused by low levels of SCFAs. This study provides strong evidence of anti-cancer activity in Euglena gracilis extracts against tobacco smoke carcinogen-induced tumorigenesis and demonstrates that this activity is linked to increased production of specific gut microbiota metabolites and the resultant induction of cell cycle arrest and apoptosis of lung carcinoma cells.

The Impact of Passive Smoking on Salivary Glutathione Peroxidase and Selenium in Relation to Dental Caries Severity among Five Years Old Children.

Background: It had been found that passive smoking may have the same harmful effect as tobacco cigarettes smoking. Aims: This study was conducted to determine the effect of passive smoking on salivary glutathione peroxidase and selenium in relation to dental caries severity. Settings and Design: The sample consisted of 120 children aged 5 years old, classified into four groups according to the number of cigarettes smoked by their fathers daily: Passive smoking children of 5-10 cigarettes, those of 10-15 cigarettes daily, those of 15-20 cigarettes daily and non-passive smoking children of no smokers indoor (the control group). The sample was further classified according to dental caries severity into three groups: mild (DMFS values <4), moderate (DMFS values from 4 to 8) and severe (DMFS values >8). Methods and Material: Stimulated saliva was collected, and salivary glutathione peroxidase and selenium were chemically analysed. Results and Conclusions: Glutathione peroxidase and selenium were higher among non-passive smoking children than passive smoking children and they were higher among children with mild caries severity than in children with moderate or severe caries severity (p < 0.01). Passive smoking had significant effect in both salivary glutathione peroxidase and selenium (p < 0.01), while dental caries had non-significant effect on them (p > 0.05). In conclusion, passive smoking had deleterious effect in salivary glutathione peroxidase and selenium, while dental caries did not have effect on these two variables. There is no interaction between both passive smoking and dental caries in neither glutathione peroxidase nor selenium, so the effect of passive smoking on these two variables can exceed the effect of dental caries on them.

Regulation of oxidative stress and inflammatory responses in human retinal pigment epithelial cells.

Age-related macular degeneration (AMD) is an eye disease, which causes impaired vision that can lead to blindness. The incidence of AMD increases with age. Retinal pigment epithelial (RPE) cells maintain retinal homeostasis and support the functionality of photoreceptors. In the pathogenesis of AMD, the degeneration of the RPE cells precedes photoreceptor cell death. RPE cells are susceptible to oxidative stress, and chronic inflammation involving nucleotide-binding domain, leucine-rich repeat and pyrin domain 3 (NLRP3) inflammasome activation and impaired autophagy are challenges faced by aged RPE cells in AMD. There are two types of AMD, dry (85-90%) and wet (10-15%) disease forms. Choroidal neovascularization is typical for wet AMD, and anti-vascular endothelial growth factor (anti-VEGF) injections are used to prevent the progression of the disease but there is no curative treatment. There is no cure for the dry disease form, but antioxidants have been proposed as a potential treatment option. Ageing is the most important risk factor of AMD, and tobacco smoke is the most important environmental risk factor that can be controlled. Hydroquinone is a cytotoxic, immunotoxic, carcinogenic and pro-oxidative component of tobacco smoke. The aim of this PhD thesis was to study hydroquinone-induced oxidative stress and NLRP3 inflammasome activation in human RPE cells (ARPE-19 cells). An age-related eye disease study (AREDS) formulation (incl. omega-3 fatty acids, vitamin C and E, copper, zinc, lutein and zeaxanthin), which is clinically investigated p.o. dosing combination of dietary supplements for AMD patients, has been evaluated as a possible treatment and restraining option for AMD. Resvega (4.1.1, Table 2) is a similar kind of product to AREDS with added resveratrol, and many of the components incorporated within Resvega can be considered as belonging to the normal antioxidative defence system of the retina. Another aim was to evaluate the effects of Resvega on hydroquinone-induced oxidative stress or NLRP3 inflammasome activation induced by impaired protein clearance. The results of this study reveal that hydroquinone elevated the activity of NADPH oxidase which subsequently mediated the production of reactive oxygen species (ROS) and predisposed RPE cells to degeneration by reducing levels of vascular endothelial growth factor (VEGF) and pigment epithelium-derived factor (PEDF). Hydroquinone induced an NLRP3-independent IL-18 release and NLRP3 accumulation inside the IL-1α-primed cells. Resvega treatment reduced the extent of hydroquinone-induced ROS production and NLRP3 inflammasome activation evoked by impaired protein clearance. Thus, Resvega alleviated hydroquinone- and impaired protein clearance-induced stress in human RPE cells, but more studies are needed, for example, to reveal the most optimal route of administration for targeting the cells in the retina, since both oxidative stress and NLRP3 inflammasome activation are important contributors to the development of AMD and represent significant treatment targets.

