Smoke Exposure Research Articles

Current smoking is related to severe damage in systemic lupus erythematosus patients

Objective To assess the relationship between smoking exposure and organ damage accrual measured by Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index for Systemic Lupus Erythematosus score (SLICC-SDI) in consecutive patients with systemic lupus erythematosus (SLE) from Argentina. Methods 623 consecutive SLE patients (fulfilling ≥4, 1997 ACR criteria) were included in this cross-sectional study. Sociodemographic and disease related variables including SLICC-SDI score and smoking status were collected. Patients currently smoking were considered “smokers”, and “non-smokers” those who never smoked and former smokers. SLICC-SDI was divided into two categories: <3 and ≥3 was defined as severe damage. Results Six hundred and 23 patients were included in the analysis, 89% women. Eighty-four per cent were non-smokers and 16 % were current smokers 83 percent of patients had SLICC-SDI <3 and 17 % had SLICC-SDI ≥3. Twenty one percent of patients with SLICC-SDI ≥3 and 15% with <3 SLICC-SDI were current smokers ( p 0.081). In the multiple regression analysis, current smoking (OR 1.82, CI 95% 1.01-3.31, p 0.046), older age (OR 1.04, CI 95% 1.00-1.05, p 0.034), disease duration (OR 1.03, CI 95% 1.00-1.07, p 0.021) and cyclophosphamide exposure (OR 2.97, CI 95% 1.49-5.88, p 0.002) were related to SLICC-SDI ≥3. Conclusion In our sample of patients, current smoking, older age, disease duration and cyclophosphamide were related to severe damage (SLICC-SDI ≥3).

Addressing tobacco screening and treatment among racially and ethnically minoritized parents in pediatric clinics: barriers and facilitators.

Household secondhand smoke (SHS) exposure remains a significant health issue for racially and ethnically minoritized children in the United States. Delivering parental tobacco treatment during pediatric primary care visits can reduce children's SHS exposure. This study examined current tobacco screening practices and health system stakeholder perceptions of facilitators and barriers to addressing tobacco use during pediatric visits among racially and ethnically minoritized parents. We conducted 25 semi-structured interviews with clinicians, staff, and health system leaders from 5 pediatric primary care clinics in Minneapolis-St. Paul, Minnesota. The study was informed by the Health Equity Implementation Framework. Interviews were analyzed using both directed content and thematic analysis. Participants identified multilevel facilitators and barriers to addressing parental tobacco use in minoritized families. Within the clinical encounter, barriers included linguistic and cultural barriers, health system navigational challenges, medical mistrust, low levels of clinician and staff knowledge, skills, and confidence, time constraints, and lack of alignment with external metrics. Facilitators centered on leveraging interpreters' cultural knowledge and the presence of culturally-congruent clinicians and staff to reduce medical mistrust and stigma, developing linguistically and culturally relevant resources, and integrating prompts and resources into the electronic health record. Participants described how lessons from previous system change mechanisms would facilitate this work. Addressing health system, training and resources, and linguistic and cultural barriers among clinicians and staff is essential to strengthen their capacity to address household SHS exposure among racially and ethnically minoritized populations as a component of pediatric preventive care. Clinicians and health system staff perceive unique barriers to identifying and addressing parental tobacco use among racially and ethnically minoritized parents during pediatric primary care visits. Solutions to expand tobacco treatment access to minoritized parents in pediatric settings must attend to clinician training needs on tobacco treatment, embedding clinical encounter resources and reminders that match the linguistic and cultural needs and preferences of their patient populations, and increasing access to high quality interpreting services and culturally-congruent staff.

