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Interest in lifetime lung function trajectories has increased in the context of emerging evidence that chronic obstructive pulmonary disease (COPD) can arise from multiple disadvantaged lung function pathways, including those that stem from poor lung function in childhood. To our knowledge, no previous study has investigated both obstructive and restrictive lifetime patterns concurrently, while accounting for potential overlaps between them. We aimed to investigate lifetime trajectories of the FEVUsing z scores from spirometry measured at ages 7, 13, 18, 45, 50, and 53 years in the Tasmanian Longitudinal Health Study (n=2422), we identified six FEVThe prevalence of the four lifetime spirometry patterns was as follows: low FEVTo our knowledge, this is the first study to characterise lifetime phenotypes of obstruction and restriction simultaneously using objective data-driven techniques and unique life course spirometry measures of FEVNational Health and Medical Research Council of Australia, The University of Melbourne, Clifford Craig Medical Research Trust of Tasmania, The Victorian, QueenslandTasmanian Asthma Foundations, The Royal Hobart Hospital, Helen MacPherson Smith Trust, and GlaxoSmithKline.

Background/Objective Obesity is a risk factor for multimorbidity, including depression and possibly anxiety. However, it is currently unclear how patterns of change in BMI over the life course differentially influence the magnitude in risk of depression and anxiety in mid-adulthood. We aimed to examine associations between BMI trajectories from childhood to adulthood and the risk of depression and anxiety in middle age. Methods In the Tasmanian Longitudinal Health Study (n = 2416), five distinct BMI trajectories were previously defined from age 5 to 45 years using group-based modelling. At age 53, current depression and anxiety were assessed using the Patient Health Questionnaire and the Generalized Anxiety Disorder scale, respectively. Logistic regression models adjusted for potential confounders estimated associations between BMI trajectories and these outcomes. Results Those belonging to the child average-increasing (OR = 2.24; 95%CI: 1.24, 4.06) and persistently high (OR = 2.64; 1.26, 5.52) trajectories were more likely to have depression in middle age, compared to the persistently average trajectory. However, the odds of experiencing greater severity of depressive symptoms was highest in the child average-increasing group (OR = 2.36; 1.59, 3.49). Despite finding no evidence of association between BMI trajectories and current anxiety, we observed less severe symptoms in the child high-decreasing trajectory (OR = 0.68; 0.51, 0.91). Conclusion We found an increased risk of depression in middle age among individuals with a persistently high BMI from childhood to mid-adulthood and individuals with an average BMI in childhood which then increased consistently throughout adulthood. Encouragingly, resolving childhood adiposity by adulthood was associated with lesser anxiety symptoms. Taken together, these findings highlight the need to target mental health screening and treatment towards high-risk BMI trajectory groups and the importance of early interventions to prevent and resolve excess weight.

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.

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.

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.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).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.Eczema is common both in children and adults. The proportion of severe eczema in children was substantial.

The extent to which biomarkers of asthma activity persist in spontaneous asthma remission and whether such markers are associated with future respiratory outcomes remained unclear. We investigated the association between sub-clinical inflammation in adults with spontaneous asthma remission and future asthma relapse and lung function decline.The Tasmanian Longitudinal Health Study is a population-based cohort (n = 8583). Biomarkers of systemic inflammation were measured on participants at age 45, and latent profile analysis was used to identify cytokine profiles. Bronchial hyperresponsiveness (BHR) and nitric oxide products in exhaled breath condensate (EBC NOx) were measured at age 50. Participants with spontaneous asthma remission at ages 45 (n = 466) and 50 (n = 318) were re-evaluated at age 53, and associations between baseline inflammatory biomarkers and subsequent asthma relapse and lung function decline were assessed.We identified three cytokine profiles in adults with spontaneous asthma remission: average (34%), Th2-high (42%) and Th2-low (24%). Compared to the average profile, a Th2-high profile was associated with accelerated decline in post-BD FEVBHR and serum inflammatory cytokines have prognostic value in adults with spontaneous asthma remission. At-risk individuals with BHR, Th2-high or Th2-low cytokine profiles may benefit from closer monitoring and on-going follow-up.

