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Background: About half of the population in developing countries are exposed to indoor pollution such as combustion fuels at present. Chronic obstructive pulmonary disease (COPD) is one of the leading causes of mortality globally and the primary cause of COPD in women is indoor air pollution exposure, while tobacco smoking is the leading cause in men. The aim of this systematic review and meta-analysis is to evaluate the correlation between the indoor air pollution and deaths related to COPD and COPD prevalence in South Asia. Methods: A systematic search on studies with sufficient statistical power has been conducted from 1985 until 30 June 2020, in English electronic databases following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines in MEDLINE and PubMed databases with the terms Chronic Obstructive Pulmonary disease COPD or Chronic Bronchitis or Emphysema or COPD Deaths or Chronic Obstructive Lung Disease or Airflow Obstruction or Chronic Airflow Obstruction or Airflow Obstruction, Chronic or Bronchitis, Chronic and Mortality or Death or Deceased was conducted. Studies were eligible if they were Prospective controlled or non-controlled trials conducted in Southern Asia/ Asia and Retrospective studies conducted in Southern Asia/ Asia. Results: The results have concluded that long term exposure to indoor pollution had a significant effect on COPD deaths as well as its symptoms. Odd’s ratio was in a range of 1.05 (Randomized controlled trials) to 7.87 (Cross sectional studies) for all the studies mentioned. Meta-analysis observed a significantly higher Odds Ratio of 2.13 for COPD mortality and 2.08 for COPD prevalence on exposure to indoor air pollution. Conclusion: Exposure to solid fuel smoke is consistently and significantly correlated with COPD mortality and COPD prevalence in South Asian countries, in spite of heterogeneity observed in the studies included. For performing domestic tasks, initiatives are to be taken to reduce dependency on solid fuel by using cleaner alternatives or comparatively cleaner technology.

Background Chronic obstructive pulmonary disease (COPD) has the highest increased risk due to household air pollution arising from biomass fuel burning. However, knowledge on COPD patho-mechanisms is mainly limited to tobacco smoke exposure. In this study, a repeated direct wood smoke (WS) exposure was performed using normal- (bro-ALI) and chronic bronchitis-like bronchial (bro-ALI-CB), and alveolar (alv-ALI) lung mucosa models at air–liquid interface (ALI) to assess broad toxicological end points. Methods The bro-ALI and bro-ALI-CB models were developed using human primary bronchial epithelial cells and the alv-ALI model was developed using a representative type-II pneumocyte cell line. The lung models were exposed to WS (10 min/exposure; 5-exposures over 3-days; n = 6–7 independent experiments). Sham exposed samples served as control. WS composition was analyzed following passive sampling. Cytotoxicity, total cellular reactive oxygen species (ROS) and stress responsive NFkB were assessed by flow cytometry. WS exposure induced changes in gene expression were evaluated by RNA-seq (p ≤ 0.01) followed by pathway enrichment analysis. Secreted levels of proinflammatory cytokines were assessed in the basal media. Non-parametric statistical analysis was performed. Results 147 unique compounds were annotated in WS of which 42 compounds have inhalation toxicity (9 very high). WS exposure resulted in significantly increased ROS in bro-ALI (11.2%) and bro-ALI-CB (25.7%) along with correspondingly increased NFkB levels (bro-ALI: 35.6%; bro-ALI-CB: 18.1%). A total of 1262 (817-up and 445-down), 329 (141-up and 188-down), and 102 (33-up and 69-down) genes were differentially regulated in the WS-exposed bro-ALI, bro-ALI-CB, and alv-ALI models respectively. The enriched pathways included the terms acute phase response, mitochondrial dysfunction, inflammation, oxidative stress, NFkB, ROS, xenobiotic metabolism of AHR, and chronic respiratory disorder. The enrichment of the ‘cilium’ related genes was predominant in the WS-exposed bro-ALI (180-up and 7-down). The pathways primary ciliary dyskinesia, ciliopathy, and ciliary movement were enriched in both WS-exposed bro-ALI and bro-ALI-CB. Interleukin-6 and tumor necrosis factor-α were reduced (p < 0.05) in WS-exposed bro-ALI and bro-ALI-CB. Conclusion Findings of this study indicate differential response to WS-exposure in different lung regions and in chronic bronchitis, a condition commonly associated with COPD. Further, the data suggests ciliopathy as a candidate pathway in relation to WS-exposure.

