Search

BackgroundMobile technology interventions (MTI) are becoming increasingly popular in the management of chronic health behaviors. Most MTI allow individuals to monitor medication use, record symptoms, or store and activate disease-management action plans. Therefore, MTI may have the potential to improve low adherence to medication and action plans for individuals with asthma, which is associated with poor clinical outcomes. ObjectiveA systematic review and meta-analysis were conducted to evaluate the efficacy of MTI on clinical outcomes as well as adherence in individuals with asthma. As the use of evidence-based behavior change techniques (BCT) has been shown to improve intervention effects, we also conducted exploratory analyses to determine the role of BCT and engagement with MTI as moderators of MTI efficacy. MethodsWe searched electronic databases for randomized controlled trials up until June 2016. Random effect models were used to assess the effect of MTI on clinical outcomes as well as adherence to preventer medication or symptom monitoring. Mixed effects models assessed whether the features of the MTI (ie, use of BCT) and how often a person engaged with MTI moderated the effects of MTI. ResultsThe literature search located 11 studies meeting the inclusion criteria, with 9 providing satisfactory data for meta-analysis. Compared with standard treatment, MTI had moderate to large effect sizes (Hedges g) on medication adherence and clinical outcomes. MTI had no additional effects on adherence or clinical outcomes when compared with paper-based monitoring. No moderator effects were found, and the number of studies was small. A narrative review of the two studies, which are not included in the meta-analysis, found similar results. ConclusionsThis review indicated the efficacy of MTI for self-management in individuals with asthma and also indicated that MTI appears to be as efficacious as paper-based monitoring. This review also suggested a need for robust studies to examine the effects of BCT use and engagement on MTI efficacy to inform the evidence base for MTI in individuals with asthma.

Background: Historical data on smoking can enhance our comprehension of the effectiveness of past tobacco control policies and play a key role in developing targeted public health interventions. This study was undertaken to assess trends in smoking initiation and cessation in Australia for the period 1910–2005. Methods: Rates of smoking initiation and cessation were calculated for participants in two population-based cohorts, the Busselton Health Study and the Tasmanian Longitudinal Health Study. The effects of time trends, gender and age group were evaluated. Results: Of the 29,971 participants, 56.8% ever smoked. In males, over the period 1910–1999, the rate of smoking initiation in young adolescents remained high with a peak in the 1970s; in older adolescents it peaked in the 1940s and then declined; in young adults it showed a steady decline. In females, the rate of smoking initiation in young adolescents rose sharply in the 1960s and peaked in the 1970s, in older adolescents it increased throughout the period, and in young adults it declined after 1970. In the period 1930–2005, 27.3% of 9,605 people aged 36–50 years who smoked ceased smoking. Rates of cessation in this age group increased throughout but decreased in males after 1990 and plateaued around 2000 in females. Conclusion: Our findings show substantial variation in the efficacy of tobacco control policies across age groups, with a notable lack of success among the younger population. [ABSTRACT FROM AUTHOR]

Rationale: The term "pre–chronic obstructive pulmonary disease" ("pre-COPD") refers to individuals at high risk of developing COPD who do not meet conventional spirometric criteria for airflow obstruction. New approaches to identifying these individuals are needed, particularly in younger populations. Objectives: To determine whether lung function thresholds and respiratory symptoms can be used to identify individuals at risk of developing COPD. Methods: The Tasmanian Longitudinal Health Study comprises a population-based cohort first studied in 1968 (at age 7 yr). Respiratory symptoms, pre- and post-bronchodilator (BD) spirometry, diffusing capacity, and static lung volumes were measured in a subgroup at age 45, and the incidence of COPD was assessed at age 53. For each lung function measure, z-scores were calculated using Global Lung Function Initiative references. The optimal threshold for best discrimination of COPD incidence was determined by the unweighted Youden index. Measurements and Main Results: Among 801 participants who did not have COPD at age 45, the optimal threshold for COPD incidence by age 53 was pre-BD FEV1/FVC z-score less than −1.264, corresponding to the lowest 10th percentile. Those below this threshold had a 36-fold increased risk of developing COPD over an 8-year follow-up period (risk ratio, 35.8; 95% confidence interval, 8.88 to 144), corresponding to a risk difference of 16.4% (95% confidence interval, 3.7 to 67.4). The sensitivity was 88%, and the specificity was 87%. Positive and negative likelihood ratios were 6.79 and 0.14, respectively. Respiratory symptoms, post-BD spirometry, diffusing capacity, and static lung volumes did not improve on the classification achieved by pre-BD FEV1/FVC alone. Conclusions: This is the first study, to our knowledge, to evaluate the discriminatory accuracy of spirometry, diffusing capacity, and static lung volume thresholds for COPD incidence in middle-aged adults. Our findings support the inclusion of pre-BD spirometry in the physiological definition of pre-COPD and indicate that pre-BD FEV1/FVC at the 10th percentile accurately identifies individuals at high risk of developing COPD in community-based settings. [ABSTRACT FROM AUTHOR]

