In Utero Exposure to Environmental Tobacco Smoke Increases Neuroinflammation in Offspring

The embryonic stage is the most vulnerable period for congenital abnormalities. Due to its prolonged developmental course, the central nervous system (CNS) is susceptible to numerous genetic, epigenetic, and environmental influences. During embryo implantation, the CNS is more vulnerable to external influences such as environmental tobacco smoke (ETS), increasing the risk for delayed fetal growth, sudden infant death syndrome, and immune system abnormalities. This study aimed to evaluate the effects of in utero exposure to ETS on neuroinflammation in the offspring of pregnant mice challenged or not with lipopolysaccharide (LPS). After the confirmation of mating by the presence of the vaginal plug until offspring birth, pregnant C57BL/6 mice were exposed to either 3R4F cigarettes smoke (Kentucky University) or compressed air, twice a day (1h each), for 21 days. Enhanced glial cell and mixed cell cultures were prepared from 3-day-old mouse pups. After cell maturation, both cells were stimulated with LPS or saline. To inhibit microglia activation, minocycline was added to the mixed cell culture media 24 h before LPS challenge. To verify the influence of in utero exposure to ETS on the development of neuroinflammatory events in adulthood, a different set of 8-week-old animals was submitted to the Autoimmune Experimental Encephalomyelitis (EAE) model. The results indicate that cells from LPS-challenged pups exposed to ETS in utero presented high levels of proinflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNFα) and decreased cell viability. Such a proinflammatory environment could modulate fetal programming by an increase in microglia and astrocytes miRNA155. This scenario may lead to the more severe EAE observed in pups exposed to ETS in utero.

Environmental tobacco smoke and carotid intima–media thickness in healthy children and adolescents: a systematic review

Thicker carotid intima–media thickness (CIMT) has been a valid predictor for atherosclerosis development. A significant association between environmental tobacco smoke (ETS) and thickening of CIMT has been demonstrated in adults, whereas such association has scarcely been reviewed in paediatric population. The dominate electronic databases, including MEDLINE (Ovid), PubMed, Embase, CINAHL, Web of Science, Scopus, were searched from inception. Reference lists of retrieved articles were further scanned as to avoid any missing literatures. Newcastle-Ottawa scale was used to assess the quality of the included studies. Qualitative synthesis analyses were performed on the selected studies. 331 articles were retrieved, and 4 were finally selected. All four studies investigated the association between postnatal ETS and CIMT in children, and three of them reported a statistically significant positive association. Three studies investigated the association between prenatal maternal ETS and CIMT, and one of the three found a positive association. Two studies explored the association between postnatal maternal ETS and CIMT, one reported a positive association. Two studies used serum cotinine measurement to quantify ETS and demonstrated potential dose-response relationship with CIMT. ETS exposure may play an independent role in the development of cardiovascular risks in healthy children and adolescents. In the consideration of the great burden of respiratory and cardiovascular diseases, there is an urgent need of effective surveillance for paediatric population’s ETS exposure to reduce smoke exposure.

Genetic Polymorphism of Cyp2a6 and Cyp2a13 Genes and Environmental Tobacco Smoke Induced Lung Cancer Risk in Indonesian Female Never Smokers

BACKGROUND: The presence of nicotine metabolite in the urine of subjects exposed to tobacco smoke represents the nicotine metabolism activity in environmental tobacco smokers. CYP2A6 and CYP2A13 are known as the main enzymes responsible for nicotine metabolism and xenobiotic activity in tobacco smoke-related lung cancer. AIM: The aim of this study is to analyze the relationship between genetic polymorphism of CYP26 and CYP2A13 genes and environmental tobacco smoke-induced lung cancer risk in Indonesian females never smoker. METHODS: This is a case-control study with two-stage of distinguishing polymorphism detection. Restriction fragment length polymorphism polymerase chain reaction from venous blood extraction was performed to examine the CYP2A6 and CYP2A13 polymorphism. Logistic regression test in Epi Info-7 software was carried out to examine genetic polymorphism of CYP2A6 and CYP2A13 genes and environmental tobacco smoke-induced lung cancer risk in Indonesian female never smokers. RESULTS: A total of 203 participants enrolled in this study with the first stage of CYP2A6 polymorphism involved 101 subjects showed no significant correlation between the genotypes of CYP2A6 and the incidence of lung cancer. On the other hand, there was a significant correlation between genotypes of CYP2A13 and the incidence of lung cancer (p < 0.05). People with the genotype CT have a 2.7 higher risk for developing lung cancer compare with genotype CC. Allele *1B was the most common allele in CYP2A6. Allele C has more frequencies and has 0.62 times the risk for developing lung cancer compared with allele T with a wide range of confidence intervals (0.73–3.52). CONCLUSIONS: There was a significant correlation between polymorphism CYP213 with the incidence of lung cancer among female lung cancer never smoker. However, the results show no significant relationship between CYP2A6 genetic polymorphism and lung cancer incidence.

