Smoke Exposure Research Articles

Association between urinary cotinine level and hypertensive disorders of pregnancy in women with uterine myoma: findings from the Japan Environment and Children's Study.

The effect of smoking on hypertensive disorders of pregnancy is a public concern. Recent evidence suggests that the risk of hypertensive disorders of pregnancy is influenced by the presence of uterine fibroids. We explored the association between maternal smoking exposure and the risk of hypertensive disorders of pregnancy in relation to the presence of uterine fibroids using data from Japan's largest birth cohort study. This study focused on first-time mothers, and the study population comprised 2752 and 35,294 first-time mothers with and without uterine fibroids, respectively. Hypertensive disorders of pregnancy was categorized as early-onset (before 34 weeks) and late-onset (after 34 weeks). Maternal smoking exposure was assessed by measuring the urinary cotinine concentration during the mid-trimester. Participants were classified into four quartiles based on their urinary cotinine levels as follows: Q1 (low concentration) to Q4 (high concentration). Multivariate analysis adjusted for potential confounders revealed that in women without uterine fibroids, the Q3 urinary cotinine level was associated with a modified risk of early-onset hypertensive disorders of pregnancy (adjusted odds ratio: 0.63, 95% confidence interval: 0.44-0.89). Conversely, for women with uterine fibroids, Q4 urinary cotinine level was associated with an increased risk of hypertensive disorders of pregnancy (adjusted odds ratio: 1.68, 95% confidence interval: 1.05-2.72). In conclusion, this study indicated that the impact of maternal smoking exposure varied based on the presence of uterine fibroids, underscoring the importance of personalized preconception care.

Smoking Cessation and Incident Cardiovascular Disease

The association between smoking cessation and cardiovascular disease (CVD) risk in relation to cumulative smoking exposure remains poorly understood. To evaluate the associations among smoking cessation, lifetime smoking burden, and CVD risk according to the number of years elapsed after smoking cessation. This retrospective cohort study of the Korean National Health Insurance Service database investigated smoking duration and intensity between January 2006 and December 2008. Participants were categorized by self-reported smoking habits as current, ex-, or never-smokers. Smoking records were updated every 2 years until December 2019, with participants whose smoking status changed or whose smoking status was unclear excluded. Data analysis was performed between June and December 2022. Time-updated self-reported smoking status, years since quitting, and cumulative smoking amount (pack-years [PY]). The primary outcome was incidence and hazard ratio of CVD (composite of cardiovascular death, myocardial infarction, stroke, and heart failure). Overall, 5 391 231 participants (39.9% male; mean [SD] age, 45.8 [14.7] years; 853 756 [15.8%] current smokers, 104 604 [1.9%] ex-smokers, and 4 432 871 [82.2%] never smokers) were followed up for a mean (SD) of 4.2 (4.4) years. The median (IQR) baseline cumulative smoking amounts were 14.0 (7.5-20.0) PY in current smokers and 10.5 (5.3-20.0) PY in ex-smokers. The median (IQR) duration of smoking cessation was 4 (2-8) years for ex-smokers. Regardless of continued smoking, a dose-dependent association was evident between smoking and incident CVD. Compared with current smokers, ex-smokers with a lifetime smoking burden of less than 8 PY (light ex-smokers) experienced a significant reduction in CVD risk within 10 years of cessation, with a CVD risk similar to that of never-smokers. Conversely, ex-smokers with at least 8 PY (heavy ex-smokers) exhibited a slower decline in CVD risk than light ex-smokers, requiring more than 25 years for the residual CVD risk to disappear. In this cohort study, smoking and CVD risk exhibited a dose-dependent association, with light ex-smokers having a CVD risk similar to that of never-smokers relatively soon after smoking cessation. For heavy ex-smokers, greater than 25 years might be required for the residual CVD risk to align with that of never-smokers.

The Ability of Indigenous Plants in Alleviating Rheumatoid Arthritis: A Comprehensive Review.

