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Background: Recent evidence suggests that parental exposures before conception can increase the risk of asthma in offspring. Objective(s): We investigated the association between parents' preconception body mass index (BMI) trajectories from childhood to adolescence and subsequent risk of asthma in their offspring. Method(s): Using group-based trajectory modeling from the Tasmanian Longitudinal Health Study, we identified BMI trajectories for index participants (parents) when aged 4 years to 15 years. Multinomial regression models adjusted for potential confounders were utilized to estimate the association between these early-life parents' BMI trajectories and asthma phenotypes in their subsequent offspring. Result(s): The main analysis included 1822 parents and 4208 offspring. Four BMI trajectories from age 4 years to 15 years were identified as the best-fitting model: low (8.8%), normal (44.1%), above normal (40.2%), and high (7.0%). Associations were observed between father's high BMI trajectory and risk of asthma in offspring before the age of 10 years (relative risk ratio [RRR] =1.70 [95% CI = 0.98-2.93]) and also asthma ever (RRR = 1.72 [95% CI = 1.00-2.97]), especially allergic asthma ever (RRR = 2.05 [95% CI = 1.12-3.72]). These associations were not mediated by offspring birth weight. No associations were observed for maternal BMI trajectories and offspring asthma phenotypes. Conclusion(s): This cohort study over 6 decades of life and across 2 generations suggests that the high BMI trajectory in fathers, well before conception, increased the risk of asthma in their offspring.Copyright © 2022 American Academy of Allergy, Asthma & Immunology

Background and objective Different lung function trajectories through life can lead to COPD in adulthood. This study investigated whether circulating levels of biomarkers can differentiate those with accelerated (AD) from normal decline (ND) trajectories. Methods The Tasmanian Longitudinal Health Study (TAHS) is a general population study that measured spirometry and followed up participants from ages 7 to 53 years. Based on their forced expiratory volume in 1 s (FEV1) trajectories from age 7 to 53 years, this analysis included those with COPD at age 53 years (60 with AD and 94 with ND) and controls (n=720) defined as never-smokers with an average FEV1 trajectory. Circulating levels of selected biomarkers determined at 53 and 45 years of age were compared between trajectories. Results Results showed that CC16 levels (an anti-inflammatory protein) were lower and C-reactive protein (CRP) (a pro-inflammatory marker) higher in the AD than in the ND trajectory. Higher CC16 levels were associated with a decreased risk of belonging to the AD trajectory (OR=0.79 (0.63-0.98) per unit increase) relative to ND trajectory. Higher CRP levels were associated with an increased risk of belonging to the AD trajectory (OR=1.07, 95% CI: 1.00-1.13, per unit increase). Levels of CC16 (area under the curve (AUC) =0.69, 95% CI: 0.56-0.81, p=0.002), CRP (AUC=0.63, 95% CI: 0.53-0.72, p=0.01) and the combination of both (AUC=0.72, 95% CI: 0.60-0.83, p<0.001) were able to discriminate between the AD and ND trajectories. Other quantified biomarkers (interleukin (IL)-4, IL-5, IL-6, IL-10 and tumour necrosis factor-alpha (TNF-alpha)) were not significantly different between AD, ND and controls. Conclusions Circulating levels of CRP and CC16 measured in late adulthood identify different lung function trajectories (AD versus ND) leading to COPD at age 53 years.Copyright © The authors 2021.

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. Method(s): Ambient air pollution exposures (distance from a major road, nitrogen dioxide [NO2], fine particulate matter with an aerodynamic diameter <=2.5 microm [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. Result(s): 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 microg/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(s): Increased exposure to residential ambient air pollutants was associated with an increased odds of eczema, only in males, and aeroallergen sensitization in both genders.Copyright © 2021 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd.

