Search Results (142)

Background: Exposure to secondhand smoke (SHS) during pregnancy has been linked to adverse maternal and perinatal outcomes. Preterm birth is one of the most critical complications. However, the evidence of an association between SHS exposure and preterm birth remains inconclusive. Objectives: our aim was to identify the prevalence of exposure to secondhand smoke among pregnant women and investigate the association between exposure to SHS and preterm birth. Methods: A cross-sectional study was conducted in Madinah, Saudi Arabia, from October to December 2024. A self-administered questionnaire was distributed among women in the postnatal ward to assess sociodemographic and pregnancy-related variables and exposure to SHS. Results: A total of 469 women were included in the study. About 33.7% of the women reported that their husbands currently smoked tobacco, with 51% smoking indoors; 21% of the women did not impose smoking restrictions at home. Pregnant women exposed to SHS had more than twice the odds of preterm birth compared to unexposed women (OR = 2.09; 95% CI: 1.06–4.13; p = 0.03). Conclusions: SHS exposure increased the risk of preterm birth among pregnant women in Madinah. These findings emphasize the essential need for preventive strategies to diminish SHS exposure in residential and public environments. Full article

Background: Previous studies have demonstrated that involuntary smoking (e.g., secondhand smoke [SHS] and thirdhand smoke [THS]) is not only associated with an increased risk of several physical health problems, such as cardiovascular disease and cancer, but also impacts mental health, including depression and anxiety. However, the relationships between SHS and THS exposure and non-suicidal self-injury (NSSI), suicidal ideation (SI), and suicide attempts (SAs) remain unclear. Methods: Participants were recruited at a Chinese vocational college via voluntary online surveys conducted on campus. Self-reported SHS exposure was determined by the frequency of contact with smokers or detecting tobacco odors in living environments, while THS was assessed through regular contact with smoker-contaminated surfaces (e.g., clothing, furniture, textiles). Logistic regression analysis was performed to evaluate the associations of SHS and THS exposure with the prevalence of NSSI, SI, and SAs in never-smoking participants. Results: The study included 5716 participants (mean age = 19.3 years; females, 85.4%). The prevalence of SHS and THS exposure was 87.6% and 77.4%, with 8.8% reporting ≥15 min of SHS exposure on at least one day per week. After controlling for potential covariates, exposure to SHS (≥15 min on at least one day per week) was significantly associated with the odds of SAs (OR [95%CI] = 1.85 [1.17–2.91]). Additionally, daily THS exposure was significantly associated with increased past-year NSSI prevalence (2.35 [1.29–4.28]) compared to those without THS exposure, with similar associations observed for SI (2.11 [1.28–3.48]) and SAs (2.40 [1.23–4.69]). Conclusions: Exposure to SHS and THS was significantly associated with increased likelihood of NSSI, SI, and SAs among young adults at a Chinese vocational college. Further studies are needed to validate these associations across more diverse populations. Full article

This study aims to explore the link between exposure to tobacco smoke among nonsmokers and the risk of lung cancer in the United States. We searched six databases for studies on second-hand smoke (SHS) and lung cancer following PRISMA guidelines. Following the random effects model and specific statistical methods, our meta-analysis analyzed studies based on SHS exposure type. A total of 19 eligible studies were included in the review and 15 in the meta-analysis. We covered exposure from parents (childhood), spouses and partners (household), and work-related exposure (colleagues), with higher risk among non-smoking children and domestic partners. Findings reveal a consistent link between SHS exposure and increased lung cancer risk for this population (exposure effect sizes: 1.05–3.11). Analysis of childhood SHS exposure reveals a distinct increased risk associated with parental exposure. For nonsmokers living with smoking spouses, there is a marked 41% increase in risk. Higher risk was associated with more and more prolonged SHS exposure. Exposure to SHS in the workplace shows a correlation with lung cancer risk. Our findings highlight increased SHS-related lung cancer risk, particularly among non-smoking children and domestic partners, intensifying with the amount and duration of exposure, indicating the significant impact of SHS within domestic environments. Full article