BackgroundRecent evidence suggests that parental exposures before conception can increase the risk of asthma in offspring.ObjectiveWe investigated the association between parents' preconception body mass index (BMI) trajectories from childhood to adolescence and subsequent risk of asthma in their offspring.MethodsUsing 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.ResultsThe 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.ConclusionThis 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.

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.

Coal mine lung dust disease (CMDLD) and artificial stone (AS) silicosis are preventable diseases which have occurred in serious outbreaks in Australia recently. This has prompted a TSANZ review of Australia's approach to respiratory periodic health surveillance. While regulating respirable dust exposure remains the foundation of primary and secondary prevention, identification of workers with early disease assists with control of further exposure, and with the aims of preserving lung function and decreasing respiratory morbidity in those affected. Prompt detection of an abnormality also allows for ongoing respiratory specialist clinical management. This review outlines a medical framework for improvements in respiratory surveillance to detect CMDLD and AS silicosis in Australia. This includes appropriate referral, improved data collection and interpretation, enhanced surveillance, the establishment of a nationwide Occupational Lung Disease Registry and an independent advisory group. These measures are designed to improve health outcomes for workers in the coal mining, AS and other dust‐exposed and mining industries.

Background The association between grass pollen exposure and early markers of asthma exacerbations such as lung function changes and increase in airway inflammation is limited. We investigated the associations between short-term grass pollen exposure and lung function and airway inflammation in a community-based sample, and whether any such associations were modified by current asthma, current hay fever, pollen sensitization, age, and other environmental factors. Methods Cross-sectional and short-term analyses of data from the Melbourne Atopy Cohort Study (MACS) participants (n = 936). Lung function was assessed using spirometry. Airway inflammation was assessed by fractional exhaled nitric oxide (FeNO) and exhaled breath condensate pH and nitrogen oxides (NOx). Daily pollen counts were collected using a volumetric spore trap. The associations were examined by linear regression. Results Higher ambient levels of grass pollen 2 days before (lag 2) were associated with lower mid-forced expiratory flow (FEF25%-75%) and FEV1/FVC ratio (Coef. [95% CI] = −119 [−226, −11] mL/s and −1.0 [−3.0, −0.03] %, respectively) and also 3 days before (lag 3). Increased levels of grass pollen a day before (lag 1) were associated with increased FeNO (4.35 [−0.1, 8.7] ppb) and also at lag 2. Adverse associations between pollen and multiple outcomes were greater in adults with current asthma, hay fever, and pollen sensitization. Conclusion Grass pollen exposure was associated with eosinophilic airway inflammation 1-2 days after exposure and airway obstruction 2-3 days after exposure. Adults and individuals with asthma, hay fever, and pollen sensitization may be at higher risk.

The heterogeneity of development and progression of eczema suggests multiple underlying subclasses for which aetiology and prognosis may vary. A better understanding may provide a comprehensive overview of eczema development and progression in childhood. Thus, we aimed to determine longitudinal eczema subclasses based on assessments and identify their associations with risk factors and allergic outcomes.A total of 619 participants with a family history of allergic disease were assessed at 24 time-points from birth to 12 years. At each time, eczema was defined as the report of current rash treated with topical steroid-based preparations. Longitudinal latent class analysis was used to determine eczema subclasses. Subsequent analyses using regression models assessed the associations between eczema subclasses and potential risk factors and allergic outcomes at 18- and 25-year follow-ups (eczema, allergic rhinitis, asthma and allergic sensitization).We identified five eczema subclasses 'early-onset persistent', 'early-onset resolving', 'mid-onset persistent', 'mid-onset resolving' and 'minimal eczema'. Filaggrin null mutations were associated with the early-onset persistent (OR = 2.58 [1.09-6.08]) and mid-onset persistent class (OR = 2.58 [1.32-5.06]). Compared with 'minimal eczema', participants from early-onset persistent class had higher odds of eczema (OR = 11.8 [5.20-26.6]) and allergic rhinitis (OR = 3.13 [1.43-6.85]) at 18 and at 25 years eczema (OR = 9.37 [3.17-27.65]), allergic rhinitis (OR = 3.26 [1.07-9.93]) and asthma (OR = 2.91 [1.14-7.43]). Likewise, mid-onset persistent class had higher odds of eczema (OR = 2.59 [1.31-5.14]), allergic rhinitis (OR = 1.70 [1.00-2.89]) and asthma (OR = 2.00 [1.10-3.63]) at 18 and at 25 years eczema (OR = 6.75 [3.11-14-65]), allergic rhinitis (OR = 2.74 [1.28-5.88]) and asthma (OR = 2.50 [1.25-5.00]). Allergic and food sensitization in early life was more common in those in the persistent eczema subclasses.We identified five distinct eczema subclasses. These classes were differentially associated with risk factors, suggesting differences in aetiology, and also with the development of allergic outcomes, highlighting their potential to identify high-risk groups for close monitoring and intervention.