Background: Human milk oligosaccharides (HMO) are a diverse range of sugars secreted in breast milk that have direct and indirect effects on immunity. The profiles of HMOs produced differ between mothers. Objective(s): We sought to determine the relationship between maternal HMO profiles and offspring allergic diseases up to age 18 years. Method(s): Colostrum and early lactation milk samples were collected from 285 mothers enrolled in a high-allergy-risk birth cohort, the Melbourne Atopy Cohort Study. Nineteen HMOs were measured. Profiles/patterns of maternal HMOs were determined using LCA. Details of allergic disease outcomes including sensitization, wheeze, asthma, and eczema were collected at multiple follow-ups up to age 18 years. Adjusted logistic regression analyses and generalized estimating equations were used to determine the relationship between HMO profiles and allergy. Result(s): The levels of several HMOs were highly correlated with each other. LCA determined 7 distinct maternal milk profiles with memberships of 10% and 20%. Compared with offspring exposed to the neutral Lewis HMO profile, exposure to acidic Lewis HMOs was associated with a higher risk of allergic disease and asthma over childhood (odds ratio asthma at 18 years, 5.82; 95% CI, 1.59-21.23), whereas exposure to the acidic-predominant profile was associated with a reduced risk of food sensitization (OR at 12 years, 0.08; 95% CI, 0.01-0.67). Conclusion(s): In this high-allergy-risk birth cohort, some profiles of HMOs were associated with increased and some with decreased allergic disease risks over childhood. Further studies are needed to confirm these findings and realize the potential for intervention.Copyright © 2020 American Academy of Allergy, Asthma & Immunology

Introduction: We investigated if long-term household air pollution (HAP) is associated with asthma and lung function decline in middle-aged adults, and whether these associations were modified by glutathione S-transferase (GST) gene variants, ventilation and atopy. Material(s) and Method(s): Prospective data on HAP (heating, cooking, mould and smoking) and asthma were collected in the Tasmanian Longitudinal Health Study (TAHS) at mean ages 43 and 53 years (n=3314). Subsamples had data on lung function (n=897) and GST gene polymorphisms (n=928). Latent class analysis was used to characterise longitudinal patterns of exposure. Regression models assessed associations and interactions. Result(s): We identified seven longitudinal HAP profiles. Of these, three were associated with persistent asthma, greater lung function decline and % reversibility by age 53 years compared with the "Least exposed" reference profile for those who used reverse-cycle air conditioning, electric cooking and no smoking. The "All gas" (OR 2.64, 95% CI 1.22-5.70), "Wood heating/smoking" (OR 2.71, 95% CI 1.21-6.05) and "Wood heating/gas cooking" (OR 2.60, 95% CI 1.11-6.11) profiles were associated with persistent asthma, as well as greater lung function decline and % reversibility. Participants with the GSTP1 Ile/Ile genotype were at a higher risk of asthma or greater lung function decline when exposed compared with other genotypes. Exhaust fan use and opening windows frequently may reduce the adverse effects of HAP produced by combustion heating and cooking on current asthma, presumably through increasing ventilation. Conclusion(s): Exposures to wood heating, gas cooking and heating, and tobacco smoke over 10 years increased the risks of persistent asthma, lung function decline and % reversibility, with evidence of interaction by GST genes and ventilation.Copyright © ERS 2021

Background: Longitudinal trajectories of asthma and allergies from childhood to adulthood might be differentially associated with lung function and chronic obstructive pulmonary disease (COPD), but associations with extrapulmonary comorbidities have not been well investigated. We aimed to assess these trajectories and examine their associations with lung function outcomes and profiles of comorbidities. Method(s): In this prospective cohort study, data for asthma and related allergic conditions (ie, eczema, hay fever, and food allergy) were prospectively collected from the Tasmanian Longitudinal Health Study for participants aged 7-53 years originally recruited in Tasmania, Australia. All surviving individuals in the database with contact details were invited in the most recent follow-up (mean age 53 years). There were no exclusion criteria. With use of latent class analysis, we identified longitudinal trajectories of asthma and allergic conditions from 7-53 years, and profiles of self-reported extrapulmonary conditions recorded at 53 years. The associations between asthma and allergy trajectories and morbidity profiles and lung function at 53 years were investigated with regression models. Finding(s): Between Sept 3, 2012, and Nov 8, 2016, of 6128 individuals invited, 3609 (58.9%) individuals were enrolled. We identified five asthma and allergy trajectories: minimal and least asthma and allergies (n= 1767 [49.0%]); late-onset hay fever, no asthma (n=1065 [29.5%]); early-onset remitted asthma and allergies (n=236 [6.5%]); late-onset asthma and allergies (n=317 [8.8%]); and early-onset persistent asthma and allergies (n=224 [6.2%]); and four profiles of extrapulmonary morbidities: minimal or least disease (n=2206 [61.1%]); dominant mental health disorders (n=861 [23.9%]); dominant cardiovascular diseases or risks (n=424 [11.7%]); and multiple disorders (n=117 [3.2%]). The late-onset asthma and allergies trajectory was predominantly associated with the multiple disorde