Rheumatoid Arthritis is a long-lasted, inflammatory, systemic autoimmune disease that predominantly manifests in people between the ages of 30 and 50 Rheumatoid arthritis is characterized by more than a half-hour of morning stiffness in the affected joints, fever, soreness, swelling, weight loss, tiredness, warm joints, and subcutaneous rheumatoid nodules. Hormonal, genetic, epigenetic, reproductive, and neuroendocrine risk factors, as well as comorbid host variables, are the categories of host-related risk factors associated with the evolution of RA. Additional risk variables that have been linked to RA include food, environmental variables, socioeconomic status, smoking, microbiome, infection agents, and other airborne exposures. The objective of RA therapies is to minimise joint deformity and destruction, minimise discomfort and inflammation in the joints, and maximise joint function.Growing data suggests that the course of Rheumatoid Arthritis is affected by the minimisation of disease activity caused by disease-modifying medications, and that patients may benefit from early antirheumatic medication delivery that modifies illness. While numerous herbs have been explored for their anti-inflammatory properties, it is important to note that not all herbs have been thoroughly researched. This review focuses on seventeen native plant species that have shown either promising or established anti-arthritic effects based on preclinical and clinical studies where available. The review highlights the biochemical and immunological attributes of these herbs, summarizing their therapeutic potential for RA management while also acknowledging the limitations and gaps in current research. This examination provides insights into the potential of these herbal treatments for RA and calls for further research to explore their efficacy and safety in greater depth.

Sensors for Smoking Detection in Epidemiological Research: Scoping Review.

The use of wearable sensors is being explored as a challenging way to accurately identify smoking behaviors by measuring physiological and environmental factors in real-life settings. Although they hold potential benefits for aiding smoking cessation, no single wearable device currently achieves high accuracy in detecting smoking events. Furthermore, it is crucial to emphasize that this area of study is dynamic and requires ongoing updates. This scoping review aims to map the scientific literature for identifying the main sensors developed or used for tobacco smoke detection, with a specific focus on wearable sensors, as well as describe their key features and categorize them by type. According to the PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews) protocol, an electronic search was conducted on the PubMed, MEDLINE, and Web of Science databases, using the following keywords: ("biosensors" OR "biosensor" OR "sensors" OR "sensor" OR "wearable") AND ("smoking" OR "smoke"). Among a total of 37 studies included in this scoping review published between 2012 and March 2024, 16 described sensors based on wearable bands, 15 described multisensory systems, and 6 described other strategies to detect tobacco smoke exposure. Included studies provided details about the design or application of wearable sensors based on an elastic band to detect different aspects of tobacco smoke exposure (eg, arm, wrist, and finger movements, and lighting events). Some studies proposed a system composed of different sensor modalities (eg, Personal Automatic Cigarette Tracker [PACT], PACT 2.0, and AutoSense). Our scoping review has revealed both the obstacles and opportunities linked to wearable devices, offering valuable insights for future research initiatives. Tackling the recognized challenges and delving into potential avenues for enhancement could elevate wearable devices into even more effective tools for aiding smoking cessation. In this context, continuous research is essential to fine-tune and optimize these devices, guaranteeing their practicality and reliability in real-world applications.

Effect of BMI on Caries Assessed by Structural Equation Modelling in an Adult Brazilian Population.

Compare different behavioural, environmental and socioeconomic factors for caries with transversal data to decompose the direct and indirect effects of body mass index (BMI) in relation to coronal and root caries. This cross-sectional study used a representative sample of 1002 individuals aged ≥ 35 years living in Porto Alegre. Questionnaires recorded age, sex, educational level, tooth brushing frequency and access to dental services. Oral examination assessed gingival bleeding and recession, coronal and root caries. Height and weight were collected to calculate the BMI. The structural equation modelling approach was used, and standardised coefficients (SC) to direct, indirect and total effects were calculated. The prevalence of excessive body weight was 71.17%, of which 40.09% were overweight and 31.07% were obese. The overall prevalence of coronal and root caries was 99.83 and 36.95, respectively. No direct link between BMI and coronal or root caries was observed. For coronal caries, positive SC was found for age (0.56; p < 0.01) and sex (female) (0.14; p < 0.01). For root caries, positive SC was detected for age (0.34; p < 0.01), smoking exposure (0.17; p < 0.01) and gingivitis (0.08; p < 0.01). Overweight and obese adults should not be regarded at higher risk for dental caries.

