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.

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.

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.

Exposure to Crude Oil-Related Volatile Organic Compounds Associated with Lung Function Decline in a Longitudinal Panel of Children.

BACKGROUND: Children in the affected area were exposed to large amounts of volatile organic compounds (VOCs) from the Hebei Spirit oil spill accident. OBJECTIVES: We investigated the lung function loss from the exposure to VOCs in a longitudinal panel of 224 children 1, 3, and 5 years after the VOC exposure event. METHODS: Atmospheric estimated concentration of total VOCs (TVOCs), benzene, toluene, ethylbenzene, and xylene for 4 days immediately after the accident were calculated for each village (n = 83) using a modeling technique. Forced expiratory volume in 1 s (FEV1) as an indicator of airway status was measured 1, 3, and 5 years after the exposure in 224 children 4~9 years of age at the exposure to the oil spill. Multiple linear regression and linear mixed models were used to evaluate the associations, with adjustment for smoking and second-hand smoke at home. RESULTS: Among the TVOCs (geometric mean: 1319.5 mg/m3·4 d), xylene (9.4), toluene (8.5), ethylbenzene (5.2), and benzene (2.0) were dominant in the order of air concentration level. In 224 children, percent predicted FEV1 (ppFEV1), adjusted for smoking and second-hand smoke at home, was 100.7% after 1 year, 96.2% after 3 years, and 94.6% after 5 years, and the loss over the period was significant (p < 0.0001). After 1 and 3 years, TVOCs, xylene, toluene, and ethylbenzene were significantly associated with ppFEV1. After 5 years, the associations were not significant. Throughout the 5 years' repeated measurements in the panel, TVOCs, xylene, toluene, and ethylbenzene were significantly associated with ppFEV1. CONCLUSIONS: Exposure to VOCs from the oil spill resulted in lung function loss among children, which remained significant up to 5 years after the exposure.

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.

Computational Insights into ß-Carboline Inhibition of Monoamine Oxidase A.

Monoamine oxidases (MAOs) are an important group of enzymes involved in the degradation of neurotransmitters and their imbalanced mode of action may lead to the development of various neuropsychiatric or neurodegenerative disorders. In this work, we report the results of an in-depth computational study in which we performed a static and a dynamic analysis of a series of substituted ß-carboline natural products, found mainly in roasted coffee and tobacco smoke, that bind to the active site of the MAO-A isoform. By applying molecular docking in conjunction with structure-based pharmacophores and molecular dynamics simulations coupled with dynamic pharmacophores, we extensively investigated the geometric aspects of MAO-A binding. To gain insight into the energetics of binding, we used the linear interaction energy (LIE) method and determined the key anchors that allow productive ß-carboline binding to MAO-A. The results presented herein could be applied in the rational structure-based design and optimization of ß-carbolines towards preclinical candidates that would target the MAO-A enzyme and would be applicable especially in the treatment of mental disorders such as depression.

Embryonic exposure to benzo[a]pyrene causes age-dependent behavioral alterations and long-term metabolic dysfunction in zebrafish.

Polycyclic aromatic hydrocarbons (PAH) are products of incomplete combustion which are ubiquitous pollutants and constituents of harmful mixtures such as tobacco smoke, petroleum and creosote. Animal studies have shown that these compounds exert developmental toxicity in multiple organ systems, including the nervous system. The relative persistence of or recovery from these effects across the lifespan remain poorly characterized. These studies tested for persistence of neurobehavioral effects in AB* zebrafish exposed 5-120 h post-fertilization to a typical PAH, benzo[a]pyrene (BAP). Study 1 evaluated the neurobehavioral effects of a wide concentration range of BAP (0.02-10 µM) exposures from 5 to 120 hpf during larval (6 days) and adult (6 months) stages of development, while study 2 evaluated neurobehavioral effects of BAP (0.3-3 µM) from 5 to 120 hpf across four stages of development: larval (6 days), adolescence (2.5 months), adulthood (8 months) and late adulthood (14 months). Embryonic BAP exposure caused minimal effects on larval motility, but did cause neurobehavioral changes at later points in life. Embryonic BAP exposure led to nonmonotonic effects on adolescent activity (0.3 µM hyperactive, Study 2), which attenuated with age, as well as startle responses (0.2 µM enhanced, Study 1) at 6 months of age. Similar startle changes were also detected in Study 2 (1.0 µM), though it was observed that the phenotype shifted from reduced pretap activity to enhanced posttap activity from 8 to 14 months of age. Changes in the avoidance (0.02-10 µM, Study 1) and approach (reduced, 0.3 µM, Study 2) of aversive/social cues were also detected, with the latter attenuating from 8 to 14 months of age. Fish from study 2 were maintained into aging (18 months) and evaluated for overall and tissue-specific oxygen consumption to determine whether metabolic processes in the brain and other target organs show altered function in late life based on embryonic PAH toxicity. BAP reduced whole animal oxygen consumption, and overall reductions in total basal, mitochondrial basal, and mitochondrial maximum respiration in target organs, including the brain, liver and heart. The present data show that embryonic BAP exposure can lead to neurobehavioral impairment across the life-span, but that these long-term risks differentially emerge or attenuate as development progresses.