BackgroundChronic bronchitis in childhood is associated with a diagnosis of asthma and/or bronchiectasis a few years later, however, consequences into middle-age are unknown.ObjectiveTo investigate the relationship between childhood bronchitis and respiratory-related health outcomes in middle-age.DesignCohort study from age 7 to 53 years.SettingGeneral population of European descent from Tasmania, Australia.Participants3202 participants of the age 53-year follow-up (mean age 53, range 51–55) of the Tasmanian Longitudinal Health Study cohort who were born in 1961 and first investigated at age 7 were included in our analysis.Statistical methodsMultivariable linear and logistic regression. The association between parent reported childhood bronchitis up to age 7 and age 53-year lung conditions (n=3202) and lung function (n=2379) were investigated.ResultsAmong 3202 participants, 47.5% had one or more episodes of childhood bronchitis, classified according to severity based on the number of episodes and duration as: ‘non-recurrent bronchitis’ (28.1%); ‘recurrent non-protracted bronchitis’ (18.1%) and ‘recurrent-protracted bronchitis’ (1.3%). Age 53 prevalence of doctor-diagnosed asthma and pneumonia (p-trend ConclusionIn this cohort born in 1961, one or more episodes of childhood bronchitis was a frequent occurrence. ‘Recurrent-protracted bronchitis’, while uncommon, was especially linked to multiple respiratory outcomes almost five decades later, including asthma, pneumonia and raised lung gas transfer. These findings provide insights into the natural history of childhood ‘bronchitis’ into middle-age.

Background: A global increase in asthma and COPD incidence has occurred, the cause is unknown. One potential relationship that has yet to be explored is the interaction between blood pressure (BP) and lung function in children 5-17 years old. Our purpose is to assess the relationship between hypotension, hypertension, and lung function in children 5 to 17 years old. Methods: Participants were recruited from elementary and middle schools from 7 cities in northeastern China (N=6,797). BP was categorized into 3 groups: hypotensive (th percentile or 10 years), normotensive and hypertensive (>95th percentile) based on American Academy of Pediatrics standards. Spirometry measured lung function in forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), peak expiratory flow (PEF), and maximum mid expiratory flow (MMEF). Associations were assessed using logistic regression analysis. Results: Decreases in FVC , FEV1, PEF, and MMEF were noted in hypotensive children. Higher FVC, FEV1, PEF, and MMEF were noted among children ³ 10 with hypertension, while children Conclusions: Our findings suggest that, in this study population, hypotension may be associated with decreased lung function, and the increased lung function may be associated with hypertension in children. Future studies are needed to confirm temporality as this is the first study to explore these relationships in children which requires in depth investigation.

