Search

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. Method(s): 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. Result(s): 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(s): 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.Copyright © 2019 Asian Pacific Society of Respirology

Rationale: Interactions between early life and adult insults on lung function decline are not well understood, with most studies investigating prebronchodilator (pre-BD) FEV1 decline. Objective(s): To investigate relationships between adult risk factors and pre- and post-BD lung function decline and their potential effect modification by early life and genetic factors. Method(s): Multiple regression was used to examine associations between adult exposures (asthma, smoking, occupational exposures, traffic pollution, and obesity) and decline in both pre- and post-BD spirometry (forced expiratory volume in 1 s [FEV1], forced vital capacity [FVC], and FEV1/FVC) between ages 45 and 53 years in the Tasmanian Longitudinal Health Study (n = 857). Effect modification of these relationships by childhood respiratory risk factors, including low childhood lung function and GST (glutathione S-transferase) gene polymorphisms, was investigated. Result(s): Baseline asthma, smoking, occupational exposure to vapors/gases/dusts/fumes, and living close to traffic were associated with accelerated decline in both pre- and post-BD FEV1. These factors were also associated with FEV1/FVC decline. Occupational exposure to aromatic solvents was associated with pre-BD but not post-BD FEV1 decline. Maternal smoking accentuated the effect of personal smoking on pre- and post-BD FEV1 decline. Lower childhood lung function and having the GSTM1 null allele accentuated the effect of occupational exposure to vapors/gases/ dusts/fumes and personal smoking on post-BD FEV1 decline. Incident obesity was associated with accelerated decline in FEV1 and more pronounced in FVC. Conclusion(s): This study provides new evidence for accentuation of individual susceptibility to adult risk factors by low childhood lung function, GSTM1 genotype, and maternal smoking.Copyright © 2020 by the American Thoracic Society

Background: Lifetime lung function is related to quality of life and longevity. Over the lifespan, individuals follow different lung function trajectories. Identification of these trajectories, their determinants, and outcomes is important, but no study has done this beyond the fourth decade. Method(s): We used six waves of the Tasmanian Longitudinal Health Study (TAHS) to model lung function trajectories measured at 7, 13, 18, 45, 50, and 53 years. We analysed pre-bronchodilator FEV1 z-scores at the six timepoints using group-based trajectory modelling to identify distinct subgroups of individuals whose measurements followed a similar pattern over time. We related the trajectories identified to childhood factors and risk of chronic obstructive pulmonary disease (COPD) using logistic regression, and estimated population-attributable fractions of COPD. Finding(s): Of the 8583 participants in the original cohort, 2438 had at least two waves of lung function data at age 7 years and 53 years and comprised the study population. We identified six trajectories: early below average, accelerated decline (97 [4%] participants); persistently low (136 [6%] participants); early low, accelerated growth, normal decline (196 [8%] participants); persistently high (293 [12%] participants); below average (772 [32%] participants); and average (944 [39%] participants). The three trajectories early below average, accelerated decline; persistently low; and below average had increased risk of COPD at age 53 years compared with the average group (early below average, accelerated decline: odds ratio 35.0, 95% CI 19.5-64.0; persistently low: 9.5, 4.5-20.6; and below average: 3.7, 1.9-6.9). Early-life predictors of the three trajectories included childhood asthma, bronchitis, pneumonia, allergic rhinitis, eczema, parental asthma, and maternal smoking. Personal smoking and active adult asthma increased the impact of maternal smoking and childhood asthma, respectively, on the early below average

