Caroline J. Lodge

Description:The prevalence of pollen-induced health problems is expected to increase as climate change worsens.1 Previous research has found that adults had worse pollen-induced airway impairment compared to children.2 We hypothesized that different lifestyle and environmental factors and/or lung aging may explain why the different health impacts of pollen across age groups. To the best of our knowledge, no adult population-based study has assessed the relationships between ambient pollen exposure and post-bronchodilator (BD) lung function as a measure of fixed airflow obstruction, or gas transfer as a measure of parenchymal damage. Studies that investigated pre-BD lung function in adults have reported no significant changes in and out of the pollen season, but the sample sizes were small and only stratified by asthma and/or seasonal allergic rhinitis.2 However, there are more individual, lifestyle and environmental factors to consider that may interact with each other and pollen on lung function. Using data collected from the 6th decade follow-up (mean age: 53 years; n = 2471) of the population-based Tasmanian Longitudinal Health Study (TAHS) conducted between 2012 and 2016, we assessed cross-sectional relationships between the temperate grass pollen season and lung function using regression. Temperate grass pollen season was used as a proxy because daily pollen counts were available for a subset of participants only. We defined ‘in season’ as from October to December, as pollen levels were insignificant outside this period.1 Lung function measurements (pre- and post-BD spirometry & gas transfer) were converted to z-scores using Global Lung Initiative reference values. All models included adjustments for temperature and humidity as a priori confounders. We also examined potential interactions with current allergic disease (hay fever, asthma, pollen allergy, eczema), current chronic rhinosinusitis (CRS), grass pollen sensitisation [skin prick test (SPT)≥3 mm], inhaled corticosteroid (ICS) use, traffic-related air pollution (TRAP), smoking, urbanisation, and residential greenness using likelihood ratio tests. For more detailed definitions and results including summary statistics of environmental factors (where available), please refer to the Supplementary Materials. We found that lung function testing, comparing in to out of the grass pollen season, was associated with a lower pre- and post-BD FEV1/FVC (forced expiratory volume in 1 s and forced vital capacity ratio) and FEF25–75 % (mid-forced expiratory flow) as an index of smaller airway calibre, only in certain subgroups, namely: smokers with asthma/hay fever, people with asthma/hay fever who did not use ICS in the past 12 months, and in those with co-existing allergic diseases or living 200 m from major roads (Fig. 1). People with asthma who also smoked or did not recently use ICS additionally had lower pre-/post-BD FEV1 (Table 1). No evidence of interaction was found with CRS, residential greenness, NO2 or PM2.5.

Description:Background: Allergic sensitization and respiratory infections commonly occur in childhood. Interplay between them in asthma development is known as the 'two-hit' hypothesis. There has been no previous investigation of this hypothesis on adult lung function. Objective: In a birth cohort at high risk for allergic diseases, we investigated interactions between these two factors and lung function outcomes into adulthood. Methods: Allergic sensitization was assessed at age 24 months by skin prick testing to aero and food allergens. Respiratory infection was defined as cough, rattle or wheeze measured by frequent questionnaires up to age 24 months. Regression models were utilized to identify interactions between these exposures and associations with lung function at ages 12, 18 and 25 years. Results: At age 25 years, those sensitized at age 2 years(n = 118) demonstrated reductions in pre-bronchodilator FEV1 of 0.06(95% CI: -0.12, 0.00, z-score units, p = .055) for each additional month of respiratory infections. Those not sensitized (n = 120) had increases in pre-bronchodilator FEV1 of 0.07 (95% CI: 0.02, 0.13, z-score units, p = .012) for each additional month of respiratory infection(pinteraction = .012). Similar findings were noted for FEV1/FVC ratio(pinteraction = .011), FEF25-75(pinteraction = .007) and absolute change in pre and post bronchodilator lung function. At 18 years, findings were similar; however, there was less evidence for interactions at 12 years. Conclusions: Our study findings support the 'two-hit' hypothesis of interactions between early-life allergic sensitization and increasing respiratory infections, and impairment in lung function up to age 25 years. Early childhood respiratory infections however had different impacts on lung function depending upon the presence or absence of allergic sensitization.

