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Background and Objective: The association between birth weight, particularly relative to gestational age, and adult lung function is uncertain. We investigated the associations between birth weight relative to gestational age and measures of lung function in middle age, and mediation of these associations by adult height. Methods: Participants in the Tasmanian Longitudinal Health Study who had both known birth weight and lung function assessment at age 45 years were included (n = 849). Linear regression models were fitted to investigate the association between small for gestational age and birth weight with post‐bronchodilator lung function measures (forced expiratory volume in 1 second [FEV1], forced vital capacity [FVC], FEV1/FVC, diffusing capacity for carbon monoxide [DLco], residual volume [RV] and total lung capacity [TLC]), adjusting for potential confounders. The contribution of adult height as a mediator of these associations was investigated. Results: Compared with infants born with normal weight for gestational age, those born small for gestational age had reduced FEV1 (coefficient: −191 ml [95%CI: −296, −87]), FVC (−205 ml [−330, −81]), TLC (−292 ml [−492, −92]), RV (−126 ml [−253, 0]) and DLco (−0.42 mmol/min/kPa [−0.79, −0.041]) at age 45 years. However, they had comparable FEV1/FVC. For every 1 kg increase in birth weight, lung function indices increased by an average of 117 ml (95%CI: 40, 196) for FEV1, 124 ml (30, 218) for FVC, 215 ml (66, 365) for TLC and 0.36 mmol/min/kPa (0.11, 0.62) for DLco, independent of gestational age, but again not for FEV1/FVC. These associations were significantly mediated by adult height (56%–90%). Conclusion: Small for gestational age was associated with reduced lung function that is likely due to smaller lungs with little evidence of any specific parenchymal impairment. [ABSTRACT FROM AUTHOR]

Background: Experimental challenge studies have shown that pollen can have early and delayed effects on the lungs and airways. Here, we qualitatively and quantitatively synthesize the evidence of outdoor pollen exposure on various lung function and airway inflammation markers in community‐based studies. Methods: Four online databases were searched: Medline, Web of Science, CINAHL and Google Scholar. The search strategy included terms relating to both exposure and outcomes. Inclusion criteria were human‐based studies published in English that were representative of the community. Additionally, we only considered cross‐sectional or short‐term longitudinal studies which investigated pollen exposure by levels or season. Study quality assessment was performed using the Newcastle‐Ottawa scale. Meta‐analysis was conducted using random‐effects models. Results: We included 27 of 6551 studies identified from the search. Qualitative synthesis indicated associations between pollen exposure and predominantly type‐2 inflammation in both the upper and lower airways, but little evidence for lung function changes. People with ever asthma and/or seasonal allergic rhinitis (SAR) were at higher risk of such airway inflammation. Meta‐analysis confirmed a positive relationship between pollen season, eosinophilia and eosinophil cationic protein (ECP) in people with ever SAR but the results between studies were highly variable. Heterogeneity was reduced after further subgrouping by age, and the forest plots indicated that eosinophilic airway inflammation to outdoor pollen exposure increased with age. Conclusion: Among people with ever asthma and ever SAR, exposure to increased ambient pollen triggers type‐2 upper and lower airway inflammation rather than a non‐specific or innate inflammation. These findings can lead to the formulation of specific pollen immunotherapy for susceptible individuals. Future research should be directed towards investigating lagged associations and effect modifications using larger and more generalized populations. Systematic review registration: CRD42020146981 (PROSPERO). [ABSTRACT FROM AUTHOR]

COPD is a seriously disabling respiratory condition that inexorably progresses to disability and mortality. It affects approximately 10% of the population globally with a greater prevalence at advanced ages. Airway bacterial infections complicate the disease course in most COPD patients, leading to increased symptoms, more rapid decline in lung function, acute exacerbations and reduced quality of life. With increasing bacterial resistance to antibiotics and adverse effects of conventional treatments, new effective non‐antibiotic antimicrobial therapies are urgently needed to manage COPD. Hypoxia‐inducible factor (HIF)‐1α is an important transcriptional regulator of cellular responses to hypoxia, oxidants and inflammation, and is overexpressed in the lungs of COPD patients. Recent evidence shows that increased HIF‐1α expression can upregulate the platelet‐activating factor receptor (PAFR) on the airway epithelial surface that is increased in smokers and particularly COPD patients. The receptor is utilized by PAFR‐dependent bacteria (Streptococcus pneumoniae, Haemophilus influenzae and Pseudomonas aeruginosa) to induce infection in both the respiratory and gastrointestinal (GI) tracts. However, the importance and mechanism of HIF‐1α in augmenting PAFR‐dependent bacterial infections in COPD are poorly understood. Here, we review the evidence for the roles of local tissue hypoxia‐induced inflammation, HIF‐1α and PAFR in facilitating bacterial infections in COPD. Blocking PAFR may provide a novel antimicrobial approach to manage bacterial infections in COPD. [ABSTRACT FROM AUTHOR]

Background and objective: Obstructive sleep apnoea (OSA) and asthma are associated, and nocturnal breathing difficulty that is usually identified as asthma‐like symptoms can be present in both conditions. We investigated how nocturnal asthma‐like symptoms (NAS) and bronchial hyper‐reactivity (BHR) contribute to the association between OSA risk and current asthma, which is currently unknown but a clinically important question. Methods: We used data from 794 middle‐aged participants in a population‐based cohort who provided information on OSA risk (defined by a STOP‐Bang questionnaire score of at least 3), current asthma and NAS, and underwent methacholine bronchial challenge testing. Using regression models, we examined the association between OSA risk and current asthma‐NAS subgroups and investigated any effect modification by BHR. Results: The participants were aged 50 years (49.8% male). OSA risk was associated with NAS with or without current asthma (odds ratio (OR): 2.6; 95% CI = 1.3–5.0; OR: 4.2; 95% CI = 1.1–16.1, respectively), but not with current asthma in the absence of NAS. BHR was associated with current asthma with or without NAS (OR: 2.9; 95% CI = 1.4–5.9; OR: 3.4; 95% CI = 2.0–7.0, respectively) but not with NAS in the absence of current asthma. The associations between OSA risk and current asthma were neither modified nor mediated by BHR. Conclusion: Our findings suggest that some of the nocturnal symptoms perceived as asthma may be OSA symptoms. Patients with nocturnal asthma symptoms should be considered for possible OSA. We assessed the roles of nocturnal asthma‐like symptoms (NAS) and bronchial hyper‐reactivity (BHR) in obstructive sleep apnoea (OSA)–asthma association. OSA is associated with NAS with or without the presence of asthma, but BHR is not associated with NAS when asthma is absent. Some NAS perceived as nocturnal asthma could be symptoms of OSA. See relatedEditorial [ABSTRACT FROM AUTHOR]