Bronchodilator reversibility (BDR) is often used as a diagnostic test for adult asthma. However, there has been limited assessment of its diagnostic utility. We aimed to determine the discriminatory accuracy of common BDR cut-offs in the context of current asthma and asthma-COPD overlap (ACO) in a middle-aged community sample. The Tasmanian Longitudinal Health Study is a population-based cohort first studied in 1968 (n=8583). In 2012, participants completed respiratory questionnaires and spirometry (n=3609; mean age 53 years). Receiver operating characteristic (ROC) curves were fitted for current asthma and ACO using continuous BDR measurements. Diagnostic parameters were calculated for different categorical cut-offs. Area under the ROC curve (AUC) was highest when BDR was expressed as change in forced expiratory volume in 1 s (FEV1) as a percentage of initial FEV1, as compared with predicted FEV1. The corresponding AUC was 59% (95% CI 54-64%) for current asthma and 87% (95% CI 81-93%) for ACO. Of the categorical cut-offs examined, the European Respiratory Society/American Thoracic Society threshold (12% from baseline and 200 mL) was assessed as providing the best balance between positive and negative likelihood ratios (LR+ and LR-, respectively), with corresponding sensitivities and specificities of 9% and 97%, respectively, for current asthma (LR+ 3.26, LR- 0.93), and 47% and 97%, respectively, for ACO (LR+ 16.05, LR- 0.55). With a threshold of 12% and 200 mL from baseline, a positive BDR test provided a clinically meaningful change in the post-test probability of disease, whereas a negative test did not. BDR was more useful as a diagnostic test in those with co-existent post-bronchodilator airflow obstruction (ACO).Copyright © ERS 2021.

Little is known about the association between ambient temperature and DNA methylation, which is a potential biological process through which ambient temperature affects health. This study aimed to evaluate the association between ambient temperature and DNA methylation across human genome. We included 479 Australian women, including 132 twin pairs and 215 sisters of these twins. Blood-derived DNA methylation was measured using the HumanMethylation450 BeadChip array. Data on average ambient temperature during eight different exposure windows [lag0d (the blood draw day), lag0-7d (the current day and previous seven days prior to blood draw), lag0-14d, lag0-21d, lag0-28d, lag0-90d, lag0-180d, and lag0-365d)] was linked to each participant's home address. For each cytosine-guanine dinucleotide (CpG), we evaluated the association between its methylation level and temperature using generalized estimating equations (GEE), adjusting for important covariates. We used comb-p and DMRcate to identify differentially methylated regions (DMRs). We identified 31 CpGs at which blood DNA methylation were significantly associated with ambient temperature with false discovery rate [FDR] < 0.05. There were 82 significant DMRs identified by both comb-p (Sidak p-value < 0.01) and DMRcate (FDR < 0.01). Most of these CpGs and DMRs only showed association with temperature during one specific exposure window. These CpGs and DMRs were mapped to 85 genes. These related genes have been related to many human chronic diseases or phenotypes (e.g., diabetes, arthritis, breast cancer, depression, asthma, body height) in previous studies. The signals of short-term windows (lag0d and lag0-21d) showed enrichment in biological processes related to cell adhesion. In conclusion, short-, medium-, and long-term exposures to ambient temperature were all associated with blood DNA methylation, but the target genomic loci varied by exposure window. These differential methylation signals may serve as potential bio

Background: DNA methylation is a potential biological mechanism through which residential greenness affects health, but little is known about its association with greenness and whether the association could be modified by genetic background. We aimed to evaluate the association between surrounding greenness and genome-wide DNA methylation and potential gene-greenness interaction effects on DNA methylation. Method(s): We measured blood-derived DNA methylation using the HumanMethylation450 BeadChip array (Illumina) for 479 Australian women, including 66 monozygotic, 66 dizygotic twin pairs, and 215 sisters of these twins. Surrounding greenness was represented by Normalized Difference Vegetation Index (NDVI) and Enhanced Vegetation Index (EVI) within 300, 500, 1000 or 2000 m surrounding participants' home addresses. For each cytosine-guanine dinucleotide (CpG), the associations between its methylation level and NDVI or EVI were evaluated by generalized estimating equations, after adjusting for age, education, marital status, area-level socioeconomic status, smoking behavior, cell-type proportions, and familial clustering. We used comb-p and DMRcate to identify significant differentially methylated regions (DMRs). For each significant CpG, we evaluated the interaction effects of greenness and single-nucleotide polymorphisms (SNPs) within +/-1 Mb window on its methylation level. Result(s): We found associations between surrounding greenness and blood DNA methylation for one CpG (cg04720477, mapped to the promoter region of CNP gene) with false discovery rate [FDR] < 0.05, and for another 9 CpGs with 0.05 <= FDR < 0.10. For two of these CpGs, we found 33 SNPs significantly (FDR < 0.05) modified the greenness-methylation association. There were 35 significant DMRs related to surrounding greenness that were identified by both comb-p (Sidak p-value < 0.01) and DMRcate (FDR < 0.01). Those CpGs and DMRs were mapped to genes related to many human diseases, such as mental health

