Asthma is a globally significant non-communicable disease with major public health consequences for both children and adults, including high morbidity, and mortality in severe cases. We have summarized the evidence on asthma trends, environmental determinants, and long-term impacts while comparing these epidemiological features across childhood asthma and adult asthma. While asthma incidence and prevalence are higher in children, morbidity, and mortality are higher in adults. Childhood asthma is more common in boys while adult asthma is more common in women, and the reversal of this sex difference in prevalence occurs around puberty suggesting sex hormones may play a role in the etiology of asthma. The global epidemic of asthma that has been observed in both children and adults is still continuing, especially in low to middle income countries, although it has subsided in some developed countries. As a heterogeneous disease, distinct asthma phenotypes, and endotypes need to be adequately characterized to develop more accurate and meaningful definitions for use in research and clinical settings. This may be facilitated by new clustering techniques such as latent class analysis, and computational phenotyping methods are being developed to retrieve information from electronic health records using natural language processing (NLP) algorithms to assist in the early diagnosis of asthma. While some important environmental determinants that trigger asthma are well-established, more work is needed to define the role of environmental exposures in the development of asthma in both children and adults. There is increasing evidence that investigation into possible gene-by-environment and environment-by-environment interactions may help to better uncover the determinants of asthma. Therefore, there is an urgent need to further investigate the interrelationship between environmental and genetic determinants to identify high risk groups and key modifiable exposures. For children, asthma may impair airway development and reduce maximally attained lung function, and these lung function deficits may persist into adulthood without additional progressive loss. Adult asthma may accelerate lung function decline and increase the risk of fixed airflow obstruction, with the effect of early onset asthma being greater than late onset asthma. Therefore, in managing asthma, our focus going forward should be firmly on improving not only short-term symptoms, but also the long-term respiratory and other health outcomes.

Coal workers’ pneumoconiosis (CWP), as part of the spectrum of coal mine dust lung disease (CMDLD), is a preventable but incurable lung disease that can be complicated by respiratory failure and death. Recent increases in coal production from the financial incentive of economic growth lead to higher respirable coal and quartz dust levels, often associated with mechanization of longwall coal mining. In Australia, the observed increase in the number of new CWP diagnoses since the year 2000 has necessitated a review of recommended respirable dust exposure limits, where exposure limits and monitoring protocols should ideally be standardized. Evidence that considers the regulation of engineering dust controls in the mines is lacking even in high‐income countries, despite this being the primary preventative measure. Also, it is a global public health priority for at‐risk miners to be systemically screened to detect early changes of CWP and to include confirmed patients within a central registry; a task limited by financial constraints in less developed countries. Characteristic X‐ray changes are usually categorized using the International Labour Office classification, although future evaluation by low‐dose HRCT) chest scanning may allow for CWP detection and thus avoidance of further exposure, at an earlier stage. Preclinical animal and human organoid‐based models are required to explore potential re‐purposing of anti‐fibrotic and related agents with potential efficacy. Epidemiological patterns and the assessment of molecular and genetic biomarkers may further enhance our capacity to identify susceptible individuals to the inhalation of coal dust in the modern era.

Young children are particularly vulnerable to otitis media (OM) which globally affects over 80% of children below the age of 3 years. Although there is convincing evidence for an association between environmental tobacco smoke exposure and OM in children, the relationship with ambient air pollution is not clear. We aimed to systematically review the literature on the relationship between ambient air pollution exposure and OM in children. A systematic search was performed in PubMed and EMBASE databases. Of 934 references identified, 24 articles were included. There is an increasing body of evidence supporting an association between higher ambient air pollution exposure and a higher risk of OM in children. While NO₂ showed the most consistent association with OM, other specific pollutants showed inconsistent associations. Studies were mainly conducted in high/middle income countries with limited evidence from low-income countries. Although there was a general consensus that higher air pollution exposure is associated with a greater prevalence of OM, the evidence for associations with specific pollutants is inconsistent. More well-designed studies on associations between specific air pollutants as risk factors for OM are warranted, especially in low income countries with high air pollution levels.