Background and Objective: Early‐life risk factors for obstructive sleep apnoea (OSA) are poorly described, yet this knowledge may be critical to inform preventive strategies. We conducted the first study to investigate the association between early‐life risk factors and OSA in middle‐aged adults. Methods: Data were from population‐based Tasmanian Longitudinal Health Study cohort (n = 3550) followed from 1st to 6th decades of life. Potentially relevant childhood exposures were available from a parent‐completed survey at age 7‐years, along with previously characterized risk factor profiles. Information on the primary outcome, probable OSA (based on a STOP‐Bang questionnaire cut‐off ≥5), were collected when participants were 53 years old. Associations were examined using logistic regression adjusting for potential confounders. Analyses were repeated using the Berlin questionnaire. Results: Maternal asthma (OR = 1.5; 95% CI 1.1–2.0), maternal smoking (OR = 1.2; 1.05, 1.5), childhood pleurisy/pneumonia (OR = 1.3; 1.04, 1.7) and frequent bronchitis (OR = 1.2; 1.01, 1.5) were associated with probable OSA. The risk‐factor profiles of 'parental smoking' and 'frequent asthma and bronchitis' were also associated with probable OSA (OR = 1.3; 1.01, 1.6 and OR = 1.3; 1.01–1.9, respectively). Similar associations were found for Berlin questionnaire‐defined OSA. Conclusions: We found novel temporal associations of maternal asthma, parental smoking and frequent lower respiratory tract infections before the age of 7 years with adult OSA. While determination of their pathophysiological and any causal pathways require further research, these may be useful to flag the risk of OSA within clinical practice and create awareness and vigilance among at‐risk groups. This study provides the first known evidence for individual and profiled early‐life and childhood risk factors for OSA in adults. It shows that early exposures to smoking and lower respiratory tract infections could be risks for adult OSA, which may stimulate future research and help flag future risk of OSA. See relatededitorial [ABSTRACT FROM AUTHOR]

See relatedarticle [ABSTRACT FROM AUTHOR]

Purpose: To assess misclassification in adults reporting childhood asthma. Methods: The Tasmanian Asthma Survey commenced in 1968 when 8,583 7-year-old children attending school in Tasmania (participants) were studied. In 1991–1993, a stratified sample of 1,494 participants was studied. Their recall of childhood asthma was compared to their parents' prospectively gathered report. Results: Where participants had childhood asthma, those with current asthma, severe eczema, or hay fever were less likely to misclassify while females were more likely to misclassify. Where participants had no childhood asthma, misclassification was associated with current asthma, hay fever, or allergies. Conclusions: Retrospective self-assessment of childhood asthma is unreliable. [ABSTRACT FROM AUTHOR]

Because bronchial hyperresponsiveness has been linked to the bronchiolitis obliterans syndrome (BOS), we determined PD20 methacholine (PD20(M)), PD15 hypertonic saline (PD15(HS)) and their dose-response slopes (DRSM and DRSHS) in 8 single and 18 double lung transplant recipients within 1 year of lung transplantation and examined the relationship to bronchoalveolar lavage cell profiles and subsequent development of BOS. Twenty-two patients (81%) had a positive methacholine and 6 (25%) a positive hypertonic saline challenge. A positive PD15(HS) was associated with an increased risk for BOS at 2 years (odds ratio 12.6, 95% confidence interval 1.3–123.5, p < 0.05), and time to BOS was significantly and negatively related to DRSHS (r = -0.5, p < 0.05) — that is, the greater the response, the shorter the time to BOS. Interestingly, DRSHS correlated positively with recipient:donor total lung capacity ratio (r = 0.5, p < 0.05), but there was no relationship between either challenge result and airway inflammation. Methacholine hyperresponsiveness is common after lung transplantation but is not prognostic, whereas response to hypertonic saline may reflect recipient:donor size matching and provide useful information regarding the potential for BOS development. [Copyright &y& Elsevier]

The complex nature of chronic bronchitis (CB) and changing definitions have contributed to challenges in understanding its aetiology and burden. In children, CB is characterised by persistent airway inflammation often linked to bacterial infections and is therefore termed "protracted bacterial bronchitis" (PBB). Longitudinal studies suggest that CB in childhood persists into adulthood in a subgroup. It can also be associated with future chronic respiratory diseases including asthma, bronchiectasis, and chronic obstructive pulmonary disease (COPD). Adult CB is traditionally associated with smoking, occupational exposures, and lower socioeconomic status. The interplay between risk factors, childhood CB, adult CB, and other chronic respiratory diseases is intricate, requiring comprehensive longitudinal studies for a clearer understanding of the natural history of CB across the lifespan. Such longitudinal studies have been scarce to date given the logistic challenges of maintaining them over time. In this review, we summarise current evidence on the evolution of the definitions, pathophysiology, risk factors, and consequences of childhood and adulthood chronic bronchitis. [ABSTRACT FROM AUTHOR]

Background and Objective: Little is known about the association between ambient air pollution and idiopathic pulmonary fibrosis (IPF) in areas with lower levels of exposure. We aimed to investigate the impact of air pollution on lung function and rapid progression of IPF in Australia. Methods: Participants were recruited from the Australian IPF Registry (n = 570). The impact of air pollution on changes in lung function was assessed using linear mixed models and Cox regression was used to investigate the association with rapid progression. Results: Median (25th–75th percentiles) annual fine particulate matter (<2.5 μm, PM2.5) and nitrogen dioxide (NO2) were 6.8 (5.7, 7.9) μg/m3 and 6.7 (4.9, 8.2) ppb, respectively. Compared to living more than 100 m from a major road, living within 100 m was associated with a 1.3% predicted/year (95% confidence interval [CI] −2.4 to −0.3) faster annual decline in diffusing capacity of the lungs for carbon monoxide (DLco). Each interquartile range (IQR) of 2.2 μg/m3 increase in PM2.5 was associated with a 0.9% predicted/year (95% CI −1.6 to −0.3) faster annual decline in DLco, while there was no association observed with NO2. There was also no association between air pollution and rapid progression of IPF. Conclusion: Living near a major road and increased PM2.5 were both associated with an increased rate of annual decline in DLco. This study adds to the evidence supporting the negative effects of air pollution on lung function decline in people with IPF living at low‐level concentrations of exposure. [ABSTRACT FROM AUTHOR]

Purpose: Little is known about the impact of co-morbidities on health-related quality of life (HRQoL) for people with idiopathic pulmonary fibrosis (IPF). We aimed to investigate the relative contribution of co-morbidities to HRQoL of people with IPF. Methods: N = 157 participants were recruited from the Australian IPF Registry (AIPFR). Health state utilities (HSUs), and the super-dimensions of physical and psychosocial scores were measured using the Assessment of Quality of Life-8-Dimensions (AQoL-8D). The impact of co-morbidities on HRQoL was investigated using linear regression and general dominance analyses. Results: A higher number of co-morbidities was associated with lower HSUs (p trend = 0.002). Co-morbidities explained 9.1% of the variance of HSUs, 16.0% of physical super-dimensional scores, and 4.2% of psychosocial super-dimensional scores. Arthritis was associated with a significant reduction on HSUs (β = − 0.09, 95% confidence interval [CI] − 0.16 to − 0.02), largely driven by reduced scores on the physical super-dimension (β = − 0.13, 95% CI − 0.20 to − 0.06). Heart diseases were associated with a significant reduction on HSUs (β = − 0.09, 95% CI − 0.16 to − 0.02), driven by reduced scores on physical (β = − 0.09, 95% CI − 0.16 to − 0.02) and psychosocial (β = -0.10, 95% CI − 0.17 to − 0.02) super-dimensions. Conclusions: Co-morbidities significantly impact HRQoL of people with IPF, with markedly negative impacts on their HSUs and physical health. A more holistic approach to the care of people with IPF is important as better management of these co-morbidities could lead to improved HRQoL in people with IPF. [ABSTRACT FROM AUTHOR]