BACKGROUND: High surrounding greenness has many health benefits and might contribute to slower biological aging. However, very few studies have evaluated this from the perspective of epigenetics. OBJECTIVE(S): We aimed to evaluate the association between surrounding greenness and biological aging based on DNA methylation. METHOD(S): We derived Horvath's DNA methylation age (DNAmAge), Hannum's DNAmAge, PhenoAge, and GrimAge based on DNA methylation measured in peripheral blood samples from 479 Australian women in 130 families. Measures of DNAmAge acceleration (DNAmAgeAC) were derived from the residuals after regressing each DNAmAge metric on chronological age. Greenness was represented by satellite-derived Normalized Difference Vegetation Index (NDVI) and Enhanced Vegetation Index (EVI) metrics within 300-, 500-, 1,000-, and 2,000-m buffers surrounding par-ticipant addresses. Greenness-DNAmAgeAC associations were estimated using a within-sibship design fitted by linear mixed effect models, adjusting for familial clustering and important covariates. RESULT(S): Greenness metrics were associated with significantly lower DNAmAgeAC based on GrimAge acceleration, suggesting slower biological aging with higher greenness based on both NDVI and EVI in 300-2,000 m buffer areas. For example, each interquartile range increase in NDVI within 1,000 m was associated with a 0.59 (95% CI: 0.18, 1.01)-year decrease in GrimAge acceleration. Greenness was also inversely associated with three of the eight components of GrimAge, specifically, DNA methylation-based surrogates of serum cystatin-C, serum growth differentiation factor 15, and smoking pack years. Associations between greenness and biological aging measured by Horvath's and Hannum's DNAmAgeAC were less consistent, and depended on neighborhood socioeconomic status. No significant associations were estimated for PhenoAge acceleration. DISCUSSION: Higher surrounding greenness was associated with slower biological aging, as indicat

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

Introduction Smoking is a leading cause of premature deaths globally. The health benefits of smoking cessation are many. However, majority of quit attempts are unsuccessful. One way to potentially improve success rates is to evaluate new combinations of existing smoking cessation therapies that may work synergistically to decrease the intensity of withdrawal symptoms and cravings. Aims To evaluate the feasibility, efficacy and safety of the combination of varenicline and nicotine replacement therapy (NRT) lozenges versus varenicline alone in assisting hospitalised smokers to quit. Methods and analysis This is a multicentre, randomised, placebo-controlled trial. Adults with a history of smoking >=10 cigarettes per day on average in the 4 weeks prior to their hospitalisation will be recruited. Participants will be randomly assigned to either the intervention group and will receive varenicline and NRT lozenges, or the control group and will receive varenicline and placebo lozenges. All participants will be actively referred to behavioural support from telephone Quitline. Participants are followed up at 1 and 3 weeks and 3, 6 and 12 months from the start of treatment. The primary outcome is carbon monoxide validated prolonged abstinence from 2 weeks to 6 months after treatment initiation. Secondary outcomes include self-reported and biochemically validated prolonged and point prevalence abstinence at 3, 6 and 12 months, self-reported adverse events, withdrawal symptoms and cravings, adherence to treatment, Quitline sessions attended and others. According to the Russell Standard, all randomised participants will be accounted for in the primary intention-to-treat analysis. Ethics and dissemination The trial will be conducted in compliance with the protocol, the principles of Good Clinical Practice, the National Health and Medical Research Council National Statement on Ethical Conduct in Human Research (updated 2015) and the Australian Code for the Responsible Conduct of R