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.

Molecular signatures of organic particulates as tracers of emission sources.

Chemical signature of airborne particulates and deposition dusts is subject of study since decades. Usually, three complementary composition markers are investigated, namely, (i) specific organic compounds; (ii) concentration ratios between congeners, and (iii) percent distributions of homologs. Due to its intrinsic limits (e.g., variability depending on decomposition and gas/particle equilibrium), the identification of pollution sources based on molecular signatures results overall restricted to qualitative purposes. Nevertheless, chemical fingerprints allow drawing preliminary information, suitable for successfully approaching multivariate analysis and valuing the relative importance of sources. Here, the state-of-the-art is presented about the molecular fingerprints of non-polar aliphatic, polyaromatic (PAHs, nitro-PAHs), and polar (fatty acids, organic halides, polysaccharides) compounds in emissions. Special concern was addressed to alkenes and alkanes with carbon numbers ranging from 12 to 23 and ≥ 24, which displayed distinct relative abundances in petrol-derived spills and exhausts, emissions from microorganisms, high vegetation, and sediments. Long-chain alkanes associated with tobacco smoke were characterized by a peculiar iso/anteiso/normal homolog fingerprint and by n-hentriacontane percentages higher than elsewhere. Several concentration ratios of PAHs were identified as diagnostic of the type of emission, and the sources of uncertainty were elucidated. Despite extensive investigations conducted so far, the origin of uncommon molecular fingerprints, e.g., alkane/alkene relationships in deposition dusts and airborne particles, remains quite unclear. Polar organics resulted scarcely investigated for pollution apportioning purposes, though they looked as indicative of the nature of sources. Finally, the role of humans and living organisms as actual emitters of chemicals seems to need concern in the future.

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.

The dynamic change of urinary selenium concentration during pregnancy and influencing factors: A longitudinal study.

BACKGROUND: Selenium concentration of one spot urine sample cannot reflect selenium status during whole pregnancy. Studies on variations of urinary selenium concentration at different stages of pregnancy are limited. AIM: To assess variations of urinary selenium concentrations during three trimesters of pregnancy and to explore the influencing factors. METHODS: This study included 2613 pregnant women from a birth cohort study (Wuhan, China) enrolled between October 2014 and October 2016. Selenium concentrations of urine samples collected at three trimesters were measured. We used a generalized linear mixed effects model to observe the changes in urinary selenium concentration during pregnancy and its influencing factors. RESULTS: The median value (range) of gestational weeks at urine sample collection was 11 (9-14), 24 (15-27), and 34 (28-41) respectively. Urine selenium concentration varied across trimesters (geometric mean: 16.34, 17.65 and 18.83 µg/g creatinine, respectively), with an upward trend (ß = -0.145, 95%CI: -0.164, -0.126) (ß = -0.066, 95%CI: -0.083, -0.048). The concentrations of urinary selenium increased with the increasing of educational level [ß (95%CI): ≤ 9 years = -0.105 (-0.163, -0.047); 10-12 years = -0.086(-0.126, -0.047); > 12 years = reference]. Pregnant women who rarely or only took multivitamins in the first trimester [ß (95% CI): rarely = -0.076 (-0.144, -0.007); only in the first three months of pregnancy = -0.104 (-0.170, -0.038); always = reference], or were not exposed to passive smoking during pregnancy（ߠ= -0.093, 95% CI: - 0.173, - 0.014), or exercised three to four days per week for the first three months before delivery（ߠ= -0.074, 95% CI: - 0.140, - 0.008) had lower urinary selenium concentrations. Pregnant women who took calcium supplements after the third month of pregnancy had higher urinary selenium levels（ߠ= 0.114, 95% CI: 0.059, 0.169). CONCLUSIONS: Urine selenium concentrations of pregnant women showed an upward trend across trimesters. Educational level, calcium or multivitamin supplementation, passive smoking, and physical exercise might impact urine selenium levels.