Objectives: Fibrotic interstitial lung disease (ILD) includes a large group of conditions that lead to scarring of the lungs. The lack of available 5-level EuroQol 5D (EQ5D) data has limited the ability to conduct economic evaluations in ILD. The purpose of this study was to develop and validate a mapping algorithm that predicts EQ5D utilities from commonly collected pulmonary function measurements (forced vital capacity [FVC] and diffusing capacity of the lung for carbon monoxide [DLCO]) in fibrotic ILDs. Methods: EQ5D utility and pulmonary function measurements from the Canadian Registry for Pulmonary Fibrosis were included. Ordinary least squares (OLS), beta regression, two-part, and tobit models were used to map EQ5D utilities from FVC or DLCO. Model performance was assessed by comparing the predicted and observed utilities. Subgroup analyses were also conducted to test how well models performed across different patient characteristics. The models were then externally validated in the Australian Idiopathic Pulmonary Fibrosis Registry. Results: The OLS model performed as well as other more complex models (root mean squared error: 0.17 for FVC and 0.16 for DLCO). As with the other models, the OLS algorithm performed well across the different subgroups (except for EQ5D utilities < 0.5) and in the external validation cohort. Conclusion: We developed a mapping algorithm that predicts EQ5D utilities from FVC and DLCO, with the intent that this algorithm can be applied to clinical trial populations and real-world cohorts that have not prioritized collection of health-related utilities. The mapping algorithm can be used in future economic evaluations of potential ILD therapies. [ABSTRACT FROM AUTHOR]

Background/Objectives: Eczema is a common chronic debilitating skin condition in childhood. Data on the epidemiology and natural history of eczema across the life course are lacking. This analysis aimed to describe these epidemiological features in Australian children and adults. Methods: Data collected on eczema from four Australian cohort studies were analysed: namely HealthNuts, Melbourne Atopic Cohort Study (MACS), Tasmanian Longitudinal Health Study (TAHS) and the Australian arm of the European Community Respiratory Health Survey (ECRHS). Results: Among children aged under 6 years, 28.8%–35.6% have ever‐had eczema, and 16.7%–26.6% had 'current eczema'. Among those aged 6–12 years, 14.6%–24.7% had 'current eczema' with 12.0%–18.5% of those at ages of 6 and 10 years classified as having moderate‐to‐severe eczema according to the Scoring of Atopic Dermatitis (SCORAD) index. In adults, the prevalence of 'eczema ever' ranged between 13.8% and 48.4%. The 12‐month period prevalence of eczema was 15.1% at age 18, while current eczema was 8.5% at an average age of 51, and 8.8% at an average age 53 years. Eczema was more common among young boys, but this difference became non‐significant for older children and early adolescents. In contrast, eczema was more common for adult women than men. Conclusions: Eczema is common both in children and adults. The proportion of severe eczema in children was substantial. [ABSTRACT FROM AUTHOR]

Purpose: Idiopathic pulmonary fibrosis (IPF) is a progressive and debilitating chronic lung disease with a high symptom burden, which has a substantial impact on health-related quality of life (HRQoL). Our study aimed to assess the suitability of the EuroQol five-dimension (EQ-5D-5L) and the Assessment of Quality of Life- eight-dimension (AQoL-8D) questionnaires in measuring HRQoL as health state utility values (HSUVs) in an Australian IPF cohort. Methods: Data for estimation of health state utility values (HSUVs) were collected from participants of the Australian IPF Registry (AIPFR) using self-administered surveys which included the EQ-5D-5L and the AQoL-8D. Data on lung function and disease specific HRQoL instruments were collected from the AIPFR. Performance of the two instruments was evaluated based on questionnaire practicality, agreement between the two instruments and test performance (internal and construct validity). Results: Overall completion rates for the EQ-5D-5L and AQoL-8D were 96% and 85%, respectively. Mean (median) HSUVs were 0.65 (0.70) and 0.69 (0.72) for the EQ-5D-5L and AQoL-8D, respectively. There was reasonable agreement between the two instruments based on the Bland–Altman plot mean difference (−0.04) and intraclass correlation coefficient (0.84), however there were some fundamental differences. A larger range of values was observed with the EQ-5D-5L (−0.57–1.00 vs 0.16–1.00). The EQ-5D-5L had a greater divergent sensitivity and efficacy in relation to assessing HSUVs between clinical groupings. The AQoL-8D ,however, had a higher sensitivity to measure psychosocial aspects of HRQoL in IPF. Conclusion: The EQ-5D-5L demonstrated superior performance when compared to AQoL-8D in persons with IPF. This may be attributable to the high symptom burden which is physically debilitating to which the EQ-5D-5L may be more sensitive. [ABSTRACT FROM AUTHOR]

Background and objective: Prediction of disease course in patients with progressive pulmonary fibrosis remains challenging. The purpose of this study was to assess the prognostic value of lung fibrosis extent quantified at computed tomography (CT) using data‐driven texture analysis (DTA) in a large cohort of well‐characterized patients with idiopathic pulmonary fibrosis (IPF) enrolled in a national registry. Methods: This retrospective analysis included participants in the Australian IPF Registry with available CT between 2007 and 2016. CT scans were analysed using the DTA method to quantify the extent of lung fibrosis. Demographics, longitudinal pulmonary function and quantitative CT metrics were compared using descriptive statistics. Linear mixed models, and Cox analyses adjusted for age, gender, BMI, smoking history and treatment with anti‐fibrotics were performed to assess the relationships between baseline DTA, pulmonary function metrics and outcomes. Results: CT scans of 393 participants were analysed, 221 of which had available pulmonary function testing obtained within 90 days of CT. Linear mixed‐effect modelling showed that baseline DTA score was significantly associated with annual rate of decline in forced vital capacity and diffusing capacity of carbon monoxide. In multivariable Cox proportional hazard models, greater extent of lung fibrosis was associated with poorer transplant‐free survival (hazard ratio [HR] 1.20, p < 0.0001) and progression‐free survival (HR 1.14, p < 0.0001). Conclusion: In a multi‐centre observational registry of patients with IPF, the extent of fibrotic abnormality on baseline CT quantified using DTA is associated with outcomes independent of pulmonary function. [ABSTRACT FROM AUTHOR]

We have established that EMT is an active process throughout the airway tree in smokers and even more so in airways in COPD. (Comment on: Proliferation Genes Repressed by TGF- Are Downstream of Slug/Snail2 in Normal Bronchial Epithelial Progenitors and are Deregulated in COPD. EMT in basal epithelial cells was first postulated as active in human airways disease in lung transplant recipients as part of the development of Bronchiolitis Obliterans Syndrome (BOS) in chronic lung allograft dysfunction/rejection [[2]]. [Extracted from the article]

The chronic respiratory non-communicable diseases, asthma and chronic obstructive pulmonary disease (COPD) are among the leading causes of global mortality and morbidity. Individuals suffering from these diseases are particularly susceptible to respiratory infections caused by bacterial and/or viral pathogens, which frequently result in exacerbation of symptoms, lung function decline, frequent hospital emergency visits and increased socioeconomic burden. Human rhinoviruses (HRV) remain the major viral pathogen group implicated in exacerbations of both asthma and COPD. The rhinoviral entry into the host lung epithelium is facilitated primarily by the adhesion site ("receptor") intercellular adhesion molecule-1 (ICAM-1), coincidentally expressed on the respiratory epithelium in these conditions. Multiple observations of increased airway ICAM-1 protein in asthmatics, smokers and smoking-related COPD have been recorded in the literature. However, the lack of robust therapies for COPD in particular has triggered a renewed interest in assessing receptor antagonism-based anti-viral strategies for treatment of intercurrent viral infections in those with pre-existing chronic lung diseases. Given the crucial role ICAM-1 plays in facilitating HRV adhesion and, thus, transmissibility to the host respiratory system, as well as the up-regulation of ICAM-1 by smoking, we summarize the role of HRV in smoking-induced COPD and especially highlight the role of ICAM-1 in epithelial viral adhesion and chronic lung disease progression. Further, the review also sheds light specifically on evolving precision therapeutic strategies in blocking ICAM-1 for preventing viral adhesion and exacerbations of COPD. [ABSTRACT FROM AUTHOR]