Description:Objective: The impact of household air pollution (HAP) on obstructive sleep apnoea (OSA) was unclear from the literature. We aimed to investigate the associations between HAP exposure over 10 years and OSA in middle-aged adults. Methods: Using the Tasmanian Longitudinal Health Study (TAHS), seven longitudinal HAP profiles were previously identified using information on household heating, cooking, mould, active and passive smoking exposure collected at two ages spanning 10 years (at mean ages 43 and 53 years). Probable OSA was only measured at 53 years using validated STOP-Bang, Berlin and OSA-50 questionnaires. Medically diagnosed OSA was self-reported. Multivariable logistic regression was used to assess the associations between HAP profiles and each definition of OSA, adjusting for age, sex, socioeconomic status and ambient air pollution. Results: Compared with the "Least exposed" profile, characterised by reverse-cycle air conditioning, electric cooking and no smoking exposure, the "Wood and gas heating/gas cooking/smoking" profile was associated with both probable OSA defined using OSA-50 (aOR=2.39, 95%CI 1.61-3.53) and medically diagnosed OSA (aOR=2.31, 1.06-5.05). The "All gas" and "Wood heating/smoking" profiles were associated with OSA-50-defined probable OSA (aOR=1.35, 1.01-1.79; aOR=1.47, 1.10-1.96 respectively). Additionally, the "All gas" profile was associated with incident medically diagnosed OSA (aOR=2.15, 1.06-4.38). Conclusions: Sustained exposure to wood and gas heating and gas cooking especially when combined with tobacco smoke increased the risk of OSA over 10 years in middle age. Our study strengthens the rationale for including the potential adverse effects of HAP on mid-life OSA within public educational programs and guidelines.

Description:Background: Skin lipids are crucial components of the skin barrier. Individuals with atopic dermatitis (AD or eczema) have a different skin lipid profile from those without. However, whether altered skin lipids precede and predict the subsequent risk of AD remained unclear, especially for different AD phenotypes. Objective: We sought to examine the relationship between skin lipids and subsequent AD and AD phenotypes in infants. Methods: Skin lipids from the forearms of 133 infants with family history of allergic disease were sampled using tape strips at age 6 weeks. Lipids were quantified using liquid chromatography-tandem mass spectrometry. AD by age 1 year was diagnosed using modified UK Working Party Criteria. Allergic sensitization was assessed using skin prick tests. Associations and predictive discrimination were estimated using univariable logistic regression. Potential causation was explored using multivariable logistic regression. Results: Reduced levels of 6 protein-bound ω-hydroxyl sphingosine (POS) ceramides with C30 and C32 fatty acids at 6 weeks were associated with increased risk of AD by age 1 year. In univariate models, a number of POS ceramides predicted subsequent AD, such as PO30:0-C20S (area under the curve, 0.65; 95% CI, 0.55-0.75). After confounders were adjusted, only PO30:0-C20S was associated with AD (adjusted odds ratio, 0.62; 95% CI, 0.39-0.96 per 1-SD increase), and a trend for AD without sensitization (adjusted odds ratio, 0.57; 95% CI, 0.31-1.05) but not AD with sensitization (adjusted odds ratio, 0.76; 95% CI, 0.39-1.47). Conclusions: Reduced levels of POS ceramides are associated with the development of nonatopic AD, suggesting that these lipids may play a role in the pathogenesis of AD and may be useful predictive biomarkers. Interventions that increase POS ceramides may reduce the incidence of AD.

Description:Objective: The impact of lifetime body mass index (BMI) trajectories on adult lung function abnormalities has not been investigated previously. We investigated associations of BMI trajectories from childhood to mid-adulthood with lung function deficits and COPD in mid-adulthood. Methods: Five BMI trajectories (n = 4194) from age 5 to 43 were identified in the Tasmanian Longitudinal Health Study. Lung function outcomes were defined using spirometry at 45 and 53 years. Associations between these BMI trajectories and lung function outcomes were investigated using multivariable regression. Results: Compared to the average BMI trajectory, the child's average-increasing BMI trajectory was associated with greater FVC decline from 45 to 53 years (β = -178 mL; 95% CI -300.6, -55.4), lower FRC, ERV and higher TLco at 45 years, lower FVC (-227 mL; -345.3, -109.1) and higher TLco at 53 years. The High BMI trajectory was also associated with lower FRC, ERV and higher TLco at 45 years, while spirometric restriction (OR = 6.9; 2.3, 21.1) and higher TLco at 53 years. The low BMI trajectory was associated with an obstructive picture: lower FEV1 (-124 mL; -196.4, -51.4) and FVC (-91 mL; -173.4, -7.7), and FEV1/FVC (-1.2%; -2.2, -0.1) and higher ERV and lower TLco at 45 and 53 years. A similar pattern was found at 53 years. No associations were observed with spirometrically defined COPD. Conclusions: Our findings revealed contrasting lung function abnormalities were associated with high, subsequently increasing, and low BMI trajectories. These results emphasise the importance of tracking changes in BMI over time and the need to maintain an average BMI trajectory (BMI-Z-score 0 at each time point) throughout life.