Wildfire Smoke Exposure During Pregnancy: Consensus-Building to Co-Create a Community-Engaged Study

Relative to other Oregon counties, Klamath County experiences worse air quality due to wildfire smoke, as well as elevated rates of infant mortality and low birthweight. Klamath County Public Health (KCPH) raised concerns that wildfire smoke is a contributor to poor infant health. Thus, we built a multidisciplinary team and designed a community-engaged research (CEnR) project to capture community and individual-level exposure to wildfire smoke contaminants, alongside perinatal health outcomes. Through partnerships, we identified 24 individuals across academic, public health, and community organizations that met five times over three months to develop a study design. We initially used a modified Delphi method, but adjusted our approach to find multidisciplinary areas of agreement across a highly diverse team. Our team used structured meetings, surveys, and iterative feedback to build consensus on a study design. KCPH and our community partners reviewed and approved all proposed activities to ensure community input was integrated. The resultant study, trialed in Klamath County, included the use of environmental, residential, and personal samplers and health surveys with a cohort of pregnant individuals during the wildfire season. We discuss the advantages and challenges of building a multidisciplinary CEnR study in a rural county disproportionately impacted by wildfire smoke and infant mortality.

Cigarette smoke alters calcium flux to induce PP2A membrane trafficking and endothelial cell permeability.

Alveolar capillary barrier disruption induces local edema and inflammation that impairs pulmonary function and promotes alveolar destruction in COPD. This study aimed to determine how cigarette smoke modulated the serine-threonine phosphatase protein phosphatase 2A (PP2A) to alter the barrier function of human lung microvascular endothelial cells (HLMVECs). Cigarette smoke exposure lowered overall PP2A activity and enhanced endothelial permeability in HLMVECs. However, directly decreasing PP2A activity with Fostriecin significantly reduced endothelial cell permeability. Protein fractionation studies determined that cigarette smoke diminished cytosolic PP2A activity but increased membrane and cytoskeletal activity. These changes coincided with the translocation of PP2A to the membrane, which reduced occludin phosphorylation in the membrane. Cigarette smoke decreased protein tyrosine phosphatase 1B (PTP1B) activity, a PP2A activator which also counters calcium intracellular influx. The decrease in PTP1B activity correlated with reduced calcium efflux in endothelial cells and these changes in calcium flux regulated PP2A activity. Indeed, culturing endothelial cells in low calcium medium prevented the decrease in cytosolic PP2A activity mediated by cigarette smoke. Together, these findings outline a mechanism whereby cigarette smoke acts via calcium to traffic PP2A from the cytosol to the membrane where it dephosphorylates occludin to increase endothelial cell permeability.

Clearing the air: Heightened perception of harm from secondhand cannabis smoke exposure is associated with no in-home cannabis smoking in a 21-country convenience sample.

As countries adopt more lenient cannabis use policies, perception of harm from secondhand cannabis smoke (SHCS) exposure is decreasing and most cannabis smoking is taking place at home. We quantified the relationship of reported in-home cannabis smoking with perceived harm from SHCS exposure. The analytic sample comprised 28,154 adult respondents, from 21 countries, to the annual cross-sectional Global Drug Survey (2021) of users of licit or illicit drugs. Respondents reported perception of harm to non-smoking residents from SHCS exposure and past 30-day cannabis smoking in the home by anyone. Logistic regression estimated covariate-adjusted odds ratios and 95 % confidence intervals of in-home cannabis smoking (yes/no). The association between harm perception and in-home cannabis smoking by country of residence was also quantified. Sixty-one percent reported no in-home cannabis smoking in the last 30 days; mean perception of harm of SHCS exposure on a 10-point scale was 5.2. Those at the 75th (vs 25th) percentile of perceived harm had 70 % higher odds (OR = 1.7, 95 % CI = 1.6-1.8) of no in-home cannabis smoking. In all countries of residence, higher perception of harm was associated with reporting no in-home cannabis smoking, although not all were statistically significant. The strongest association was seen in Sweden (OR = 3.9, 95 % CI = 1.5-11.9) and New Zealand (OR = 2.3, 95 % CI = 2.0-2.7). Respondents who perceived SHCS as harmful were less likely to report in-home cannabis smoking. If this association subsequently proves causal, increasing awareness of the harms associated with SHCS exposure could substantially reduce residential cannabis secondhand smoke exposure.