Background and objective: Idiopathic pulmonary fibrosis (IPF) is one of the most common forms of interstitial lung diseases. While studies have been conducted in other countries to determine the epidemiological burden of IPF, there is limited information in Australia. Our study aimed to address this gap and generate the first estimates for the mortality, incidence and prevalence of IPF in Australia. Methods: Estimates were generated by utilizing the novel Mortality Incidence Analysis Model (MIAMOD) method and software based on the illness–death model. Data inputs included population estimates and mortality data from the Australian Bureau of Statistics (ABS) for the period 1997–2015 and participant data from the Australian IPF Registry (AIPFR). Projections were estimated for a 10‐year period up to 2025. Results: Overall crude and age‐standardized estimates for mortality were 5.9 and 6.3 per 100,000 population; incidence, 10.4 and 11.2 per 100,000 population; and prevalence, 32.6 and 35.1 per 100,000 population. Crude and age‐standardized mortality, incidence and prevalence increased over the study period; however, they demonstrated a decreasing trend over the projected period. Persons older than 70 years constituted 9% of the population; however, they accounted for approximately 82%–83% of all deaths, incident and prevalent cases. All estimates were higher in males than in females. Conclusion: Our study provides the first estimates for incidence, prevalence and mortality of IPF in Australia. By reporting national estimates for IPF, our study addresses an information gap important for policy, planning and to help optimize the allocation of resources for the management of patients with IPF. [ABSTRACT FROM AUTHOR]

Background and objective The role of indoor air pollution as a risk factor for asthma and respiratory symptoms in middle age is unclear. We investigated associations between indoor air pollution sources and (i) asthma phenotypes and (ii) asthma-related respiratory symptoms in middle-aged adults. Methods Subjects ( n = 5729) who participated in the 2004 survey of the Tasmanian Longitudinal Health Study completed respiratory and home environment questionnaires. Associations between indoor air pollution sources, and asthma phenotypes and asthma-related respiratory symptoms were estimated. Results Recent mould in the home was associated with current asthma (odds ratio ( OR) 1.26; 95% confidence interval 1.06-1.50), wheeze ( OR 1.34; 1.17-1.54) and nocturnal chest tightness ( OR 1.30; 1.12-1.51). Stratified by atopy and gender, recent mould was associated with current non-atopic asthma only in males ( OR 3.73; 1.29-10.80). More rooms affected by mould were associated with significant trends for current asthma, wheeze and nocturnal chest tightness. Home environmental tobacco smoke was associated with doctor-diagnosed asthma ( OR 1.25; 1.02-1.53), wheeze ( OR 1.69; 1.41-2.03), nocturnal chest tightness ( OR 1.54; 1.26-1.88), with current asthma only in non-smokers ( OR 2.09; 95%: 1.30-3.35) and with current asthma only in males ( OR 1.74; 95%: 1.25-2.42). Among heating appliances, reverse cycle air conditioning was negatively associated with doctor-diagnosed asthma ( OR 0.84; 0.70-1.00). Neither electric nor gas stove use was associated with either asthma phenotype or with asthma-related respiratory symptoms. Conclusions In middle age, reducing home exposure to mould and environmental tobacco smoke might reduce asthma and asthma-related respiratory symptoms. [ABSTRACT FROM AUTHOR]

Despite the challenges of diagnosing and managing adult patients with chronic cough, a systematic synthesis of evidence on aetiological risk factor is lacking. We systematically searched PubMed and EMBASE to synthesize the current evidence for longitudinal associations between a wide range of risk factors and chronic cough in the general adult population, following the meta‐analysis of observational studies in epidemiology (MOOSE) guidelines. The Newcastle–Ottawa scale was used to assess the quality of the included studies. Fixed‐effect meta‐analysis was conducted where appropriate. Of 26 eligible articles, 16 domains of risk factors were assessed. There was consistent evidence that asthma (pooled adjusted OR [aOR] = 3.01; 95% CI: 2.33–3.70; I2 = 0%; number of articles [N] = 3) and low education levels/socioeconomic status (SES) (pooled aOR = 1.46; 95% CI: 1.20–1.72; I2 = 0%; N = 3) were associated with an increased risk of chronic cough after adjusting for smoking and other confounders. While continuous smoking was associated with chronic cough (aOR = 1.81; 95% CI: 1.36–2.26; I2 = 57%; N = 3), there was too little evidence to draw conclusions for occupational exposures, outdoor air pollution, early‐life exposures, diet, snoring and other chronic conditions, including obesity, chronic obstructive pulmonary disease, gastro‐oesophageal reflux disease and chronic pain. Asthma, persistent smoking and lower education/SES were associated with an increased risk of chronic cough. Longitudinal associations between other factors frequently mentioned empirically (i.e., occupational exposures, air pollution and chronic respiratory conditions) need further investigation, ideally with objective and standardized measurement. [ABSTRACT FROM AUTHOR]

Microsomal epoxide hydrolase (EPHX1) is an important gene because of its role in the metabolism of components of cigarette smoke; thus it may be an important potential modifier of the risk of developing smoking-related lung disease, such as chronic obstructive pulmonary disease (COPD). Several studies have investigated EPHX1 and COPD, but some of these studies have potentially been affected by genotyping error. We investigated the influence of single nucleotide polymorphisms (SNPs) in EPHX1 on well-characterized COPD and intermediate phenotypes. A total of 1,232 participants completed a detailed respiratory questionnaire and spirometry. From this sample, 72 COPD cases (FEV1/FVC < 0.70 and FEV1 < 80% predicted) and 220 control subjects (no respiratory symptoms and normal lung function) were selected for analysis. The EPHX1 exon 3 and EPHX1 exon 4 polymorphisms were carefully genotyped to avoid error using several methods. We found that the EPHX1 exon 3 polymorphism was not associated with an increased risk of COPD, nor was the EPHX1 exon 4 polymorphism. In addition, none of the EPHX1 haplotypes were associated with an increased risk of any COPD phenotype. This finding, along with doubt shed on the accuracy of other studies that have demonstrated positive associations, suggests that a strong role for the EPHX1 polymorphisms in respiratory disease is unlikely. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) has a high level of morbidity. There is limited information about levels of physical activity among community dwelling subjects with the disease and its association with lung function and quality of life. In this study, 176 subjects with COPD were recruited from general practices. Physical activity was measured over 7 days using pedometers, quality-of-life using the St. George's Respiratory Questionnaire, and lung function using spirometry, 124 subjects, 60% male, aged 70 ± 8 years were included in the analysis. Physical activity levels were low, median steps/day for males = 3,621,IQR = 4,247 and for females = 4,287,IQR = 3,063. Overall physical activity (median steps/day = 3,716,IQR = 3682) was significantly associated with the forced expiratory volume in one second (r = 0.39, p [ABSTRACT FROM AUTHOR]

Adjustment for psychosocial and family problems is common in epidemiological research. Recursive partitioning algorithms, such as CHi Square Automatic Interaction Detection (CHAID), can be used to explore complex interactions between these factors and predictor and outcome variables. We investigated the nature of interactions between asthma management variables and psychosocial problems and how these interactions changed the risk of asthma mortality; 50 cases of asthma death and 201 emergency department controls were recruited. A validated questionnaire was used to collect data. An extended version of CHAID was used to identify statistically significant ( p = 0.05) interactions controlling for asthma severity. Family problems were associated with increased risk of mortality for patients aged > 31 years (OR = 6.5; 95% CI 2.6–16.1) but not for younger patients. Males were at increased risk overall, but females with family problems (OR = 4.3; 95% CI 1.7–10.7) were at greater risk then males (OR = 3.1; 95% CI 1.2–7.9) with family problems. Alcohol use increased risk of mortality for individuals with verbal instructions (OR = 5.4; 95% CI 1.5–19.5) or without a written action plan (OR = 4.4; 95% CI 1.0–19.4). Individuals with severe asthma and who reported having lung function tests were at increased risk for mortality if family (OR = 8.2; 95% CI 1.6–41.6) or financial problems (OR = 11.5; 95% CI 2.0–65.9) were present. This analysis highlights some important interactions and the magnitude of additional risk for mortality associated with psychosocial or family problems. Psychosocial problems need to be identified and addressed as part of asthma management, because even with best practice, these problems place patients at an increased risk of dying. [ABSTRACT FROM AUTHOR]