Rationale: Childhood risk factors for long-term lung health often coexist and their specific patterns may affect subsequent lung function differently. Objective(s): To identify childhood risk factor profiles and their influence on lung function and chronic obstructive pulmonary disease (COPD) in middle age, and potential pathways. Method(s): Profiles of 11 childhood respiratory risk factors, documented at age 7, were identified in 8,352 participants from the Tasmanian Longitudinal Health Study using latent class analysis. We investigated associations between risk profiles and post-bronchodilator lung function and COPD at age 53, mediation by childhood lung function and adult asthma, and interaction with personal smoking. Result(s): Six risk profiles were identified: 1) unexposed or least exposed (49%); 2) parental smoking (21.5%); 3) allergy (10%); 4) frequent asthma, bronchitis (8.7%); 5) infrequent asthma, bronchitis (8.3%); and 6) frequent asthma, bronchitis, allergy (2.6%). Profile 6 was most strongly associated with lower forced expiratory volume in 1 second (FEV1) (2261; 95% confidence interval, 2373 to 2148 ml); lower FEV1/forced vital capacity (FVC) (23.4; 24.8 to 21.9%) and increased COPD risk (odds ratio, 4.9; 2.1 to 11.0) at age 53. The effect of profile 6 on COPD was largely mediated by adult active asthma (62.5%) and reduced childhood lung function (26.5%). Profiles 2 and 4 had smaller adverse effects than profile 6. Notably, the effects of profiles 2 and 6 were synergistically stronger for smokers. Conclusion(s): Profiles of childhood respiratory risk factors predict middle-age lung function levels and COPD risk. Specifically, children with frequent asthma attacks and allergies, especially if they also become adult smokers, are the most vulnerable group. Targeting active asthma in adulthood (i.e., a dominant mediator) and smoking (i.e., an effect modifier) may block causal pathways and lessen the effect of such established early-life exposures.Copyrigh

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-alpha (TNF-alpha) 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.Copyright © 2017 by the authors.Licensee MDPI, Basel, Switzerland.

Introduction/Aim: Individuals with different patterns of lung function growth and decline may have different risks for developing COPD. We investigated trajectories of lung function from childhood to middle age and their associated childhood factors. Method(s): Using 2142 subjects from the Tasmanian Longitudinal Health Study, pre-bronchodilator FEV1, measured at 7, 13, 18, 45, 50 and 53 years, was modelled with Group Based Trajectory Modelling. Logistic regression was used to investigate the relationship between childhood factors and trajectory groups. Result(s): The best fit model showed six distinct trajectories (Figure 1). Based on initial lung function at 7 years, lung function growth and decline rates, the trajectories were labelled as "early low, reduced growth, accelerated decline" (7.4%; n = 159), "early normal/high, normal growth, accelerated decline" (5%; n = 107), "early low, normal growth, normal decline" (28.7%; n = 615), "early low, accelerated growth, normal decline" (4.2%, n = 90), "persistently high" (14%; n = 300) and "normal" (40.7%; n = 871). The first three trajectories had increased risk of COPD (post-bronchodilator FEV1/ FVC < LLN) at age 53 years compared with the "normal" group. Childhood asthma, bronchitis, pneumonia/pleurisy, maternal asthma and maternal smoking were positively associated with these three trajectories while negative associations were observed for breast feeding and childhood overweight (Figure presented). Conclusion(s): This is the first study to develop lung function trajectories from childhood to middle age in a general population. We identified three trajectories for increased risk of COPD: (1) only accelerated lung decline in adulthood, (2) low initial lung function in childhood with normal growth and normal decline, and (3) low initial lung function in childhood with reduced growth and accelerated decline. Important modifiable childhood risk factors for these three trajectories included exposure to maternal smoking in

We aimed to systematically review the Berlin questionnaire as a screening tool for obstructive sleep apnea. We systematically searched PubMed, Embase, and Scopus databases, reviewed articles reporting the Berlin questionnaire's diagnostic utility as measured against type-1 polysomnography, and performed meta-analyses where possible. Thirty five eligible articles showed that the Berlin questionnaire's diagnostic utility varied by study population, definition of hypopnea used, and apnea-hypopnea index threshold used. It had good sensitivity and specificity for detecting clinically relevant obstructive sleep apnea as well as any obstructive sleep apnea in the sleep clinic population. Despite limited evidence, it showed modest to high sensitivity for detecting clinically relevant obstructive sleep apnea or any obstructive sleep apnea in other clinical and general population subgroups. Its specificity was relatively low. Possible reasons for variability in reported diagnostic utility of the Berlin questionnaire are multifaceted. We conclude that the Berlin questionnaire is useful as a clinical screening test and epidemiological tool in the sleep clinic population. Despite limited evidence, it likely has potential clinical and research utility in other populations. Adopting more consistent methodological definitions and focussing more on the general population and specific clinical populations to determine its usefulness as a clinical or epidemiological screening tool are recommended.Copyright © 2017