Abstract 4122507: Fetal Socioeconomic and Environmental Exposures Influence Fetal Brain Growth and Risk of Neonatal Brain Injury in Congenital Heart Disease

Introduction: Fetuses with CHD have smaller total brain volume (TBV) and are at risk for acquired brain white matter injury (WMI), both of which are linked to neurodevelopmental impairments. Social determinants of health (SDOH) and other fetal environmental factors have been linked to fetal brain health in other populations. Our aim was to test our hypothesis that these exposures influence fetal brain growth and postnatal WMI risk in severe CHD. Methods: Our prospective longitudinal cohort study enrolled fetuses with severe CHD to undergo fetal brain MRI and postnatal pre-operative brain MRI. Participants completed home environment surveys on individual SDOH and exposures. Community SDOH metrics were determined using Child Opportunity Index (COI) based on home address. An ‘at risk’ fetus composite was created if there was exposure to: personal/household smoking, welfare/food stamps, or poverty. TBV was calculated at both time points. Presence/degree of WMI was determined on postnatal MRI. Repeated measures analysis and logistic regression were performed to determine association between individual and community SDOH metrics with rate of TBV growth and risk of WMI. Results: 55 participants enrolled (54 fetal scans: mean GA 33.9 wks, 95%CI: 33.7,34.1; 47 neonatal scans: mean GA 39.3 wks 95%CI: 38.9,39.6). Fetal sex, smoking exposure, and several individual SDOH were associated with TBV growth. Adjusting for fetal sex and GA at scan, rate of TBV growth was slower with smoking exposure (coeff: -5.2, 95%CI: -10.3, -0.2, p= 0.04) and trended towards significance for those with welfare/food stamps or poverty. ‘At risk’ fetuses had slower rate of TBV growth than those without risk (coeff: -2.5, 95%CI: -5.0, -0.07, p= 0.04) (Figure 1). There were lower odds of pre-operative WMI with high COI compared to low after adjusting for GA at scan (OR= 0.16, 95%CI: 0.03, 0.9, p= 0.04). Conclusion: Smoking exposure and individual-level SDOH influence brain growth, while community COI is associated with risk of postnatal pre-op WMI in CHD. Our findings identify targets for intervention to optimize brain growth and outcomes in the CHD population, including smoking cessation programs, and nutritional and needs assessment during pregnancy.

Metabolic Effects of Sodium Thiosulfate During Resuscitation from Trauma and Hemorrhage in Cigarette-Smoke-Exposed Cystathionine-γ-Lyase Knockout Mice

Background: Acute and chronic pre-traumatic cigarette smoke exposure increases morbidity and mortality after trauma and hemorrhage. In mice with a genetic deletion of the H2S-producing enzyme cystathione-γ-lyase (CSE−/−), providing exogenous H2S using sodium thiosulfate (Na2S2O3) improved organ function after chest trauma and hemorrhagic shock. Therefore, we evaluated the effect of Na2S2O3 during resuscitation from blunt chest trauma and hemorrhagic shock on CSE−/− mice with pre-traumatic cigarette smoke (CS) exposure. Since H2S is well established as being able to modify energy metabolism, a specific focus was placed on whole-body metabolic pathways and mitochondrial respiratory activity. Methods: Following CS exposure, the CSE−/− mice underwent anesthesia, surgical instrumentation, blunt chest trauma, hemorrhagic shock for over 1 h (target mean arterial pressure (MAP) ≈ 35 ± 5 mmHg), and resuscitation for up to 8 h comprising lung-protective mechanical ventilation, the re-transfusion of shed blood, fluid resuscitation, and continuous i.v. noradrenaline (NoA) to maintain an MAP ≥ 55 mmHg. At the start of the resuscitation, the mice randomly received either i.v. Na2S2O3 (0.45 mg/gbodyweight; n = 14) or the vehicle (NaCl 0.9%; n = 11). In addition to the hemodynamics, lung mechanics, gas exchange, acid–base status, and organ function, we quantified the parameters of carbohydrate, lipid, and protein metabolism using a primed continuous infusion of stable, non-radioactive, isotope-labeled substrates (gas chromatography/mass spectrometry) and the post-mortem tissue mitochondrial respiratory activity (“high-resolution respirometry”). Results: While the hemodynamics and NoA infusion rates did not differ, Na2S2O3 was associated with a trend towards lower static lung compliance (p = 0.071) and arterial PO2 (p = 0.089) at the end of the experiment. The direct, aerobic glucose oxidation rate was higher (p = 0.041) in the Na2S2O3-treated mice, which resulted in lower glycemia levels (p = 0.050) and a higher whole-body CO2 production rate (p = 0.065). The mitochondrial respiration in the heart, kidney, and liver tissue did not differ. While the kidney function was comparable, the Na2S2O3-treated mice showed a trend towards a shorter survival time (p = 0.068). Conclusions: During resuscitation from blunt chest trauma and hemorrhagic shock in CSE−/− mice with pre-traumatic CS exposure, Na2S2O3 was associated with increased direct, aerobic glucose oxidation, suggesting a switch in energy metabolism towards preferential carbohydrate utilization. Nevertheless, treatment with Na2S2O3 coincided with a trend towards worsened lung mechanics and gas exchange, and, ultimately, shorter survival.

