James Markos

The Interplay between the Effects of Lifetime Asthma, Smoking, and Atopy on Fixed Airflow Obstruction in Middle Age

RATIONALE The contribution by asthma to the development of fixed airflow obstruction (AO) and the nature of its effect combined with active smoking and atopy remain unclear. OBJECTIVES To investigate the prevalence and relative influence of lifetime asthma, active smoking, and atopy on fixed AO in middle age. METHODS The population-based Tasmanian Longitudinal Health Study cohort born in 1961 (n = 8,583) and studied with prebronchodilator spirometry in 1968 was retraced (n = 7,312) and resurveyed (n = 5,729 responses) from 2002 to 2005. A sample enriched for asthma and chronic bronchitis underwent a further questionnaire, pre- and post-bronchodilator spirometry (n = 1,389), skin prick testing, lung volumes, and diffusing capacity measurements. Prevalence estimates were reweighted for sampling fractions. Multiple linear and logistic regression were used to assess the relevant associations. MEASUREMENTS AND MAIN RESULTS Main effects and interactions between lifetime asthma, active smoking, and atopy as they relate to fixed AO were measured. The prevalence of fixed AO was 6.0% (95% confidence interval [CI], 4.5-7.5%). Its association with early-onset current clinical asthma was equivalent to a 33 pack-year history of smoking (odds ratio, 3.7; 95% CI, 1.5-9.3; P = 0.005), compared with a 24 pack-year history for late-onset current clinical asthma (odds ratio, 2.6; 95% CI, 1.03-6.5; P = 0.042). An interaction (multiplicative effect) was present between asthma and active smoking as it relates to the ratio of post-bronchodilator FEV(1)/FVC, but only among those with atopic sensitization. CONCLUSIONS Active smoking and current clinical asthma both contribute substantially to fixed AO in middle age, especially among those with atopy. The interaction between these factors provides another compelling reason for atopic individuals with current asthma who smoke to quit.

Ambient wood smoke, traffic pollution and adult asthma prevalence and severity.

The impact of ambient wood smoke and traffic‐related air pollution on adult asthma has not been well studied. This paper aims to investigate associations between exposure to ambient wood smoke, traffic‐related air pollution and current asthma/asthma severity in middle age, and whether any associations are modified by atopic status.

Mother's smoking and complex lung function of offspring in middle age: A cohort study from childhood

Existing evidence that supports maternal smoking to be a potential risk factor for chronic obstructive pulmonary disease (COPD) for adult offspring has barely been mentioned in major guideline documents, suggesting a need for more robust and consistent data. We aimed to examine whether such early life exposure can predispose to COPD in middle age, possibly through its interaction with personal smoking.

Domestic airborne pollutants and asthma and respiratory symptoms in middle age

The role of indoor air pollution as a risk factor for asthma and respiratory symptoms in middle age is unclear. We investigated associations between indoor air pollution sources and (i) asthma phenotypes and (ii) asthma‐related respiratory symptoms in middle‐aged adults.

Cohort Profile: The Tasmanian Longitudinal Health STUDY (TAHS).

Melanie C Matheson,, Michael J Abramson, Katrina Allen, Geza Benke, John A Burgess, James G Dowty, Bircan Erbas, Iain H Feather, Peter A Frith, Graham G Giles, Lyle C Gurrin, Garun S Hamilton, John L Hopper, Alan L James, Mark A Jenkins, David P Johns, Caroline J Lodge, Adrian J Lowe, James Markos, Stephen C Morrison, Jennifer L Perret, Melissa C Southey, Paul S Thomas, Bruce R Thompson, Richard Wood-Baker, Eugene Haydn Walters and Shyamali C Dharmage;* for the TAHS investigator group

Ambient wood smoke exposure and respiratory symptoms in Tasmania, Australia

Wood smoke exposure has been associated with adverse respiratory health outcomes, with much of the current research focused on wood smoke from domestic heating and cooking. This study examined the association between respiratory symptoms and outdoor wood smoke in Launceston, Tasmania, where ~30% of homes use wood burners for domestic heating. This ecological study examined data from participants of the 2004 Tasmanian Longitudinal Health Study postal survey and compared the prevalence of respiratory symptoms in Launceston (n=601) with that in Hobart (n=1071), a larger Tasmanian city with much less wood smoke. Multivariate logistic regression models were used to investigate the associations of interest while adjusting for gender, atopy, history of allergic disease and current smoking status. There were no significant differences in symptom prevalence between Launceston and Hobart. Two subgroup analyses, which examined participants with pre-existing chronic respiratory disease, and those who reported actively using a wood burner in their home, also did not find significant differences. Any impact of wood smoke on non-specific respiratory symptoms might have been overshadowed by other important determinants of respiratory health, such as vehicle exhaust and tobacco smoking, or were too small to have been detected. However, the lack of detectable differences in symptom prevalence might also reflect the success of regulatory action by local governments to reduce wood smoke emissions in Launceston. The results of other epidemiological studies support an association between ambient wood smoke exposure and adverse respiratory health. Further investigations of wood smoke exposure in Australian settings are needed to investigate the lack of significant associations found in this study, especially studies of indoor air quality and health impacts in children and elderly populations.