Financial Insecurity and Food Insecurity among U.S. Children with Secondhand and Thirdhand Smoke Exposure.

Objectives: Smokers with financial and food insecurity may find it difficult to quit smoking and reduce their children's tobacco smoke exposure (TSE). The objective was to examine the associations between child TSE and financial and food insecurity among U.S. school-aged children. Methods: We examined the 2018−2019 National Survey of Children's Health data on 17,484 children 6−11 years old. Children were categorized into TSE groups: (1) No TSE: did not live with a smoker; (2) thirdhand smoke (THS) exposure alone: lived with a smoker who did not smoke inside the home; or (3) secondhand smoke (SHS) and THS exposure: lived with a smoker who smoked inside the home. We conducted weighted logistic, ordinal, and linear regression analyses to assess the relationships between child TSE status and financial and food insecurity, adjusting for covariates. Results: Overall, 13.1% and 1.8% of children had THS exposure alone and SHS and THS exposure, respectively. Compared to children with no TSE, children with THS exposure alone were at 2.17 increased odds (95% CI = 1.83, 2.58, p < 0.001) and children with SHS and THS exposure were at 2.24 increased odds (95% CI = 1.57, 3.19, p < 0.001) of having financial insecurity. Children with THS exposure alone were at 1.92 increased odds (95% CI = 1.58, 2.33, p < 0.001) and children with SHS and THS exposure were at 2.14 increased odds (95% CI = 1.45, 3.16, p < 0.001) of having food insecurity. Conclusions: Children with TSE are at increased risk of experiencing financial and food insecurity. When developing tobacco interventions, a holistic approach to tobacco control that addresses ways to decrease financial and food hardships may improve outcomes.

What is the association between secondhand smoke (SHS) and possible obstructive sleep apnea: a meta-analysis.

BACKGROUND: Association between smoking and sleep apnea is well-known from previous studies. However, the influence of secondhand smoke (SHS), which is a potential risk factor of obstructive sleep apnea (OSA), remains unclear. Our aim was to investigate the relationship between SHS and OSA using a meta-analysis. MATERIALS AND METHODS: For the meta-analysis, searches were performed in MEDLINE, EMBASE, and Web of Science databases on January 10, 2022, by combining various keywords including "SHS exposure" and "OSA". Data were extracted using defined inclusion and exclusion criteria. Fixed-effects model meta-analyses were used to pool risk ratio (RR) estimates with their 95% confidence intervals (CI). I2 was used to assess heterogeneity. Moreover, we performed subgroup meta-analyses of children-adults, and smoker fathers and mothers. RESULTS: In total, 267 articles were obtained through an electronic search. Twenty-six articles were included in our analysis according to the inclusion and exclusion criteria. We found evidence of an association between SHS exposure and possible OSA (RR 1.64, 95% CI 1.44-1.88). The results of the subgroup analyses showed that children passive smokers (RR 1.84, 95% CI 1.60-2.13) were at greater risks of possible OSA than adult passive smokers (RR 1.35, 95% CI 1.21-1.50). Also, significant differences were observed in mothers with smoking exposure (RR 2.61, 95% CI 1.62-4.21, p < 0.0001), as well as in fathers with smoking exposure (RR 2.15, 95% CI 0.98-4.72, p = 0.06). SHORT CONCLUSION: Our meta-analysis confirmed that SHS exposure is significantly associated with OSA. In the subgroup analyses, the association of SHS and possible OSA was significant in both children and adults, as well as in smoker mothers and fathers.

RAGE signaling during tobacco smoke-induced lung inflammation and potential therapeutic utility of SAGEs.