Lady health workers smoking cessation initiative in rural Pakistan

Abstract Background In Pakistan, tobacco smoking and indoor smoke from cooking fires pose significant health risks. Lady Health Workers (LHWs) play a crucial role in improving healthcare access, particularly in rural areas. This study aimed to explore the practicality of training LHWs to deliver health education aimed at reducing household exposure to tobacco smoke and indoor biomass smoke, while also documenting baseline exposure levels and assessing the immediate impact on household awareness and intentions to reduce exposure. The Program Over 170 LHWs were trained and equipped with health education resources to raise awareness about the risks of tobacco and biomass smoke exposure. The training was designed to be integrated into their routine duties. Results Over 24 weeks, the program was delivered to 25,760 households in Gujranwala district. Approximately half of these households had at least one person who smoked, with 90% smoking indoors. Many (85%) households used indoor cooking fires. Only 24% of household head-women were aware of the health risks associated with indoor smoke exposure. Awareness of less harmful alternatives to smoking was low. Most households had someone who wanted to stop smoking and 51 women and 146 men agreed to try a tobacco harm reduction (THR) product. Primary health units’ staff appreciated the project, especially the training provided. They believed the program could be sustainable, and LHWs expressed interest in continuing it. Conclusion The study demonstrated the practicality of training LHWs to deliver health education on reducing tobacco and biomass smoke exposure in rural settings. The program effectively raised awareness and showed potential for sustainable integration into existing healthcare structures, highlighting the value of community-centric approaches in low-resource settings.

Abstract 4136285: Large-Scale Proteomics Identifies Novel Shared Biomarkers of Heart Failure and Cancer: the Atherosclerosis Risk in Communities (ARIC) Study

Introduction: There is a bidirectional relationship between cancer and cardiovascular disease risk. Identifying proteins associated with both cancer and heart failure (HF) may provide insight into common biological pathways underlying both conditions. Methods: Among 10,136 participants in the community-based ARIC cohort study who were free of HF and cancer at study visit 2 (1990-92) and had aptamer-based proteomics (SomaScan v4), we assessed the association of 4,955 plasma proteins with incident HF and with incident site-specific cancer ascertained by cancer registry linkage supplemented with medical records (lung, post-menopausal breast, prostate, colorectal, and hematologic) using multivariable Cox models adjusted for demographics, clinical characteristics, and social determinants of health. Two-sample cis-Mendelian randomization ( cis- MR) was performed to evaluate potential causal effects of proteins on HF, left ventricular (LV) function, and site-specific cancer. Results: Mean age at baseline was 56±6; 54% were female; and 24% reported black race. Over a median follow-up of 10 [IQR 10, 10] years, there were 604 incident HF events and 1,207 incident cancers (169 lung, 85 hematologic, 105 colorectal, 206 breast, 288 prostate). Using a Bonferroni significance threshold (p < 1.0x10 -5 ), 23 proteins were associated with both HF and lung cancer, 2 with HF and hematologic malignancy, 1 with HF and colorectal cancer, and none with HF and breast or prostate cancer. Six proteins remained significantly associated with both HF and lung cancer after further adjustment for pack-years of smoking (Figure). In cis- MR of these six proteins, ICAM5 and MMP12 showed potential causal effect on LV volume and lung adenocarcinoma, and PLAUR showed potential causal effect on HF and lung adenocarcinoma. Conclusion: Among various types of cancer, proteins associated with lung cancer showed the greatest overlap with proteins associated with HF, which was largely accounted for by smoking exposure. We uncovered a set of 6 plasma proteins associated with both incident HF and lung cancer after accounting for smoking. MR identified proteins with potential causal effects on both lung adenocarcinoma and LV size (ICAM5, MMP12) and HF (PLAUR).