Apoptosis is critical in placental development, and its dysregulation is linked to pregnancy complications such as intrauterine growth restriction (IUGR) and preeclampsia (PE). Environmental exposures, particularly secondhand smoke (SHS) and e-cigarettes (eCigs), may contribute to placental dysfunction through apoptotic pathways. This study examined the effects of SHS and eCig exposure on placental apoptosis and growth-regulatory proteins in a murine model. C57BL/6 pregnant mice were exposed to SHS or eCigs at two critical gestational time points: early trophoblast invasion (E12.5 to E18.5) and established invasion (E14.5 to E18.5). Placental tissues were collected and analyzed for pro-apoptotic and anti-apoptotic markers, heat shock proteins, insulin-like growth factor-binding proteins (IGFBPs), and growth regulators. SHS exposure increased pro-apoptotic markers (BAD, Fas/FasL) and decreased mitochondrial function markers (cytochrome c), indicating compromised cellular survival. Both SHS and eCig exposure reduced anti-apoptotic markers (BCL-2, HSP27, survivin) and growth regulators (IGF-1, IGFBPs). SHS and eCig exposure create a pro-apoptotic environment in the placenta, potentially impairing fetal development through altered apoptotic and growth-regulatory pathways. These findings underscore the risks of environmental exposures during pregnancy, highlighting the need for strategies to minimize maternal exposure to SHS and eCigs. Full article

This study aimed to investigate the impact of alcohol (A), secondhand cigarette smoking (ShS), and their combined effect on liver antioxidant activity and hepatic damage in rats with induced apical periodontitis (AP). Thirty-five female Wistar rats were randomly allocated into five groups (n = 7): (1) control (rats without ShS, alcoholic diet, or AP), (2) control-AP (induced AP only), (3) ShS-AP (ShS exposure and induced AP), (4) A-AP (alcoholic diet and induced AP), and (5) A+ShS-AP (alcoholic diet, ShS exposure, and induced AP). Alcohol was administered through semi-voluntary intake, while ShS exposure involved the daily inhalation of cigarette smoke. The experimental period lasted 8 weeks, with AP induction occurring in the 4th week following molar pulp exposure. Liver samples were collected post-euthanasia for histomorphometric and antioxidant marker analyses. All AP-induced groups exhibited increased liver sinusoidal dilation compared to the control group (p < 0.05). AP significantly reduced total antioxidant capacity (FRAP) across all groups (p < 0.05). In AP-induced groups, FRAP levels were further decreased in ShS-AP and A+ShS-AP compared to control-AP (p < 0.05). AP also led to a decrease in the glutathione defense system (p < 0.05). Rats with alcohol exposure (A-AP and A+ShS-AP) showed reduced glutathione peroxidase activity (p < 0.05). Glutathione reductase activity was comparable in the control and control-AP groups (p > 0.05), but significantly decreased in the alcohol and ShS-exposed groups (p < 0.05). Apical periodontitis can relate to morphological changes in the liver’s sinusoidal spaces and impairment of liver’s antioxidant capacity of rats, particularly when combined with chronic alcohol consumption and exposure to cigarette smoke. Full article

Background: Several studies have documented the detrimental impacts of secondhand smoke (SHS) exposure to a range of pediatric respiratory conditions, including asthma, bronchitis, and reduced lung function. The aim of the study was to investigate the influence of SHS exposure on lung function, physical fitness, and body mass index (BMI) in children aged 10 to 14 years. Methods: This cross-sectional study included children aged 10 to 14 years at the Elementary School “Trilj” in Trilj, Croatia. Data on SHS exposure were collected using a questionnaire. Antropometric and spirometry measurements were performed. Physical fitness was assessed using the shuttle run (BEEP) test. Results: This study included 157 children, 89 (56.69%) boys and 68 (43.31%) girls. Children exposed to every day SHS in households had significantly lower values of forced vital capacity (FVC), forced expiratory volume in one second (FEV1), FEV1/FVC, peak expiratory flow (PEF) (p < 0.001) and higher z-score BMI levels (p = 0.018) in comparison to unexposed children. Logistic regression showed that children unexposed to SHS had higher odds for better results in the BEEP test (OR 62.45, 95% CI 21.26–179.24, p < 0.001). Children with poorer physical fitness, expressed by lower BEEP score levels, had significantly lower FVC, FEV1, FEV1/FVC, and PEF (p < 0.001). Conclusions: Every day SHS exposure in children was associated with poorer lung function, higher BMI, and poorer physical fitness. Full article