Despite the growing body of evidence on lung function trajectories over the life course and their risk factors, the literature has not been systematically synthesized. Publications related to lung function trajectories were identified from PubMed, EMBASE and CINAHL databases. Two authors independently identified publications for inclusion according to predefined selection criteria. Studies that modelled lung function trajectories and reported associated exposures were included. Meta-analyses could not be conducted due to heterogeneity in the exposures and methods used to model lung function trajectories. Nine publications were eligible for inclusion of which four used group-based trajectory modelling to model lung function trajectories, while five used latent profile analysis. Studies with repeated lung function measurements over the life course identified more trajectories than others. Only one study spanning from childhood to middle age reported catch-up trajectory. The following childhood risk factors for subnormal lung function trajectories were observed in at least across two studies: low birth weight, early wheezing, asthma, allergic sensitization, eczema, allergic rhinitis, lower respiratory tract infections, family history of asthma and second-hand smoke exposure. Adult active asthma and personal cigarette smoking were observed to be associated with accelerated decline lung trajectories. Our review identified 10 risk factors associated with the growth, catch-up, reduced plateau and decline trajectories of lung function. Intervention directed at childhood asthma and infections, and tobacco smoke exposure at all ages would help promote lung health and prevent subnormal lung function trajectories. [ABSTRACT FROM AUTHOR]

Purpose: Idiopathic pulmonary fibrosis (IPF) is a progressive and universally fatal lung disease, characterised by increasing fibrosis of the lung parenchyma. In this study, we aimed to quantify the health state utility values (HSUVs) for Australians with IPF and to identify the factors affecting these HSUVs. Methods: Participants of the Australian IPF Registry (AIPFR), with data on EuroQoL five dimension—five level (EQ-5D-5L) profiles were included. Pulmonary function tests (PFTs) were used to assess disease severity using three IPF -based classification systems. Stepwise multivariable linear regression models assessed the relationship between HSUVs and important demographic and clinical parameters.Query Results: A total of 155 participants provided data for the analysis of HSUVs. For our base case, HSUVs ranged from − 0.57 to 1.00. Mean HSUVs for all participants was 0.65 (95% CI 0.61–0.70). In general, HSUVs decreased with increasing disease severity under all disease severity classification systems. Multivariable linear regression demonstrated a negative association between HSUVs, disease severity and having more than 2 comorbidities. Conclusions: Our study has shown that EQ-5D-5L has exhibited discriminatory sensitivity for the study population. We have demonstrated that disease severity and having more than two comorbidities was associated with lower HSUVs in Australians with IPF. Our findings support early diagnosis and appropriate evidence-based treatment to slow or prevent IPF progression; and identification and treatment of associated comorbidities to potentially improve health-related quality of life in people with IPF. [ABSTRACT FROM AUTHOR]

Background: There is limited information on risk factors for eczema in adults. Recent evidence suggests that air pollution may be associated with increased incidence of eczema in adults. We aimed to assess this possible association. Methods: Ambient air pollution exposures (distance from a major road, nitrogen dioxide [NO2], fine particulate matter with an aerodynamic diameter ≤2.5 µm [PM2.5]) were assessed for the residential address of Tasmanian Longitudinal Health Study participants at ages 43 and 53 years. Eczema incidence (onset after age 43 years), prevalence (at 53 years), and persistence were assessed from surveys, while IgE sensitization was assessed using skin prick tests. The presence or absence of eczema and sensitization was classified into four groups: no atopy or eczema, atopy alone, non‐atopic eczema, and atopic eczema. Adjusted logistic and multinomial regression models were fitted to estimate associations between ambient air pollution and eczema, and interaction by sex was assessed. Results: Of 3153 participants in both follow‐ups, 2369 had valid skin prick tests. For males, a 2.3 ppb increase in baselineNO2was associated with increased odds of prevalent eczema (OR = 1.15 [95% CI 0.98–1.36]) and prevalent atopic eczema (OR = 1.26 [1.00–1.59]). These associations were not seen in females (p for interaction = 0.08, <0.01). For both sexes, a 1.6 µg/m3 increase in PM2.5 exposure at follow‐up was associated with increased odds of aeroallergen sensitization (OR = 1.15 [1.03–1.30]). Conclusion: Increased exposure to residential ambient air pollutants was associated with an increased odds of eczema, only in males, and aeroallergen sensitization in both genders. [ABSTRACT FROM AUTHOR]

Background: Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease characterized by fibrosis and progressive loss of lung function. The pathophysiological pathways involved in IPF are not well understood. Abnormal lipid metabolism has been described in various other chronic lung diseases including asthma and chronic obstructive pulmonary disease (COPD). However, its potential role in IPF pathogenesis remains unclear.Methods: In this study, we used ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS) to characterize lipid changes in plasma derived from IPF patients with stable and progressive disease. We further applied a data-independent acquisition (DIA) technique called SONAR, to improve the specificity of lipid identification.Results: Statistical modelling showed variable discrimination between the stable and progressive subjects, revealing differences in the detection of triglycerides (TG) and phosphatidylcholines (PC) between progressors and stable IPF groups, which was further confirmed by mass spectrometry imaging (MSI) in IPF tissue.Conclusion: This is the first study to characterise lipid metabolism between stable and progressive IPF, with results suggesting disparities in the circulating lipidome with disease progression. [ABSTRACT FROM AUTHOR]

Background and objective: Early menarche is increasing in prevalence worldwide, prompting clinical and public health interest on its links with pulmonary function. We aimed to investigate the relationship between early menarche and lung function in middle age. Methods: The population‐based Tasmanian Longitudinal Health Study (born 1961; n = 8583), was initiated in 1968. The 5th Decade follow‐up data (mean age: 45 years) included age at menarche and complex lung function testing. The 6th Decade follow‐up (age: 53 years) repeated spirometry and gas transfer factor. Multiple linear regression and mediation analyses were performed to determine the association between age at menarche and adult lung function and investigate biological pathways, including the proportion mediated by adult‐attained height. Results: Girls reporting an early menarche (<12 years) were measured to be taller with greater lung function at age 7 years compared with those reporting menarche ≥12 years. By 45 years of age, they were shorter and had lower post‐bronchodilator (BD) forced expiratory volume in 1 s (adjusted mean difference: −133 mL; 95% CI: −233, −33), forced vital capacity (−183 mL; 95% CI: −300, −65) and functional residual capacity (−168 mL; 95% CI: −315, −21). Magnitudes of spirometric deficits were similar at age 53 years. Forty percent of these total effects were mediated through adult‐attained height. Conclusion: Early menarche was associated with reduced adult lung function. This is the first study to investigate post‐BD outcomes and quantify the partial role of adult height in this association. This is the first longitudinal study with data on key early life confounders to link early age at menarche to lung function deficits in middle age and provide novel evidence on potential biological pathways contributing to this link. [ABSTRACT FROM AUTHOR]