BACKGROUND: Smoke exposure culminates as a progressive lung complication involving airway inflammation and remodeling. While primary smoke poses the greatest risk, nearly half of the US population is also at risk due to exposure to secondhand smoke (SHS). METHODS: We used WT, RAGE-/- (KO), and Tet-inducible lung-specific RAGE overexpressing transgenic (TG) mice to study the role of RAGE during short-term responses to SHS. We evaluated SHS effects in mice with and without semi-synthetic glycosaminoglycan ethers (SAGEs), which are anionic, partially lipophilic sulfated polysaccharide derivatives known to inhibit RAGE signaling. TG Mice were weaned and fed doxycycline to induce RAGE at postnatal day (PN) 30. At PN40, mice from each line were exposed to room air (RA) or SHS from three Kentucky 3R4F research cigarettes via a nose-only delivery system (Scireq Scientific, Montreal, Canada) five days a week and i.p. injections of PBS or SAGE (30 mg/kg body weight) occurred three times per week from PN40-70 before mice were sacrificed on PN70. RESULTS: RAGE mRNA and protein expression was elevated following SHS exposure of control and TG mice and not detected in RAGE KO mice. Bronchoalveolar lavage fluid (BALF) analysis revealed RAGE-mediated influence on inflammatory cell diapedesis, total protein, and pro-inflammatory mediators following exposure. Lung histological assessment revealed indistinguishable morphology following exposure, yet parenchymal apoptosis was increased. Inflammatory signaling intermediates such as Ras and NF-κB, as well as downstream responses were influenced by the availability of RAGE, as evidenced by RAGE KO and SAGE treatment. CONCLUSIONS: These data provide fascinating insight suggesting therapeutic potential for the use of RAGE inhibitors in lungs exposed to SHS smoke.

Association between secondhand smoke and peripheral arterial disease: a meta-analysis of cross-sectional studies.

PURPOSE: The association between secondhand smoke (SHS) and peripheral arterial disease (PAD) was inconsistent and the studies were relatively scarce, hence, we conducted a meta-analysis of the association between SHS and PAD. MATERIALS AND METHODS: We systematically searched three electronic databases (PubMed, EMBASE, and Web of Science), and calculated the pooled prevalence risk ratio (RR) and estimated standard error by random effect model from the meta-analysis. Furthermore, we performed a subgroup meta-analysis according to the location of SHS exposure. RESULTS: We initially identified 502 articles from the electronic database, and 6 articles, cross-sectional data from 4 cross-sectional studies and 2 prospective cohort studies, were included in the meta-analysis. Among these six articles, two studies showed a significant correlation between SHS exposure and PAD, whereas no study showed a negative correlation between SHS exposure and PAD. In the meta-analysis, pooled prevalence showed a significant association between SHS exposure and PAD (RR = 1.23; 95% confidence interval [CI] 1.08-1.41; z = 3.02, p = 0.003). In the subgroup analysis based on location of SHS exposure, the prevalence RR of PAD at home was 1.30 (95% CI 1.14-1.49, Z-3.99, p < 0.0001). The prevalence RR in the subgroup of SHS exposure at work was not significant (RR = 0.89; 95% CI 0.55-1.44; z = 0.48, p = 0.63). CONCLUSION: Exposure to SHS was significantly and positively associated with PAD. Moreover, we found a significant association between exposure to SHS and PAD at home, but the association was not significant at work.

The mutagenic effect of tobacco smoke on male fertility.

Despite the association between tobacco use and the harmful effects on general health as well as male fertility parameters, smoking remains globally prevalent. The main content of tobacco smoke is nicotine and its metabolite cotinine. These compounds can pass the blood-testis barrier, which subsequently causes harm of diverse degree to the germ cells. Although controversial, smoking has been shown to cause not only a decrease in sperm motility, sperm concentration, and an increase in abnormal sperm morphology, but also genetic and epigenetic aberrations in spermatozoa. Both animal and human studies have highlighted the occurrence of sperm DNA-strand breaks (fragmentation), genome instability, genetic mutations, and the presence of aneuploids in the germline of animals and men exposed to tobacco smoke. The question to be asked at this point is, if smoking has the potential to cause all these genetic aberrations, what is the extent of damage? Hence, this review aimed to provide evidence that smoking has a mutagenic effect on sperm and how this subsequently affects male fertility. Additionally, the role of tobacco smoke as an aneugen will be explored. We furthermore aim to incorporate the epidemiological aspects of the aforementioned and provide a holistic approach to the topic.