Overcoming Challenges to Adopting Smoke-Free Multi-Unit Housing Policies in a Large U.S. Metropolitan Area: Insights and Recommendations From Affected Groups in 20 Los Angeles County Cities.

Community members and non-academic partners ("affected groups") were asked to identify factors that can influence public support, impede adoption, and mitigate challenges related to adopting local smoke-free multi-unit housing policies. A series of key informant interviews were conducted with affected groups from a large U.S. metropolitan area. 20 cities in Los Angeles County without a smoke-free multi-unit housing ordinance. Interviewees were recruited from affected groups with knowledge about their community's civic and political landscape (n = 63). Data were collected and analyzed using thematic analysis to identify, code and compare themes. Most interviewees indicated civic groups, those who do not smoke, and/or groups who are educated about the negative health effects of secondhand smoke exposure would be more likely to support smoke-free multi-unit housing policies. Interviewees reported several challenges to policy adoption, including competing city priorities, public disengagement, and the cost and social burden of enforcing these ordinances. To overcome them, interviewees recommended working synergistically with local governments to build diverse coalitions, educate the public, and develop clear enforcement plans. Insights and recommendations from affected groups in 20 U.S. cities suggest that communicating with the public and priming impacted communities to support smoke-free multi-unit housing policies are promising interventions for protecting at-risk families from secondhand smoke exposure in their homes.

Beyond Injuries: February 6th Kahramanmaras Earthquakes and Other Patients Transported by Ambulance.

This study evaluates the Emergency Medical Service system and overall emergency preparedness by analyzing ambulance-transported patients during the February 6, 2023 earthquakes, focusing on those without earthquake-related injuries (medical emergencies and traumas not caused by earthquakes). A retrospective, observational case series was conducted, involving patients aged 18 and above transported by ambulance between February 6 and March 6, 2023. Patient demographic characteristics, vital signs, diagnoses, treatments, and outcomes were recorded. Predisposing factors for ambulance transportation including post-earthquake health facility issues, housing problems, hygiene, heating, and smoke exposure were meticulously analyzed. The study included 1872 patients, with a 55.4% hospitalization rate and a 13.7% mortality rate. Cardiovascular emergencies were the primary reason for admission (28.9%). Patients from the hospital in the study's location form Group 1, whereas those from other earthquake-affected provinces constitute Group 2. Significant predisposing factors for ambulance transportation included post-earthquake health facilities (P < 0.001), housing problems (P < 0.001), hygiene (P < 0.001), heating (P = 0.001), and smoke exposure (P < 0.001). In Group 2, pneumonia (P = 0.001), soft tissue infection (P = 0.002), sepsis (P = 0.004), carbon monoxide poisoning (P < 0.001), and diabetic emergencies (P = 0.013) were statistically significantly more frequent. Analyzing post-earthquake ambulance-transported patients is vital to comprehend the demand for emergency health care and address post-disaster health care challenges.

Cumulative effect of lifetime smoking history on arterial stiffness and subclinical atherosclerosis in patients with arterial hypertension