BackgroundClassifying individuals at high chronic obstructive pulmonary disease (COPD)-risk creates opportunities for early COPD detection and active intervention.ObjectiveTo develop and validate a statistical model to predict 10-year probabilities of COPD defined by post-bronchodilator airflow obstruction (post-BD-AO; forced expiratory volume in 1 s/forced vital capacitySettingGeneral Caucasian populations from Australia and Europe, 10 and 27 centres, respectively.ParticipantsFor the development cohort, questionnaire data on respiratory symptoms, smoking, asthma, occupation and participant sex were from the Tasmanian Longitudinal Health Study (TAHS) participants at age 41–45 years (n=5729) who did not have self-reported COPD/emphysema at baseline but had post-BD spirometry and smoking status at age 51–55 years (n=2407). The validation cohort comprised participants from the European Community Respiratory Health Survey (ECRHS) II and III (n=5970), restricted to those of age 40–49 and 50–59 with complete questionnaire and spirometry/smoking data, respectively (n=1407).Statistical methodRisk-prediction models were developed using randomForest then externally validated.ResultsArea under the receiver operating characteristic curve (AUCROC) of the final model was 80.8% (95% CI 80.0% to 81.6%), sensitivity 80.3% (77.7% to 82.9%), specificity 69.1% (68.7% to 69.5%), positive predictive value (PPV) 11.1% (10.3% to 11.9%) and negative predictive value (NPV) 98.7% (98.5% to 98.9%). The external validation was fair (AUCROC 75.6%), with the PPV increasing to 17.9% and NPV still 97.5% for adults aged 40–49 years with ≥1 respiratory symptom. To illustrate the model output using hypothetical case scenarios, a 43-year-old female unskilled worker who smoked 20 cigarettes/day for 30 years had a 27% predicted probability for post-BD-AO at age 53 if she continued to smoke. The predicted risk was 42% if she had coexistent active asthma, but only 4.5% if she had quit after age 43.ConclusionThis novel and validated risk-prediction model could identify adults aged in their 40s at high 10-year COPD-risk in the general population with potential to facilitate active monitoring/intervention in predicted ‘COPD cases’ at a much earlier age.

The prevalence of allergic diseases has been increasing for several decades. This has been partly attributed to changing environmental factors such as exposure to traffic-related air pollution (TRAP) and nutrient deficiencies, including vitamin D. Furthermore, population-based studies have suggested that air pollution may contribute to vitamin D deficiency [1], while vitamin D levels may modify pollution-driven asthma symptoms in paediatric obesity [2]. Vitamin D supplementation has also been shown to reduce the effects of pollution on asthma and other chronic respiratory diseases [3]. To date, few mechanistic studies have aimed to identify the pathways that may explain these interactions., This study provides novel insights into mechanisms of traffic-related air pollution-induced allergy by down-regulation via complement regulators (CFI, PROS1 and PLG) and its interaction with vitamin D deficiency via the complement inhibitor PLG https://bit.ly/3x0jYOw

Prematurity has been linked to reduced lung function up to age 33 years, but its long-term effects on lung function and chronic obstructive pulmonary disease (COPD) are unknown. To address this question, we investigated associations between prematurity, lung function, and COPD in the sixth decade of life using data from the Tasmanian Longitudinal Health Study (TAHS).Data were analysed from 1445 participants in the TAHS. Lung function was measured at 53 years of age. Gestational ages were very preterm (28 weeks to32 weeks), moderate preterm (32 weeks to34 weeks), late preterm (34 weeks to37 weeks) and term (≥37 weeks). Linear and logistic regression models were fitted to investigate associations of prematurity with lung function measures (FEVOf 3565 individuals with available data on gestational age from the TAHS cohort, 1445 (41%) participants were included in this study, 740 (51%) of whom were female. Compared with term birth, very to moderate preterm birth was significantly associated with an increased risk of COPD at age 53 years (odds ratio 2·9 [95% CI 1·1-7·7]). Very-to-moderate preterm birth was also associated with lower post-bronchodilator FEVThis is the first study to investigate the effect of prematurity on lung function into middle-age. Data show that very-to-moderate prematurity is associated with obstructive lung function deficits including COPD well into the sixth decade of life and that this effect is compounded by personal smoking.National Health and Medical Research Council (NHMRC) of Australia, European Union's Horizon 2020, The University of Melbourne, Clifford Craig Medical Research Trust of Tasmania, The Victorian, QueenslandTasmanian Asthma Foundations, The Royal Hobart Hospital, Helen MacPherson Smith Trust, and GlaxoSmithKline.

