Environmental Tobacco Smoke Exposure Research Articles

Prevalence of Wheezing and Its Association with Environmental Tobacco Smoke Exposure among Rural and Urban Preschool Children in Mpumalanga Province, South Africa

Background: This study aimed to investigate the prevalence of wheezing and its association with environmental tobacco smoke exposure among rural and urban preschool children in Mpumalanga province, South Africa, an area associated with poor air quality. Methods: In this study, parents/caregivers of preschool children (n = 3145) completed a modified International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire. Data were analysed using multiple logistic regression models. Results: The overall prevalence of Wheeze Ever was 15.14%, with a higher prevalence in urban preschoolers than rural preschoolers (20.71% vs. 13.30%, p < 0.000). Moreover, the total prevalence of Asthma Ever was 2.34%. The prevalence was greater in urban preschoolers than in rural preschoolers (3.92% vs. 1.81%, p < 0.001). In the final adjusted model, both urban- and rural-area children who lived with one or more people who smoked in the same household (WE: OR 1.44, 95% CI 1.11–1.86) (CW: OR 2.09, 95% CI 1.38–3.16) and (AE: OR 2.49, 95% CI 1.12–5.54) were found to have an increased likelihood of having Wheeze Ever, Current Wheeze, and Asthma Ever as compared to those who lived with non-smokers. Conclusions: The implementation of smoking limits and prohibition is crucial in areas that are frequented or utilized by children. Hence, it is imperative for healthcare providers to actively champion the rights of those who do not smoke within the society, while also endorsing legislative measures aimed at curtailing the extent of tobacco smoke exposure.

Environmental tobacco smoke exposure exaggerates bleomycin-induced collagen overexpression during pulmonary fibrogenesis.

Environmental tobacco smoke (ETS) is known to cause lung inflammatory and injurious responses. Smoke exposure is associated with the pathobiology related to lung fibrosis, whereas the mechanism that ETS exposure augments pulmonary fibrogenesis is unclear. We hypothesized that ETS exposure could exacerbate fibrotic responses via collagen dynamic dysregulation and complement activation. C57BL/6J and p16-3MR mice were exposed to ETS followed by bleomycin administration. ETS exposure exacerbated bleomycin-induced collagen and lysyl oxidase overexpression in the fibrotic lesion. ETS exposure also led to augmented bleomycin-induced upregulation of C3 and C3AR, which are pro-fibrotic markers. Moreover, overexpressed collagens and C3 levels were highly significant in males than females. The old mice (17 months old) were exposed to ETS and treated with bleomycin to induce fibrogenesiswhich is considered as an aging-associated disease. Fewer gene and protein dysregulations trends were identified between ETS exposure with the bleomycin group and the bleomycin alone group in old mice. Based on our findings, we suggested that ETS exposure increases the risk of developing severe lung fibrotic responses via collagen overexpression and lysyl oxidase-mediated collagen stabilization in the fibrotic lesion,and potentially affected the complement system activation induced by bleomycin. Further, male mice were more susceptible than females during fibrogenesis exacerbation. Thus ETS and bleomycin induced lung fibrotic changes via collagen-lysyl oxidase in anage-dependent mechanism.

Tobacco use and risk of acute stroke in 32 countries in the INTERSTROKE study: a case–control study