Interaction of Passive Smoking and Diet Habits on Vitamin D Deficiency among Women of Reproductive Age in Rural Central China.

Objective: Maternal dietary undernutrition is known to be associated with the risk of vitamin D (VD) deficiency. However, whether the risk of VD deficiency in women of reproductive age is influenced by the interaction between passive smoking and inadequate nutrition remains unknown. The aim of this study is to explore the interaction between passive smoking and dietary undernutrition on the risk of VD deficiency. Methods: A population-based case−control study including 1151 non-pregnant women of reproductive age between 18 and 40 years old was conducted in Henan Province, China from 2009 to 2010. Blood samples and information on exposure factors were collected. The prevalence of VD deficiency was estimated based on a result of serum 25-hydroxyvitamin D [25(OH)D] < 26.0 ng/mL. A multivariate logistic regression analysis was performed to explore the risk of VD deficiency. Results: The prevalence of VD deficiency was 61.5%. After adjusting for potential confounding factors, the interactions between passive smoking and no nutritional supplementation, passive smoking and insufficient egg intake, and passive smoking and insufficient milk dairy products intake were associated with the risk of VD deficiency, and the adjusted ORs were 3.40 (95% CI 2.26−5.13), 2.87 (95% CI 2.20−4.10), and 2.18 (95% CI 1.33−3.58), respectively. The interaction coefficients were calculated to be 2.35, 2.79, and 1.70, respectively, indicating there were significant interaction effects, as all of the coefficients were higher than 1. Conclusions: Our findings present that the risk of VD deficiency was potentially influenced by interactions between passive smoking and inadequate nutrition. Passive smoking might strengthen the effect of inadequate nutrition on the risk of VD deficiency among rural women of reproductive age. More attention should be paid to the health education and nutritional status improvement of women of reproductive age, especially in rural areas of developing countries.

Protective effect of Palmijihwanghwan in a mouse model of cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease.

BACKGROUND: Palmijihwanghwan (PJH) is a traditional medicine and eight constituents derived from PJH possess anti-inflammatory activities. However, the scientific evidence for its potential as a therapeutic agent for inflammatory lung disease has not yet been studied. In this study, we examined the protective effect of PJH in a mouse model of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke (CS) with lipopolysaccharide (LPS). METHODS: Mice received CS exposure for 8 weeks and intranasal instillation of LPS on weeks 1, 3, 5 and 7. PJH (100 and 200 mg/kg) was administrated daily 1 h before CS treatment for the last 4 weeks. RESULTS: Compared with CS plus LPS-exposed mice, mice in the PJH-treated group showed significantly decreased inflammatory cells count and reduced inflammatory cytokines including interleukin-1 beta (IL-1ß), IL-6 and tumor necrosis factor alpha (TNF-α) levels in broncho-alveolar lavage fluid (BALF) and lung tissue. PJH also suppressed the phosphorylation of nuclear factor kappa B (NF-κB) and extracellular signal-regulated kinase1/2 (ERK1/2) caused by CS plus LPS exposure. Furthermore, CS plus LPS induced increases in matrix metallopeptidase (MMP)-7, MMP-9, and transforming growth factor-ß (TGF-ß) expression and collagen deposition that were inhibited in PJH-treated mice. CONCLUSIONS: This study demonstrates that PJH prevents respiratory inflammation and airway remodeling caused by CS with LPS exposure suggesting potential therapy for the treatment of COPD.

Intrauterine and postnatal exposure to tobacco and wood smoke on hypothalamic development and cognition: an integrative review of the literature / Exposición intrauterina y postnatal al humo de tabaco y de leña en el desarrollo hipotalámico y la cognición: una revisión integrativa de la literatura

SUMMARY: Exposure to air pollution and its pollutants has been associated with important effects on human health since the first years of life, thus it has been seen that exposure to tobacco smoke and wood smoke is directly related to cardiovascular and pulmonary diseases, respiratory and cancers. However, exposure to air pollution during fetal development and its effects on brain structure and function during early childhood and adolescence have been little studied. In this review we have analyzed the literature on prenatal exposure to tobacco and wood smoke and its relationship with hypothalamic development and cognition in the first years of life.The molecular, morphological and physiological aspects of the relationship between pre- and postnatal exposure to tobacco and wood smoke with neural developmental, cognitive and behavioral problems during early childhood and adolescence have not yet been fully clarified. The information available in the scientific literature based on antecedents obtained from epidemiological studies has been negatively affected by confounding variables and great methodological challenges that make it impossible to affirm an exact causal relationship with certainty.