Rationale: The term “pre–chronic obstructive pulmonary disease” (“pre-COPD”) refers to individuals at high risk of developing COPD who do not meet conventional spirometric criteria for airflow obstruction. New approaches to identifying these individuals are needed, particularly in younger populations. Objectives: To determine whether lung function thresholds and respiratory symptoms can be used to identify individuals at risk of developing COPD. Methods: The Tasmanian Longitudinal Health Study comprises a population-based cohort first studied in 1968 (at age 7 yr). Respiratory symptoms, pre- and post-bronchodilator (BD) spirometry, diffusing capacity, and static lung volumes were measured in a subgroup at age 45, and the incidence of COPD was assessed at age 53. For each lung function measure, z-scores were calculated using Global Lung Function Initiative references. The optimal threshold for best discrimination of COPD incidence was determined by the unweighted Youden index. Measurements and Main Results: Among 801 participants who did not have COPD at age 45, the optimal threshold for COPD incidence by age 53 was pre-BD FEV1/FVC z-score less than −1.264, corresponding to the lowest 10th percentile. Those below this threshold had a 36-fold increased risk of developing COPD over an 8-year follow-up period (risk ratio, 35.8; 95% confidence interval, 8.88 to 144), corresponding to a risk difference of 16.4% (95% confidence interval, 3.7 to 67.4). The sensitivity was 88%, and the specificity was 87%. Positive and negative likelihood ratios were 6.79 and 0.14, respectively. Respiratory symptoms, post-BD spirometry, diffusing capacity, and static lung volumes did not improve on the classification achieved by pre-BD FEV1/FVC alone. Conclusions: This is the first study, to our knowledge, to evaluate the discriminatory accuracy of spirometry, diffusing capacity, and static lung volume thresholds for COPD incidence in middle-aged adults. Our findings support the inclusion of pre-BD spirometry in the physiological definition of pre-COPD and indicate that pre-BD FEV1/FVC at the 10th percentile accurately identifies individuals at high risk of developing COPD in community-based settings.

Background Despite chronic obstructive pulmonary disease (COPD) being a major global cause of mortality and hospitalisation, it is often undiagnosed or inaccurately diagnosed in clinical settings. Objective To systematically synthesise all peer-reviewed papers from primary healthcare settings that have reported data on: (1) undiagnosed COPD, that is, patients with respiratory symptoms and postbronchodilator airflow obstruction consistent with COPD, without a formal clinician’s diagnosis of COPD either documented in health records or reported by patients and (2) ‘overdiagnosed COPD’, that is, clinician’s diagnosis without postbronchodilator airflow obstruction. Methods Studies investigating these diagnostic metrics in patients from primary healthcare clinics (according to predefined inclusion/exclusion criteria) were sourced from Medline and Embase and assessed for bias (Johanna Briggs Institute tools for prevalence studies and case series). Meta-analyses of studies of adequate sample size used random effect modelling stratified by risk factor categories. Results Of 26 eligible articles, 21 cross-sectional studies investigated 3959 cases of spirometry-defined COPD (with or without symptoms), and 5 peer-reviewed COPD case series investigated 7381 patients. The prevalence of spirometry-confirmed COPD without a diagnosis documented in their health records was 14%–26% in studies of symptomatic smokers (N=3). 1 in 4 patients taking inhaled therapies (25% (95% CI 22% to 28%), N=2) and 1 in 6 smokers irrespective of symptoms (16% (95% CI 14% to 18%), N=6) fulfilled diagnostic spirometry criteria but did not report receiving a COPD-related diagnosis. In an adequately powered series of COPD cases documented in primary healthcare records (N=4), only between 50% and 75% of subjects had any airflow obstruction on postbronchodilator spirometry performed by study researchers, therefore, COPD was clinically ‘overdiagnosed’ in 25%–50% of subjects. Discussion Although data were heterogeneous and of modest quality, undiagnosed COPD was common in primary healthcare, especially for symptomatic smokers and patients treated with inhaled therapies. In contrast, frequent COPD ‘overdiagnosis’ may represent treatment of asthma/reversible component or another medical diagnosis. PROSPERO registration number CRD42022295832.

Systemic inflammation is an integral part of chronic obstructive pulmonary disease (COPD), and air pollution is associated with cardiorespiratory mortality, yet the interrelationships are not fully defined. We examined associations between nitrogen dioxide (NO₂) exposure (as a marker of traffic-related air pollution) and pro-inflammatory cytokines, and investigated effect modification and mediation by post-bronchodilator airflow obstruction (post-BD-AO) and cardiovascular risk. Data from middle-aged participants in the Tasmanian Longitudinal Health Study (TAHS, n = 1389) were analyzed by multivariable logistic regression, using serum interleukin (IL)-6, IL-8 and tumor necrosis factor-α (TNF-α) as the outcome. Mean annual NO₂ exposure was estimated at residential addresses using a validated satellite-based land-use regression model. Post-BD-AO was defined by post-BD forced expiratory ratio (FEV₁/FVC) < lower limit of normal, and cardiovascular risk by a history of either cerebrovascular or ischaemic heart disease. We found a positive association with increasing serum IL-6 concentration (geometric mean 1.20 (95% CI: 1.1 to 1.3, p = 0.001) per quartile increase in NO₂). This was predominantly a direct relationship, with little evidence for either effect modification or mediation via post-BD-AO, or for the small subgroup who reported cardiovascular events. However, there was some evidence consistent with serum IL-6 being on the causal pathway between NO₂ and cardiovascular risk. These findings raise the possibility that the interplay between air pollution and systemic inflammation may differ between post-BD airflow obstruction and cardiovascular diseases.