Smoking is a major risk factor for the global burden of stroke. We have previously reported a global population attributable risk (PAR) of stroke of 12.4% associated with current smoking. In this study we aimed to explore the association of current tobacco use with different types of tobacco exposure and environmental tobacco smoke (ETS) exposure on the risk of stroke and stroke subtypes, and by regions and country income levels. The INTERSTROKE study is a case-control study of acute first stroke and was undertaken with 13,462 stroke cases and 13,488 controls recruited between January 11, 2007 and August 8, 2015 in 32 countries worldwide. Association of risk of tobacco use and ETS exposure were analysed with overall stroke, ischemic and intracerebral hemorrhage (ICH), and with TOAST etiological stroke subtypes (large vessel, small vessel, cardioembolism, and undetermined). Current smoking was associated with an increased risk of all stroke (odds ratio [OR] 1.64, 95% CI 1.46-1.84), and had a stronger association with ischemic stroke (OR 1.85, 95% CI 1.61-2.11) than ICH (OR 1.19 95% CI 1.00-1.41). The OR and PAR of stroke among current smokers varied significantly between regions and income levels with high income countries (HIC) having the highest odds (OR 3.02 95% CI 2.24-4.10) and PAR (18.6%, 15.1-22.8%). Among etiological subtypes of ischemic stroke, the strongest association of current smoking was seen for large vessel stroke (OR 2.16, 95% CI 1.63-2.87) and undetermined cause (OR 1.97, 95% CI 1.55-2.50). Both filtered (OR 1.73, 95% CI 1.50-1.99) and non-filtered (OR 2.59, 95% CI 1.79-3.77) cigarettes were associated with stroke risk. ETS exposure increased the risk of stroke in a dose-dependent manner, exposure for more than 10h per week increased risk for all stroke (OR 1.95, 95% CI 1.69-2.27), ischemic stroke (OR 1.89, 95% CI 1.59-2.24) and ICH (OR 2.00, 95% CI 1.60-2.50). There are significant variations in the magnitude of risk and PAR of stroke according to the types of tobacco used, active and ETS exposure, and countries with different income levels. Specific strategies to discourage tobacco use by any form and to build a smoke free environment should be implemented to ease the global burden of stroke. The Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, Canadian Stroke Network, Swedish Research Council, Swedish Heart and Lung Foundation, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, and through unrestricted grants from several pharmaceutical companies with major contributions from Astra Zeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), MERCK, Sharp and Dohme, Swedish Heart and Lung Foundation, UK Chest, and UK Heart and Stroke.

Association between Outdoor and Indoor Air Pollution Sources and Atopic Eczema among Preschool Children in South Africa.

The objective of the study was to investigate the association between outdoor and indoor air pollution sources and atopic eczema among preschool children in South Africa. A cross-sectional design, following the International Study of Asthma and Allergies in Childhood (ISAAC) Phase III protocol, was applied. The study was conducted in Mabopane and Soshanguve Townships in the City of Tshwane Metropolitan Municipality in Gauteng, South Africa. A total population of 1844 preschool children aged 7 years and below participated in the study; 1840 were included in the final data analysis. Data were analyzed using multilevel logistic regression analysis. The prevalence of eczema ever (EE) and current eczema symptoms (ESs) was 11.9% and 13.3%, respectively. The use of open fires (paraffin, wood, or coal) for cooking and heating increased the likelihood of EE (OR = 1.63; 95% CI: 0.76-3.52) and current ESs (OR = 1.94; 95% CI: 1.00-3.74). Environmental tobacco smoke (ETS) exposure at home increased the likelihood of EE (OR = 1.66; 95% CI: 1.08-2.55) and current ESs (OR = 1.61; 95% CI: 1.07-2.43). Mothers or female guardians smoking cigarettes increased the likelihood of EE (OR = 1.50; 95% CI: 0.86-2.62) and current ESs (OR = 1.23; 95% CI: 0.71-2.13). The use of combined building materials in homes increased the likelihood of EE, and corrugated iron significantly increased the likelihood of current ESs. The frequency of trucks passing near the preschool children's residences on weekdays was found to be associated with EE and current ESs, with a significant association observed when trucks passed the children's residences almost all day on weekdays. Atopic eczema was positively associated with exposure to outdoor and indoor air pollution sources.

Unraveling the link: environmental tobacco smoke exposure and its impact on infertility among American women (18-50 years).

The detrimental effects of environmental tobacco smoke (ETS) on women's reproductive health have been widely recognized. However, the detailed association between exposure to environmental tobacco smoke and the incidence of infertility remains under-explored. This investigation focuses on exploring this potential connection. For this analysis, we extracted data from the US National Health and Nutrition Examination Survey (NHANES) database, covering the years 2013 to 2018, focusing on individuals with recorded serum cotinine levels and infertility information. ETS exposure and fertility status were analyzed as independent and dependent variables, respectively. We applied weighted multivariate logistic regression method to evaluate the impact of ETS on infertility, including subgroup analyses for more detailed insights. The study encompassed 3,343 participants. Logistic regression analysis revealed a notable positive correlation between ETS exposure and infertility, with an odds ratio (OR) of 1.64 (95% Confidence Interval [CI]: 1.14-2.36). We observed a non-linear relationship between ETS exposure and infertility risk. Notably, infertility risk increased by 64% in serum cotinine levels above 0.136 compared to that in serum cotinine levels below 0.011. Further, subgroup analysis and interaction tests showed consistent results across different segments, underscoring the robustness of the ETS-infertility link. Our findings suggest that environmental tobacco smoke exposure may be a contributing factor to infertility. These results reinforce the recommendation for women in their reproductive years to avoid ETS exposure, especially when planning for pregnancy.

