Air pollution is one of the leading causes of early deaths worldwide, with particulate matter (PM) as an emerging factor contributing to this trend. PM is classified based on its physical size, which ranges from PM (diameter ≤10 μm) to PM (≤2.5 μm) and PM (≤0.5 μm). Smaller-sized PM can move freely through the air and readily infiltrate deep into the lungs, intensifying existing health issues and exacerbating complications. Lung complications are the most common issues arising from PM exposure due to the primary site of deposition in the respiratory system. Conditions such as asthma, COPD, idiopathic pulmonary fibrosis, lung cancer and various lung infections are all susceptible to worsening due to PM exposure. PM can epigenetically modify specific target sites, further complicating its impact on these conditions. Understanding these epigenetic mechanisms holds promise for addressing these complications in cases of PM exposure. This involves studying the effect of PM on different gene expressions and regulation through epigenetic modifications, including DNA methylation, histone modifications and microRNAs. Targeting and manipulating these epigenetic modifications and their mechanisms could be promising strategies for future treatments of lung complications. This review mainly focuses on different epigenetic modifications due to PM exposure in the various lung complications mentioned above.

Advance care planning (ACP) is a complex and iterative communication process between patients, surrogates and clinicians that defines goals of care that may include, but is not limited to, documentation of advance directives. The aim of ACP is to promote patient-centred care tailored to the patient's clinical situation through informed preparation for the future and improved communication between patient, clinicians and surrogates, if the latter need to make decisions on patient's behalf.The aim of this article is to review research related to ACP in acute and chronic respiratory failure, regarding the process, communication, shared decision-making, implementation and outcomes.Research has produced controversial results on ACP interventions due to the heterogeneity of measures and outcomes, but positive outcomes have been described regarding the quality of patient-physician communication, preference for comfort care, decisional conflict and patient-caregiver congruence of preferences and improved documentation of ACP or advance directives.The main barriers to ACP in chronic respiratory failure are the uncertainty of prognosis (particularly in the organ failure trajectory), the choice of the best timing for initiation and the lack of training of healthcare workers. In acute respiratory failure, the ACP process can be very short, should include the patient whenever possible, and is based on a discussion of treatments appropriate to the patient's functional status prior to the event ( assessment of frailty) and clear communication of the likely consequences of possible options.All healthcare worker dealing with patients with serious illnesses should have training in communication skills to promote engagement in ACP discussions.

The main monogenic causes of pulmonary fibrosis in adults are mutations in telomere-related genes. These mutations may be associated with extrapulmonary signs (hepatic, haematological and dermatological) and typically present radiologically as usual interstitial pneumonia or unclassifiable fibrosis. In children, the monogenic causes of pulmonary fibrosis are dominated by mutations in surfactant-related genes. These mutations are not associated with extrapulmonary signs and often manifest radiologically as unclassifiable fibrosis with cysts that can lead to chest wall deformities in adults. This review discusses these mutations, along with most of the monogenic causes of interstitial lung disease, including interferon-related genes, mutations in genes causing cystic lung disease, Hermansky-Pudlak syndrome, pulmonary alveolar proteinosis, lysinuric protein intolerance and lysosomal storage disorders, and their pulmonary and extrapulmonary manifestations.

Extracellular vesicles (EVs) released by various cells play crucial roles in intercellular communication within the respiratory system. This review explores the historical context and significance of research into extracellular vesicles. Categorised into exosomes (sized 30-150 nm), microvesicles (sized 50-1000 nm) and apoptotic bodies (sized 500-2000nm), based on their generation mechanisms, extracellular vesicles carry diverse cargoes of biomolecules, including proteins, lipids and nucleic acids. Respiratory ailments are the primary contributors to both mortality and morbidity across various populations globally, significantly impacting public health. Recent studies have underscored the pivotal role of extracellular vesicles, particularly their cargo content, in mediating intercellular communication between lung cells in respiratory diseases. This comprehensive review provides insights into extracellular vesicle mechanisms and emphasises their significance in major respiratory conditions, including acute lung injury, COPD, pulmonary hypertension, pulmonary fibrosis, asthma and lung cancer.

In adults with serious respiratory illness, breathlessness is prevalent and associated with reduced health-related quality of life. The aim of this review was to assess the impact of breathing techniques on breathlessness in adults with serious respiratory illness.

Sub-optimal inhaler adherence undermines the efficacy of pharmacotherapy in COPD. Digitalised care pathways are increasingly used to improve inhaler-use behaviour remotely. This review investigated the feasibility and impact of remote electronic inhaler adherence monitoring (EIM) and intervention platforms on clinical outcomes in COPD.