Abstract Introduction Although the effect of smoking status on blood pressure (BP) changes is well known an adverse association between cumulative smoke exposure (by pack-years) and functional and structural changes in arteries of patients with high BP has not been consistently demonstrated. Aim of the study was to explore the contributions of cumulative smoke exposure to the vascular consequences of arterial hypertension. Methods Indices of vascular function and structure including carotid-femoral pulse wave velocity (PWV), augmentation index (AIx) and carotid intima media thickness (cIMT) were measured in 485 adults aged less than 60 years old without a history of cardiovascular disease. The cohort was divided into three groups according to office systolic BP (SBP) and diastolic BP (DBP): normal (SBP &amp;lt;130 and DBP &amp;lt;85 mmHg, n=242), high normal (130≤SBP&amp;lt;140 or DBP 85≤DBP&amp;lt;90mmHg, n=96), and hypertension (SBP≥140 or DBP≥90mmHg, n=147). The cohort was subdivided according to pack-years of smoking history as never smokers (0.0 pack-years), light smokers (&amp;lt;20 pack-years), moderate smokers (20-40 pack-years), and heavy smokers (&amp;gt; 40 pack-years). Results The three BP groups had similar age and metabolic parameters (body mass index, fasting blood glucose and LDL-C). Figure shows PWV, AIx and carotid IMT by smoking exposure, stratified by BP level. The lowest PWV level was observed in never smokers with normal BP; whereas heavy smokers with hypertension exhibited the highest PWV. Also of note, heavy smokers with normal BP exhibited comparable PWV to light and never smokers with hypertension. Furthermore, in smokers with more than 20 pack-years tobacco exposure, PWV was higher among patients with high normal BP compared to subjects with normal BP (all P&amp;lt;0.01). In contrast to the monotonic increases in PWV and AIx by BP and pack-years smoking history, carotid IMT was generally similar among BP groups on the basis of cumulative exposure category. This finding may indicate a plateau in subclinical atherosclerotic burden over cumulative tobacco exposure for all BP categories. Conclusion Tobacco cumulative exposure adversely modify the effect of BP on arterial stiffness. Given that most adults who smoke start before the age 18 years, efforts to promote smoking cessation should continue to target younger adults with high BP.BP, tobacco exposure-vascular changes

Protecting Young Lives: A Systematic Review of the Impact of Secondhand Smoke Exposure and Legislative Measures on Children's Health

Protecting Young Lives: A Systematic Review of the Impact of Secondhand Smoke Exposure and Legislative Measures on Children's Health

Exploring the associations of tobacco smoking and serum cotinine levels with selected inflammatory markers in adults with HIV in South Africa

This study examined the associations between tobacco smoking and serum cotinine levels, an objective biochemical measure of tobacco smoke exposure, with markers of inflammation, i.e., interferon-gamma (IFN-γ), interleukin 10 (IL-10), interleukin 2 (IL-2) and tumour necrosis factor-alpha (TNF-α) in people living with HIV (PLWH).These specific markers were selected because of their hypothesised associations with smoking, PLWH and their outcomes. In a random sample of ≥ 18-year-old PLWH receiving care at 17 public healthcare facilities across the Western Cape Province in South Africa, data collection included self-reported smoking history, and serum levels of cotinine and selected inflammatory markers. The inflammatory marker data were log transformed because of the skewedness of their distribution. Linear regression models (1) adjusted for age and gender, and (2) fully adjusted for age, gender, current alcohol use, body mass index and CD4 counts were used to examine the associations between smoking tobacco or serum cotinine and inflammatory markers. Level of significance was p < 0.05. Among 749 PLWH who were mainly women (79%), the mean age was 38.5 (8.9) years and similar when stratified by smoking status. Serum cotinine levels exhibited a striking discrepancy, with a median of 154 ng/mL among current smokers, in stark contrast to the consistent median values of 10 ng/mL observed among past and never smokers. In regression models adjusted for age and gender, current smoking and frequent smoking were associated with lower IL-2 but higher TNF-α. Log-cotinine exhibited associations with IFN-γ, IL-10, and TNF-α, while cotinine levels ≥ 10 ng/mL compared to < 10 ng/mL were associated with higher IFN-γ and TNF-α. In fully adjusted models, log-cotinine and cotinine levels ≥ 10 ng/mL displayed significant associations with higher IFN-γ and lower IL-2. This study underscores the importance of investigating the interplay between smoking tobacco or serum cotinine levels with pro-inflammatory cytokines in PLWH. It signals the need for comprehensive research to unravel the potential synergistic impacts of smoking tobacco and HIV infection on chronic inflammation and immune dysregulation, shedding light on critical avenues for intervention and management strategies.

