Decline in Lung Function in the Busselton Health Study: the Effects of Asthma and Cigarette Smoking
Asthma in adults may be associated with chronic airflow obstruction, possibly resulting from airway disease in early life and/or a greater rate of decline in lung function in adult life compared with those with asthma. Treatment and cigarette smoking may also influence the rate of decline of lung function. The aim of this analysis was to examine the level and rate of decline in lung function in relationship to asthma and cigarette smoking in adults. Subjects (n = 9,317) had participated as adults (> 18 years) in one or more of the cross-sectional Busselton Health Surveys between 1966 and 1981 or in the follow-up study of 1994/1995. The effects of sex, doctor-diagnosed asthma, smoking status, and anthropometric data on the level and rate of decline in FEV1 were examined in a linear mixed effects model. At the age of 19 years, FEV1 was reduced in subjects with asthma but was similar in smokers and nonsmokers. Males, taller subjects, smokers, and subjects with asthma had greater declines in FEV1 with age. Smoking and asthma had additive but not multiplicative effects on decline. Thus, asthma is associated with reduced lung function at the beginning of adult life as well as an increased rate of decline during adult life.
Available from: Romola S Bucks
- "The Shire has been the site of repeated cross-sectional surveys of adults from 1966 to 2009, with participation rates ranging from 64 to 91% . Health surveys have previously focused on specific systems or diseases: respiratory [14,15]; cardiovascular [16-18]; gastrointestinal ; endocrine ; iron metabolism [21,22]; cancer mortality ; the “metabolic syndrome” ; dementia and diabetes  and genetic epidemiology [13,26-28]. "
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ABSTRACT: The global trend of increased life expectancy and increased prevalence of chronic and degenerative diseases will impact on health systems. To identify effective intervention and prevention strategies, greater understanding of the risk factors for and cumulative effects of chronic disease processes and their effects on function and quality of life is needed.The Busselton Healthy Ageing Study aims to enhance understanding of ageing by relating the clustering and interactions of common chronic conditions in adults to function. Longitudinal (3--5 yearly) follow-up is planned.Methods/design: Phase I (recruitment) is a cross-sectional community-based prospective cohort study involving up to 4,000 'Baby Boomers' (born from 1946 to 1964) living in the Busselton Shire, Western Australia. The study protocol involves a detailed, self-administered health and risk factor questionnaire and a range of physical assessments including body composition and bone density measurements, cardiovascular profiling (blood pressure, ECG and brachial pulse wave velocity), retinal photography, tonometry, auto-refraction, spirometry and bronchodilator responsiveness, skin allergy prick tests, sleep apnoea screening, tympanometry and audiometry, grip strength, mobility, balance and leg extensor strength. Cognitive function and reserve, semantic memory, and pre-morbid intelligence are assessed. Participants provide a fasting blood sample for assessment of lipids, blood glucose, C-reactive protein and renal and liver function, and RNA, DNA and serum are stored. Clinically relevant results are provided to all participants. The prevalence of risk factors, symptoms and diagnosed illness will be calculated and the burden of illness will be estimated based on the observed relationships and clustering of symptoms and illness within individuals. Risk factors for combinations of illness will be compared with those for single illnesses and the relation of combinations of illness and symptoms to cognitive and physical function will be estimated.
This study will enable a thorough characterization of multiple disease processes and their risk factors within a community-based sample of individuals to determine their singular, interactive and cumulative effects on ageing. The project will provide novel cross-sectional data and establish a cohort that will be used for longitudinal analyses of the genetic, lifestyle and environmental factors that determine whether an individual ages well or with impairment.
Available from: Helmi Ben Saad
- "Smoking, shown to be detrimental to health for many years    , has an adverse effect on the first second forced expiratory volume (FEV 1 ) throughout a lifetime, reducing the maximal FEV 1 achieved, bringing forward the age of onset of decline in FEV 1 , and hastening the rate of decline . The single most useful intervention to improve lung function in smokers, with or without, chronic obstructive pulmonary disease is smoking cessation. "
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ABSTRACT: Introduction: Interpretation of ‘‘lung age’’ data relies upon comparison of the chronological
lung age (CLA) with the estimated lung age (ELA) predicted from published reference équations [7–10].
Aim: To test the applicability of the published reference equations in healthy non-smoker Tunisian aged 19–90 years.
Population and methods: Published reference equations were applied to the spirometry results of 540 adults (364 women). Two methods of comparison were applied: (i) Determination, according each equation, of the percentages of subjects having a deltaLungAge (=ELA–CLA) >Upper-Limit-of-Normal (ULN). (ii) Bland and Altman comparison, for the same age range as in the corresponding study, between CLA and ELA.
Results: The mean ± SD (95% confidence interval) of the total sample CLA and height were 48.8 ±13.1 (47.7–49.9) years and 164± 10 (163–165) cm. (i) The percentages of healthy subjects with a deltaLungAge > ULN varied from 1% (Newbury) to 64% (Hansen) in men, and from 20% (Yamaguchi) to 51% (Hansen, Morris and Temple) for women. (ii) Mean ± SD ELA was significantly underestimated by 17 ± 19 years (Hansen), by 12 ±23 years (Morris and Temple) and was significantly overestimated by 4± 19 years (Newbury). Mean ± SD ELA from Yamaguchi et al.  was not statistically different from the CLA (1 ±14 years).
Conclusion: The published reference equations did not reliably predict CLA data in the Tunisian population. Awaiting the establishment of reliable equation proper to North African population, we recommend the use of the Yamaguchi et al.’s  reference equations.
Available from: Mendes Carlos Maurício Cardeal
- "The relationship between asthma and COPD appears to be bidirectional and complex. Asthma patients who smoke are known to have more frequent exacerbations, a poorer response to ICs, and early functional impairment, and sometimes it is difficult to distinguish between COPD and severe asthma, the inflammation of which can mimic the neutrophilic inflammation of COPD.(
) Paradoxically, a high frequency of eosinophilic bronchitis has been described in patients with stable COPD.(
) There is evidence of a subgroup of COPD patients who have a greater response to high doses of ICs, a positive bronchodilator response, frequent exacerbations, and an FEV1 < 50% of the predicted value. However, it is necessary to establish the profile of these patients more accurately, reducing the side effects and costs related to the use of high doses of ICs in nonresponding patients.( "
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ABSTRACT: To determine the prevalence of atopy and to evaluate clinical, laboratory, and radiological profiles in patients with COPD.
This was a cross-sectional study involving outpatients with stable COPD (defined by the clinical history and a post-bronchodilator FEV1/FVC < 70% of the predicted value). The patients completed a questionnaire regarding clinical characteristics and atopy, after which they underwent nasal lavage cytology, skin prick testing, chest X-rays, arterial blood gas analyses, and determination of total serum IgE.
Of the 149 subjects studied, 53 (35.6%), 49 (32.8%), and 88 (59.1%) presented with nasal eosinophilia, a positive skin prick test result, and symptoms of allergic rhinitis, respectively. Correspondence analysis confirmed these findings, showing two distinct patterns of disease expression: atopy in patients with COPD that was less severe; and no evidence of atopy in those with COPD that was more severe (reduced FEV1 and hyperinflation). There was a statistically significant association between nasal eosinophilia and a positive bronchodilator response.
Using simple and reproducible methods, we were able to show that there is a high frequency of atopy in patients with COPD. Monitoring inflammation in the upper airways can be a useful tool for evaluating respiratory diseases in the elderly and in those with concomitant asthma and COPD, a clinical entity not yet fully understood.
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