Exposure to cigarette smoke is known to induce disease during pregnancy. Recent evidence showed that exposure to secondhand smoke (SHS) negatively impacts fetal and placental weights, leading to the development of intrauterine growth restriction (IUGR). Electronic cigarettes (eCigs) represent a phenomenon that has recently emerged, and their use is also steadily rising. Even so, the effects of SHS or eCigs during gestation remain limited. In the present study, we wanted to characterize the effects of SHS or eCig exposure at two different important gestational points during mouse pregnancy. C57/Bl6 mice were exposed to SHS or eCigs via a nose-only delivery system for 4 days (from 14.5 to 17.5 gestational days (dGA) or for 6 days (from 12.5 dGA to 17.5 dGA)). At the time of necropsy (18.5 dGA), placental and fetal weights were recorded, maternal blood pressure was determined, and a dipstick test to measure proteinuria was performed. Placental tissues were collected, and inflammatory molecules in the placenta were identified. Treatment with SHS showed the following: (1) a significant decrease in placental and fetal weights following four days of exposure, (2) higher systolic and diastolic blood pressure following six days of exposure, and (3) increased proteinuria after six days of exposure. Treatment with eCigs showed the following: (1) a significant decrease in placental weight and fetal weight following four or six days of exposure, (2) higher systolic and diastolic blood pressure following six days of exposure, and (3) increased proteinuria after six days of exposure. We also observed different inflammatory markers associated with the development of IUGR or PE. We conclude that the detrimental effects of SHS or eCig treatment coincide with the length of maternal exposure. These results could be beneficial in understanding the long-term effects of SHS or eCig exposure in the development of placental diseases. Full article

The receptor for advanced glycation end-products (RAGE) has a central function in orchestrating inflammatory responses in multiple disease states including chronic obstructive pulmonary disease (COPD). RAGE is a transmembrane pattern recognition receptor with particular interest in lung disease due to its naturally abundant pulmonary expression. Our previous research demonstrated an inflammatory role for RAGE following acute exposure to secondhand smoke (SHS). However, chronic inflammatory mechanisms associated with RAGE remain ambiguous. In this study, we assessed transcriptional outcomes in mice exposed to chronic SHS in the context of RAGE expression. RAGE knockout (RKO) and wild-type (WT) mice were delivered nose-only SHS via an exposure system for six months and compared to control mice exposed to room air (RA). We specifically compared WT + RA, WT + SHS, RKO + RA, and RKO + SHS. Analysis of gene expression data from WT + RA vs. WT + SHS showed FEZ1, Slpi, and Msln as significant at the three-month time point; while RKO + SHS vs. WT + SHS identified cytochrome p450 1a1 and Slc26a4 as significant at multiple time points; and the RKO + SHS vs. WT + RA revealed Tmem151A as significant at the three-month time point as well as Gprc5a and Dynlt1b as significant at the three- and six-month time points. Notable gene clusters were functionally analyzed and discovered to be specific to cytoskeletal elements, inflammatory signaling, lipogenesis, and ciliogenesis. We found gene ontologies (GO) demonstrated significant biological pathways differentially impacted by the presence of RAGE. We also observed evidence that the PI3K-Akt and NF-κB signaling pathways were significantly enriched in DEGs across multiple comparisons. These data collectively identify several opportunities to further dissect RAGE signaling in the context of SHS exposure and foreshadow possible therapeutic modalities. Full article

Background: Pregnant women exposed to second-hand smoke (SHS) are at increased risk of poor birth outcomes. We piloted multicomponent behavioural intervention and trial methods in Bangalore, India, and Comilla, Bangladesh. Methods: A pilot individual randomised controlled trial with economic and process evaluation components was conducted. Non-tobacco-using pregnant women exposed to SHS were recruited from clinics and randomly allocated to intervention or control (educational leaflet) arms. The process evaluation captured feedback on the trial methods and intervention components. The economic component piloted a service use questionnaire. The primary outcome was saliva cotinine 3 months post-intervention. Results: Most pregnant women and many husbands engaged with the intervention and rated the components highly, although the cotinine report elicited some anxiety. Forty-eight (Comilla) and fifty-four (Bangalore) women were recruited. The retention at 3 months was 100% (Comilla) and 78% (Bangalore). Primary outcome data were available for 98% (Comilla) and 77% (Bangalore). Conclusions: The multicomponent behavioural intervention was feasible to deliver and was acceptable to the interventionists, pregnant women, and husbands. With the intervention, it was possible to recruit, randomise, and retain pregnant women in Bangladesh and India. The cotinine data will inform sample size calculations for a future definitive trial. Full article