IntroductionAir pollution is a significant global health concern, with studies from the USA and Europe linking long-term exposure to respiratory issues and poor school attendance in children. While Indian cities experience much higher pollution levels, the impact on lung development in Indian children remains unclear. This study aims to assess the burden of impaired lung function in Indian children and identify key factors contributing to pollution-induced lung injury.Methods and analysisThis longitudinal, prospective cohort study is conducted in four cities categorised by particulate matter 2.5 (PM2.5) levels: ‘very high’ (Delhi), ‘high’ (Mumbai, Bangalore) and ‘moderate’ (Mysore). A total of 4000 participants (1000 from each city) will be included in the study. Participants will complete a structured questionnaire covering sociodemographics, asthma and allergy history (International Study of Asthma and Allergies in Childhood core questionnaire), dietary intake (24-hour recall and Food Frequency Questionnaire), Physical Activity-C Questionnaire and air pollution exposure. Spirometry and Forced Oscillation Technique will be used to assess lung function. Blood samples will be collected for identification of biomarkers to predict lung impairment. After quality checks, data will be compiled, summarising pulmonary function parameters alongside covariates and confounders. Analysis of Variance (ANOVA) will assess between-city and within-city differences in lung function.We anticipate a higher prevalence of reduced lung function in children residing in cities with very high and high PM2.5 levels compared with the moderately polluted city. Findings from this study could establish normal age-appropriate lung function reference values for Indian urban children, aiding in clinical diagnosis.If a reliable biomarker for identifying children at risk of lung impairment is available, it could serve as an early predictor of poor lung health in asymptomatic children.Ethics and disseminationThe approval from individual site institutional review board (IRB) is obtained prior to initiation of the study from institutional ethics committee, St. John’s Medical College and Hospital, Bangalore; institutional ethics committee, JSS Medical College, Mysore; institute ethics committee, Indian Institute of Technology Bombay and institute ethics committee, All India Institute of Medical Sciences. Findings from this study will be disseminated through conference presentations, peer-reviewed publications and establishment of normal age-appropriate lung function reference values for children living in urban India.

Background: Chronic Obstructive Pulmonary Disease (COPD) is a major global health challenge, primarily driven by exposures to tobacco smoke and biomass smoke. While Tobacco-Smoke-Induced COPD (TSCOPD) has been extensively studied, the diagnostic challenges and distinct pathogenesis of Biomass-Smoke-Induced COPD (BSCOPD), particularly in low- and middle-income countries, remain underexplored. Objective: To explore the differences in clinical manifestations, pulmonary function, and inflammatory profiles between BSCOPD and TSCOPD and highlight the diagnostic complexities of BSCOPD. Methods: This review analyzes the current literature comparing BSCOPD with TSCOPD, focusing on distinctive pathophysiological mechanisms, inflammatory markers, and oxidative stress processes. Results: BSCOPD presents differences in clinical presentation, with less emphysema, smaller airway damage, and higher rates of pulmonary hypertension compared to TSCOPD. BSCOPD is also characterized by bronchial hyperresponsiveness and significant hypoxemia, unlike TSCOPD, which exhibits severe airflow obstruction and emphysema. Additionally, the inflammatory profile of BSCOPD includes distinct mucous hypersecretion and airway remodeling. Conclusions: The unique genetic, epigenetic, and oxidative stress mechanisms involved in BSCOPD complicate its diagnosis and management. Biomass smoke’s underrecognized impact on accelerated lung aging and exacerbation mechanisms emphasizes the need for targeted research to refine diagnostic criteria and management strategies for BSCOPD. Future directions: Further research should focus on identifying specific biomarkers and molecular pathways to enhance early diagnosis and improve clinical outcomes in populations exposed to biomass smoke.