Impacts of environmental tobacco smoke on the onset and progression of multiple sclerosis: a systematic review.

Unlike cigarette smoking, environmental tobacco smoke (ETS) has not been as well described as an environmental risk for Multiple sclerosis (MS) nor as a risk factor for disease progression. We systematically reviewed the association between ETS and the risk of onset and/or progression of MS. We systematically screened MedLine/PubMed, Science Direct, LILACs, and SciELO searching for publications between January 1st, 2010, and July 5, 2021, with the following keywords: "multiple sclerosis and smoking"; "multiple sclerosis and passive smoking"; "multiple sclerosis and secondhand smoking". Fifteen articles were included in this review, which consisted of systematic reviews with meta-analysis (N = 2), systematic reviews (N = 2), and observational studies (N = 11). Both meta-analyses reported an impact of ETS on MS onset among secondhand smokers. One of the systematic reviews selected two observational studies showing the association between ETS and MS development, and one study that did not find a significant association between ETS and the risk of MS development. The other systematic review identified selected eight articles showing a relationship between ETS and MS. Seven observational studies reported higher odds of MS onset when associated with ETS. Four observational studies did not show a relationship between ETS and MS onset or progression. Most articles showed a positive association between ETS exposure and the risk of developing MS. On the other hand, an association between ETS and a higher risk for MS progression could not be established.

Maternal environmental tobacco smoke exposure and adverse birth outcomes in Egypt: a cross sectional study

Maternal environmental tobacco smoke exposure and adverse birth outcomes in Egypt: a cross sectional study

Association between environmental tobacco smoke exposure and diabetes: Results from the NHANES 2013–2016 and mendelian randomization analysis

The relationship between environmental tobacco smoke (ETS) exposure at different locations and diabetes remains unclear. We explored the abovementioned associations and combined mendelian randomization (MR) techniques to further investigate the causality. In this observational study, data collected by the National Health and Nutrition Examination Survey (NHANES) 2013–2016 were assessed, which included nonsmokers aged ≥20 years (n = 3749). Subsequently, MR analysis was performed using the inverse variance weighted (IVW) approach to assess the causal connection between different locations of ETS exposure and diabetes from the UK Biobank, DIAbetes Genetic Replication And Meta-analysis (DIAGRAM) consortium, and FinnGen datasets. Multivariate logistic regression analyses demonstrated that exposure to ETS outside the home was positively associated with diabetes in nonsmokers over 60 years (OR = 2.19; 95%CI, 1.19–4.02, p = 0.018). This positive connection was sustained in a subgroup analysis among females (OR = 3.19; 95%CI, 1.48–6.88, p = 0.006) but not in males. In the MR analysis, exposure to ETS outside the home was linked with an elevated risk of type 2 diabetes mellitus (OR = 4.52; 95%CI: 1.54–13.32, p = 0.006) according to the IVW outcomes. Findings from our observational study identified exposure to ETS outside the home might be associated with an increased risk of diabetes in nonsmokers, and further MR analysis revealed the causal associations between genetically predicted ETS exposure outside the home on T2DM.These findings assist the need for targeted strategies, including more compulsory smoke-free policies, to address this issue effectively.

Tobacco smoke exposure in early childhood and later risk of inflammatory bowel disease: A Scandinavian birth cohort study.

To examine the association between early-life smoking exposure and later risk of inflammatory bowel disease (IBD). We followed 115,663 participants from the Norwegian Mother, Father and Child (MoBa) and All Babies in Southeast Sweden (ABIS) cohorts from birth (1997-2009) through 2021. IBD was identified through national patient registers. Validated questionnaire data defined maternal smoking during pregnancy, maternal environmental tobacco smoke (ETS) exposure during pregnancy, and child ETS exposure by age 12 and 36 months. Cox regression was used to estimate adjusted hazard ratios (aHRs) for sex, maternal age, education level, parental IBD and origin. Cohort-specific estimates were pooled using a random-effects model. During 1,987,430 person-years of follow-up, 444 participants developed IBD (ABIS, n=112; MoBa, n=332). Any vs. no maternal smoking during pregnancy yielded a pooled aHR of 1.30 (95%CI=0.97-1.74) for offspring IBD. Higher level of maternal smoking during pregnancy (compared to no smoking, average ≥6 cigarettes/day: pooled aHR=1.60 [95%CI 1.08-2.38]) was associated with offspring IBD, whereas a lower smoking level was not (average 1-5 cigarettes/day: pooled aHR=1.09 [95%CI=0.73-1.64]). Child ETS exposure in the first year of life was associated with later IBD (any vs. no ETS, pooled aHR=1.32 [95%CI=1.03-1.69]). Estimates observed for child ETS exposure by 36 months were similar but not statistically significant. In this prospective Scandinavian cohort study, children exposed to higher levels of maternal smoking during pregnancy or ETS during the first year of life were at increased risk of later IBD.

