Search

Cough is a common yet heterogeneous condition. Little is known about the characteristics and course of cough in general populations. We aimed to investigate cough subclasses, their characteristics from childhood across six decades of life, and potential treatable traits in a community-based cohort.

Cough is the most common symptom leading to medical consultation. Chronic cough results in significant health care costs, impairs quality of life, and may indicate the presence of a serious underlying condition. Here, we present a summary of an updated position statement on cough management in the clinical consultation. Assessment of children and adults requires a focused history of chronic cough to identify any red flag cough pointers that may indicate an underlying disease. Further assessment with examination should include a chest x‐ray and spirometry (when age > 6 years). Separate paediatric and adult diagnostic management algorithms should be followed. Management of the underlying condition(s) should follow specific disease guidelines, as well as address adverse environmental exposures and patient/carer concerns. First Nations adults and children should be considered a high risk group. The full statement from the Thoracic Society of Australia and New Zealand and Lung Foundation Australia for managing chronic cough is available at https://lungfoundation.com.au/resources/cicada‐full‐position‐statement. Algorithms for assessment and diagnosis of adult and paediatric chronic cough are recommended.High quality evidence supports the use of child‐specific chronic cough management algorithms to improve clinical outcomes, but none exist in adults.Red flags that indicate serious underlying conditions requiring investigation or referral should be identified.Early and effective treatment of chronic wet/productive cough in children is critical.Culturally specific strategies for facilitating the management of chronic cough in First Nations populations should be adopted.If the chronic cough does not resolve or is unexplained, the patient should be referred to a respiratory specialist or cough clinic.

BackgroundObservational studies suggest that total testosterone (TT) and sex hormone-binding globulin (SHBG) may have beneficial effects on lung function, but these findings might be spurious due to confounding and reverse causation. We addressed these limitations by using multivariable Mendelian randomisation (MVMR) to investigate the independent causal effects of TT and SHBG on lung function.MethodsWe first identified genetic instruments by performing genome-wide association analyses of TT and SHBG in the large UK Biobank, separately in males and females. We then assessed the independent effects of TT and SHBG on forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC using one-sample MVMR. We addressed pleiotropy, which could bias MVMR, using several methods that account for it. We performed subgroup MVMR analyses by obesity, physical activity and menopausal status, and assessed associations between TT and SHBG with lung function decline. Finally, we compared the MVMR results with those of observational analyses in the UK Biobank.FindingsIn the MVMR analyses, there was evidence of pleiotropy, but results were consistent when accounting for it. We found a strong beneficial effect of TT on FVC and FEV1in both males and females, but a moderate detrimental effect of SHBG on FEV1and FEV1/FVC in males only. Subgroup analyses suggested stronger effects of TT among obese and older males. The observational analyses, in line with previous studies, agreed with MRMV for TT, but not for SHBG.InterpretationThese findings suggest that testosterone improves lung function in males and females, while SHBG has an opposite independent effect in males.

BackgroundThere is growing interest in the joint effects of hazardous trace elements (HTEs) on lung function deficits, but the data are limited. This is a critical research gap given increased global industrialisation.MethodsA national cross-sectional study including spirometry was performed among 2112 adults across 11 provinces in China between 2020 and 2021. A total of 27 HTEs were quantified from urine samples. Generalised linear models and quantile-based g-computation were used to explore the individual and joint effects of urinary HTEs on lung function, respectively.ResultsOverall, there were negative associations between forced expiratory volume in 1 s (FEV1) and urinary arsenic (As) (z-score coefficient, −0.150; 95% CI, −0.262 to –0.038 per 1 ln-unit increase), barium (Ba) (−0.148, 95% CI: −0.258 to –0.039), cadmium (Cd) (−0.132, 95% CI: −0.236 to –0.028), thallium (Tl) (−0.137, 95% CI: −0.257 to –0.018), strontium (Sr) (−0.147, 95% CI: −0.273 to –0.022) and lead (Pb) (−0.121, 95% CI: −0.219 to –0.023). Similar results were observed for forced vital capacity (FVC) with urinary As, Ba and Pb and FEV1/FVC with titanium (Ti), As, Sr, Cd, Tl and Pb. We found borderline associations between the ln-quartile of joint HTEs and decreased FEV1(−20 mL, 95% CI: −48 to +8) and FVC (−14 mL, 95% CI: −49 to+2). Ba and Ti were assigned the largest negative weights for FEV1and FVC within the model, respectively.ConclusionOur study investigating a wide range of HTEs in a highly polluted setting suggests that higher urinary HTE concentrations are associated with lower lung function, especially for emerging Ti and Ba, which need to be monitored or regulated to improve lung health.