RESUMEN: La exposición a la contaminación del aire se ha asociado con importantes efectos en la salud humana desde los primeros años de vida. Estudios han demostrado con certeza que la exposición al humo de tabaco y humo de leña está directamente relacionada con enfermedades cardiovasculares, pulmonares, respiratorias y cánceres. Sin embargo, la exposición a la contaminación del aire durante el desarrollo fetal y sus efectos a posteriori sobre la estructura y función del cerebro durante la primera infancia y la adolescencia son aún desconocidos. En esta revisión analizamos la literatura sobre la exposición prenatal al tabaco y al humo de leña y su relación con el desarrollo hipotalámico y la cognición en los primeros años de vida. Los aspectos moleculares, morfológicos y fisiológicos de la asociación entre la exposición pre y postnatal al humo de tabaco o al humo de leña con problemas del desarrollo neurológico normal, cognitivos y de comportamiento durante la primera infancia y la adolescencia aún no se han aclarado completamente. La información disponible en la literatura científica basada en antecedentes obtenidos de estudios epidemiológicos ha sido afectada negativamente por variables de confusión y grandes desafíos metodológicos que hacen imposible afirmar una relación directa y causal exacta con certeza.

Risk factors associated with congenital anomalies among newborns in southwestern Ethiopia: A case-control study.

INTRODUCTION: Human embryo is well protected in the uterus by the embryonic membrane, although teratogens may cause developmental disruptions after maternal exposure to them during early pregnancy. Most of the risk factors contributing to the development of congenital anomalies are uncertain; however, genetic factors, environmental factors and multifactorial inheritance are found to be risk factors. Regardless of their clinical importance, there are little/no studies conducted directly related to predisposing risk factors in southwestern Ethiopia. OBJECTIVE: The study aimed to determine the associated risk factors with congenital anomalies among newborns in southwestern Ethiopia. METHODS: Case-control study was conducted on newborns and their mothers in six purposively selected hospitals in southwestern Ethiopia from May 2016 to May 2018. Data was collected after evaluation of the neonates for the presence of congenital anomalies using the standard pretested checklist. The data was analyzed using SPSS version 25.0. P <0.01 was set as statistically significant. RESULTS: Risk factors such as unidentified medicinal usage in the first three months of pregnancy (AOR = 3.435; 99% CI: 2.012-5.863), exposure to pesticide (AOR = 3.926; 99% CI: 1.266-12.176), passive smoking (AOR = 4.104; 99% CI: 1.892-8.901), surface water as sources of drinking (AOR = 2.073; 99% CI: 1.221-3.519), folic acid supplementation during the early pregnancy (AOR = 0.428; 99% CI: 0.247-0.740) were significantly associated with the congenital anomalies. CONCLUSIONS: In this study, risk factors such as passive smoking, exposure to pesticides, chemicals and use of surface water as a source of drinking during early pregnancy had a significant association with congenital anomalies. There is a need to continuously provide health information for the community on how to prevent and control predisposing risk factors.

Interactive Effects of Omega-3 Polyunsaturated Fatty Acids and Secondhand Smoke in Mice and Human Subjects.