The impact of wildfire smoke exposure on excess mortality and later-life socioeconomic outcomes: the Great Fire of 1910

AbstractThe Great Fire of 1910 in the northwestern United States burnt more than 1.2 million hectares in just two days and stands as one of the largest wildfires ever recorded. While it is known for having led to the introduction of a rigorous fire suppression regime that lasted for much of the twentieth century, it also generated a considerable amount of smoke far beyond the burnt areas that is likely to have impacted the health of those exposed. This paper examines the short- and long-term impact of this fire-sourced smoke pollution on children, combining historical data with smoke emission and dispersion modelling. The econometric results indicate a 119% increase in excess mortality during the week of the fire and a decrease of 4–14% in later-life socioeconomic status scores 20 and 30 years after the event. This research offers novel insights into wildfire smoke repercussions on health and long-run human capital formation in a setting where avoidance behaviour was minimal.

In utero, childhood, and adolescence tobacco smoke exposure, physical activity, and chronic kidney disease incidence in adulthood: evidence from a large prospective cohort study

BackgroundThe adverse effects of early-life tobacco smoke exposure on chronic kidney disease (CKD) risk remain unclear. This study aimed to investigate the associations of early-life tobacco smoke exposure with CKD incidence in adulthood, and further explore the modification effects of physical activity (PA).MethodsA total of 352,883 participants were included from the UK Biobank. The information on early-life tobacco smoke exposure was assessed by employing in utero tobacco smoke exposure and age of smoking initiation. Weekly moderate-to-vigorous physical activity (MVPA) was calculated for each individual. Cox proportional hazard regression was fitted to estimate the hazard ratio (HR) and 95% confidence interval (CI) of CKD risk, and to investigate the modification effects of MVPA.ResultsCKD incidence significantly increased in participants with in utero tobacco smoke exposure (HR: 1.08, 95% CI: 1.04, 1.12). Compared with never-smokers, we found a monotonic increase in the risk of CKD with smoking initiation across adulthood (HR: 1.21, 95% CI: 1.16, 1.27), adolescence (HR: 1.29, 95% CI: 1.24, 1.35), and childhood (HR: 1.34, 95% CI: 1.25, 1.43) (P trend < 0.001). Additionally, we identified joint cumulative effects of MVPA and early-life tobacco smoke exposure on incident CKD. Compared with never-smokers with recommended MVPA, prenatal or childhood tobacco smokers without recommended MVPA had the highest CKD risk, and the HRs (95% CIs) were 1.17 (1.10, 1.24) and 1.51 (1.36, 1.68), respectively.ConclusionsEarly-life tobacco smoke exposure may contribute to CKD incidence in adulthood, and the observed associations could be modified by MVPA. These findings provide important information on CKD prevention in the participant’s early life while urging a more rapid and powerful need for tobacco control among pregnant couples, children, and adolescents.

Effect of Nicotine on Pulmonary Pathogenic Bacteria.