Increased tobacco taxation associated with decreased consumption and bladder cancer incidence.

The temporal relationship between smoking exposure and bladder cancer (BC) diagnosis remains ill-defined. This study aims to cross-correlate and temporally associate changes in United States (US) tobacco tax and consumption with BC incidence. US tobacco consumption, tobacco tax data, and BC incidence rates from 1975-2019 were retrieved. A cross-correlation lag time for tobacco tax and consumption on BC incidence was calculated while controlling for national health expenditure. Proxied lag weighted semi-log linear models to determine the rate of change in BC incidence rates associated with a 1% change in tobacco tax percentages on a national and state level. A 1% increase in tobacco tax was associated with a 1.77% decrease in BC incidence over a 6-year period (R2=0.9687, p=0.00044). 22 states had a statistically significant decline in BC incidences correlated with increasing tobacco taxation. Reduction in BC incidence >0.5% were observed in states along the Western and Eastern US borders. Montana, Utah, Nebraska, Arkansas, and Tennessee did not have decreasing BC incidences from tobacco tax increases. California had the most drastic decline in BC incidence (1.98%). Nationally, tobacco consumption decrease in 1 pack per capita was associated with a 0.47% decrease in BC incidence over a 28-year period (R2=0.984, p=0.00011). Declining US tobacco consumption may indicate significant reduction in BC incidence through 2047. Primary prevention through adaptation of state-legislated tax changes may contribute to a reduction in BC incidence in states lying within the Central US. A national tobacco tax initative can be considered given the improvement in population health.

Exposure to secondhand smoke among school-going adolescents in Malaysia: Results from the National Health and Morbidity Survey (NHMS) 2022: Adolescent Health Survey (AHS).

The adverse effects of secondhand smoke (SHS) exposure on health have been well established. Using the NHMS 2002: Adolescent Health Survey (AHS), this study attempts to evaluate the extent and factors associated with SHS exposure among Malaysian school-going adolescents. We conducted the NHMS 2022: AHS to gather a representative sample of school-age teenagers. We employed a cross-sectional study design and a multi-stage sampling procedure. We utilized a pre-validated self-administered questionnaire to collect data from the selected respondents. The data analysis included adjusted odds ratios (AORs) with 95% confidence intervals (95% CIs). Additionally, we investigated the possible two-way interactions between the independent variables. The SHS prevalence was 42.0%. Exposure to secondhand smoke (SHS) was associated with male gender (AOR=1.28; 95 CI: 1.20-1.38), older age (AOR=1.46; 95% CI: 1.33-1.60), Malay (AOR=1.88; 95% CI: 1.49-2.37), Bumiputra Sabah (AOR=2.23; 95% CI: 1.67-2.99), Bumiputra Sarawak (AOR=2.43; 95% CI: 1.80-3.28), and Chinese ethnicity (AOR=2.89; 95 CI: % 2.30-3.64), as well as current smoking (AOR=2.78; 95% CI: 2.50-3.09), having separated or divorced parents (AOR=1.12; 95% CI: 1.02-1.23), and parental tobacco product use (AOR=4.75; 95% CI: 4.44-5.08). We found significant interactions between: 1) Age group with gender and ethnicity; 2) Gender and ethnicity; and 3) Parental smoking status with gender, response to tobacco use, parents' marital status, and ethnicity. Parental characteristics, sociodemographic characteristics, and SHS exposure are strongly correlated. In addition, there is evidence of smoking displacement to the house from other areas by parents/guardians. This study offers a fresh perspective on how these variables influence the likelihood of SHS exposure for Malaysian school-age teenagers. More efforts should focus on parental variables and sociodemographic traits, especially parental smoking cessation support.