Active smoking and secondhand smoke (SHS) exposure increase the risk of cardiovascular morbidity and mortality. Active smoking is associated with reduced levels of omega-3 polyunsaturated fatty acids (n-3 PUFA) and studies show that n-3 PUFA supplementation can improve smoking-induced vascular dysfunction. However, the relationship between n-3 PUFA and SHS exposure has not been studied. Fat-1 transgenic mice, which convert n-6 to n-3 PUFA, were fed diets with n-3 PUFA or without (n-6 PUFA diet), exposed to air or SHS for 4 weeks, and vasoreactivity, antioxidant indices, and omega-3 index (percent eicosapentaenoic + docosahexaenoic acids in RBC) measured. Compared to air-exposed mice, SHS-enhanced aortic constriction in mice fed the n-6 PUFA diet (omega-3 index, 5.9 ± 0.2%; mean ± SE), but not in mice fed the n-3 PUFA diet (omega-3 index, 7.8 ± 0.6%). SHS also significantly induced mRNA expression of cytochrome P4501A1, NADPH:quinone oxidoreductase, heme oxygenase-1, and angiotensinogen in adipose tissue, and increased antioxidant capacity only in mice on the n-6 PUFA diet. Notably, SHS reduced the omega-3 index by 1.0 percentage point (p = 0.003), compared to air-exposed mice irrespective of diet. Additionally, we recruited human nonsmokers (NS) with and without SHS exposure (n = 40) 19-40 years old and measured the omega-3 index and antioxidant capacity. In human subjects SHS exposure was associated with a significantly lower omega-3 index (NS, 4.4 ± 1.1%; NS + SHS, 3.2 ± 1.0%; mean ± SD, p = 0.002) and higher antioxidant capacity (p < 0.001) than unexposed NS. Thus, SHS exposure is associated with lower levels of n-3 PUFA in mice and humans; however, an omega-3 index of ~ 8% in mice has vasoprotective and antioxidant properties.

Sex-specific effects of in utero and adult tobacco smoke exposure.

Tobacco smoke has harmful effects on a multiorgan level. Exposure to smoke, whether in utero or environmental, significantly increases susceptibility. This susceptibility has been identified to be divergent between males and females. However, there remains a distinct lack of thorough research into the relationship between sex and exposure to tobacco. Females tend to generate a more significant response than males during adulthood exposure. The intrauterine environment is meticulously controlled, and exposure to tobacco presents a significant factor that contributes to poor health outcomes and susceptibility later in life. Analysis of these effects in relation to the sex of the offspring is yet to be holistically reviewed and summarized. In this review, we will delineate the time-dependent relationship between tobacco smoke exposure and sex-specific disease susceptibility. We further outline possible biological mechanisms that may contribute to the identified pattern.

Chronic Maternal Tobacco Smoke Exposure and/or Alpha-Lipoic Acid Treatment Causes Long-Term Deterioration of Testis and Sexual Behavior in Adult Male Rats.

BACKGROUND: Tobacco use during pregnancy is known to have several negative effects on the offspring's reproductive health in the long term. The use of alpha-lipoic acid (ALA) as a dietary supplement during pregnancy has increased greatly in recent years and has been known to have positive effects on various pregnancy outcomes including miscarriage, diabetic embryopathy, preterm delivery, and congenital malformations. AIM: To evaluate the effects of tobacco smoke exposure (TSE) on sexual behavior, reproductive parameters, and testicles in adult male rats and to reveal the possible role of ALA administration on these parameters. METHODS: Pregnant rats (n = 7 per group) were treated with tobacco smoke (TS), ALA (20 mg/kg), and TS + ALA for a total of 11 weeks. The following parameters were compared with 8 control rats: puberty parameters, sexual behavior; levels of serum gonadotropins and testosterone, total antioxidant status, and total oxidant status; the expression of the apoptotic protease-activating factor-1 and caspase 9 mRNA levels in the testis; and assessment of immunohistochemistry and terminal deoxynucleotidyl transferase dUTP nick end labeling assay of testis. MAIN OUTCOME MEASURE: Sexual behavior, changes in puberty parameters, and hormonal and genetic alterations were the outcomes analyzed in this study. RESULTS: Maternal TSE caused a significant decrease in the number of intromissions compared to the control group. Similarly, ALA decreased erectile function in sexual behavior by decreasing the number of intromissions and intromission ratio in the ALA group compared to the control group. In addition, TSE and ALA treatment caused an impairment of some consummatory sexual behaviors. Also, in parallel with this inhibitory effect, the age of pubertal onset was significantly delayed in the TS + ALA group compared to other groups. Also, histopathological changes in testicular tissue, oxidative stress markers, apoptotic index, and mRNA levels of apoptosis-related genes increased in all treatment groups. CLINICAL IMPLICATIONS: The use of ALA and/or tobacco products during pregnancy may adversely affect the reproductive health of male newborns in the long term. STRENGTHS & LIMITATIONS: To the best of our knowledge, this study is the first to show the effects of maternal ALA treatment and/or TSE on the sexual behavior and reproductive parameters in male rats; however, the study is based on an animal model, and the present findings partially reflect the characteristics of human sexual behavior. CONCLUSION: Maternal TSE and/or ALA treatment may impair sexual behavior in adulthood in male rats because of testicular damage caused by oxidative stress during gonadal development. Yardimci A, Akkoc RF, Tektemur A, et al. Chronic Maternal Tobacco Smoke Exposure and/or Alpha-Lipoic Acid Treatment Causes Long-Term Deterioration of Testis and Sexual Behavior in Adult Male Rats. J Sex Med 2020;17:1835-1847.