Rationale & Aim: There is increasing interest in lung function trajectories but the focus to date has been on obstructive patterns without taking restrictive patterns into account. We investigated these patterns concurrently over the lifespan Methods: Using group-based trajectory modelling of spirometry collected from 7 to 53 years in the Tasmanian Longitudinal Health Study (n=2,438), 6 FEV1/FVC and 5 FVC trajectories were identified. Three FEV1/FVC trajectories were collectively recognised as ‘low’ and one FVC trajectory as ‘low’. Based on whether trajectories of FEV1/FVC and FVC were ‘low’, 4 patterns of lifetime spirometry trajectories were identified. Risk factors and consequences of these patterns were investigated Results: The prevalence of the lifetime patterns were: low FEV1/FVC-only 25.8%; low FVC-only 10.4%; both low FEV1/FVC and low FVC, labelled as ‘mixed’ 3.5%, and neither low (60.2%). Those with the mixed pattern had the highest prevalence of COPD at age 53 years (36.9%) followed by the low FEV1/FVC-only pattern (21.6%). Those with the mixed pattern had the highest prevalence of parental asthma, childhood respiratory illnesses, adult asthma and mental health disorders. Those with the low FVC-only pattern had low total lung capacity and residual volume and had the highest prevalence of childhood underweight, adult obesity, diabetes and cardiovascular conditions Conclusion: We identified physiological patterns of lifetime spirometric airway obstruction, restriction and both/mixed. Mixed and obstructive patterns identify those who may benefit from early interventions. The restrictive pattern identifies those at higher risk of multi-morbidity by middle-age

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, In the general population, two circulating biomarkers (CRP and CC16) are associated with different lung function trajectories leading to COPD in adulthood https://bit.ly/3wqWfb3

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.

IntroductionAdult spirometry following community-acquired childhood pneumonia has variably been reported as showing obstructive or non-obstructive deficits. We analysed associations between doctor-diagnosed childhood pneumonia/pleurisy and more comprehensive lung function in a middle-aged general population cohort born in 1961.MethodsData were from the prospective population-based Tasmanian Longitudinal Health Study cohort. Analysed lung function was from ages 7 years (prebronchodilator spirometry only, n=7097), 45 years (postbronchodilator spirometry, carbon monoxide transfer factor and static lung volumes, n=1220) and 53 years (postbronchodilator spirometry and transfer factor, n=2485). Parent-recalled histories of doctor-diagnosed childhood pneumonia and/or pleurisy were recorded at age 7. Multivariable linear and logistic regression were used.ResultsAt age 7, compared with no episodes, childhood pneumonia/pleurisy-ever was associated with reduced FEV1:FVC for only those with current asthma (beta-coefficient or change in z-score=−0.20 SD, 95% CI −0.38 to –0.02, p=0.028, p interaction=0.036). At age 45, for all participants, childhood pneumonia/pleurisy-ever was associated with a restrictive pattern: OR 3.02 (1.5 to 6.0), p=0.002 for spirometric restriction (FVC less than the lower limit of normal plus FEV1:FVC greater than the lower limit of normal); total lung capacity z-score −0.26 SD (95% CI −0.38 to –0.13), pDiscussionFor this community-based population, doctor-diagnosed childhood pneumonia and/or pleurisy were associated with obstructed lung function at age 7 for children who had current asthma symptoms, but with evidence of ‘smaller lungs’ when in middle age.

Introduction The study aim was to examine the association of snoring and nocturnal gastro-oesophageal reflux (nGOR) with respiratory symptoms and lung function, and if snoring and/or nGOR associated with a steeper decline in lung function. Methods Data from the third visit of the European Community Respiratory Health Survey (ECRHS) was used for cross-sectional analysis. Pre- and post-bronchodilator spirometry was performed, and information on sleep, nGOR and respiratory symptoms was collected (n=5715). Habitual snoring and nGOR were assessed by questionnaire reports. Pre-bronchodilator spirometry from ECRHS I, II and III (20 years follow-up) were used to analyse lung function changes by multivariate regression analysis. Results Snoring and nGOR were independently associated with a higher prevalence of wheeze, chest tightness, breathlessness, cough and phlegm. The prevalence of any respiratory symptom was 79% in subjects with both snoring and nGOR versus 56% in those with neither (p, Middle-aged adults with habitual snoring have a steeper decline in lung function over 10 years compared to controls. Habitual snorers with nocturnal gastro-oesophageal reflux have a higher prevalence of nocturnal respiratory symptoms than controls. http://ow.ly/YsiK30odcMY