Association between PRKG1 Gene and Gene-Environment Interactions with Pediatric Asthma

ABSTRACT Objective To investigate the relationship between single nucleotide polymorphisms (SNPs) of cGMP-dependent protein kinase I (PRKG1) gene and gene-environment interactions with bronchial asthma in children. Methods 109 asthma patients and 158 healthy controls from the General Hospital of Northern Theater Command were enrolled, based case–control study. The iMLDR® multiple SNP typing technique was applied to detect the genotypes of rs7903366, rs7081864, rs7070958 and rs7897633 in PRKG1 gene. The percentage of eosinophils (EOS%) in peripheral blood and serum immunoglobulin E (IgE) in the case group were also measured. Gene-environment interactions were examined using the generalized multi-factor dimensionality reduction (GMDR) method. Results There were polymorphisms in four SNPs of PRKG1 gene in the case and control groups. The genotype and allele frequencies distribution of rs7897633 demonstrated statistical significance (p < 0.05). There were no statistically significant differences in EOS% and IgE among genotypes at the four SNPs of PRKG1 gene (p > 0.05). The haplotypes CAGA and TGAC presented significant association with asthma risk (p < 0.05). The four-factor model indicated a potential gene-environment interaction in rs7897633, allergen exposure, residence, and environmental tobacco smoke (ETS) exposure (p < 0.05). Conclusions The rs7897633 in PRKG1 gene was associated with susceptibility to childhood asthma, and C allele is a protective factor. The haplotype CAGA had a protective effect against asthma risk and TGAC was linked to the high risk of developing asthma. Moreover, the interaction of rs7897633, allergen exposure, residence, and ETS exposure conferred susceptibility to childhood asthma.

Comprehensive evaluation of smoking exposures and their interactions on DNA methylation

BackgroundSmoking impacts DNA methylation, but data are lacking on smoking-related differential methylation by sex or dietary intake, recent smoking cessation (<1 year), persistence of differential methylation from in utero smoking exposure, and effects of environmental tobacco smoke (ETS). MethodsWe meta-analysed data from up to 15,014 adults across 5 cohorts with DNA methylation measured in blood using Illumina’s EPIC array for current smoking (2,560 exposed), quit <1 year (500 exposed), in utero (286 exposed), and ETS exposure (676 exposed). We also evaluated the interaction of current smoking with sex or diet (fibre, folate, and vitamin C). FindingsUsing false discovery rate (FDR<0.05), 65,857 CpGs were differentially methylated in relation to current smoking, 4,025 with recent quitting, 594 with in utero exposure, and 6 with ETS. Most current smoking CpGs attenuated within a year of quitting. CpGs related to in utero exposure in adults were enriched for those previously observed in newborns. Differential methylation by current smoking at 4-71 CpGs may be modified by sex or dietary intake. Nearly half (35-50%) of differentially methylated CpGs on the 450K array were associated with blood gene expression. Current smoking and in utero smoking CpGs implicated 3,049 and 1,067 druggable targets, including chemotherapy drugs. InterpretationMany smoking-related methylation sites were identified with Illumina’s EPIC array. Most signals revert to levels observed in never smokers within a year of cessation. Many in utero smoking CpGs persist into adulthood. Smoking-related druggable targets may provide insights into cancer treatment response and shared mechanisms across smoking-related diseases. FundingIntramural Research Program of the National Institutes of Health, Norwegian Ministry of Health and Care Services and the Ministry of Education and Research, Chief Scientist Office of the Scottish Government Health Directorates and the Scottish Funding Council, Medical Research Council UK and the Wellcome Trust

Association of GAB1 gene with asthma susceptibility and the efficacy of inhaled corticosteroids in children