Effects of fixed oil of Caryocar coriaceum Wittm. Seeds on the respiratory system of rats in a short-term secondhand-smoke exposure model.

ETHNOPHARMACOLOGICAL RELEVANCE: Pequi fruit are obtained from the pequi tree (Caryocar coriaceum), from which the pulp and nut are used in order to extract an oil that is commonly used in popular medicine as an antiinflammatory agent, particularly for the treatment of colds, bronchitis and bronchopulmonary infections. Making use of the fixed oil of Caryocar coriaceum (FOCC), an attractive alternative for the treatment of diseases caused by exposure to environmental tobacco smoke. AIM OF THE STUDY: To evaluate whether oral intake FOCC provides beneficial effects in the respiratory system of rats submitted to a short-term secondhand smoke (SHS) exposure model. MATERIALS AND METHODS: The experiments were performed on Wistar rats divided into 4 groups; in the SHS + O and SHS + T groups, the animals were pretreated orally with 0.5 mL of FOCC (SHS + O) or vehicle (Tween-80 [1%] solution) (SHS + T). Immediately after pretreatment, the animals were submitted to the SHS exposure protocol, for a total period of 14 days. Exposures were performed 6 times per day, with a duration of 40 min per exposure (5 cigarettes per exposure), followed by a 1-h interval between subsequent exposures. In the AA + O and AA + T groups, animals were submitted to daily oral pretreatment with 0.5 mL of FOCC (AA + O) or vehicle (AA + T). These animals were then subjected to the aforementioned exposure protocol, but using ambient air. After the exposure period, we investigated the effects of FOCC in respiratory mechanics in vivo (Newtonian resistance -RN, tissue elastance -H, tissue resistance -G, static compliance -CST, inspiratory capacity -IC, PV loop area) histopathology and lung parenchymal morphometry in vitro (polymorphonuclear cells -PMN, mean alveolar diameter -Lm, bronchoconstriction index -BCI), temporal evolution of subjects' masses, and percent composition of the FOCC. RESULTS: Regarding the body mass of the animals, the results demonstrated an average body mass gain of 10.5 g for the animals in the AA + T group, and 15.5 g for those in the AA + O group. On the other hand, the body mass of animals in the SHS + T and SHS + O suffered an average loss of 14.4 and 4.75 g, respectively. Regarding respiratory system analyzes, our results demonstrated significant changes in all respiratory mechanics variables and lung parenchyma morphometry analyzed for the SHS + T group when compared to the AA + T group (p < 0,05), confirming the establishment of pulmonary injury induced by SHS exposure. We also observed that rats pretreated orally with FOCC (SHS + O) showed improvement in all variables when compared to the SHS + T group (p < 0,05), thus demonstrating the effectiveness of FOCC in preventing lung damage induced by short-term SHS exposure. CONCLUSION: In conclusion, our results demonstrate that FOCC was able to prevent lung injury in rats submitted to short-term SHS exposure.

Fructus mume Protects Against Cigarette Smoke Induced Chronic Cough Guinea Pig.