BackgroundUnderstanding the natural history of abnormal spirometric patterns at different stages of life is critical to identify and optimise preventive strategies. We aimed to describe characteristics and risk factors of restrictive and obstructive spirometric patterns occurring before 40 years (young onset) and between 40 and 61 years (mid-adult onset).MethodsWe used data from the population-based cohort of the European Community Respiratory Health Survey (ECRHS). Prebronchodilator forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) were assessed longitudinally at baseline (ECRHS1, 1993–1994) and again 20 years later (ECRHS3, 2010–2013). Spirometry patterns were defined as: restrictive if FEV1/FVC≥LLN and FVC<10th percentile, obstructive if FEV1/FVC

Food allergy is considered a precursor to asthma in the context of the atopic march, but the relationship between infant food allergy phenotypes and lung function and asthma in childhood is unclear. We aimed to examine the association between food sensitisation and challenge-confirmed food allergy in infancy, as well as persistent and resolved food allergy up to age 6 years, and the risk of lung function deficits and asthma at age 6 years.

Early childhood respiratory infections, including pneumonia, are an important global public health issue, with more than 40 million annual cases resulting in approximately 650 000 deaths. A growing number of published studies have examined the effects of early childhood lower respiratory tract infections (LRTIs) or pneumonia on lung function, particularly as part of large early-life exposure studies. To our knowledge, there is no published systematic review of these data. We searched PubMed, Embase, and Web of Science for studies published between database inception and May 12, 2022. Case-control, cohort, and cross-sectional studies were included if they reported forced expiratory volume in 1 s (FEV1) or forced vital capacity (FVC) values of participants older than 5 years. Article titles and abstracts were screened in Rayyan before retrieval, assessment, and data extraction of the full text. Primary outcome measures were differences in mean FEV1or FVC values between exposed groups (ie, children aged ≤5 years with LRTIs) and non-exposed groups. This study is registered with PROSPERO, CRD42021265295. Database searches yielded 3070 articles, and 14 studies were included in this systematic review, providing a total of 23 276 participants, including 9969 children and 13 307 adults. Eight of 14 articles reported significant reductions in FEV1values, and six of 12 studies reported reductions in FVC values in children and adults with a history of early childhood LRTIs or pneumonia, compared with unexposed controls (p<0·05). Most studies reporting reductions in lung function described deficits consistent with a restrictive spirometry pattern. Only two of 14 studies reported data from low-income and middle-income countries or disadvantaged populations in middle-income and high-income countries, and there were scarce data available on the effect of LRTI severity and recurrence on lung function. LRTIs in early childhood could be associated with a restrictive spirometry pattern in later childhood and adulthood. Data are needed from low-income and middle-income nations, and from disadvantaged populations in middle-income and high-income countries in which early childhood respiratory infection burden is disproportionately high. Data are also needed on the effect of LRTI severity and recurrence on future lung function.

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 FEV1/forced vital capacity (FVC) ratio, FVC, and their combinations, relate these combined trajectory groups to static lung volume and gas transfer measurements, and investigate both risk factors for and consequences of these combined trajectory groups.