Immune system benefits of pulmonary rehabilitation in chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a respiratory disease characterized by pulmonary and systemic inflammation. Inflammatory mediators show relationships with shortness of breath, exercise intolerance and health related quality of life. Pulmonary rehabilitation (PR), a comprehensive education and exercise training programme, is the most effective therapy for COPD and is associated with reduced exacerbation and hospitalization rates and increased survival. Exercise training, the primary physiological intervention within PR, is known to exert a beneficial anti-inflammatory effect in health and chronic diseases. The question of this review article is whether exercise training can also make such a beneficial anti-inflammatory effect in COPD. Experimental studies using smoke exposure mice models suggest that the response of the immune system to exercise training is favourably anti-inflammatory. However, the evidence about the response of most known inflammatory mediators (C-reactive protein, tumour necrosis factor α, interleukin 6, interleukin 10) to exercise training in COPD patients is inconsistent, making it difficult to conclude whether regular exercise training has an anti-inflammatory effect in COPD. It is also unclear whether COPD patients with more persistent inflammation are a subgroup that would benefit more from hypothesized immunomodulatory effects of exercise training (i.e., personalized treatment). Nevertheless, it seems that PR combined with maintenance exercise training (i.e., lifestyle change) might be more beneficial in controlling inflammation and slowing disease progress in COPD patients, specifically in those with early stages of disease.

Predicting exacerbations in severe preschool wheezers.

Simple clinical indices, complex composite phenotyping/endotyping and telehome monitoring now allow us to evaluate the risk of preschool wheezing on a population or individual level. We herein discuss the usefulness of clinical markers which involve underlying issues such as in utero smoke exposure, the pathophysiology of viral-immunological-allergic interactions, and changes in airway epithelium, mesenchyme and smooth muscle cells. The most important unmet need in this age group remains disease-modifying interventions.

FSP1 Acts in Parallel with GPX4 to Inhibit Ferroptosis in COPD.

Glutathione peroxidase 4 (GPX4) has recently been reported to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Ferroptosis suppressor protein-1 (FSP1) is a protein that defends against ferroptosis in parallel with GPX4, but its role in the pathogenesis of COPD remains unexplored, and further research is needed. Normal and COPD lung tissues were obtained from lobectomy and lung transplant specimens, respectively. FSP1-overexpressing mice were established by monthly transfection with AAV9-FSP1 through modified intranasal administration. The expression of FSP1, GPX4, and prostaglandin-endoperoxide synthase 2 (PTGS2) was measured by Western blotting, immunohistochemistry and other methods. The correlation between FSP1 and ferroptosis and the role of FSP1 in COPD were explored by screening the expression of ferroptosis-related genes in a COPD cell model after the inhibition and overexpression of FSP1. We then explored the underlying mechanism of low FSP1 expression in patients with COPD in vitro by methylated RNA immunoprecipitation (MeRIP)-qPCR. We found that cigarette smoke exposure can lead to an increase in lipid peroxide production and ultimately ferroptosis, which is negatively regulated by FSP1 activity. FSP1 overexpression can prevent ferroptosis and alleviate emphysema. Next, we found that decreased FSP1 expression was caused by increased m6A modification of FSP1 mRNA. Moreover, the level of FSP1 decreased in a YTHDF2-dependent manner. These results indicate that METTL3-induced FSP1 mRNA methylation leading to low FSP1 expression is a potential therapeutic target for COPD. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Effect of polyunsaturated fatty acids intake on the occurrence of current asthma among children and adolescents exposed to tobacco smoke: NHANES 2007–2018