The use of the Ratio of Oxygen Saturation (ROX) index to predict the success of high-flow nasal oxygenation (HFNO) is well established. The ROX can also predict the need for intubation, mortality, and is easier to calculate compared with APACHE II. In this prospective study, the primary aim is to compare the ROX (easily administered in resource limited setting) to APACHE II for clinically relevant outcomes such as mortality and the need for intubation. Our secondary aim was to identify thresholds for the ROX index in predicting outcomes such as the length of ICU stay and failure of non-invasive respiratory support therapies and to assess the effectiveness of using the ROX (day 1 at admission, day 2, and day 3) versus Acute physiology and chronic health evaluation (APACHE) II scores (at admission) in patients with Coronavirus Disease 2019 (COVID-19) pneumonia and Acute Respiratory Distress Syndrome (ARDS) to predict early, late, and non-responders. After screening 208 intensive care unit patients, a total of 118 COVID-19 patients were enrolled, who were categorized into early (n = 38), late (n = 34), and non-responders (n = 46). Multinomial logistic regression, receiver operating characteristic (ROC), Multivariate Cox regression, and Kaplan–Meier analysis were conducted. Multinomial logistic regressions between late and early responders and between non- and early responders were associated with reduced risk of treatment failures. ROC analysis for early vs. late responders showed that APACHE II on admission had the largest area under the curve (0.847), followed by the ROX index on admission (0.843). For responders vs. non-responders, we found that the ROX index on admission had a slightly better AUC than APACHE II on admission (0.759 vs. 0.751). A higher ROX index on admission [HR (95% CI): 0.29 (0.13–0.52)] and on day 2 [HR (95% CI): 0.55 (0.34–0.89)] were associated with a reduced risk of treatment failure. The ROX index can be used as an independent predictor of early response and mortality outcomes to HFNO and NIV in COVID-19 pneumonia, especially in low-resource settings, and is non-inferior to APACHE II.

High-flow nasal cannula (HFNC) and ventilator-delivered non-invasive mechanical ventilation (NIV) were used to treat acute respiratory distress syndrome (ARDS) due to COVID-19 pneumonia, especially in low- and middle-income countries (LMICs), due to lack of ventilators and manpower resources despite the paucity of data regarding their efficacy. This prospective study aimed to analyse the efficacy of HFNC versus NIV in the management of COVID-19 ARDS. A total of 88 RT-PCR-confirmed COVID-19 patients with moderate ARDS were recruited. Linear regression and generalized estimating equations (GEEs) were used for trends in vital parameters over time. A total of 37 patients were on HFNC, and 51 were on NIV. Patients in the HFNC group stayed slightly but not significantly longer in the ICU as compared to their NIV counterparts (HFNC vs. NIV: 8.00 (4.0–12.0) days vs. 7.00 (2.0–12.0) days; p = 0.055). Intubation rates, complications, and mortality were similar in both groups. The switch to HFNC from NIV was 5.8%, while 37.8% required a switch to NIV from HFNC. The resolution of respiratory alkalosis was better with NIV. We conclude that in patients with COVID-19 pneumonia with moderate ARDS, the duration of treatment in the ICU, intubation rate, and mortality did not differ significantly with the use of HFNC or NIV for respiratory support.

Acute exacerbations of COPD (AECOPD) are clinically significant events having therapeutic and prognostic consequences. However, there is a lot of variation in its clinical manifestations described by phenotypes. The phenotypes of AECOPD were categorized in this study based on pathology and exposure. In our cross-sectional study, conducted between 1 January 2016 to 31 December 2020, the patients were categorized into six groups based on pathology: non-bacterial and non-eosinophilic; bacterial; eosinophilic; bacterial infection with eosinophilia; pneumonia; and bronchiectasis. Further, four groups were classified based on exposure to tobacco smoke (TS), biomass smoke (BMS), both, or no exposure. Cox proportional-hazards regression analyses were performed to assess hazard ratios, and Kaplan–Meier analysis was performed to assess survival, which was then compared using the log-rank test. The odds ratio (OR) and independent predictors of ward admission type and length of hospital stay were assessed using binomial logistic regression analyses. Of the 2236 subjects, 2194 were selected. The median age of the cohort was 67.0 (60.0 to 74.0) and 75.2% were males. Mortality rates were higher in females than in males (6.2% vs. 2.3%). AECOPD-B (bacterial infection) subjects [HR 95% CI 6.42 (3.06–13.46)], followed by AECOPD-P (pneumonia) subjects [HR (95% CI: 4.33 (2.01–9.30)], were at higher mortality risk and had a more extended hospital stay (6.0 (4.0 to 9.5) days; 6.0 (4.0 to 10.0). Subjects with TS and BMS-AECOPD [HR 95% CI 7.24 (1.53–34.29)], followed by BMS-AECOPD [HR 95% CI 5.28 (2.46–11.35)], had higher mortality risk. Different phenotypes have different impacts on AECOPD clinical outcomes. A better understanding of AECOPD phenotypes could contribute to developing an algorithm for the precise management of different phenotypes.