Exposure to cigarette smoke significantly enhances susceptibility to bacterial infections by inducing physiological and structural alterations, including immune system dysregulation. This exposure also augments bacterial virulence including biofilm formation, leading to severe infectious diseases and antibiotic resistance. Notably, cigarette smoke exposure increases the incidence of pneumonia by up to 2.5-fold and tuberculosis by up to 4.1-fold. Nicotine, a primary constituent of cigarette smoke, has been extensively characterized for its immunomodulatory effects. However, despite the wealth of knowledge on nicotine's impact on the host immune response, there is a paucity of data regarding its direct effects on various pulmonary pathogens. In the present review, we discuss the main findings in this field.

Wildfire Smoke: Health Effects, Mechanisms, and Mitigation.

Wildfires are becoming more frequent and intense on a global scale, raising concerns about their acute and long-term effects on human health. We conducted a systematic review of the current epidemiological evidence on wildfire health risks and a meta-analysis to investigate the association between wildfire smoke exposure and various health outcomes. We discovered that wildfire smoke increases the risk of premature deaths and respiratory morbidity in the general population. Meta-analysis of cause-specific mortality and morbidity revealed that wildfire smoke had the strongest associations with cardiovascular mortality (RR: 1.018, 95% CI: 1.014-1.021), asthma hospitalization (RR: 1.054, 95% CI: 1.026-1.082), and asthma emergency department visits (RR: 1.117, 95% CI: 1.035-1.204) in the general population. Subgroup analyses of age found that adults and elderly adults were more susceptible to the cardiopulmonary effects of wildfire smoke. Next, we systematically addressed the toxicological mechanisms of wildfire smoke, including direct toxicity, oxidative stress, inflammatory reactions, immune dysregulation, genotoxicity and mutations, skin allergies, inflammation, and others. We discuss wildfire smoke risk mitigation strategies including public health interventions, regulatory measures, and personal actions. We conclude by highlighting current research limitations and future directions for wildfire research, such as elucidating the complex interactions of wildfire smoke components on human health, developing personalized risk assessment tools, and improving resilience and adaptation strategies to mitigate the health effects of wildfires in changing climate.

Using sensory and instrumental analysis to assess the impact of grape smoke exposure on different red wine varietals in California

This study is an investigation of the impact of volatile phenols (VPs) released from burning wood during wildfires on grape composition and the resulting wines. Baseline levels of VPs in grapes and sensory differences between smoke-impacted wines and non-smoke-impacted wines were determined. The differences were related to different levels of smoke taint marker compounds in different wine matrices, using modified descriptive analysis (DA), multivariate statistics, gas chromatography mass spectrometry (GC-MS) and liquid chromatography-triple quadrupole tandem mass spectrometry (LC-QqQ-MS) of the free and total VPs, and individual bound glycosides, respectively. Across two DA panels, Cabernet Sauvignon, Cabernet Franc, Petite Verdot, Merlot, Syrah, Malbec, and Zinfandel wines made from grape originating from different areas in California were evaluated. The results show sensory differences between highly smoke-impacted and non-impacted wines with wines made from highly smoke-impacted grapes characterized as smoky, barbeque, medicinal, and having a retro-nasal ashtray character. Low smoke-impact wines based on free and total VP concentrations were not significantly different from the non-impacted wines when rated through descriptive analysis. The amount of smoke exposure was the largest contributor to smoke impact determined by sensory evaluation, but the different wine matrices from different locations and varietals also played an important role in determining the level of perceived smoke impact. The results of this study will contribute to our understanding of smoke impact and how it influences wine characteristics by relating smoke marker indicator compounds to wine sensory attributes.

Associations Between Mosaic Loss of Sex Chromosomes and Incident Hospitalization for Atrial Fibrillation in the United Kingdom.