Fructus mume was recorded in the Chinese Pharmacopoeia and traditional Chinese medical books for chronic cough, but the effect and related constituents are still unknown. Thus, we investigated the protect effects and the relevant constituents of F. mume in a guinea pig model with chronic cough induced by cigarette smoke (CS). The organic acids and polysaccharides in F. mume were detected by high performance liquid chromatography, gel permeation chromatography, and gas chromatography-mass spectrometry. The guinea pigs were orally administrated with vehicle or the water extract of Fructus mume (FW) during the 14 days of CS exposure. Citric acid induced coughs were automatically measured by Buxco system. The differential cells in bronchoalveolar lavage fluid (BALF) and histopathological changes in lung tissue were assessed by hematoxylin and eosin staining. The tumor necrosis factor alpha (TNF-α) and interleukin-8 (IL-8) levels in lung tissue were detected via enzyme-linked immunosorbent assay. The mucus productions in tracheas were determined with Alcian blue-periodic acid Schiff staining. The results suggested relatively high concentration of citric acid, chlorogenic acid, and neochlorogenic acid in F. mume, and high proportion of galactose and glucose and lower molecular weight of polysaccharides. Administration of FW significantly reduced the cough frequency, decreased inflammatory cells in BALF and lung tissue, and attenuated the thickening of airway epithelium and submucosa compared with CS-exposure group. Moreover, the overproduction of TNF-α and IL-8 in lung tissues, and mucus in central airways of CS-induced guinea pigs was markedly inhibited by FW. The extract could also protect against CS exposure-induced chronic cough in guinea pigs by reducing coughs, airways inflammation, and mucus overproduction.

Phytochemical study, molecular docking, genotoxicity and therapeutic efficacy of the aqueous extract of the stem bark of Ximenia americana L. in the treatment of experimental COPD in rats.

ETHNOPHARMACOLOGICAL RELEVANCE: Ximenia americana L. is popularly known as yellow plum, brave plum or tallow wood. All the parts of this plant are used in popular medicine. Its reddish and smooth bark are used to treat skin infections, inflammation of the mucous membranes and in the wound healing process. OBJECTIVE: Verification of phytochemical profile, the molecular interaction between flavonoid, (-) epi-catechin and 5-LOX enzyme, by means of in silico study, the genotoxic effect and to investigate the pharmacological action of the aqueous extract of the stem bark of X. americana in pulmonary alterations caused by experimental COPD in Rattus norvegicus. MATERIALS AND METHODS: The identification of secondary metabolites was carried out by TLC and HPLC chromatographic methods, molecular anchoring tests were applied to analyze the interaction of flavonoid present in the extract with the enzyme involved in pulmonary inflammation process and the genotoxic effect was assessed by comet assay and micronucleus test. For induction of COPD, male rats were distributed in seven groups. The control group was exposed only to ambient air and six were subjected to passive smoke inhalations for 20 min/day for 60 days. One of the groups exposed to cigarette smoke did not receive treatment. The others were treated by inhalation with beclomethasone dipropionate (400 mcg/kg) and aqueous and lyophilized extracts of X. americana (500 mg/kg) separately or in combination for a period of 15 days. The structural and inflammatory pulmonary alterations were evaluated by histological examination. Additional morphometric analyses were performed, including the alveolar diameter and the thickness of the right ventricle wall. RESULTS: The results showed that the aqueous extract of the bark of X. americana possesses (-) epi -catechin, in silico studies with 5-LOX indicate that the EpiC ligand showed better affinity parameters than the AracA ligand, which is in accordance with the results obtained in vivo studies. Genotoxity was not observed at the dose tested and the extract was able to stagnate the alveolar enlargement caused by the destruction of the interalveolar septa, attenuation of mucus production and decrease the presence of collagen fibers in the bronchi of animals submitted to cigarette smoke. CONCLUSION: Altogether, the results proved that the aqueous extract of X. americana presents itself as a new option of therapeutic approach in the treatment of COPD.

Does smoking increase the anesthetic requirement?

Background/aim: To examine the effects of active and passive smoking on perioperative anesthetic and analgesic consumption. Materials and methods: Patients were divided into three groups: group S, smokers; group PS, passive smokers; and group NS, individuals who did not have a history of smoking and were not exposed to smoke. All patients underwent the standard total intravenous anesthesia method. The primary endpoint of this study was determination of the total amount of propofol and remifentanil consumed. Results: The amount of propofol used in induction of anesthesia was significantly higher in group S compared to groups PS and NS. Moreover, the total consumption of propofol was significantly higher in group S compared to groups PS and NS. The total propofol consumption of group PS was significantly higher than that of group NS (P = 0.00). Analysis of total remifentanil consumption showed that remifentanil use was significantly higher in group S compared to group NS (P = 0.00). Conclusion: The amount of the anesthetic required to ensure equal anesthetic depth in similar surgeries was higher in active smokers and passive smokers compared to nonsmokers.