ObjectivesThere is a scarcity of evidence on occupational exposures that may increase eczema in adults. We aimed to investigate potential associations between occupational exposures and eczema in middle-aged adults.MethodsA lifetime work history calendar was collected from the Tasmanian Longitudinal Health Study participants when they were at age 53. Their work history was collated with the occupational asthma-specific job exposure matrix to define ever-exposure and cumulative exposure unit-years since no eczema job exposure matrix is available. Eczema was determined using the report of flexural rash that was coming and going for at least 6 months in the last 12 months. Skin prick tests were used to further subgroup eczema and atopic eczema (AE) or non-AE (NAE). Logistic and multinomial regression models were used to investigate the associations.ResultsEczema prevalence was 9.1%. Current occupational exposure to animals (adjusted OR, aOR=3.06 (95% CI 1.43 to 6.58)), storage mites (aOR=2.96 (95% CI 1.38 to 6.34)) and endotoxin (aOR=1.95 (95% CI 1.04 to 3.64)) were associated with increased risk of current eczema. Furthermore, increased odds of NAE were associated with current exposure to animals (aOR=5.60 (95% CI 1.45 to 21.7)) and storage mites (aOR=5.63 (95% CI 1.45 to 21.9)). Current exposures to isocyanates (aOR=5.27 (95% CI 1.17 to 23.7)) and acrylates (aOR=8.41 (95% CI 1.60 to 44.3)) were associated with AE. There was no evidence of associations between cumulative exposures and eczema prevalence. Cumulative exposure to metalworking fluids (aOR=1.10 (95% CI 1.01 to 1.22)) was associated with NAE and acrylates (aOR=1.24 (95% CI 1.04 to 1.46)) with AE.ConclusionsIn this exploratory assessment, multiple occupational exposures were associated with current eczema in middle-aged adults. Raising awareness and limiting these exposures during an individual’s productive working life will likely have various health benefits, including reducing eczema prevalence.

ObjectivesAdverse occupational exposures can accelerate age-related lung function decline. Some longitudinal population-based studies have investigated this association. This study aims to examine this association using findings reported by longitudinal population-based studies.MethodsOvid Medline, PubMed, Embase, and Web of Science were searched using keywords and text words related to occupational exposures and lung function and 12 longitudinal population-based studies were identified using predefined inclusion criteria. The quality of the studies was assessed using the Newcastle-Ottawa Scale. Lung function decline was defined as annual loss of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) or the ratio (FEV1/FVC). Fixed and random-effects meta-analyses were conducted to calculate pooled estimates for ever and cumulative exposures. Heterogeneity was assessed using the I2test, and publication bias was evaluated using funnel plots.ResultsEver exposures to gases/fumes, vapours, gases, dusts, fumes (VGDF) and aromatic solvents were significantly associated with FEV1decline in meta-analyses. Cumulative exposures for these three occupational agents observed a similar trend of FEV1decline. Ever exposures to fungicides and cumulative exposures to biological dust, fungicides and insecticides were associated with FEV1decline in fixed-effect models only. No statistically significant association was observed between mineral dust, herbicides and metals and FEV1decline in meta-analyses.ConclusionPooled estimates from the longitudinal population-based studies have provided evidence that occupational exposures are associated with FEV1decline. Specific exposure control and respiratory health surveillance are required to protect the lung health of the workers.

Following evidence from randomized controlled trials, patients with bronchiectasis unrelated to cystic fibrosis receive long-term azithromycin to reduce acute respiratory exacerbations. However, the period when azithromycin is effective and which patients are likely to most benefit remain unknown.

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).

There are limited longitudinal data on the population prevalence of allergic conditions during childhood, and few studies have incorporated the reference standard oral food challenge to confirm food allergy.