Asthma is a polygenic disease that may onset during childhood. Inhaled corticosteroids (ICS) are the main therapy in asthma, although their efficacy varies among individuals. Nuclear factor κB (NF-κB) is an important target of ICS treatment of asthma. Recent research has reported that GRB2 associated binding protein 1 (GAB1) gene may participate in the pathogenesis of asthma by regulating the NF-κB pathway. Therefore, we used the technique of an improved multiplex ligation detection reaction to sequence GAB1 gene and investigated the involvement of Single-nucleotide variants (SNVs) in GAB1 gene in asthma and ICS efficacy in asthmatic children. We found no differences between asthma cases and controls in allele or genotype frequencies of GAB1. Haplotype analysis showed an increased tendency for AGGAGC frequency in asthma patients compared with controls (OR = 2.69, p = 0.018). The percentage of EOS and genotype distribution of rs1397527 were associated (p = 0.007). The EOS percentage was higher in GT genotype when compared to the GG genotype (5.50 vs 3.00, Bonferroni adjusted p = 0.005). After 12-weeks ICS treatment, GAB1 rs1397527 TT and GT genotype carriers had a smaller change in forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) than GG carriers (p = 0.009), and rs3805236 GG and AG genotype carriers also had a smaller change in FEV1/FVC than AA carriers (p = 0.025). For ICS response, the frequency of GG genotype of rs1397527 was significantly higher in good responders (p = 0.038). The generalized multifactor dimensionality reduction (GMDR) analysis showed a best significant four-order model (rs1397527, allergen exposure, environmental tobacco smoke exposure, and pet exposure) involving gene-environment interactions (p = 0.001). In summary, we found that GAB1 SNVs were not associated with asthma susceptibility. Haplotype AGGAGC was a risk factor for asthma. GAB1 variants were associated with eosinophils and ICS response in asthmatics. Furthermore, gene-environment interaction was observed.

Polygenic Risk Score, Environmental Tobacco Smoke, and Risk of Lung Adenocarcinoma in Never-Smoking Women in Taiwan

Estimating absolute risk of lung cancer for never-smoking individuals is important to inform lung cancer screening programs. To integrate data on environmental tobacco smoke (ETS), a known lung cancer risk factor, with a polygenic risk score (PRS) that captures overall genetic susceptibility, to estimate the absolute risk of lung adenocarcinoma (LUAD) among never-smokers in Taiwan. The analyses were conducted in never-smoking women in the Taiwan Genetic Epidemiology Study of Lung Adenocarcinoma, a case-control study. Participants were recruited between September 17, 2002, and March 30, 2011. Data analysis was performed from January 17 to July 15, 2022. A PRS was derived using 25 genetic variants that achieved genome-wide significance (P < 5 × 10-8) in a recent genome-wide association study, and ETS was defined as never exposed, exposed at home or at work, and exposed at home and at work. The Individualized Coherent Absolute Risk Estimator software was used to estimate the lifetime absolute risk of LUAD in never-smoking women aged 40 years over a projected 40-year span among the controls by using the relative risk estimates for the PRS and ETS exposures, as well as age-specific lung cancer incidence rates for never-smokers in Taiwan. Likelihood ratio tests were conducted to assess an additive interaction between the PRS and ETS exposure. Data were obtained on 1024 women with LUAD (mean [SD] age, 59.6 [11.4] years, 47.9% ever exposed to ETS at home, and 19.5% ever exposed to ETS at work) and 1024 controls (mean [SD] age, 58.9 [11.0] years, 37.0% ever exposed to ETS at home, and 14.3% ever exposed to ETS at work). The overall average lifetime 40-year absolute risk of LUAD estimated using PRS alone was 2.5% (range, 0.6%-10.3%) among women never exposed to ETS. When integrating both ETS and PRS data, the estimated absolute risk was 3.7% (range, 0.6%-14.5%) for women exposed to ETS at home or work and 5.3% (range, 1.2%-12.1%) for women exposed to ETS at home and work. A super-additive interaction between ETS and the PRS (P = 6.5 × 10-4 for interaction) was identified. This study found differences in absolute risk of LUAD attributed to genetic susceptibility according to levels of ETS exposure in never-smoking women. Future studies are warranted to integrate these findings in expanded risk models for LUAD.