Risk Assessment of Passive Smoking Based on Analysis of Hair Nicotine and Cotinine as Exposure Biomarkers by In-Tube Solid-Phase Microextraction Coupled On-Line to LC-MS/MS

Passive smoking due to environmental tobacco smoke is a serious public health concern because it increases the risk of lung cancer and cardiovascular disease. However, the current status and effect of passive smoking in various lifestyles are not fully understood. In this study, we measured hair nicotine and cotinine levels as exposure biomarkers in non-smokers and assessed the risk from the actual situation of passive smoking in different lifestyle environments. Nicotine and cotinine contents in hair samples of 110 non-smoker subjects were measured by in-tube solid-phase microextraction with on-line coupling to liquid chromatography-tandem mass spectrometry, and self-reported lifestyle questionnaires were completed by the subjects. Nicotine and cotinine were detected at concentrations of 1.38 ng mg−1 and 12.8 pg mg−1 respectively in the hair of non-smokers, with levels significantly higher in subjects who reported being sensitive to tobacco smoke exposure. These levels were also affected by type of food intake and cooking method. Nicotine and cotinine in hair are useful biomarkers for assessing the effects of passive smoking on long-term exposure to environmental tobacco smoke, and our analytical methods can measure these exposure levels in people who are unaware of passive smoking. The results of this study suggest that the environment and places of tobacco smoke exposure and the lifestyle behaviors therein are important for the health effects of passive smoking.

Parental Knowledge, Attitude, and Practice on Tobacco Use, Smoking Cessation, and Children's Environmental Tobacco Smoke Exposure

Background: Environmental tobacco smoke (ETS) exposure in children ranks one of the major public health problems in our time. Poor parental knowledge, attitude, and practice (KAP) on ETS often contribute to worse exposure of the kids. Thus, we aimed to document parental KAP regarding tobacco use, smoking cessation and children's ETS exposure, and to analyse how knowledge and attitude relate to practice.Methods: Self-administered KAP questionnaires were distributed to smoking parents recruited from the pediatric unit at the Prince of Wales Hospital, which provides pediatric service to a population of 1.2 million in Hong Kong. The 60-item questionnaire had a range of 0–38 for knowledge, 0–44 for attitude, and 0–40 for practice. Descriptive analyses were performed for KAP response, regression analyses were performed for the exploration of associations and identification of predictive indicators.Results: 145 smoking parents (mean age: 38.0 ± 6.7 yrs.; male: 85.5%) were included. Less than half (39.3%) of them reported a smoke-free policy at home. Among those parents who had private cars, less than half (45.2%) of them had smoke-free policy in their car that they never smoked in the car. Only 25.5% of the participants correctly answered ≥70% of the knowledge questions, and 11.8 % of the participants gave favorable responses to ≥70% of the attitude questions. The total knowledge and the total attitudes score were positively associated (r = 0.49, 95% CI: 0.35–0.79, p &lt; 0.001), yet they were only modestly correlated with parental practice on children's ETS exposure. By multivariate regressions, potential predictive factors for more favorable parental KAP included higher household income, lower parental nicotine dependence level and breastfeeding practice.Conclusions: Parental KAP related to tobacco use and children's ETS exposure needs improvement to address the significant gap between recommended and actual practice. The weak association between knowledge and practice suggested that parental education alone is not adequate to combat ETS exposure in children.

Analysis of Diabetes Mellitus and Environmental Tobacco Smoke (ETS) Exposure as Lung Tuberculosis Risk Factors

Indonesia, is the country with the second highest lung TB case in the world. Some studies suggest there is a relationship between TB and diabetes. The smoking habit is also linked because it can damage the lung defense mechanism thereby facilitating the entry of TB germs. This research was conducted to analyze diabetes mellitus and exposure to environmental tobacco smoke (ETS) as risk factors for pulmonary tuberculosis. This research is a quantitative analytic study with Case Control conducted in the TB Endemic Region in Palembang, namely the work area of ​​the Kertapati Health Center, Sei Selincah Health Center and 23 ilir Health Center in February to December 2018. Data were obtained from primary data obtained from questionnaires and examinations physical. The data obtained are presented in the form of a master tabulation and processed using the Chi-square test and T-test analysis. In this study showed no significant relationship between blood sugar levels when with tuberculosis status (p = 0.075).

Association of Environmental tobacco smoke exposure with depression among non-smoking adults

Background Depression is a psychological dysfunction that impairs health and quality of life. However, whether environmental tobacco smoke exposure (ETSE) is associated with depression is poorly understood. This study was designed to evaluate the association of ETSE with depression among non-smoking adults in the United States. Method Using the 2015–2016 United States National Health and Nutrition Examination Survey (NHANES), we identified 2623 adults (females – 64.2%, males – 35.8%) who had never smoked and applied multivariable adjusted-logistic regression to determine the adjusted odds ratio (aOR) and 95% confidence interval (CI) at P < 0.05 for the association of ETSE with depression adjusting for relevant confounders. Results Mean age of respondents was 46.5 ± 17.9 years, 23.5% reported ETSE, and 4.7% reported depression. Also, aORs for the association of ETSE with depression were 1.992 (1.987, 1.997) among females and 0.674 (0.670, 0.677) among males. When we examined the association by age groups, the aORs were 1.792 (1.787, 1.796) among young adults (< 60 years) and 1.146 (1.140, 1.152) among older adults (≥60 years). Conclusions We found that ETSE was associated with higher odds of depression among females but not among males.