Exposure to secondhand smoke (SHS) during fetal development results in negative postnatal effects, including altered organ development, changes in metabolism, and increased risk of respiratory illness. Previously, we found the induction of intrauterine growth restriction (IUGR) dependent on the expression of the receptor for advanced glycation end-products (RAGE) in mice treated with SHS. Furthermore, antenatal SHS exposure increases RAGE expression in the fetal lung. Our objective was to determine the postnatal effects of antenatal SHS treatment in 4- and 12-week-old offspring. Pregnant animals were treated with SHS via a nose-only delivery system (Scireq Scientific, Montreal, Canada) for 4 days (embryonic day 14.5 through 18.5), and offspring were evaluated at 4 or 12 weeks of age. Animal and organ weights were measured, and lungs were histologically characterized. Blood pressure and heart rates were obtained, and RAGE protein expression was determined in the lungs of control and treated animals. We observed the following: (1) significant decreases in animal, liver, and heart weights at 4 weeks of age; (2) increased blood pressure in 4-week-old animals; and (3) increased RAGE expression in the lungs of the 4-week-old animals. Our results suggest an improvement in these metrics by 12 weeks postnatally such that measures were not different regardless of RA or SHS exposure. Increased RAGE expression in lungs from 4-week-old mice antenatally treated with SHS suggests a possible role for this important smoke-mediated receptor in establishing adult disease following IUGR pregnancies. Full article

Chemotherapy and radiotherapy resistance are major obstacles in the long-term efficacy of head and neck squamous cell carcinoma (HNSCC) treatment. Secondhand smoke (SHS) exposure is common and has been proposed as an independent predictor of HNSCC recurrence and disease-free survival. However, the underlying mechanisms responsible for these negative patient outcomes are unknown. To assess the effects of SHS exposure on cisplatin efficacy in cancer cells, three distinct HNSCC cell lines were exposed to sidestream (SS) smoke, the main component of SHS, at concentrations mimicking the nicotine level seen in passive smokers’ saliva and treated with cisplatin (0.01–100 µM) for 48 h. Compared to cisplatin treatment alone, cancer cells exposed to both cisplatin and SS smoke extract showed significantly lower cisplatin-induced cell death and higher cell viability, IC₅₀, and indefinite survival capacity. However, SS smoke extract exposure alone did not change cancer cell viability, cell death, or cell proliferation compared to unexposed control cancer cells. Mechanistically, exposure to SS smoke extract significantly reduced the expression of cisplatin influx transporter CTR1, and increased the expression of multidrug-resistant proteins ABCG2 and ATP7A. Our study is the first to document that exposure to SHS can increase cisplatin resistance by altering the expression of several proteins involved in multidrug resistance, thus increasing the cells’ capability to evade cisplatin-induced cell death. These findings emphasize the urgent need for clinicians to consider the potential role of SHS on treatment outcomes and to advise cancer patients and caregivers on the potential benefits of avoiding SHS exposure. Full article

Chronic sinusitis (CS) is characterized by sinonasal inflammation, mucus overproduction, and edematous mucosal tissue. CS impacts one in seven adults and estimates suggest up to 15% of the general U.S. population may be affected. This research sought to assess a potential role for receptors for advanced glycation end-products (RAGE), an inflammatory receptor expressed in tissues exposed to secondhand smoke (SHS). Human sinus tissue sections were stained for RAGE and S100s, common RAGE ligands. Wild-type mice and mice that over-express RAGE in sinonasal epithelium (RAGE TG) were maintained in room air (RA) or exposed to secondhand smoke (SHS) via a nose-only delivery system five days a week for 6 weeks. Mouse sections were stained for RAGE and tissue lysates were assayed for cleaved caspase 3, cytokines, or matrix metalloproteases. We discovered increased RAGE expression in sinus tissue following SHS exposure and in sinuses from RAGE TG mice in the absence of SHS. Cleaved caspase-3, cytokines (IL-1β, IL-3, and TNF-α), and MMPs (-9 and -13) were induced by SHS and in tissues from RAGE TG mice. These results expand the inflammatory role of RAGE signaling, a key axis in disease progression observed in smokers. In this relatively unexplored area, enhanced understanding of RAGE signaling during voluntary and involuntary smoking may help to elucidate potential therapeutic targets that may attenuate the progression of smoke-related CS. Full article