BackgroundHigh body mass index (BMI) trajectories from childhood to adulthood are associated with the development of some chronic diseases, but whether such trajectories influence adult asthma has not been investigated to date. Therefore, we investigated associations between BMI trajectories from childhood to middle age (5–43 years) and incidence, persistence and relapse of asthma from ages 43 to 53 years.MethodsIn the Tasmanian Longitudinal Health Study (n=4194), weight and height were recorded at eight time-points between 5 and 43 years of age. BMI trajectories were developed using group-based trajectory modelling. Associations between BMI trajectories and asthma incidence, persistence and relapse from age 43 to 53 years, bronchial hyperresponsiveness (BHR) at age 50 years, and bronchodilator responsiveness at age 53 years were modelled using multiple logistic and linear regression.ResultsFive distinct BMI trajectories were identified: average, low, child high-decreasing, child average-increasing and high. Compared with the average trajectory, child average-increasing and high trajectories were associated with increased risk of incident asthma (OR 2.6, 95% CI 1.1–6.6 and OR 4.4, 95% CI 1.7–11.4, respectively) and BHR in middle age (OR 2.9, 95% CI 1.1–7.5 and OR 3.5, 95% CI 1.1–11.4, respectively). No associations were observed for asthma persistence or relapse.ConclusionsParticipants with child average-increasing and high BMI trajectories from childhood to middle age were at higher risk of incident adult asthma. Thus, encouraging individuals to maintain a normal BMI over the life course may help reduce the burden of adult asthma.

Rationale The naturally occurring age-dependent decline in lung function accelerates after menopause, likely due to the change of the endocrine balance. Although increasing evidence shows suboptimal lung health in early life can increase adult susceptibility to insults, the potential effect of poor childhood lung function on menopause-dependent lung function decline has not yet been investigated. Objectives To study whether menopause-dependent lung function decline, assessed as forced vital capacity (FVC) and forced expiratory volume in one second (FEV1), is determined by childhood lung function. Methods The Tasmanian Longitudinal Health Study, a cohort born in 1961, underwent spirometry at age seven. At ages 45 and 50 serum samples, spirometry and questionnaire data were collected (N = 506). We measured follicle stimulating and luteinizing hormones to determine menopausal status using latent profile analysis. The menopause-dependent lung function decline was investigated using linear mixed models, adjusted for anthropometrics, occupational level, smoking, asthma, asthma medication and study year, for the whole study population and stratified by tertiles of childhood lung function. Measurements and Main Results The overall menopause-dependent lung function decline was 19.3 mL/y (95%CI 2.2 to 36.3) for FVC and 9.1 mL/y (-2.8 to 21.0) for FEV1. This was most pronounced (pinteraction=0.03) among women within the lowest tertile of childhood lung function [FVC 22.2 mL/y (1.1 to 43.4); FEV1 13.9 mL/y (-1.5 to 29.4)]. Conclusions Lung function declines especially rapidly in postmenopausal women who had poor low lung function in childhood. This provides novel insights into respiratory health during reproductive aging and emphasizes the need for holistic public health strategies covering the whole lifespan.

Grass pollen exposure is a risk factor for childhood asthma hospital attendances. However, its short-term influence on lung function, especially among those with other allergic conditions, has been less well-studied.To investigate this association in a population-based sample of children.Within the HealthNuts cohort, 641 children performed spirometry during the grass pollen season. Grass pollen concentration was considered on the day of testing (lag 0), up to 3 days before (lag 1-lag 3), and cumulatively (lag 0-3). We used linear regression to assess the relevant associations and examined potential interactions with current asthma, hay fever or eczema, and food allergy.Associations were observed only in children with allergic disease (P value for interaction ≤ 0.1). In children with food allergy, grass pollen concentration was associated with a lower ratio of forced expiratory volume in 1 second to forced vital capacity (FEVA proactive approach needs to be enforced to manage susceptible children, especially those with food allergy, before high-grass pollen days.