Aim: To identify the level of non-pharmacological care received by middle-aged adults with current asthma in Australia and to identify its association with clinical measures. Methods: The Tasmanian Longitudinal Health Study (TAHS) is a population-based cohort first studied in 1968 (n = 8583). In 2010, when participants were aged 49 years, a stratified sample enriched for asthma and bronchitis underwent clinical assessments including respiratory questionnaires and lung function testing (n = 836). Current asthma was defined as self-reported asthma symptoms and/or healthcare utilization in the last 12 months. Multivariable linear regression and log-binomial models were used to assess the relevant associations. Results: Of the entire TAHS cohort, 15.6% (95% CI 13.4–18.2%) had current asthma. Of these, 37.9% (95% CI 30.5–45.9%) had seen a general practitioner for their asthma and 16.5% (95% CI 11.5–23.1%) had discussed their asthma with a pharmacist in the last 12 months. Written asthma action plans (AAPs) were reported by 17.9% (95% CI 12.9–23.2%), verbal AAPs by 53.8% (95% CI 45.9–61.6%) and doctor-assessments of inhaler technique by 42.7% (95% CI 35.2–50.5%). Adults with asthma of greater severity were more likely to have received verbal AAPs (p-trend =0.02). In contrast, adults with lower spirometry were more likely to have received verbal AAPs (p = 0.04), written AAPs (p = 0.001) and education on inhaler technique (p = 0.04). Conclusion: Despite an established evidence base and recommendations in local and international guidelines, non-pharmacological asthma management remains sub-optimal in the middle-aged adult asthma population. [ABSTRACT FROM AUTHOR]

Summary: Background: Markers of microbial exposure are thought to be associated with risk of allergic sensitization; however, the associations are inconsistent and may be related to gene‐environment interactions. Objective: To examine the relationship between polymorphisms in the CD14 gene and allergic sensitization and whether sibling exposure, as a marker of microbial exposure, modified this relationship. Methods: We used data from the Tasmanian Longitudinal Health Study and the Melbourne Atopy Cohort Study. Two CD14 polymorphisms were genotyped. Allergic sensitization was defined by a positive response to a skin prick test. Sibling exposure was measured as cumulative exposure to siblings before age 6 months, 2 and 4 years. Logistic regression and multi‐level mixed‐effects logistic regression were used to examine the associations. Effect estimates across the cohorts were pooled using random‐effects meta‐analysis. Results: CD14 SNPs were not individually associated with allergic sensitization in either cohort. In TAHS, cumulative sibling exposure before age 6 months, 2 and 4 years was each associated with a reduced risk of allergic sensitization at age 45 years. A similar effect was observed in MACS. Meta‐analysis across the two cohorts showed consistent evidence of an interaction between cumulative sibling exposure before 6 months and the rs5744455‐SNP (P = 0.001) but not with the rs2569190‐SNP (P = 0.60). The pooled meta‐analysis showed that the odds of sensitization with increasing cumulative exposure to sibling before 6 months of age was 20.9% smaller in those with the rs5744455‐C‐allele than the T‐allele (OR = 0.83 vs 1.05, respectively). Conclusion and Clinical Relevance: Cumulative sibling exposure reduced the risk of sensitization from childhood to middle age in genetically susceptible individuals. [ABSTRACT FROM AUTHOR]

Background: Asthma and allergic diseases are heterogeneous. Measurement of biomarkers in exhaled breath condensate (EBC) may help to discriminate between different phenotypes and may assist with clinical prognostication. Objectives: We aimed to assess associations between total nitric oxide products (NOx) in EBC and different allergic phenotypes and lung function in young and middle‐aged adults. Methods: Cross‐sectional analyses were nested within two Australian longitudinal studies, the Melbourne Atopy Cohort Study (MACS, mean age 17.8 years) and the Tasmanian Longitudinal Health Study (TAHS, mean age 49.4 years). Levels of EBC NOx were determined by Griess‐reaction fluorescent method. Associations were assessed between EBC NOx and different allergic phenotypes, lung function and airway reactivity. Results: Atopy, with or without asthma or rhinitis, was associated with increased EBC NOx levels particularly in individuals with poly‐aero‐sensitization. These findings were generally consistent across the two age groups. In the older cohort, use of ICS in the previous 12 months masked the association between sensitization and EBC NOx (OR = 0.64, 95% CI = 0.21‐1.96, p for interaction = 0.05). Conclusions and clinical relevance: In these population‐based samples, EBC NOx was most strongly associated with atopic sensitization, rather than either current asthma or rhinitis, possibly indicating underlying increased airway inflammation associated with atopy. Therefore, EBC NOx could be a key predictor of atopy in both young and middle‐aged adults, regardless of the presence of concomitant asthma or rhinitis. [ABSTRACT FROM AUTHOR]

Objective: Atopy is associated with asthma, but cross-sectional studies suggest this association may be weaker in older adults. It remains unclear if atopy predicts asthma later in adult life. We aimed to investigate whether atopy in young adults predicted asthma 20 years later and to quantify the contemporaneous relationship of atopy and asthma as adults age. Methods: Participants of the European Community Respiratory Health Survey (ECRHS) in Melbourne aged 20-44 years were followed for 20 years and completed questionnaires, skin prick tests (SPT) and allergen specific immunoglobulin E measurement at a baseline and two subsequent surveys. Using logistic regression and generalized estimating equations, we tested if atopy at baseline predicted current asthma later in life and estimated the association between current atopy measured at each survey and current asthma, while adjusting for potential confounders. Results: The analysis included 220 participants: 50.9% male. Mean (SD) age at baseline was 35.7 (5.7) years. Asthma and atopy prevalence remained stable over 20 years. Baseline atopy (SPT) was associated with current asthma (OR 9.74, 95%CI 4.22, 22.5) over 20 years, and current atopy (SPT) with concurrent asthma (3.12; 1.70, 5.74). Conclusions: Atopy remains strongly associated with current asthma in 40 to 64 year-old adults, both prospectively and contemporaneously, but the prospective association is stronger. [ABSTRACT FROM AUTHOR]

Abstract: Background and objective: Chronic obstructive pulmonary disease (COPD) has potential origins in childhood but an association between childhood measles and post‐bronchodilator (BD) airflow obstruction (AO) has not yet been shown. We investigated whether childhood measles contributed to post‐BD AO through interactions with asthma and/or smoking in a non‐immunized middle‐aged population. Methods: The population‐based Tasmanian Longitudinal Health Study (TAHS) cohort born in 1961 (n = 8583) underwent spirometry in 1968 before immunization was introduced. A history of childhood measles infection was obtained from school medical records. During the fifth decade follow‐up (n = 5729 responses), a subgroup underwent further lung function measurements (n = 1389). Relevant main associations and interactions by asthma and/or smoking on post‐BD forced expiratory volume in 1 s/forced vital capacity (FEV1/FVC; continuous variable) and AO (FEV1/FVC < lower limit of normal) were estimated by multiple regression. Results: Sixty‐nine percent (n = 950) had a history of childhood measles. Childhood measles augmented the combined adverse effect of current clinical asthma and smoking at least 10 pack‐years on post‐BD FEV1/FVC ratio in middle age (z‐score: −0.70 (95% CI: −1.1 to −0.3) vs −1.36 (−1.6 to −1.1), three‐way interaction: P = 0.009), especially for those with childhood‐onset asthma. For never‐ and ever‐smokers of <10 pack‐years who had current asthma symptoms, compared with those without childhood measles, paradoxically, the odds for post‐BD AO was not significant in the presence of childhood measles (OR: 12.0 (95% CI: 3.4–42) vs 2.17 (0.9–5.3)). Conclusion: Childhood measles infection appears to compound the associations between smoking, current asthma and post‐BD AO. Differences between asthma subgroups provide further insight into the complex aetiology of obstructive lung diseases for middle‐aged adults. [ABSTRACT FROM AUTHOR]