Pretreatment assessment of pulmonary function: recent predictive studies using respiratory function tests

The standard guidelines for operability for pneumonectomy were established in 1975 by Olsen, Block et al. [5], following their report of 56 patients with impaired lung function who were accepted for surgery if the preoperative FEV, was z 2 1 or the predicted postoperative FEV, was > 0.8 1. If these criteria were not met, then invasive studies involving temporary unilateral pulmonary artery occlusion (TUPAO) were advocated to exclude pulmonary hypertension and arterial hypoxemia prior to attempting lung resection.

An observational study of PM10 and hospital admissions for acute exacerbations of chronic respiratory disease in Tasmania, Australia 1992-2002.

Objective Particulate matter with a diameter below 10 µ (PM10) has been a major concern in the Tamar Valley, Launceston, where wood heaters are extensively used. We examined the relationship between PM10 levels, meteorological variables, respiratory medications and hospital admissions for respiratory disease over the decade 1992–2002. Methods PM10 levels were provided by the Department of Primary Industry Water, Parks and Environment, and meteorological variables from the Bureau of Meteorology. We obtained hospital discharge codes for the Launceston General Hospital. Poisson regression was used for statistical analyses. Results Mean daily PM10 levels declined from 50.7 to 16.5 μg/m3. Hospitalisations for asthma decreased from 29 to 21 per month, whereas chronic obstructive pulmonary disease (COPD) increased and bronchitis/bronchiolitis remained unchanged. We found a 10 μg/m3 increase in PM10 to be associated with a 4% increase in admissions for acute bronchitis/bronchiolitis (p0.05), but no association with asthma or COPD was found. All respiratory diseases showed seasonal patterns of hospitalisation. Conclusions This is the first long-term study in Australia to demonstrate an association between PM10 levels and respiratory diseases. Reducing exposure to PM10 may decrease hospital admissions for respiratory diseases. Implication Better preventive measures, including sustained public health initiatives to combat air pollution, are required to reduce respiratory morbidity.

The Dose-Response Association between Nitrogen Dioxide Exposure and Serum Interleukin-6 Concentrations

Systemic inflammation is an integral part of chronic obstructive pulmonary disease (COPD), and air pollution is associated with cardiorespiratory mortality, yet the interrelationships are not fully defined. We examined associations between nitrogen dioxide (NO2) exposure (as a marker of traffic-related air pollution) and pro-inflammatory cytokines, and investigated effect modification and mediation by post-bronchodilator airflow obstruction (post-BD-AO) and cardiovascular risk. Data from middle-aged participants in the Tasmanian Longitudinal Health Study (TAHS, n = 1389) were analyzed by multivariable logistic regression, using serum interleukin (IL)-6, IL-8 and tumor necrosis factor-α (TNF-α) as the outcome. Mean annual NO2 exposure was estimated at residential addresses using a validated satellite-based land-use regression model. Post-BD-AO was defined by post-BD forced expiratory ratio (FEV1/FVC) < lower limit of normal, and cardiovascular risk by a history of either cerebrovascular or ischaemic heart disease. We found a positive association with increasing serum IL-6 concentration (geometric mean 1.20 (95% CI: 1.1 to 1.3, p = 0.001) per quartile increase in NO2). This was predominantly a direct relationship, with little evidence for either effect modification or mediation via post-BD-AO, or for the small subgroup who reported cardiovascular events. However, there was some evidence consistent with serum IL-6 being on the causal pathway between NO2 and cardiovascular risk. These findings raise the possibility that the interplay between air pollution and systemic inflammation may differ between post-BD airflow obstruction and cardiovascular diseases.

Sarcoidosis: a state of the art review from the Thoracic Society of Australia and New Zealand.

Sarcoidosis is a systemic disease of unknown aetiology, characterised by non-caseating granulomatous inflammation. It most commonly manifests in the lungs and intrathoracic lymph nodes but can affect any organ. This summary of an educational resource provided by the Thoracic Society of Australia and New Zealand outlines the current understanding of sarcoidosis and highlights the need for further research. Our knowledge of the aetiology and immunopathogenesis of sarcoidosis remains incomplete. The enigma of sarcoidosis lies in its immunological paradox of type 1 T helper cell-dominated local inflammation co-existing with T regulatory-induced peripheral anergy. Although specific aetiological agents have not been identified, mounting evidence suggests that environmental and microbial antigens may trigger sarcoidosis. Genome-wide association studies have identified candidate genes conferring susceptibility and gene expression analyses have provided insights into cytokine dysregulation leading to inflammation. Sarcoidosis remains a diagnosis of exclusion based on histological evidence of non-caseating granulomas with compatible clinical and radiological findings. In recent years, endobronchial ultrasound-guided transbronchial needle aspiration of mediastinal lymph nodes has facilitated the diagnosis, and whole body positron emission tomography scanning has improved localisation of disease. No single biomarker is adequately sensitive and specific for detecting and monitoring disease activity. Most patients do not require treatment; when indicated, corticosteroids remain the initial standard of care, despite their adverse side effect profile. Other drugs with fewer side effects may be a better long term choice (eg, methotrexate, hydroxychloroquine, azathioprine, mycophenolate), while tumour necrosis factor-α inhibitors are a treatment option for patients with refractory disease.