Asthma is one of the most common chronic respiratory diseases globally. Despite national and international asthma care guidelines, gaps persist in primary care. Knowledge translation (KT) electronic tools (eTools) exist aiming to address these gaps, but their impact on practice patterns and patient outcomes is variable. We aimed to conduct a nonsystematic review of the literature for key asthma care gaps and identify limitations and future directions of KT eTools optimised for use in electronic medical records (EMRs).

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Physical rehabilitation may improve health and wellbeing outcomes for some adults living with long COVID. However, individuals living with pre-existing multiple long-term conditions (MLTCs) and long COVID may have additional rehabilitation challenges. This scoping review aims to identify the available evidence describing physical rehabilitation interventions for adults living with long COVID, to systematically map the reporting of pre-existing MLTCs, and to describe the characteristics of physical rehabilitation interventions used in adults with both pre-existing long-term conditions (LTCs) and long COVID.

The advent of cystic fibrosis transmembrane conductance regulator (CFTR) modulator therapy, especially the triple therapy combining the drugs elexacaftor, tezacaftor, ivacaftor (ETI), has significantly changed the course of the disease in people with cystic fibrosis (pwCF). ETI, which is approved for the majority (80-90%) of pwCF, partially restores CFTR channel function, resulting in improved mucociliary clearance and, consequently, improved lung function, respiratory symptoms and pulmonary exacerbations. The bacterial burden of classical CF pathogens such as and is reduced without reaching eradication in the majority of infected patients. Limited data is available on less common or emerging bacterial pathogens. ETI has a positive effect on the lung microbiome but does not fully restore it to a healthy state. Due to the significant reduction in sputum production under ETI, respiratory samples such as deep-throat swabs are commonly taken, despite their inadequate representation of lower respiratory tract pathogens. Currently, there are still unanswered questions related to this new therapy, such as the clinical impact of infection with cystic fibrosis (CF) pathogens, the value of molecular diagnostic tests, the durability of the effects on respiratory infection and the role of fungal and viral infections. This article reviews the changes in bacterial lung infections and the microbiome in CF to provide evidence for the use of antibiotics in the era of ETI.

Assessing and treating respiratory muscle dysfunction is crucial for patients with both acute and chronic respiratory failure. Respiratory muscle dysfunction can contribute to the onset of respiratory failure and may also worsen due to interventions aimed at treatment. Evaluating respiratory muscle function is particularly valuable for diagnosing, phenotyping and assessing treatment efficacy in these patients. This review outlines established methods, such as measuring respiratory pressures, and explores novel techniques, including respiratory muscle neurophysiology assessments using electromyography and imaging with ultrasound.Additionally, we review various treatment strategies designed to support and alleviate the burden on overworked respiratory muscles or to enhance their capacity through training interventions. These strategies range from invasive and noninvasive mechanical ventilation approaches to specialised respiratory muscle training programmes. By summarising both established techniques and recent methodological advancements, this review aims to provide a comprehensive overview of the tools available in clinical practice for evaluating and treating respiratory muscle dysfunction. Our goal is to present a clear understanding of the current capabilities and limitations of these diagnostic and therapeutic approaches. Integrating advanced diagnostic methods and innovative treatment strategies should help improve patient management and outcomes. This comprehensive review serves as a resource for clinicians, equipping them with the necessary knowledge to effectively diagnose and treat respiratory muscle dysfunction in both acute and chronic respiratory failure scenarios.

COPD is a heterogeneous disease of the lungs characterised by restricted airflow. Chronic inflammation and recurrent bacterial infections are known to be important driving factors in exacerbations of this disease. Despite a marked increase in the number of alveolar macrophages present in the lungs of COPD patients, there is evidence of reduced clearance of pathogenic bacteria, leading to recurrent infection, exacerbation and subsequent lung function decline. This is thought to be attributed to a defect in the phagocytic capability of both alveolar and monocyte-derived macrophages in COPD. In addition to this defect, there is apparent selectivity in bacterial uptake by COPD macrophages because certain pathogenic genera, such as , and , are taken up more readily than others. The respiratory microbiome plays a key role in regulating the host immune response both in health and during chronic inflammation. In patients with COPD, there are distinct changes in the composition of the respiratory microbiome, particularly the lower respiratory tract, where dominance of clinically relevant pathogenic species is commonly observed. Whether there are links between these changes in the microbiome and dysfunctional macrophage phagocytosis has not yet been widely studied. This review aims to discuss what is currently known about these phenomena and to explore interactions between macrophages and the respiratory microbiome.