AbstractRATIONALE: On November 21, 2016 in Australia, a major thunderstorm-asthma epidemic struck Melbourne with an unprecedented number of emergency presentations, hospital admissions and fatalities.OBJECTIVESWe identified affected patients who presented to The Royal Melbourne Hospital, an adult tertiary center in North-West Melbourne. We aimed to characterize individual patient factors associated with hospital admission and identify biomarkers in patient subgroups that are at risk of being severely affected by thunderstorm-asthma.METHODSCross-sectional, retrospective analysis of demographics of 240 patients presenting to The Royal Melbourne Hospital on November 21 to 22, 2016 post thunderstorm-asthma event and clinical characteristics of 70 of those patients who subsequently attended an outpatient clinic review.RESULTSPatients were generally young adults (mean age 35 years), with seasonal rhinitis (96%) and universally (100%) sensitized to ryegrass pollen. Forty-four patients (63%) had a known diagnosis of asthma while 20% reported no previous diagnosis but had symptoms consistent with asthma. Patient characteristics associated with hospitalization were: uncontrolled asthma symptoms in the month before the thunderstorm-asthma event, symptomatic allergic rhinitis, high blood eosinophilia and lower lung function.CONCLUSIONThunderstorm-asthma affects people with seasonal rhinitis, ryegrass sensitization and can occur without prior history of asthma, with dramatic potential to inundate a healthcare system. Our data suggests that hospitalization, and thus a more severe thunderstorm-asthma exacerbation, was associated with a known history of asthma, prior uncontrolled asthma symptoms, allergic rhinitis, high eosinophil count and lower lung function. These factors may inform strategies to identify those most at risk of thunderstorm-asthma.

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.

IntroductionThere is growing interest in the impact of greenness exposure on airway diseases, but the impact of greenness on lung function in children is limited. We aimed to investigate the associations between greenness surrounding schools and lung function in children and whether these associations are modified by air pollution exposure.MethodsBetween 2012 and 2013, a cross-sectional survey and spirometry were performed among 6740 school children. Lung function patterns were determined as obstructive forced expiratory volume 1 s/forced vital capacity (FEV1/FVC <0.8) or restrictive (FEV1/FVC ≥0.8 but FVC <80% of predicted). School greenness was defined by Normalized difference vegetation index (NDVI) and soil-adjusted vegetation index. Nitrogen dioxide, sulphur dioxide and particular matter concentrations were assessed using a spatiotemporal model and national monitoring data. Two-level generalised linear models were used to investigate associations and interactions.ResultsOverall, an IQR in NDVI within 500 m was associated with higher FEV1(+57 mL 95% CI 44 to 70) and FVC (+58 mL 95% CI 43 to 73). NDVI was similarly associated with 25% reduced odds of spirometric restriction (OR: 0.75, 95% CI 0.65 to 0.86). However, among children exposed to the highest compared with the lowest quartile of particulate matter, increasing NDVI was paradoxically associated with lower −40 mL FVC (95% CI −47 to –33, p interaction<0.05).DiscussionOur findings suggest that, in this study population, greening urban areas may promote lung health in low–moderate pollution areas but not in high air pollution areas. If the findings are replicated in other moderate-to-high pollution settings, this highlights a need to have a flexible green policy.

Few studies have investigated adverse food reactions among food-allergic children in a population-based sample, which is critical for the development of evidence-based management strategies.

To evaluate associations between exposure during early life to mine fire smoke and parent‐reported indicators of respiratory and atopic illness 2–4 years later. The Hazelwood coalmine fire exposed a regional Australian community to markedly increased air pollution during February – March 2014. During June 2016 – October 2018 we conducted a prospective cohort study of children from the Latrobe Valley. Seventy‐nine children exposed to smoke in utero, 81 exposed during early childhood (0–2 years of age), and 129 children conceived after the fire (ie, unexposed). Individualised mean daily and peak 24‐hour fire‐attributable fine particulate matter (PM2.5) exposure during the fire period, based on modelled air quality and time‐activity data. Parent‐reported symptoms, medications use, and contacts with medical professionals, collected in monthly online diaries for 29 months, 2–4 years after the fire. In the in uteroexposure analysis (2678 monthly diaries for 160 children exposed in uteroor unexposed), each 10 μg/m3increase in mean daily PM2.5exposure was associated with increased reports of runny nose/cough (relative risk [RR], 1.09; 95% CI, 1.02–1.17), wheeze (RR, 1.56; 95% CI, 1.18–2.07), seeking health professional advice (RR, 1.17; 95% CI1.06–1.29), and doctor diagnoses of upper respiratory tract infections, cold or flu (RR, 1.35; 95% CI, 1.14–1.60). Associations with peak 24‐hour PM2.5exposure were similar. In the early childhood exposure analysis (3290 diaries for 210 children exposed during early childhood, or unexposed), each 100 μg/m3increase in peak 24‐hour PM2.5exposure was associated with increased use of asthma inhalers (RR, 1.26; 95% CI, 1.01–1.58). Exposure to mine fire smoke in uterowas associated with increased reports by parents of respiratory infections and wheeze in their children 2–4 years later.