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.

Association of prenatal factors and cord blood lead levels in China: A nested cohort cross-sectional study.

BACKGROUND: Lead exposure all over the world has gradually declined. As fetuses are more prone to lead exposure, even to low levels of lead exposure, it is important to monitor blood lead levels (BLLs) in pregnancy. METHODS: We obtained data on BLLs in the third trimester of pregnancy from medical records and measured cord BLLs obtained from 121 mother-child pairs in Shenyang, China from September 2019 to February 2020. We also estimated relationships between socio-demographic, lifestyle and dietary factors during pregnancy as well as cord BLLs to identify the source of lead exposure during pregnancy. BLLs was estimated by atomic absorption spectrometry through graphite furnace ionization techniques. The data which obtained by questionnaires during pregnancy included maternal sociodemographic, lifestyle, dietary factors. We have established three multivariate logistic regression models in which the dichotomous BLLs was used as the dependent variable (cord BLLs ≥20 µg/L vs <20 µg/L). RESULTS: The median and geometric mean of cord BLLs were 22.90 µg/L, 21.88 µg/L and BLLs in the third trimester of pregnancy were 25.29 µg/L, 24.66 µg/L, respectively. BLLs showed significant correlations between cord and the third trimester of pregnancy (r = 0.277, P = 0.012). Pregnant women who had not been exposed to passive smoking had lower OR (95 %) [0.43(0.19-0.94)] for cord BLLs ≥20 µg/L than pregnant women who had. Intake of docosahexaenoic acid (DHA) during third trimester of pregnancy presented an OR (95 %) [0.23(0.08-0.61)] for cord BLLs ≥20 µg/L. Consuming more whole grains (>3 times/week) and beverage (≥1 times/week) showed an OR (95%CI) for cord BLLs ≥20 µg/L of 0.09(0.02-0.53) and 0.19(0.06-0.69), respectively. CONCLUSION: This study showed the cord BLLs of Chinese are still higher than most developed countries. Passive smoking is a risk factor for cord BLLs ≥20 µg/L and supplement of DHA, whole grains and beverage consumption during pregnancy may act as a beneficial factor against having cord BLLs ≥20 µg/L.

Prenatal Exposure to Alcohol, Tobacco, and Coffee: Associated Congenital Complications and Adverse Birth Outcomes.

A few studies to date have examined the association between prenatal exposure to alcohol, tobacco, and coffee, and congenital complications/adverse birth outcomes among South Korean populations. Thus, this study analyzed the data of 1675 Korean women with birth experience within the last 3 years for pregnancy-related health and nutritional behaviors and relative outcomes. During their pregnancies, 11.58% of the study population consumed alcohol at least once, 1.43% drank throughout all three trimesters, 1.13% smoked, 25.43% were exposed to secondhand smoking, and 28.18% consumed 3 coffees or more every day. Prenatal alcohol exposure was associated with 11.24 times increased risk of birth defects/disabilities [Odds Ratio (OR): 11.24, 95% Confidence Interval (CI) 1.07-117.86] and 10.66 times increased risk of inherited metabolic diseases (OR: 10.66, 95% CI: 1.08-104.82). Prenatal secondhand smoke exposure (OR: 1.62, 95% CI: 1.01-2.62) and coffee consumption (OR: 1.92, 95% CI: 1.22-3.03) was associated with increased risk of low birth weight. Such results were in alignment with that of previous studies and confirmed that prenatal alcohol, tobacco, and coffee exposure can have detrimental neonatal and maternal consequences.

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.