Environmental tobacco smoke and children’s health: a bibliometric and altmetric analysis of 100 most cited articles

BackgroundExposure to environmental tobacco smoke (ETS) is arguably the most ubiquitous and hazardous, even at very low levels, starting in early life. The objective of this study was to describe the state of research and future trends on ETS exposure and Children’s Health (CH) topics with bibliometrics and altmetrics.MethodsAn electronic search was performed in Scopus database on January 31, 2023. Consensus was arrived on 100 most-cited articles by two reviewers. These papers were then cross matched with citations harvested from Web of Science (WoS) and Google Scholar. Altmetric Attention Score (AAS) and Dimension counts were also collected. Analysis and network visualization of authors, countries, and keywords were generated using VOSviewer software.ResultsAmong a total of 1107 articles published on ETS and CH, the 100 top-cited articles appeared in 54 journals, with Pediatrics (n = 12) contributing a maximum number of articles. The time period between 2000 and 2009 accounted for 44% of all publications. With respect to the research design employed across these studies, cross-sectional design took precedence over others accounting for approximately 40%. Predominantly, articles focused on childhood asthma; however, current research trends have shifted towards emerging fields such as children’s oral health and DNA methylation. Twitter, policy documents, and news outlets were the main platforms where outputs were discussed. The AAS was not associated with journal impact factor or access type. Weak correlations were observed between AAS and citation count in Scopus, WoS, and Google Scholar (r = 0.17 to 0.27) while a positive association existed between dimension count and the number of citations across all three databases (r = 0.84 to 0.98).ConclusionThis study demonstrates the evolution, digital dissemination and research hotspots in the field of ETS and CH, predicting the possible future research directions. High-quality studies with more specific exposure classification are warranted to better understand the relationship between ETS and CH.

Passive Smoking And The Health Of Children: A Primary Concern In Pakistan.

Dear Madam, Environmental tobacco smoke (ETS), also referred to as second-hand, involuntary, or passive smoke, is produced from the combustion of tobacco products or puffed out by active smokers. The smoke emitted from the tip of a cigarette contains about two times the concentration of nicotine, five times the concentration of Carbon monoxide, and 50 times the concentration of ammonia than active smoke1. Furthermore, amongst the exposed population, children are far more susceptible to complications associated with ETS due to their manner of exposure and developmental physiology. According to the 2014 Global Adult Tobacco Survey for Pakistan, 43.3% of households were exposed to ETS, with a significant amount of children included in that percentage2. Thus, children's health is more detrimentally impacted by ETS than adults. Exposure of children to ETS in domestic and public settings risks a higher occurrence of respiratory and middle-ear diseases. According to numerous studies, dose-dependent exposure to ETS directs more frequent and severe asthma attacks accompanied by wheezing. Moreover, it is observed that school-aged individuals who live in a smoking household tend to develop a range of lung diseases, including bronchitis, bronchiolitis, and pneumonia. Their lungs become weak, resulting in impaired pulmonary function3. With reference to a population-based cohort study conducted by Lovasi et al. (ref 4), it was evident that childhood ETS exposure from 2 or more smokers compared with none is linked with early emphysema in adulthood4. In addition, constant ETS exposure leads to swelling and obstruction of the eustachian tube, which interferes with pressure equalization leading to pain, fluid accumulation, and infection. Ear infections and middle ear fluid are the most common causes of hearing loss in children. Being the primary reason behind several disease, ETS is also known to cause acute effects on cardiovascular function in children. Compelling evidence demonstrates that childhood ETS exposure risks the accumulation of factors associated with cardiovascular diseases, including obesity, dyslipidemia, and imbalanced systolic and diastolic blood pressure5. [Exposure to hazardous chemicals found in ETS, for instance, benzopyrene, is known to accelerate the development of atherosclerosis].  Moreover, studies show convincing evidence that hypertension is common in children exposed to ETS at home. It is also observed that hypertension is a common risk factor for cardiovascular disease and cardiovascular stress hyperactivity in children with smoking parents. ---Continue