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

Rationale: The prevalence of Obstructive sleep apnoea (OSA) has increased in the recent past and there is increasing interest in its aetiology. However, there is limited and equivocal evidence that low FEV1 is associated with OSA. We aimed to determine whether lung function trajectories across the first fifty years of life were associated with OSA. Method(s): Within a whole-ofpopulation cohort (n=2,659) with spirometry assessed at ages of 7, 13, 18, 45, 50 and 53 years, we have previously identified six lung function trajectories. These trajectories were 'average', 'persistently low', 'early below average, accelerated decline', 'early low, accelerated growth, normal decline', 'below average', and 'persistently high'. Outcomes were medically confirmed OSA, and likely-OSA that was defined using the high specificity cut-off score of STOP-Bang (score >=5). Associations between lung function trajectories and confirmed or likely OSA were assessed using logistic regression models. Association between lung function trajectories and likely or confirmed OSA when accounting for the effects of COPD and asthma was also assessed using multinomial logistic regression. Result(s): Three lung function trajectories were significantly associated with likely or confirmed OSA. These were 'below average' (OR 1.4 [95%CI 1.1, 1.8] for likely OSA and 1.7 [1.1, 2.6] for confirmed OSA); 'early below average, accelerated decline' (OR 1.9 [1.2, 3.2] for likely OSA and 1.2 [0.5, 3.1] for confirmed OSA), and 'persistently low' (OR 2.2 [1.4, 3.4] for likely OSA and 2.2 [1.1, 4.5] for confirmed OSA). Consistent associations were seen between these three lung function trajectories and likely or confirmed OSA without coexisting COPD. Consistent results were also seen for Berlin Questionnaire and OSA-50 Questionnaire, as for STOP-Bang (see Table). Conclusion(s): We provide the first evidence that lung function trajectories characterized with lower lung function from childhood with or without rapid decl

Objective: To examine the utility of apnoea screening questionnaires, alone and in combination with the Epworth sleepiness scale (ESS), for detecting obstructive sleep apnoea (OSA) in primary care. Design, setting: Prospective validation study in an Australian general population cohort. Participant(s): 424 of 772 randomly invited Tasmanian Longitudinal Health Study, 6th decade follow-up participants with OSA symptoms (mean age, 52.9 years; SD, 0.9 year) who completed OSA screening questionnaires and underwent type 4 sleep studies. Main Outcome Measure(s): Clinically relevant OSA, defined as moderate to severe OSA (15 or more oxygen desaturation events/hour), or mild OSA (5-14 events/hour) and excessive daytime sleepiness (ESS >= 8); diagnostic test properties of the Berlin (BQ), STOP-Bang and OSA-50 questionnaires, alone or combined with an ESS >= 8. Result(s): STOP-Bang and OSA-50 correctly identified most participants with clinically relevant OSA (sensitivity, 81% and 86% respectively), but with poor specificity (36% and 21% respectively); the specificity (59%) and sensitivity of the BQ (65%) were both low. When combined with the criterion ESS >= 8, the specificity of each questionnaire was high (94-96%), but sensitivity was low (36-51%). Sensitivity and specificity could be adjusted according to specific needs by varying the STOP-Bang cut-off score when combined with the ESS >= 8 criterion. Conclusion(s): For people likely to trigger OSA assessment in primary care, the STOP-Bang, BQ, and OSA-50 questionnaires, combined with the ESS, can be used to rule in, but not to rule out clinically relevant OSA. Combined use of the STOP-Bang with different cut-off scores and the ESS facilitates a flexible balance between sensitivity and specificity.Copyright © 2019 AMPCo Pty Ltd

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. Objective(s): 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. Method(s): 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. Result(s): 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.Copyright © 2018 John Wiley & Sons Ltd

Rationale: Measles infection in childhood was common until immunization was widely available, and has been associated with reduced atopy in later life, but not in allergic diseases per se. There was a marked reduction in house dust mite (HDM) sensitization among young Africans aged 14-21 years who survived a measles epidemic in early childhood, compared with the reference group without clinically apparent measles but who were offered immunization 6-12 months post-epidemic (1). We had the unique opportunity to assess whether childhood measles infection modulated the relationship between childhood allergy and atopic asthma in a non-immunized Australian cohort, currently followed to middle-age. Method(s): Data were from the population-based Tasmanian Longitudinal Health Study (TAHS) cohort born in 1961. Parental report of eczema-ever was recorded at the initial 1968 survey, and measles history was recorded by Tasmanian school health records. At the 2012-2015 follow-up, atopic asthma was defined by self-reported doctor-diagnosed asthma with skin prick test (SPT) positivity to at least one food and/or aeroallergen. Multivariable regression was used including interaction terms. Result(s): Of 1,622 participants aged 51-55 years, 69.7% (n = 1,131) had parental report of measles infection in childhood. While there was no significant association with measles in the absence of childhood eczema [odds ratio (OR) 1.23 (95% confidence interval [CI]: 0.87-1.74), p=0.24], a reduced risk between childhood measles and adult atopic asthma was observed for those with childhood eczema [OR 0.48 (0.26-0.91), p=0.023, p-interaction=0.029]. This non-synergistic interaction was present for adult sensitization to HDM, cat and pollen (p-interaction=0.028, 0.036 and 0.052 respectively). A similar interaction was seen for the outcome of sensitization to HDM in middle-age, regardless of adult asthma status (p-interaction=0.003). There was also some evidence that childhood measles was associated wi