BackgroundAsthma is an airway inflammatory disease driven by multiple factors with a high incidence in children and adolescents. Environmental tobacco smoke exposure (TSE) and diet are inducing factors for asthma. The potential of omega-3 polyunsaturated fatty acids (PUFAs) to alleviate asthma symptoms by their anti-inflammatory effects has been explored. However, to date, no studies have explored the effect of dietary PUFAs intake on the asthma in children and adolescents exposed to tobacco smoke.ObjectiveWe aimed to examine the effect of dietary PUFAs intake on the current asthma in children and adolescents exposed to tobacco smoke.MethodsData of this cross-sectional were extracted from the National Health and Nutrition Examination Survey (NHANES) 2007–2018. Children and adolescents with serum cotinine concentration ≥ 0.05 ng/mL were defined to exposed to tobacco smoke. Dietary PUFAs intake information were obtained from 24 h recall interview. The weighted univariate and multivariate were utilized to explore the effect of PUFAs on the association of asthma and TSE, with adjusted odds ratios (AORs) and 95% confidence intervals (CIs). These moderating effects were further explored based on the age, gender and body mass index (BMI) and sedentary time.ResultsTotally, 7981 eligible children and adolescents were included, with the mean age of 11.96 ± 0.06 years old. Of whom, 1.024 (12.83%) had current asthma. After adjusted all covariates, we found children and adolescents with TSE had high occurrence of current asthma (AOR = 1.2, 95% CI 1.03–1.63); We also found omega-3 PUFAs intake (P for interaction = 0.010), not omega-6 PUFAs (P for interaction = 0.546), has a moderating effect on the association of TSE and current asthma. Moreover, we further observed that children and adolescents with TSE and low omega-3 PUFAs intake had high occurrence of current asthma (AOR = 1.58, 95% CI 1.19–2.10), while no significant association was found in children and adolescents with high omega-3 PUFAs intake (all P > 0.05). This moderating effect was more prominent in children and adolescents aged ≤ 12 years old (AOR = 1.62, 95% CI 1.06–2.47), girls (AOR = 2.14, 95% CI 1.15–3.98), overweight (AOR = 1.87, 95% CI 1.01–3.47) and sedentary time > 6 h (AOR = 1.96, 95% CI 1.00–3.86).ConclusionWe found dietary omega-3 PUFAs plays a moderating effect on the association of asthma and TSE in children and adolescents, especially in children and adolescents aged ≤ 12 years, girls, overweight or sedentary time > 6 h. This moderating effect suggested higher omega-3 intake has potential benefits in decreasing the occurrence of asthma in children and adolescents who exposed to tobacco smoke.

A Study on Assessing the Impact of Smoking and Occupational Exposure on COPD Severity.

Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of morbidity and mortality worldwide, with occupational exposure to respiratory hazards and smoking being significant risk factors for its development and progression. This study aimed to investigate the relationship between occupational exposure and COPD severity among patients admitted to the new medical ward of a public hospital. The research employed a cross-sectional design and involved a sample of 160 COPD patients. Data collection included patient records, face-to-face interviews, and structured questionnaires that gathered demographic information, smoking history, occupational exposure, and disease severity. Quantitative analysis methods were used, with statistical tools such as chi-square tests and correlation analysis applied to assess the relationships between variables. The chi-square test demonstrated a significant association between occupational exposure and COPD severity (χ² = 45.07, df = 8, p = 0.05). Correlation analysis revealed positive relationships between COPD severity and age (r = 0.40), smoking status (r = 0.53), and duration of occupational exposure (r = 0.69). The findings emphasize the critical role of occupational risks and smoking in exacerbating COPD and suggest the need for preventive workplace interventions and stricter regulations to reduce respiratory hazards.

Bringing the group back in: Social class and resistance in adolescent smoking.

Absolute prevalence of tobacco smoking has fallen in recent decades but inequalities by socioeconomic position (SEP) persist. Adolescence is a critical period for smoking initiation and habits formed during this period likely continue into adulthood. Explanations for inequalities in adolescent smoking have tended to focus on individualistic theories based on differentials in knowledge and psychology. These have been criticised for their blindness to processes of social stratification and social context that influence smoking behaviours. Based on previous social theories, we put forward, and test empirically, two potential structural explanations for inequalities in smoking, using nationally representative longitudinal cohort data on 6039 Irish young people aged 9-18years. Descriptive analyses confirmed the adverse SEP gradient in smoking prevalence as well as SEP gradients in variables representing individual-level characteristics and structural-level explanations. Despite lower self-esteem being associated with a higher likelihood of smoking, there was no significant indirect pathway between SEP and smoking via self-esteem. Path analyses found that differentials in exposure to parental smoking and levels of oppositional values mediate the relationship between SEP and smoking. Our results favour structural and group-based explanations for inequalities, that is, the 'smoking exposure' and 'social resistance' models, over explanations based on individual psychology.