Passive Smoking and Lung Disease in Children, Systematic Review

Background: Children's morbidity and mortality are greatly increased by passive cigarette smoke exposure. Preterm delivery, intrauterine growth retardation, perinatal death, respiratory illnesses, neurobehavioral issues, and lower academic performance have all been linked to environmental tobacco smoke (ETS) as having negative effects on children's health. This systematic review aims to comprehensively assess recent literature on prevalence of passive smoking in association with lung diseases in children. Methods: Comprehensive searches were conducted across PubMed, Web of Science, Science Direct, Cochrane Library, and Google Scholar to include pertinent literature. The Rayyan QRCI tool facilitated this systematic approach. Results: A total of 490 study articles resulted from the systematic search, and 53 duplicates were deleted. Title and abstract screening were conducted on 437 studies, and 390 studies were excluded. Forty-seven reports were sought for retrieval, and only 7 articles were not retrieved. Finally, 40 studies were screened for full-text assessment; 17 were excluded for wrong study outcomes, and 6 for the wrong population type. Seventeen eligible study articles were included in this systematic review.  Conclusion: ETS exposure has a considerable negative impact on children's morbidity and death. Children appear to be the population group most vulnerable to the negative impacts of ETS. There should be a consolidation of more efficient governmental policies and initiatives to safeguard preschoolers from ETS.

Association of environmental tobacco smoke exposure with chronic constipation: a nationwide survey (NHANES 2005-2010).

Environmental tobacco smoke (ETS) exposure has been proven to induce digestive diseases such as hepatic steatosis, cirrhosis, and gastrointestinal cancer, yet little is known about the link between ETS exposure and constipation. This study aimed to investigate the impact of ETS exposure on the risk of chronic constipation in adults aged 20years or older. This is a cross-sectional study based on population. A total number of 7705 participants from the National Health and Nutrition Examination Survey (NHANES) 2005-2010 were included. Cotinine, an alkaloid found in tobacco, serves as a reliable and precise biomarker for measuring exposure to ETS. Hence, the categorization of exposure to ETS was conducted based on serum cotinine levels, resulting in four distinct categories. The association between ETS exposure and the risk of constipation was assessed using multivariable restricted cubic spline and logistic regression with odds ratio (OR) and 95% confidence interval (CI). The weighted prevalence of constipation in this study was estimated to be 7.51% based on stool consistency, or 3.11% based on stool frequency. The fully adjusted models indicated a positive correlation between exposure to ETS and constipation as measured by stool frequency, among adults with poor dietary quality (OR (95% CI): moderate exposure: 2.49 (1.05, 5.94); high exposure: 2.36(1.13, 4.95), P for trend = 0.03), while no significant difference was observed in the subgroup with a higher healthy eating index. Furthermore, the log10-transformed serum cotinine level exhibited a non-linear inverted U-shaped association with constipation in individuals with poor dietary quality (P overall = 0.0207, P non-linear = 0.0427). Conversely, a J-shaped non-linear relationship was observed in the subgroup with a higher healthy eating index (P overall = 0.0028, P non-linear = 0.0036). Our results show that ETS exposure appears to be positively associated with stool frequency-related chronic constipation in adults with poor dietary quality.

Investigating associations between maternal stress, smoking and adverse birth outcomes: evidence from the All Our Families cohort

BackgroundIndependently, active maternal and environmental tobacco smoke exposure and maternal stress have been linked to an increased risk of preterm birth and low birth weight. An understudied relationship is the potential for interactive effects between these risk factors.MethodsData was obtained from the All Our Families cohort, a study of 3,388 pregnant women < 25 weeks gestation recruited from those receiving prenatal care in Calgary, Canada between May 2008 and December 2010. We investigated the joint effects of active maternal smoking, total smoke exposure (active maternal smoking plus environmental tobacco smoke) and prenatal stress (Perceived Stress Scale, Spielberger State-Trait Anxiety Inventory), measured at two time points (< 25 weeks and 34–36 weeks gestation), on preterm birth and low birth weight.ResultsA marginally significant association was observed with the interaction active maternal smoking and Spielberger State-Trait Anxiety Inventory scores in relation to low birth weight, after imputation (aOR = 1.02, 95%CI: 1.00-1.03, p = 0.06). No significant joint effects of maternal stress and either active maternal smoking or total smoke exposure with preterm birth were observed. Active maternal smoking, total smoke exposure, Perceived Stress Scores, and Spielberger State-Trait Anxiety Inventory scores were independently associated with preterm birth and/or low birth weight.ConclusionsFindings indicate the role of independent effects of smoking and stress in terms of preterm birth and low birthweight. However, the etiology of preterm birth and low birth weight is complex and multifactorial. Further investigations of potential interactive effects may be useful in helping to identify women experiencing vulnerability and inform the development of targeted interventions.