Lung cancer ranks as the leading cause of cancer-related deaths worldwide. There is evidence that second-hand smoke (SHS) exposure is a risk factor for the development of lung cancer in never-smokers. This systematic review and meta-analysis aims to provide the most accurate quantification of the association between SHS exposure and lung cancer risk in never-smokers.

The obesity paradox is a well-established clinical conundrum in COPD patients. This study aimed to provide an updated analysis of the relationship between body mass index (BMI) and mortality in this population.

Asthma exacerbations in children pose a significant burden on healthcare systems and families. While traditional risk assessment tools exist, artificial intelligence (AI) offers the potential for enhanced prediction models.

Lung transplantation, a critical intervention for end-stage lung diseases, is frequently challenged by post-transplant complications. Indeed, primary graft dysfunction, anastomotic complications, infections and acute and chronic rejections pose significant hurdles in lung transplantation. While evidence regarding the role of airway epithelium after lung transplantation is still emerging, its importance is becoming increasingly recognised. This review looks at the complex involvement of airway epithelium in various post-transplant complications, while emphasising the utility of airway epithelial culture as a research model. In summary, by elucidating the involvement of airway epithelium in each post-transplant complication and explaining these intricate processes, the review aims to guide specific future research efforts and therapeutic strategies aimed at improving lung transplant outcomes and enhancing patient care.

Bronchiectasis is a chronic lung condition which is characterised by recurrent chest infections, chronic sputum production and cough, and limited exercise tolerance. While bronchiectasis may be caused by various aetiologies, these features are shared by most patients with bronchiectasis regardless of the cause. This review consolidates the existing evidence on patient-managed interventions for adults with bronchiectasis, while also outlining areas for future research. Airway clearance techniques and hyperosmolar agents are key components of the bronchiectasis management and consistently recommended for clinical implementation. Questions around their prescription, such as optimal sequence of delivery, are still to be answered. Pulmonary rehabilitation and exercise are also recommended for patients with bronchiectasis. Relatively strong evidence underpins this recommendation during a clinically stable stage of the disease, although the role of pulmonary rehabilitation following an exacerbation is still unclear. Additionally, self-management programmes feature prominently in bronchiectasis treatment, yet the lack of consensus regarding their definition and outcomes presents hurdles to establishing a cohesive evidence base. Moreover, cough, a cardinal symptom of bronchiectasis, warrants closer examination. Although managing cough in bronchiectasis may initially appear risky, further research is necessary to ascertain whether strategies employed in other respiratory conditions can be safely and effectively adapted to bronchiectasis, particularly through identifying patient responder populations and criteria where cough may not enhance airway clearance efficacy and its control is needed. Overall, there is a growing recognition of the importance of patient-managed interventions in the bronchiectasis management. Efforts to improve research methodologies and increase research funding are needed to further advance our understanding of these interventions, and their role in optimising patient care and outcomes.

The shared pathobiological mechanisms driving progressive fibrosis in interstitial lung diseases (ILDs) remain unclear. Neutrophils, the most common immune cells in the human body, contain an extensive array of proteinases that are important for cell function, including tissue repair and remodelling. Increasing observational studies have reported elevated neutrophil counts in the respiratory tract and circulation of patients with ILD and suggest a role as a biomarker of disease severity. Neutrophils and their contents (including the formation of neutrophil extracellular traps (NETs)) are present in fibrotic lung tissue. Proteinases and NETs may drive fibrogenesis in animal and models and may impact transforming growth factor-β1 activation. However, the effect of neutrophil action, whether reparative or pathologically destructive to the delicate lung architecture, has yet to be determined. This review aims to summarise the current literature surrounding the potential role of the neutrophil as a biomarker and contributor to the pathogenesis of ILD. There is currently a paucity of treatment options in ILD driven by the knowledge gap underlying the overall disease mechanisms. This review concludes that neutrophils warrant further evaluation as manipulation of recruitment and function could provide a novel and much needed therapeutic strategy.

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Interstitial lung disease (ILD) encompasses a heterogeneous group of chronic lung conditions with considerable variability in prognosis and response to treatment. People with reduced muscle mass and function, known as sarcopenia, have a higher risk of mortality and adverse clinical outcomes both in the general population and in other chronic disease states. The importance of sarcopenia across the spectrum of patients with ILD is not well established.