The complex nature of chronic bronchitis (CB) and changing definitions have contributed to challenges in understanding its aetiology and burden. In children, CB is characterised by persistent airway inflammation often linked to bacterial infections and is therefore termed "protracted bacterial bronchitis" (PBB). Longitudinal studies suggest that CB in childhood persists into adulthood in a subgroup. It can also be associated with future chronic respiratory diseases including asthma, bronchiectasis, and chronic obstructive pulmonary disease (COPD). Adult CB is traditionally associated with smoking, occupational exposures, and lower socioeconomic status. The interplay between risk factors, childhood CB, adult CB, and other chronic respiratory diseases is intricate, requiring comprehensive longitudinal studies for a clearer understanding of the natural history of CB across the lifespan. Such longitudinal studies have been scarce to date given the logistic challenges of maintaining them over time. In this review, we summarise current evidence on the evolution of the definitions, pathophysiology, risk factors, and consequences of childhood and adulthood chronic bronchitis. [ABSTRACT FROM AUTHOR]

Background and Objective: Early‐life risk factors for obstructive sleep apnoea (OSA) are poorly described, yet this knowledge may be critical to inform preventive strategies. We conducted the first study to investigate the association between early‐life risk factors and OSA in middle‐aged adults. Methods: Data were from population‐based Tasmanian Longitudinal Health Study cohort (n = 3550) followed from 1st to 6th decades of life. Potentially relevant childhood exposures were available from a parent‐completed survey at age 7‐years, along with previously characterized risk factor profiles. Information on the primary outcome, probable OSA (based on a STOP‐Bang questionnaire cut‐off ≥5), were collected when participants were 53 years old. Associations were examined using logistic regression adjusting for potential confounders. Analyses were repeated using the Berlin questionnaire. Results: Maternal asthma (OR = 1.5; 95% CI 1.1–2.0), maternal smoking (OR = 1.2; 1.05, 1.5), childhood pleurisy/pneumonia (OR = 1.3; 1.04, 1.7) and frequent bronchitis (OR = 1.2; 1.01, 1.5) were associated with probable OSA. The risk‐factor profiles of 'parental smoking' and 'frequent asthma and bronchitis' were also associated with probable OSA (OR = 1.3; 1.01, 1.6 and OR = 1.3; 1.01–1.9, respectively). Similar associations were found for Berlin questionnaire‐defined OSA. Conclusions: We found novel temporal associations of maternal asthma, parental smoking and frequent lower respiratory tract infections before the age of 7 years with adult OSA. While determination of their pathophysiological and any causal pathways require further research, these may be useful to flag the risk of OSA within clinical practice and create awareness and vigilance among at‐risk groups. This study provides the first known evidence for individual and profiled early‐life and childhood risk factors for OSA in adults. It shows that early exposures to smoking and lower respiratory tract infections could be risks for adult OSA, which may stimulate future research and help flag future risk of OSA. See relatededitorial [ABSTRACT FROM AUTHOR]

Tasmania led in several areas of tobacco control legislation reform in the period 1997 to 2010. Despite this, Tasmania lagged in other crucial areas, particularly the allocation of resources for community education, mass media campaigns and cessation programmes. Key impediments were crony capitalism; the conservative ideology of "white male" politicians; cognitive dissonance of smoking politicians; a lack of perception of priority regarding the scientific research evidence about smoking risk; and delays caused by the tobacco industry. This study analyses the political situation in Tasmania and argues that evidence-based progress on tobacco control resource allocation was not established until 2013.

Background and Objective: Little is known about the association between ambient air pollution and idiopathic pulmonary fibrosis (IPF) in areas with lower levels of exposure. We aimed to investigate the impact of air pollution on lung function and rapid progression of IPF in Australia. Methods: Participants were recruited from the Australian IPF Registry (n = 570). The impact of air pollution on changes in lung function was assessed using linear mixed models and Cox regression was used to investigate the association with rapid progression. Results: Median (25th–75th percentiles) annual fine particulate matter (<2.5 μm, PM2.5) and nitrogen dioxide (NO2) were 6.8 (5.7, 7.9) μg/m3 and 6.7 (4.9, 8.2) ppb, respectively. Compared to living more than 100 m from a major road, living within 100 m was associated with a 1.3% predicted/year (95% confidence interval [CI] −2.4 to −0.3) faster annual decline in diffusing capacity of the lungs for carbon monoxide (DLco). Each interquartile range (IQR) of 2.2 μg/m3 increase in PM2.5 was associated with a 0.9% predicted/year (95% CI −1.6 to −0.3) faster annual decline in DLco, while there was no association observed with NO2. There was also no association between air pollution and rapid progression of IPF. Conclusion: Living near a major road and increased PM2.5 were both associated with an increased rate of annual decline in DLco. This study adds to the evidence supporting the negative effects of air pollution on lung function decline in people with IPF living at low‐level concentrations of exposure. [ABSTRACT FROM AUTHOR]