Impact of smoking habits on cardiovascular and neoplastic events and all-cause death in people living with HIVfrom the STOPSHIV cohort.

The study aimed to assess the impact of smoking exposure on major clinical events (MCE) in a real-life setting of people living with HIV (PWH). Observational longitudinal multicentre cohort study from Italy. Consecutive 983 PWH were enrolled in "STOP Smoking in HIV people" (STOPSHIV) projects and followed from July 2014 until September 2023. The observed MCE defined as cardiovascular (CV) events, neoplastic diseases or death for any reason was assessed according smoking status and related variables (number of cigarettes smoked daily, pack-years, Fagerström test) in participants. The association between exposure variables and the event was evaluated using the Cox proportional hazard model (hazard ratios, HR, and 95% CI). Over 6997.6 person-years of follow-up (PYFU), we found a total of 49 CV events, 61 neoplastic events, and 47 deaths. The overall incidence rate of MCE was 17.6 /1000 PYFU (95% confidence interval 14.7-21.0). All-cause death rate was 6.7 (95% CI 5.0-8.9)/1000 PYFU. In a multivariate analysis, older age (HR 1.07, CI 1.05-1.09), high Fagerström Test for Nicotine Dependence (HR 1.09, CI 1.03-1.15), a low nadir CD4 <200 cells/mm3 (HR 1.63, CI 1.10-1.41), history of previous neoplasm (HR 2.41; CI 1.34-4.43) and intravenous drug use as risk factor for HIV infection (HR 2.36; CI 1.52-3.68) were independent predictors of any MCE. Non-AIDS clinical conditions are the most observed clinical events in PWH from Italy. Smoking exposure significantly increases the risk of MCE in PWH and a high Fagerström Test for Nicotine Dependence is a predictor of MCE.

Intermittent Exercise and Cigarette Smoke Extract-Induced Pulmonary Tensegrity Dysfunction; Monitoring Elastin, Matrix Metalloproteinase-12, Transforming Growth Factor-beta 1

Background: Cigarette smoke causes inflammation of the alveoli, leading to airflow restriction and potentially irreversible changes in lung architecture, including pulmonary emphysema. This study investigates the effects of a six-week aerobic interval training regimen on elastin activity in a rat model of cigarette smoke-induced COPD (CS-COPD). Objectives: Specifically, we observe the variables matrix metalloproteinase-12 (MMP12) and transforming growth factor-beta (TGF-β1). Methods: Twenty male Wistar rats, aged eight weeks, were divided into four groups (n = 5 per group): Control, aerobic interval training (Exe), cigarette smoke extract (CSE), and CSE + Exe. The aerobic interval training (Exe) was performed for 49 min/day, five days per week for six weeks in interval form. The CSE group received an intraperitoneal (IP) injection of 150 µL of cigarette smoke extract, one day per week for six weeks. Results: The CSE and CSE + Exe groups showed a significant decrease in elastin gene expression in lung tissue compared to the healthy control group (P = 0.0002 and P = 0.0057, respectively) and the Exe group (P = 0.0002 and P = 0.0042, respectively). Additionally, the CSE group exhibited a significant increase in lung MMP12 gene expression compared to the healthy control and Exe groups (P = 0.0008 and P = 0.0013, respectively). Notably, the CSE + Exe group showed a significant decrease in MMP12 gene expression in lung tissue compared to the CSE group (P = 0.0015). Furthermore, the CSE and CSE + Exe groups demonstrated a significant increase in TGFB1 gene expression in lung tissue compared to the healthy control group (P &lt; 0.0001 and P = 0.0022, respectively) and the Exe group (P &lt; 0.0001 for both). Conclusions: Our findings indicate that the group exposed to cigarette smoke experienced a significant decrease in elastin levels, accompanied by an increase in MMP12 and TGF-β1 expression. Although aerobic interval training provided some protection against the detrimental effects of cigarette smoke exposure, it was not sufficient to fully reverse the harmful impacts of the disease.