Although there is ongoing debate regarding the impact of early postnatal exposure to antibiotics on the development of asthma, the possibility that antibiotic exposure may impair lung function has not previously been examined. Furthermore, it is unclear if specific types of antibiotics may have a greater effect, or if children with genetic mutations in the oxidative stress response glutathione S-transferase (GST) superfamily may be at greater risk.

Background and objectiveAs caesarean delivery and childhood allergy continue to rise, their inter-relationships may change. We examined whether caesarean delivery predicts allergic disease and impaired lung function in two contemporary harmonised population-based cohorts.MethodsParent-reported asthma and eczema data were drawn from two prospective Australian infant cohorts, HealthNuts (n=5276, born 2006–2010) and the Longitudinal Study of Australian Children (LSAC, n=5107, born 2003–2004) at age 6–7 years, and spirometric lung function from LSAC’s Child Health CheckPoint (n=1756) at age 11–12 years. Logistic regression estimated associations between delivery mode and current asthma and eczema at 6–7 years, and linear regression examined lung function at 11–12 years. Models were adjusted for potential confounding factors.ResultsComplete case analysis included 3135 HealthNuts and 3654 LSAC children (32.2% and 30.9% born by caesarean, respectively). An association was evident between caesarean delivery and asthma at age 6–7 years in HealthNuts (adjusted OR (aOR) 1.25, 95% CI 1.00 to 1.57) but not in LSAC (aOR 1.05, 95% CI 0.86 to 1.28), while neither study showed clear associations with eczema (HealthNuts: aOR 1.09, 95% CI 0.88 to 1.35; LSAC: aOR 0.89, 95% CI 0.69 to 1.15). Spirometric lung function parameters at age 11–12 years were similar by delivery mode. Associations were not modified by duration of breast feeding, maternal history of asthma/eczema, childcare attendance, number of older siblings or pet exposure.ConclusionsIn two unselected populations using harmonised protocols, the likely association of caesarean delivery with developing childhood allergy was small.

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), p<0.001; functional residual capacity −0.16 SD (−0.34 to –0.08), p=0.001; and residual volume −0.18 SD (−0.31 to –0.05), p=0.008. Reduced lung volumes were accompanied by increased carbon monoxide transfer coefficient at both time points (z-score +0.29 SD (0.11 to 0.49), p=0.001 and +0.17 SD (0.04 to 0.29), p=0.008, respectively).DiscussionFor 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.

IntroductionIdiopathic pulmonary fibrosis (IPF) is a lung disease of unknown cause characterised by progressive scarring, with limited effective treatment and a median survival of only 2–3 years. Our aim was to identify potential occupational and environmental exposures associated with IPF in Australia.MethodsCases were recruited by the Australian IPF registry. Population-based controls were recruited by random digit dialling, frequency matched on age, sex and state. Participants completed a questionnaire on demographics, smoking, family history, environmental and occupational exposures. Occupational exposure assessment was undertaken with the Finnish Job Exposure Matrix and Australian asbestos JEM. Multivariable logistic regression was used to describe associations with IPF as ORs and 95% CIs, adjusted for age, sex, state and smoking.ResultsWe recruited 503 cases (mean±SD age 71±9 years, 69% male) and 902 controls (71±8 years, 69% male). Ever smoking tobacco was associated with increased risk of IPF: OR 2.20 (95% CI 1.74 to 2.79), but ever using marijuana with reduced risk after adjusting for tobacco: 0.51 (0.33 to 0.78). A family history of pulmonary fibrosis was associated with 12.6-fold (6.52 to 24.2) increased risk of IPF. Occupational exposures to secondhand smoke (OR 2.1; 1.2 to 3.7), respirable dust (OR 1.38; 1.04 to 1.82) and asbestos (OR 1.57; 1.15 to 2.15) were independently associated with increased risk of IPF. However occupational exposures to other specific organic, mineral or metal dusts were not associated with IPF.ConclusionThe burden of IPF could be reduced by intensified tobacco control, occupational dust control measures and elimination of asbestos at work.