The concordance of different indices from type-4 sleep studies in diagnosing and categorising the severity of obstructive sleep apnoea is not known. This is a critical gap as type-4 sleep studies are used to diagnose obstructive sleep apnoea in some settings. Therefore, we aimed to determine the concordance between flow-based apnoea-hypopnoea index (AHIflow50%) and oxygen desaturation index (ODI3%) by measuring them concurrently. Using a random sub-sample of 296 from a population-based cohort who underwent two-channel type-4 sleep studies, we assessed the concordance between AHIflow50% and ODI3%. We compared the prevalence of obstructive sleep apnoea of various severities as identified by the two methods, and determined their concordance using coefficient Kappa(kappa). Participants were aged (mean +/- SD) 53 +/- 0.9 years (48% male). The body mass index was 28.8 +/- 5.2 kg m-2 and neck circumference was 37.4 +/- 3.9 cm. The median AHIflow50% was 5 (inter-quartile range 2, 10) and median ODI3% was 9 (inter-quartile range 4, 15). The obstructive sleep apnoea prevalence reported using AHIflow50% was significantly lower than that reported using ODI3% at all severity thresholds. Although 90% of those with moderate-severe obstructive sleep apnoea classified using AHIflow50% were identified by using ODI3%, only 46% of those with moderate-severe obstructive sleep apnoea classified using ODI3% were identified by AHIflow50%. The overall concordance between AHIflow50% and ODI3% in diagnosing and classifying the severity of obstructive sleep apnoea was only fair (kappa = 0.32), better for males (kappa = 0.42 [95% confidence interval 0.32-0.57] versus 0.22 [95% confidence interval 0.09-0.31]), and lowest for those with a body mass index >= 35 (kappa = 0.11). In conclusion, ODI3% and AHIflow50% from type-4 sleep studies are at least moderately discordant. Until further evidence is available, the use of ODI3% as the measure of choice for type-4 sleep studies is recommended cautiou

Background: Exposure to far-field radiofrequency electromagnetic fields (RF-EMF) has raised public concerns in recent decades. However, it is not known if individuals' perception towards the health risks of RF-EMF is dependent on their knowledge of the objectively measured personal RF-EMF exposure levels. Objective(s): This pilot study aimed to demonstrate the feasibility of objectively measuring personal RF-EMF exposure from mobile phone base stations (MPBS) and to determine if the risk perception of people to the potential health risk of exposure to RF-EMF from MPBS is dependent on their knowledge of personal RF-EMF exposure levels. Design(s): An experimental study was conducted in 383 adults, recruited in Melbourne, Australia. Participants were randomized to one of the three groups: 1) basic information group who were provided with basic information about RF-EMF to read prior to completing a risk perception assessment questionnaire; 2) precautionary group who were provided with an information pack which included precautionary messages; and 3) personal exposure measurement group who were provided with a summary of their quantitative RF-EMF exposure from MPBS. The same basic information about RF-EMF was also given to the precautionary and personal exposure measurement groups. Result(s): Participants had a mean (+/- SD) age of 36.9 +/- 12.5 years; 66.7% were women. Overall, 44.1% had noticed an MPBS in their neighbourhood. The mean (SD) values (from 1 to 7) for risk perceptions to RF-EMF from MPBS were 4.02 (1.67) for basic information, 3.82 (1.62) for precautionary messages, and 3.97 (1.72) for the personal exposure measurement groups. These differences were not statistically significant. Nevertheless, the personal exposure measurement group were more confident that they could protect themselves from RF-EMF than the precautionary or basic information groups. Conclusion(s): Our findings suggest that providing people with personal RF-EMF exposure measurements may not

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