Urinary nicotine metabolites are associated with cognitive impairment among the elderly in southern China.

This study comprehensively assessed the association between eight metabolites of urinary nicotine and cognitive impairment. This cross-sectional study was based on the data of Shenzhen Aging Related Disorder Cohort (SADC), including 51 elderly community data variables such as demographic characteristics, neuropsychological assessment and environmental factors, from July 2017 to November 2018. Participant's cognitive function was assessed by Mini-Mental State Examination (MMSE) scale and urinary nicotine metabolite [including cotinine N-β-D-glucuronide (CotGluc), rac 4-hydroxy-4-(3-pyridyl) butanoic acid dicyclohexylamine salt (HyPyBut), trans-3'-hydroxy cotinine O-β-D-glucuronide (OHCotGluc), and cotinine (Cot), etc.] concentrations were measured by high-performance liquid chromatography-tandem mass spectrometry (LC-MS/MS). Generalized linear models and restricted cubic spline models were used to explore the relationships between the urinary levels of nicotine metabolite and cognitive function. A total of 296 individuals aged >60 years were included. Individuals in the third quartile of CotGluc had a 0.786 point (95% CI: -1.244 - -0.329) decrease or in the highest quartile of OHCotGluc had a 0.804 point (95% CI: -1.330 - -0.278) decreased in attention and calculation compared to those in the lowest quartile (all p for trend <0.05). Compared with those in the lowest quartile, individuals in the highest quartile of CotGluc, HyPyBut, OHCotGluc and Cot, respectively, corresponded to a 1.043 point (95% CI: -2.269-0.182), 1.101 points (95% CI: -2.391-0.188), 2.318 points (95% CI: -3.615 - -1.020), and 1.460 points (95% CI: -2.726 - -0.194) decreased in MMSE total score (all p for trend <0.05). A non-linear dose-response relationship between urinary levels of CotGluc, HyPyBut, OHCotGluc or Cot and cognitive function (all overall p<0.05, non-linear p<0.05). Subgroup analysis showed that urinary levels of CotGluc, OHCotGluc or Cot were significantly negatively associated with cognitive function (all p for trend <0.05) among females and non-smokers. The findings highlight the public health implications of environmental tobacco smoke exposure, and effective interventions need to be performed for vulnerable populations.

The Role of Indoor Microbiome and Metabolites in Shaping Children's Nasal and Oral Microbiota: A Pilot Multi-Omic Analysis.

Maintaining a diverse and well-balanced nasal and oral microbiota is vital for human health. However, the impact of indoor microbiome and metabolites on nasal and oral microbiota remains largely unknown. Fifty-six children in Shanghai were surveyed to complete a questionnaire about their personal and environmental characteristics. The indoor microbiome and metabolites from vacuumed indoor dust were profiled via shotgun metagenomics and untargeted liquid chromatography-mass spectrometry (LC-MS). The nasal and oral microbiota in children was characterized using full-length 16S rRNA sequencing from PacBio. Associations between personal/environmental characteristics and the nasal/oral microbiota were calculated using PERMANOVA and regression analyses. We identified 6247, 431, and 342 microbial species in the indoor dust, nasal, and oral cavities, respectively. The overall nasal and oral microbial composition showed significant associations with environmental tobacco smoke (ETS) exposure during pregnancy and early childhood (p = 0.005 and 0.03, respectively), and the abundance of total indoor flavonoids and two mycotoxins (deoxynivalenol and nivalenol) (p = 0.01, 0.02, and 0.03, respectively). Notably, the abundance of several flavonoids, such as baicalein, eupatilin, isoliquiritigenin, tangeritin, and hesperidin, showed positive correlations with alpha diversity and the abundance of protective microbial taxa in nasal and oral cavities (p < 0.02), suggesting their potential beneficial roles in promoting nasal/oral health. Conversely, high carbohydrate/fat food intake and ETS exposure diminished protective microorganisms while augmenting risky microorganisms in the nasal/oral cavities. Further, potential microbial transfer was observed from the indoor environment to the childhood oral cavity (Moraxella catarrhalis, Streptococcus mitis, and Streptococcus salivarius), which could potentially increase virulence factors related to adherence and immune modulation and vancomycin resistance genes in children. This is the first study to reveal the association between the indoor microbiome/metabolites and nasal/oral microbiota using multi-omic approaches. These findings reveal potential protective and risk factors related to the indoor microbial environment.