Background and objective Ecological studies have suggested an association between exposure to particulate matter ≤2.5 μm (PM2.5) and coronavirus disease 2019 (COVID‐19) severity. However, these findings are yet to be validated in individual‐level studies. We aimed to determine the association of long‐term PM2.5 exposure with hospitalization among individual patients infected with severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). Methods We estimated the 10‐year (2009–2018) PM2.5 exposure at the residential zip code of COVID‐19 patients diagnosed at the University of Cincinnati healthcare system between 13 March 2020 and 30 September 2020. Logistic regression was used to determine the odds ratio (OR) and 95% CI for COVID‐19 hospitalizations associated with PM2.5, adjusting for socioeconomic characteristics and comorbidities. Results Among the 14,783 COVID‐19 patients included in our study, 13.6% were hospitalized; the geometric mean (SD) PM2.5 was 10.48 (1.12) μg/m3. In adjusted analysis, 1 μg/m3 increase in 10‐year annual average PM2.5 was associated with 18% higher hospitalization (OR: 1.18, 95% CI: 1.11–1.26). Likewise, 1 μg/m3 increase in PM2.5 estimated for the year 2018 was associated with 14% higher hospitalization (OR: 1.14, 95% CI: 1.08–1.21). Conclusion Long‐term PM2.5 exposure is associated with increased hospitalization in COVID‐19. Therefore, more stringent COVID‐19 prevention measures may be needed in areas with higher PM2.5 exposure to reduce the disease morbidity and healthcare burden., We examined the association between long‐term exposure to particulate matter ≤2.5 μm (PM2.5) and coronavirus disease 2019 (COVID‐19) outcomes in 14,783 COVID‐19 patients diagnosed at the University of Cincinnati Health System. Our results suggested that a 1‐μg/m3 increase in annual average PM2.5 between 2009 and 2018 was associated with 14%–18% higher odds of hospitalization for COVID‐19.Air Pollution and the Pandemic: Long‐term PM2.5 exposure and disease severity in COVID‐19 patients See related Editorial

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)., Using the commonly adopted threshold, a positive BDR test provides a meaningful change in post-test probability of adult asthma, whereas a negative test does not. Discriminatory accuracy is much greater in those with coexistent post-BD airflow obstruction. https://bit.ly/3gPvlm8

OBJECTIVE To investigate the association of demographic, career, and lifestyle factors with resilience and the association of resilience with mental health outcomes in Canadian veterinarians. SAMPLE 1,130 veterinarians in clinical practice across Canada. PROCEDURES An online questionnaire was used to collect participant data and included 5 validated psychometric scales to evaluate resilience (through the Connor-Davidson Resilience Scale [CD-RISC]), perceived stress (through the Perceived Stress Scale), emotional distress (through the Hospital Anxiety and Depression Scale), burnout (through the Maslach Burnout Inventory), and secondary traumatic stress (through the Professional Quality of Life Scale). A multivariable linear regression model was used to investigate associations between CD-RISC scores and demographic, career, and lifestyle characteristics. Univariable linear regression models were used to assess the relationship between resilience scores and other mental health outcomes. RESULTS The strongest positive association was between CD-RISC score and overall health. The level of satisfaction with support from friends and workplace resources had positive associations with the CD-RISC score. The presence of mental illness had the strongest negative association with the CD-RISC score. Being married, working in a small animal practice, or having an associate role were negatively associated with the CD-RISC score. The CD-RISC score had negative associations with scores for perceived stress, anxiety, depression, burnout, and secondary traumatic stress. CONCLUSIONS AND CLINICAL RELEVANCE Models provided evidence for the role of resilience in protecting against negative mental health outcomes in veterinarians. Both personal and workplace factors were associated with resilience, presenting opportunities for intervention at each of these levels.

Rationale: It is unclear if childhood bronchitis is associated with adverse respiratory outcomes in middle-age Aim: To determine the relationships between childhood bronchitis frequency/duration and clinical outcomes in middle-aged Australians Methods: Data were from the Tasmanian Longitudinal Health Study (TAHS, 1968-2016). Four categories of parent-reported bronchitis by age 7 were none (reference), non-recurrent, recurrent (>5 episodes of “loose, rattly” or chesty cough lasting 5 episodes, ≥1 month average duration). Outcomes at age 53 included chronic bronchitis (CB), asthma and pre/post-bronchodilator (BD) spirometry. Trend tests, mediation analysis and multivariable regression were used Results: Increasing childhood bronchitis severity was associated with adult asthma/pneumonia-ever (p-trend

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 sensitisation was assessed using skin prick tests. The presence or absence of eczema and sensitisation 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 baseline NO2 was associated with increased risk of prevalent eczema (OR=1.15 [95%CI 0.98-1.36]), both non-atopic (OR=1.39 [1.02-1.90]) and atopic eczema (OR=1.26 [1.00-1.59]). These associations were not seen in females (P for interaction=0.08