Background Salmeterol (a long acting beta2-agonist) is a chiral molecule. (R R )-salmeterol is responsible for pharmacological effect, but basic knowledge of enantioselective pulmonary pharmacodynamics and pharmacokinetics of salmeterol remains unknown. There are safety concerns with ( S )-enantiomers of beta2-agonists, with suggestions that these enantiomers may increase bronchial hyperresponsivneness in asthma patients. Methodology Horses (n = 12) received racemic ( rac- ) salmeterol 250 μg via inhalation. Enantioselective UPLC–MS/MS was used to determine ( R )- and ( S )-salmeterol concentrations in pulmonary epithelial lining fluid (PELF) sampled 2, 5, 10 and 15 min after administration, in central lung (endoscopic bronchial biopsy) and peripheral lung (percutaneous pulmonary biopsy) tissues (at 20 and 25 min respectively), and in plasma samples. Results Physiologically relevant tissue concentrations were found for both enantiomers, with median levels greater in central than peripheral lung (equivalent to 32 and 5 mM ( R )-salmeterol for central and peripheral lung respectively). Levels in PELF decreased around 50% over 15 min and enantioselective distribution was observed in the central lung with levels of ( R )-salmeterol around 30% higher than ( S )-salmeterol. Conclusion Salmeterol distribution is enantioselective in the central lung. This suggests duration of action is more likely associated with specific B2ADR localisation effects rather than non-specific physiochemical factors which would not be enantioselective. [ABSTRACT FROM AUTHOR]

Long-acting β2-agonists (LABAs) such as formoterol and salmeterol are used for prolonged bronchodilatation in asthma, usually in combination with inhaled corticosteroids (ICSs). Unexplained paradoxical asthma exacerbations and deaths have been associated with LABAs, particularly when used without ICS. LABAs clearly demonstrate effective bronchodilatation and steroid-sparing activity, but long-term treatment can lead to tolerance of their bronchodilator effects. There are also concerns with regard to the effects of LABAs on bronchial hyperresponsiveness (BHR), where long-term use is associated with increased BHR and loss of bronchoprotection. A complicating factor is that formoterol and salmeterol are both chiral compounds, usually administered as 50:50 racemic (rac-) mixtures of two enantiomers. The chiral nature of these compounds has been largely forgotten in the debate regarding LABA safety and effects on BHR, particularly that (S)-enantiomers of β2-agonists may be deleterious to asthma control. LABAs display enantioselective pharmacokinetics and pharmacodynamics. Biological plausibility of the deleterious effects of β2-agonists (S)-enantiomers is provided by in vitro and in vivo studies from the short-acting β2-agonist (SABA) salbutamol. Supportive clinical findings include the fact that patients in emergency departments who demonstrate a blunted response to salbutamol are more likely to benefit from (R)-salbutamol than rac-salbutamol, and resistance to salbutamol appears to be a contributory mechanism in rapid asthma deaths. More effort should therefore be applied to investigating potential enantiospecific effects of LABAs on safety, specifically bronchoprotection. Safety studies directly assessing the effects of LABA (S)-enantiomers on BHR are long overdue. [ABSTRACT FROM AUTHOR]

Background and aims Traffic Related Air Pollution (TRAP) exposure is known to exacerbate existing respiratory diseases. We investigated longer term effects of TRAP exposure for individuals with or without existing asthma, and with or without lower lung function. Methods Associations between TRAP exposure and asthma (n = 689) and lung function (n = 599) were investigated in the prospective Tasmanian Longitudinal Health Study (TAHS). TRAP exposure at age 45 years was measured using two methods based on residential address: mean annual NO 2 exposure; and distance to nearest major road. Adjusted multinomial logistic regression was used to model the association between exposure to TRAP at 45 years and changes in asthma and lung function, using three follow ups of TAHS (45, 50 and 53 years). Results For those who never had asthma by 45, living <200 m from a major road was associated with increased odds of new asthma that persisted from 50 to 53 years (adjusted Odds Ratio [aOR] 5.20; 95% CI 1.07, 25.4). Asthmatic participants at 45 had an increased risk of persistent asthma up to 53 years if they were living <200 m from a major road, compared with asthmatic participants living >200 m from a major road (aOR = 5.21; 95% CI 1.54, 17.6). Conclusion For middle aged adults, living <200 m for a major road (a marker of TRAP exposure) influences both the development and persistence of asthma. These findings have public health implications for asthma prevention strategies in primary and secondary settings. [ABSTRACT FROM AUTHOR]

Background: Perinatal events can influence the development of asthma in childhood but current evidence is contradictory concerning the effects on life-time asthma risk. Objective: To assess the relationship between birth characteristics and asthma from childhood to adulthood. Methodology: All available birth records for the Tasmanian Longitudinal Health Study (TAHS) cohort, born in 1961 were obtained from the Tasmanian State Archives and Tasmanian hospitals. Low birth weight (LBW) was defined as less than 2500 grams. Preterm birth was defined as delivery before 37 weeks' gestation. Small for gestational age (SGA) was defined as a birth weight below the 10th percentile for a given gestational age. Multivariate logistic and cox regression were used to examine associations between birth characteristics and lifetime risk of current and incident asthma, adjusting for confounders. Results: The prevalence of LBW was 5.2%, SGA was 13.8% and preterm was 3.3%. LBW (OR = 1.65, 95%CI 1.12,2.44) and preterm birth (OR = 1.81, 95%CI 0.99, 3.31) were both associated with an increased risk of current asthma between the ages of 7 to 43 years. There was no association between SGA and current asthma risk. However, SGA was associated with incident asthma (HR = 1.32, 95%CI 1.00, 1.74), and there was an interaction with sex (p value = 0.08), with males having a greater risk of incident asthma (HR = 1.70, 95%CI 1.16–2.49) than females (HR = 1.04, 95%CI 0.70–1.54). Conclusions: Preterm birth and LBW were associated with an increased risk of current asthma into middle-age. These findings are the first to demonstrate the continuing impact of these characteristics on asthma risk into middle-age. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Parkinson's Disease (PD) is a neurodegenerative disorder manifested by rest tremor, rigidity, bradykinesia, and postural instability. Recent pharmaco-epidemiological studies evaluating beta-adrenergic drug use and risk of PD have reported conflicting findings. This systematic review and meta-analyses evaluate the association between beta-adrenergic (agonists and antagonists) drugs' use and PD. An electronic literature search of eight databases was performed from inception to July 2021 to identify pharmaco-epidemiological studies (case-control and cohort) reporting the risk of PD in beta-adrenergic users compared to non-users. We used the generic inverse variance method and RevMan (5.3.5) to estimate pooled adjusted risk ratios (aRRs) of PD using a random-effects model. Of 3168 records, 15 studies (10 case-control; five cohort) with 6508,877 participants, including 87,011 PD cases, were included. In the pooled analysis (n = 10) including any beta-antagonist users, compared with non-users, the aRR for PD was 1.19 (CI: 1.05,1.35); for any beta-agonist users (n = 8) aRR for PD was 0.87 (CI: 0.78,0.97). Propranolol users had a significantly increased risk of PD (aRR:1.91; CI:1.20,3.06), whereas salbutamol use was associated with reduced risk of PD (aRR:0.95; CI:0.92,0.99). Significant heterogeneity (I2 >87%) was observed, but the majority (n = 13) of the studies were of high quality, based on the JBI tool. Beta-antagonist use was associated with a modestly increased risk of PD, whereas beta-agonist use was associated with a modest decreased risk of PD. Future epidemiological studies should address the issues of protopathic bias and indirect association using appropriate epidemiological methods. • Recent studies evaluating ꞵ-adrenergic drug use and risk of Parkinson's Disease (PD) have reported conflicting findings. • We found ꞵ-antagonist to be associated with increased risk of PD; ꞵ-agonist use was associated with a decreased risk of PD. • Future studies should address protopathic bias and indirect association using appropriate epidemiological methods. [ABSTRACT FROM AUTHOR]