Mosaic loss of chromosome Y (mLOY) in leukocytes of men reflects genomic instability from aging, smoking, and environmental exposures. A similar mosaic loss of chromosome X (mLOX) occurs among women. However, the associations between mLOY, mLOX, and risk of incident heart diseases are unclear. We estimated associations between mLOY, mLOX, and risk of incident heart diseases requiring hospitalization, including atrial fibrillation, myocardial infarction, ischemic heart disease, cardiomyopathy, and heart failure. We analyzed 190 613 men and 224 853 women with genotyping data from the UK Biobank. Among these participants, there were 37 037 men with mLOY and 13 978 women with mLOX detected using the Mosaic Chromosomal Alterations caller. Multivariable Cox regression was used to estimate hazard ratios (HRs) and 95% CIs of each incident heart disease in relation to mLOY in men and mLOX in women. Additionally, Mendelian randomization was conducted to estimate causal associations. Among men, detectable mLOY was associated with elevated risk of atrial fibrillation (HR, 1.06 [95% CI, 1.03-1.11]). The associations were apparent in both never smokers (HR, 1.07 [95% CI, 1.01-1.14]) and ever smokers (HR, 1.05 [95% CI, 1.01-1.11]) as well as men aged >60 and ≤60 years. Mendelian randomization analyses supported causal associations between mLOY and atrial fibrillation (HRMR-PRESSO, 1.15 [95% CI, 1.13-1.18]). Among postmenopausal women, we found a suggestive inverse association between detectable mLOX and atrial fibrillation risk (HR, 0.90 [95% CI, 0.83-0.98]). However, associations with mLOY and mLOX were not found for other heart diseases. Our findings suggest that mLOY and mLOX reflect sex-specific biological processes or exposure profiles related to incident atrial fibrillation requiring hospitalization.

The Potential Role of Cigarette Smoke, Elastic Fibers, and Secondary Lung Injury in the Transition of Pulmonary Emphysema to Combined Pulmonary Fibrosis and Emphysema.

Combined pulmonary fibrosis and emphysema (CPFE) is a distinct syndrome associated with heavy smoking. The fibrotic component of the disease is generally believed to be superimposed on previously existing pulmonary emphysema, but the mechanisms responsible for these changes remain poorly understood. To better understand the pathogenesis of CPFE, we performed a series of experiments that focused on the relationships between lung elastic fibers, cigarette smoke, and secondary lung injury. The results indicate that even brief smoke exposure predisposes the lung to additional forms of lung injury that may cause alveolar wall fibrosis. The proinflammatory activity of smoke-induced structural alterations in elastic fibers may contribute to this process by enhancing secondary lung inflammation, including acute exacerbations of chronic obstructive pulmonary disease. Furthermore, the levels of the unique elastin crosslinks, desmosine and isodesmosine, in blood, urine, and sputum may serve as biomarkers for the transition from pulmonary emphysema to interstitial fibrosis. While the long-term effects of these inflammatory reactions were not examined, the current studies provide insight into the potential relationships between elastic fiber injury, cigarette smoke, and secondary lung injury. Determining the mechanisms involved in combined pulmonary emphysema and fibrosis and developing a sensitive biomarker for this type of lung injury may permit timely therapeutic intervention that could mitigate the high risk of respiratory failure associated with this condition.

The prospective associations of fetal growth-related pregnancy complications with subsequent breastfeeding duration and markers of human milk production.