Work‐related asthma (WRA) is one of the most common occupational respiratory conditions, and includes asthma specifically caused by occupational exposures (OA) and asthma that is worsened by conditions at work (WEA). WRA should be considered in all adults with asthma, but especially those with new‐onset or difficult to control asthma. Improvement in asthma symptoms when away from work is suggestive of WRA. Clinical history alone is insufficient to diagnose WRA; therefore, objective investigations are required to confirm the presence of asthma and the association of asthma with work activities. Management of WRA requires pharmacotherapy similar to that of non‐WRA, however, also needs to take into account control of the causative workplace exposure. Ongoing exposure will likely lead to decline in lung function and worsening asthma control. WRA is a preventable condition but this does rely on increased awareness of WRA and thorough identification and control of all potential occupational respiratory hazards.

Summary 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. Methods 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. Findings 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 disorders profile (relative risk ratio 3·3 [95% CI 1·9–5·9]), whereas the other asthma and allergy trajectories were associated only with the dominant mental health disorders profile. Both spirometrically defined and clinical COPD were most strongly associated with the early-onset persistent asthma and allergies trajectory (odds ratio [OR] 5·3 [95% CI 3·2–8·6]) and also with the late-onset asthma and allergies trajectory (OR 3·8 [2·4–6·1]). Interpretation Distinct longitudinal trajectories of asthma and allergic disease from childhood to 53 years are associated with different profiles of extrapulmonary comorbidities and varying risk of COPD. These findings can inform a personalised approach in clinical guidelines and management focusing on treatable traits. Comorbidity profiles are a new target for early identification and intervention. Funding National Health and Medical Research Council of Australia, EU's Horizon 2020, The University of Melbourne, Clifford Craig Medical Research Trust of Tasmania, The Victorian, Queensland & Tasmanian Asthma Foundations, The Royal Hobart Hospital, Helen MacPherson Smith Trust, and GlaxoSmithKline.

IntroductionWe 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.Materials and methodsProspective 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.ResultsWe 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.ConclusionsExposures 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.

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.

Background Little information exists on the lipidemic effects of air pollution, particularly in developing countries. We aimed to investigate the associations of long-term exposure to ambient air pollutants with lipid levels and dyslipidemias in China. Methods In 2009, a total of 15,477 participants aged 18–74 years were recruited from the 33 Communities Chinese Health Study conducted in three Northeastern China cities. Total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were measured in participants' blood specimens. Three year (2006–08) average air pollution concentrations were assessed using data from 33 communities (particles with diameters ≤1.0 μm (PM 1 ) and ≤2.5 μm (PM 2.5 ) were predicted using a spatial statistical model) or 11 air monitoring stations (particles with diameters ≤10 μm (PM 10 ), sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), and ozone (O 3 )). Associations were evaluated by two-level logistic and generalized linear regression models. Results We detected many significant associations between exposure to air pollutants (especially for PM 1 and PM 2.5 ) and blood lipid levels. Most of the associations suggested deleterious effects on blood lipid markers (e.g., a 10 μg/m 3 increase in PM 1 was associated with 1.6% (95% confidence interval (CI): 1.1, 2.0), 2.9% (95% CI: −3.3, 9.3), and 3.2% (95% CI: 2.6, 3.9) higher levels of TC, TG, and LDL-C, respectively, but 1.4% (95% CI: −1.8, −0.9) lower HDL-C levels), although beneficial associations were found for O 3 . In analysis with dyslipidemias, all the observed associations suggested deleterious lipidemic effects of air pollutants, and no significant beneficial association was observed for O 3 . Stratified analyses showed that the associations were stronger in overweight or obese participants; sex and age modified the associations, but the pattern of effects was mixed. Conclusions Long-term ambient air pollution was associated with both altered lipid profiles and dyslipidemias, especially among overweight or obese participants.

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 (NO x ) 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 NO x were determined by Griess‐reaction fluorescent method. Associations were assessed between EBC NO x and different allergic phenotypes, lung function and airway reactivity. Results: Atopy, with or without asthma or rhinitis, was associated with increased EBC NO x 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 NO x (OR = 0.64, 95% CI = 0.21‐1.96, p for interaction = 0.05). Conclusions and clinical relevance: In these population‐based samples, EBC NO x 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 NO x could be a key predictor of atopy in both young and middle‐aged adults, regardless of the presence of concomitant asthma or rhinitis.