The complete correct name should read as follows Dinesh Kumar Chellappan The original article has been corrected. Correction to: Inflammopharmacology (2022) 30:725-735 https://doi.org/10.1007/s10787-022-0096... The 7th author name has been incorrectly published in the original publication. [Extracted from the article]

Objective. Anxiety and depression are common comorbidities in people with chronic obstructive pulmonary disease (COPD). While these comorbidities could potentially lead to a higher motivation to learn about self-management, they could also inhibit patients from translating this knowledge into appropriate self-management behaviours. This paper explores the moderating effects of anxiety and depression on a health-mentoring intervention, focusing on mechanisms of change (mediation).Methods. 182 COPD patients participated in an RCT, with anxiety and depression assessed by the Hospital Anxiety and Depression Scale (HADS), self-management knowledge by the Partners in Health Scale, and spontaneous physical activity using accelerometers, all measured at baseline, 6 and 12 months. The moderated mediation model tested the intervention's effect on physical activity, mediated via changes in self-management knowledge, at different levels of anxiety and depression.Results. Knowledge mediated the effect of the intervention on changes in physical activity only for participants reporting low levels of anxiety or depression. Both acted as moderators: Increased knowledge led to more physical activity among participants reporting low anxiety or depression and to less activity among highly anxious or depressed participants.Conclusion. Although health-mentoring interventions can be an effective tool to increase knowledge and physical activity among COPD patients, it is essential to take anxiety and depression into account, as increased knowledge may have detrimental effects in highly anxious or depressed participants. This suggests that patients with elevated anxiety or depression may need to be treated appropriately before engaging in chronic disease self-management interventions. [ABSTRACT FROM AUTHOR]

Background Despite the challenges of diagnosing and managing adult patients with chronic cough, a systematic synthesis of evidence on aetiological risk factor is lacking. Methods We systematically searched PUBMED and EMBASE to synthesize the current evidence for longitudinal associations between various risk factors and chronic cough in the general adult population, following the meta-analysis of observation studies in epidemiology (MOOSE) guidelines. The Newcastle-Ottawa scale was used to assess the quality of the included studies. Fixed-effect meta-analysis was conducted where appropriate. Results Of 26 eligible articles, 16 domains of risk factors were assessed. There was consistent evidence that asthma (pooled adjusted OR (aOR) = 3.01; 95%CI: 2.33-3.70; I2=0%, number of articles (N)=3) and low education levels/socioeconomic status (SES) (pooled aOR=1.46; 95%CI: 1.20-1.72; I2=0%; N = 3) were associated with an increased risk of chronic cough after adjusting for smoking and other confounders. While continuous smoking was associated chronic cough (aOR =1.81; 95%CI: 1.36,2.26; I2=57%; N = 3), there was too little evidence to draw conclusions for occupational exposures, outdoor air pollution, early-life exposures, diet, snoring and other chronic conditions. Conclusions Asthma, persistent smoking and lower education/SES were associated with increased risk of chronic cough. Longitudinal associations between other factors frequently mentioned empirically need further investigation. Key messages Our systematic review found asthma, smoking and lower education to be associated with adult chronic cough. More longitudinal studies are needed to understand other potential risk factors for adult chronic cough. [ABSTRACT FROM AUTHOR]

Background and objective Mortality and hospital separation data suggest a higher burden of chronic obstructive pulmonary disease ( COPD) in indigenous than non-indigenous subpopulations of high-income countries. This study sought to accurately measure the true prevalence of post-bronchodilator airflow obstruction and forced vital capacity reduction in representative samples of Indigenous and non-Indigenous Australians. Methods This study applies cross-sectional population-based survey of Aboriginal and non- Indigenous residents of the Kimberley region of Western Australia aged 40 years or older, following the international Burden Of Lung Disease ( BOLD) protocol. Quality-controlled spirometry was conducted before and after bronchodilator. COPD was defined as Global initiative for chronic Obstructive Lung Disease ( GOLD) Stage 2 and above (post-bronchodilator forced expiratory volume in 1 s/forced vital capacity (F EV1/ FVC) ratio <0.7 and FEV1 < 80% predicted). Results Complete data were available for 704 participants. The prevalence of COPD, adjusted for age, gender and body weight in Aboriginal participants (7.2%, 95% confidence interval ( CI) 3.9 to 10.4) was similar to that seen in non-Indigenous Kimberley participants (8.2%, 95% CI 5.7 to 10.7) and non-Indigenous residents of the remainder of Australia (7.1%, 95% CI 6.1 to 8.0). The prevalence of low FVC (<80% predicted) was substantially higher in Aboriginal compared with non-Indigenous participants (74.0%, 95% CI 69.1 to 78.8, vs 9.7%, 95% CI 7.1 to 12.4). Conclusions Low FVC, rather than airflow obstruction, characterizes the impact of chronic lung disease previously attributed to COPD in this population subject to significant social and economic disadvantage. Environmental risk factors other than smoking as well as developmental factors must be considered. These findings require further investigation and have implications for future prevention of chronic lung disease in similar populations. [ABSTRACT FROM AUTHOR]

There is little Australian epidemiologic data on idiopathic pulmonary fibrosis ( IPF), a relatively uncommon but devastating disease. The vast geographic distances in Australia have been a major impediment for collaborative research into IPF. A collaborative national effort, the Australian IPF Registry, has been formed, launched and is recruiting successfully ( n = 359, January 2014). Our experience provides unique insights for others wishing to set up IPF registries and in time for a global IPF registry. [ABSTRACT FROM AUTHOR]

Background and objective The impact of ambient wood smoke and traffic-related air pollution on adult asthma has not been well studied. This paper aims to investigate associations between exposure to ambient wood smoke, traffic-related air pollution and current asthma/asthma severity in middle age, and whether any associations are modified by atopic status. Methods Using data from the Tasmanian Longitudinal Health Study, associations between ambient wood smoke and two indices of traffic-related air pollution (frequency of heavy vehicles near the home and frequency of intense traffic noise) and current asthma/asthma severity were investigated. Unconditional logistic regression to examine current asthma and ordinal logistic regression to examine asthma severity was used. Results For asthmatics, both exposure to ambient wood smoke (odds ratio 1.11; 95% confidence interval 1.02-1.20) and being frequently exposed to heavy vehicles (odds ratio 1.80; 95% confidence interval 1.09-2.96) were associated with increased asthma severity. Neither association varied by atopic status. Conclusions In middle-aged adults, ambient wood smoke and traffic pollution were associated with increased asthma severity. These findings suggest that avoiding or limiting exposure to traffic pollution and wood smoke may help to reduce asthma. Future studies to replicate this finding are recommended and should examine specific biological mechanisms for this effect. [ABSTRACT FROM AUTHOR]

The article presents a study conducted to evaluate risk of asthma associated with occupational exposures in a population based cohort. The study includes analyzing asthma in a population using Cox proportional hazards regression. It is concluded that there is a significant association between cumulative occupational exposure to latex and new onset asthma.

The article discusses a study on the relation between childhood pneumonia and common child infectious diseases like measles, rubella and mumps on current, persisting and incident asthma from childhood to middle age. Data from Tasmanian Longitudinal Health Study (TAHS) spanning 37 years was used. It concludes that the effect of childhood pneumonia on asthma risk does not go beyond adolescent although childhood measles and pertussis can increase incident asthma risk until the end of adolescence.