There is a need for biomarkers to predict outcomes, including mortality, in interstitial lung disease (ILD). Krebs von den Lungen-6 (KL-6) and surfactant protein D (SP-D) are associated with lung damage and fibrosis in all ILDs and are related to important clinical outcomes. Though these two biomarkers have been associated with ILD outcomes, there are no studies that have evaluated their predictive potential in combination. This study aims to determine whether KL-6 and SP-D are linked to poor disease outcomes and mortality. Additionally, we plan to examine whether changes in KL-6 and SP-D concentrations correspond with changes in lung function and whether serial measurements improve their predictive potential to identify disease progression and mortality. Forty-four patients with ILD participated in a prospective 6-month longitudinal observational study. ILD patients who succumbed had the highest KL-6 levels (3990.4 U/mL (3490.0–4467.6)) and highest SP-D levels (256.1 ng/mL (217.9–260.0)), followed by those who deteriorated: KL-6 levels 1357.0 U/mL (822.6–1543.4) and SP-D levels 191.2 ng/mL (152.8–210.5). The generalized linear model (GLM) analysis demonstrated that changes in forced vital capacity (FVC), diffusing capacity of lungs for carbon monoxide (DLCO), forced expiratory volume in 1 s (FEV1), and partial pressure of arterial oxygen (PaO2) were correlated to changes in KL6 (p = 0.016, 0.014, 0.027, 0.047) and SP-D (p = 0.008, 0.012, 0.046, 0.020), respectively. KL-6 (odds ratio (OR): 2.87 (1.06–7.79)) and SPD (OR: 1.76 (1.05–2.97)) were independent predictors of disease progression, and KL-6 (hazard ratio (HR): 3.70 (1.46–9.41)) and SPD (HR: 2.58 (1.01–6.59)) were independent predictors of death by Cox regression analysis. Combined biomarkers (KL6 + SPD + CT + FVC) had the strongest ability to predict disease progression (AUC: 0.797) and death (AUC: 0.961), on ROC analysis. Elevated KL-6 and SPD levels are vital biomarkers for predicting the severity, progression, and outcomes of ILD. High baseline levels or an increase in levels over a six-month follow-up despite treatment indicate a poor prognosis. Combining KL6 and SPD with conventional measures yields a more potent prognostic indicator. Clinical studies are needed to test additional interventions, and future research will determine if this combined biomarker benefits different ethnicities globally.

Air pollutants are known to trigger asthma and wheezing-associated lower respiratory infections in children, but evidence regarding their effect on hospital admissions in India is limited. We conducted a time-series study over a period of five years to assess the role of ambient air pollutants in daily asthma-related hospital admissions in children in Mysore, India. Daily asthma and wheeze (associated with lower respiratory infections) admissions were modelled using a generalised additive model (GAM) to examine the non-linear effects and generalised linear models (GLM) for linear effects, if any. Models were adjusted by day of the week and lag days, with smooth terms for time, maximum temperature, and relative humidity, and they were stratified by sex and age group. Of the 362 children admitted, more than 50% were boys, and the mean age was 5.34 years (±4.66). The GAMs showed non-linear associations between NO2, PM2.5, and NH3. For example, a 10 µgm−3 (or 10%) increase in NO2 increased admissions by 2.42. These non-linear effects were more pronounced in boys. A linear effect was detected for PM10 with a relative risk (95% CI) of 1.028, 1.013, and 1.043 with admission. Further research is needed to explore whether these findings can be replicated in different cities in India. Air pollution needs to be controlled, and policies that focus on lower cut-off levels for vulnerable populations are necessary.

To achieve herd immunity to a disease, a large portion of the population needs to be vaccinated, which is possible only when there is broad acceptance of the vaccine within the community. Thus, policymakers need to understand how the general public will perceive the vaccine. This study focused on the degree of COVID-19 vaccine hesitancy and refusal and explored sociodemographic correlations that influence vaccine hesitancy and refusal. A cross-sectional online survey was conducted among the adult population of India. The survey consisted of basic demographic questions and questions from the Vaccination Attitudes Examination (VAX) Scale. Multinomial logistical regression was used to identify correlates of vaccine hesitancy and refusal. Of the 1582 people in the study, 9% refused to become vaccinated and 30.8% were hesitant. We found that both hesitancy and refusal predictors were nearly identical (lower socioeconomic status, female gender, and older age groups), except for three groups (subjects aged 45–64 years, those with approximate income <10,000 INR/month, and those residing in rural households) that showed slightly higher odds of vaccine hesitancy than refusal. We need to address the underlying sociodemographic determinants and formulate public awareness programs to address specific subgroups that are at higher risk of rejecting the vaccine and convert those who are undecided or hesitant into those willing to accept the vaccine.