The development of the breast for lactation occurs throughout pregnancy. It is unknown whether pregnancy complications resulting in poor fetal growth can affect breastfeeding success. We examined whether fetal growth-related pregnancy complications were associated with earlier breastfeeding cessation and changes in the concentrations of human milk biomarkers of low milk production. We used data from the Growing Up in Singapore Toward healthy Outcomes (GUSTO) study (n=954). Human milk concentrations of protein, lactose, citrate, sodium, potassium and zinc at 3 weeks postpartum were available for 180 mother-infant dyads. We examined the associations of fetal growth measures, including term infants born small-for-gestational-age (SGA) (<10th percentile), pregnancies complicated by fetal growth deceleration (FGD) (2nd - 3rd trimester fetal growth dropped between major centiles), elevated umbilical artery resistance (UAR) (> 90th percentile) or hypertensive disorders of pregnancy (HDP) with (i) risk of ceasing breastfeeding (Cox regression) and (ii) concentrations of human milk components (weighted linear regression). Adjusting for maternal education, smoking exposure, breastfeeding intentions and pre-pregnancy BMI, individuals who delivered SGA infants, and those with HDP were more likely to breastfeed for a shorter duration when compared to those with uncomplicated pregnancies (adjusted hazard ratio [95% CI]: 1.45 [1.11, 1.89] and 1.61 [1.14, 2.29], respectively); associations were not significant for FGD and UAR. SGA was not associated with concentrations of human milk biomarkers, but compared to participants with uncomplicated pregnancies, milk produced by those with HDP contained lower zinc concentrations (adjusted beta coefficient [95% CI]: -0.56 mg/L [-1.08, -0.04]). Individuals with HDP and those with SGA infants tend to breastfeed for a shorter duration; however, only HDP appeared to be associated with biomarkers of compromised milk production. Further research and support are needed to help individuals with HDP and SGA achieve their breastfeeding goals. This study was registered as NCT01174875, and can be accessed at https://clinicaltrials.gov/study/NCT01174875.

Magnitude and Correlates of Nicotine Dependence Among Brick Kiln Workers in A Rural Block of Murshidabad District, West Bengal, India

Background: Nicotine dependence, a major public health problem, causes respiratory illnesses like asthma, COPD, chronic bronchitis, pneumoconiosis (e.g. silicosis) and respiratory infections. Occupational exposure of smoke and dust among brick kiln workers, in addition to tobacco addiction result in worsening of lung function and increase the risk of mortality. This study planned to estimate the prevalence of nicotine dependence among tobacco users of a brick kiln factory and identify the factors associated with nicotine dependence among them. Methodology: A cross-sectional study was conducted for a period of one month in a brick kiln of Murshidabad district among 135 adult workers who had been consuming any form of tobacco. Nicotine dependence was assessed by interviewing the participants using Fagerstrom Test for Nicotine Dependence (FTND) and Fagerstrom Nicotine Dependence Scale for smokeless Tobacco (FTND-ST) questionnaire. Results: About, 52.6% were smokers, 24.4% were smokeless tobacco users and 23% were addicted to both. Approximately 73.6% and 78.2% were nicotine dependent among smokers and smokeless tobacco users respectively. Age, illiteracy, initiation of nicotine consumption at an adult age and long duration of consumption were found to be significantly associated with nicotine dependence. Conclusions: A high level of nicotine dependence was found among workers. Awareness generation and behavior change communication is recommended.

Secondhand Smoke Exposure in Pediatric Patients: What Is the Nurse Practitioner's Role?

Secondhand Smoke Exposure in Pediatric Patients: What Is the Nurse Practitioner's Role?

A Protocol for Modifying Progesterone to Increase Postpartum Cigarette Smoking Abstinence and Reduce Secondhand Smoke Exposure in Infants

New interventions are necessary to increase postpartum abstinence from cigarette smoking. Sex hormones, specifically progesterone, have been found to be protective against drug-taking behaviors. Our pilot double-blind, randomized, controlled trial, although underpowered, suggested a trend toward a higher prevalence of smoking abstinence among postpartum participants receiving exogenous progesterone compared to those receiving placebo. This paper outlines the protocol used in our study to evaluate the efficacy of modifying progesterone to increase postpartum smoking abstinence and, subsequently, decrease secondhand smoke exposure in infants. In the intervention arm, participants will receive open-label exogenous oral progesterone (200 mg twice daily). Using a concurrent control group that does not receive progesterone treatment, we hypothesize that progesterone treatment will increase postpartum smoking abstinence as measured using a 7-day point prevalence at six months post-treatment allocation, as well as reduce smoking-related risk factors. Secondary objectives include examining the impact of this maternal smoking intervention on infant health. In addition to describing the protocol, we also discuss the protocol changes made due to the COVID-19 pandemic. Upon completion, this study will provide new information on how sex hormones may influence smoking cessation in postpartum populations, which can have broad public health implications. Clinical Trials Registration #NCT04783857