Second-hand smoke (SHS) has adverse effects for pregnant women and foetuses. This controlled and randomized clinical trial evaluated the efficacy of a comic booklet intervention in promoting SHS avoidance among pregnant women and appropriate smoking behaviours among their male partners. We allocated 140 couples to the experimental group (EG), who received the comic booklet and a reminder sticker, and 146 couples to the control group (CG), who received usual care. The primary outcomes were women’s self-reported SHS exposure and their male partners’ smoking behaviours. Secondary outcomes included knowledge and awareness of SHS. Independent t-tests revealed that three months post-intervention, more male partners in the EG had appropriate self-reported smoking behaviours with a small effect size (Cohen’s d = 0.35, 95% CI [0.08, 0.62], p-value = 0.01). Significantly more pregnant women in the EG recognised their partners’ appropriate smoking behaviours with a nearly middle effect size (Cohen’s d = 0.43, 95% CI [0.16, 0.70], p-value ≤ 0.01). Cues to action showed a significant difference between groups with a small effect size (Cohen’s d = 0.36, 95% CI [0.09, 0.63], p-value = 0.01), as evaluated by male partners. These findings suggest that the comic booklet intervention might be effective against SHS exposure by providing several cues to action through knowledge and awareness of SHS. Full article

The receptor for advanced glycation end products (RAGE) is a key contributor to immune and inflammatory responses in myriad diseases. RAGE is a transmembrane pattern recognition receptor with a special interest in pulmonary anomalies due to its naturally abundant pulmonary expression. Our previous studies demonstrated an inflammatory role for RAGE following acute 30-day exposure to secondhand smoke (SHS), wherein immune cell diapedesis and cytokine/chemokine secretion were accentuated in part via RAGE signaling. However, the chronic inflammatory mechanisms associated with RAGE have yet to be fully elucidated. In this study, we address the impact of long-term SHS exposure on RAGE signaling. RAGE knockout (RKO) and wild-type (WT) mice were exposed to SHS using a nose-only delivery system (Scireq Scientific, Montreal, Canada) for six months. SHS-exposed animals were compared to mice exposed to room air (RA) only. Immunoblotting was used to assess the phospho-AKT and phospho-ERK activation data, and colorimetric high-throughput assays were used to measure NF-kB. Ras activation was measured via ELISAs. Bronchoalveolar lavage fluid (BALF) cellularity was quantified, and a mouse cytokine antibody array was used to screen the secreted cytokines. The phospho-AKT level was decreased, while those of phospho-ERK, NF-kB, and Ras were elevated in both groups of SHS-exposed mice, with the RKO + SHS-exposed mice demonstrating significantly decreased levels of each intermediate compared to those of the WT + SHS-exposed mice. The BALF contained increased levels of diverse pro-inflammatory cytokines in the SHS-exposed WT mice, and diminished secretion was detected in the SHS-exposed RKO mice. These results validate the role for RAGE in the mediation of chronic pulmonary inflammatory responses and suggest ERK signaling as a likely pathway that perpetuates RAGE-dependent inflammation. Additional characterization of RAGE-mediated pulmonary responses to prolonged exposure will provide a valuable insight into the cellular mechanisms of lung diseases such as chronic obstructive pulmonary disease. Full article

Thailand has successfully forwarded Article 8, Protection from Exposure to Tobacco Smoke, of the World Health Organization’s Framework Convention on Tobacco Control (WHO FCTC). It achieved its 100% smoke-free goals in public places in 2010, next pursuing other bans in outdoor places to lower particulate matter air pollution (PM_2.5). Our aim was to expose the secondhand smoke levels in vehicles since SHS is a danger to everyone, but especially to children and youth. This is the first experimental study of its kind in Thailand. We measured PM_2.5 for 20 min under four conditions in 10 typical Thai vehicles, including commonly used sedans and small pickup trucks. We used an established protocol with two real-time air monitoring instruments to record PM_2.5 increases with different vehicle air exchange and air conditioning conditions. Monitoring was recorded in the vehicle’s front and back seats. The most common Thai ventilation condition is all windows closed with fan/air conditioning (AC) in operation because of Thai tropical conditions. Mean exposure levels were three and nearly five times (49 and 72 μg/m³) the 24 h WHO standard of 15 μg/m³ in the back and front seats, respectively. These high PM_2.5 exposure levels warrant action to limit vehicle smoking for public health protection. Full article