BackgroundPrevious studies have reported an association between weight increase and excess lung function decline in young adults followed for short periods. We aimed to estimate lung function trajectories during adulthood from 20-year weight change profiles using data from the population-based European Community Respiratory Health Survey (ECRHS).MethodsWe included 3673 participants recruited at age 20–44 years with repeated measurements of weight and lung function (forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1)) in three study waves (1991–93, 1999–2003, 2010–14) until they were 39–67 years of age. We classified subjects into weight change profiles according to baseline body mass index (BMI) categories and weight change over 20 years. We estimated trajectories of lung function over time as a function of weight change profiles using population-averaged generalised estimating equations.ResultsIn individuals with normal BMI, overweight and obesity at baseline, moderate (0.25–1 kg/year) and high weight gain (>1 kg/year) during follow-up were associated with accelerated FVC and FEV1declines. Compared with participants with baseline normal BMI and stable weight (±0.25 kg/year), obese individuals with high weight gain during follow-up had −1011 mL (95% CI −1.259 to −763) lower estimated FVC at 65 years despite similar estimated FVC levels at 25 years. Obese individuals at baseline who lost weight (<−0.25 kg/year) exhibited an attenuation of FVC and FEV1declines. We found no association between weight change profiles and FEV1/FVC decline.ConclusionModerate and high weight gain over 20 years was associated with accelerated lung function decline, while weight loss was related to its attenuation. Control of weight gain is important for maintaining good lung function in adult life.

Adolescence is well recognized as a period of increased risk for severe and fatal food-induced anaphylaxis. Current Australian adrenaline autoinjector (AAI) prescription guidelines therefore suggest that consideration be given to AAI prescription in all adolescents with a food allergy. To date, however, few studies have assessed the AAI carriage behavior of adolescents prescribed AAI devices.

Lung development starts in utero and continues during childhood through to adolescence, reaching its peak in early adulthood. This growth is followed by gradual decline due to physiological lung ageing. Lung-function development can be altered by several host and environmental factors during the life course. As a result, a range of lung-function trajectories exist in the population. Below average trajectories are associated with respiratory, cardiovascular, metabolic, and mental health comorbidities, as well as with premature death. This Review presents progressive research into lung-function trajectories and assists the implementation of this knowledge in clinical practice as an innovative approach to detect poor lung health early, monitor respiratory disease progression, and promote lung health. Specifically, we propose that, similar to paediatric height and weight charts used globally to monitor children's growth, lung-function charts could be used for both children and adults to monitor lung health status across the life course. To achieve this proposal, we introduce our free online Lung Function Tracker tool. Finally, we discuss challenges and opportunities for effective implementation of the trajectory concept at population level and outline an agenda for crucial research needed to support such implementation.

Infant feeding guidelines in Australia changed in 2016 to recommend introducing common allergy-causing foods by age 1 year to prevent food allergy. Although most Australian infants now eat peanut and egg by age 6 months, some still develop food allergy despite the early introduction of allergens.

Overall early exposure to allergenic foods in the infant's diet is a new strategy for preventing food allergy to that allergen, but the optimal timing of exposure for different allergens is not known.

We previously reported that infants with Asian-born parents are 3 times more likely to have IgE-mediated food allergy than those with Australian-born parents. It is unknown whether this translates to the increased risk of other allergic diseases later in childhood and whether ancestry interacts with other risk factors for allergic disease development.