Thesis (Ph. D.)--University of Missouri--Columbia, 2001. / "December 2001." Typescript. Vita. Includes bibliographical references (leaves 163-171). Also available on the Internet.

published_or_final_version / Medicine / Master / Master of Philosophy

Work-related asthma surveillance is needed to improve management of occupational exposures, clinical recognition/diagnosis, and worker compensation policies. This work investigated asthma in relation to work by evaluating the utility of existing Canadian surveillance data in providing useful information about the burden of work-related asthma; estimating the burden of work-related asthma among Canada's adult population; and evaluating the effect of job risk on asthma after considering other potential risk factors for asthma. The working population formed samples from two Statistics Canada surveillance programs: Canadian Community Health Survey (CCHS), 2002/03 Cycle 2.1 and National Population Health Survey (NPHS), Longitudinal Component (1994/95-2002/03). Both surveys enquired about health professional-diagnosed asthma; NPHS additionally asked age at time of diagnosis, so adult-onset versus childhood-onset asthma was determined. Both surveys enquired about current job held; corresponding job codes were linked to an asthma-specific job exposure matrix to judge job risk for occupational asthma. CCHS only provided current job information, in contrast, NPHS longitudinal data was used to determine job held at time of asthma-onset. Statistical measures for asthma in relation to job risk were estimated. CCHS results were likely biased by the healthy worker effect, as it showed the opposite effect of job risk on asthma than the NPHS; higher asthma prevalence was shown for NPHS men and women in high risk jobs. NPHS results indicated a large burden of adult-onset asthma among men (19,000) and childhood-onset asthma among women (17,000) attributed to working in high risk jobs for occupational asthma. Using NPHS, adjusted and crude prevalence odds ratio estimates were compared to further assess effect of job risk on asthma. For adult-onset asthma, there was no difference between estimates (men: 1.8, women: 1.1); for childhood-onset asthma, adjusted estimates were larger than crude, respectively (men: 1.3 v 1.2, women: 2.0 v 1.7). Age of asthma-onset and job held at time of asthma-onset is necessary surveillance information for estimating work-related asthma. There may be increased risk of work" caused" asthma among men and work "exacerbated" asthma among women in high risk jobs. Considering other risk factors for asthma did not reduce effect of job risk on asthma.

Dissertation submitted in partial compliance with the requirements for the Masterà ¢ s Degree in Technology: Chiropractic, Durban University of Technology, 2008. / Objectives: To determine the short-term effect of an inhaled, short-acting 2-agonist bronchodilator on chest wall expansion (cm) and lung function parameters (FEV1, FVC and FEV1/FVC%) in chronic moderate asthmatics. To determine the short-term effect of spinal manipulation (SMT) and ribcage mobilisation on chest wall expansion (cm) and lung function parameters (FEV1, FVC and FEV1/FVC%) in chronic moderate asthmatics. To determine the short-term effect of a combination of SMT, ribcage mobilisation and an inhaled, short-acting 2-agonist bronchodilator on chest wall expansion (cm) and lung function parameters (FEV1, FVC and FEV1/FVC%) in chronic moderate asthmatics. Methods: Forty-five chronic moderate asthmatics who met all the inclusion criteria of the study were divided into three groups of fifteen each. Group A received a short-acting 2-agonist bronchodilator, Group B received SMT and ribcage mobilisation and Group C received a combination of SMT, ribcage mobilisation and a short-acting 2-agonist bronchodilator. Baseline measurements and testing included chest wall expansion and the lung function parameters FEV1, FVC and FEV1/FVC%. These measurements were repeated 15 minutes post-intervention. Data was analyzed using SPSS version 15.0. Results: There were no statistically significant changes between pre- and post-intervention in the short-acting 2-agonist bronchodilator group with respect to any of the chest wall expansion measurements. There was a statisticallly significant increase in FEV1 between pre- and post-intervention in the short-acting 2-agonist bronchodilator group (p = 0.008). There was a statistically significant increase in the mean pre- and post-intervention axillary chest wall expansion (p = 0.014) as well as the mean of the half-way measurement (p = 0.014) and the overall mean chest wall expansion value (p = 0.001) following SMT and ribcage mobilisation. There were no statistically significant changes in any of the lung function parameter values following SMT and ribcage mobilisation. There was a significant increase for the half-way measurement in chest wall expansion (p = 0.018) in the combination of SMT, ribcage mobilisation and the inhaled, short-acting 2-agonist bronchodilator group. There were no statistically significant changes in any of the lung function parameter values in the combination of SMT, ribcage mobilisation and an inhaled, short-acting 2-agonist bronchodilator. For FEV1, the effect in the short-acting 2-agonist bronchodilator group vs. the SMT and ribcage mobilisation group was statistically significant (p = 0.018). There was no statistical difference in any of the chest wall expansion measurements and FVC and FEV1/FVC% parameters between all three groups. Conclusions The results did not point specifically to one intervention over another for all outcomes. SMT and rib mobilisation had no effect on the lung function parameters, at least in the short term. There was a statisticallly significant increase in FEV1 between pre- and post-intervention in the short-acting 2-agonist bronchodilator group.

Asthma has not declined in morbidity and mortality despite significant advances in medical treatment. A literature review was conducted and a program of research was devised with the goal of improving understanding of why many appropriately treated and educated asthmatics are unable to gain adequate control of their asthma. A review of the literature found that psychological stress was a poorly understood trigger for asthmatic symptoms and a possible factor in poor asthma control. A clinic visit study of adult asthmatics found: (1) life event stress was associated with asthma quality of life but not ventilatory function, (2) asthma self-efficacy was strongly related to asthma quality of life and ventilatory function, (3) style of coping with stress appeared to buffer the effects of stress on asthma, and (4) evidence for a stress-responsive asthmatic subgroup. A subsequent longitudinal daily diary study found: (1) concurrent stress and daily asthma symptoms were strongly associated, (2) daily bronchodilator use appeared to be determined by pre-diary beliefs about disease severity and controllability, (3) stress could precede (within one day) increases in asthma symptoms and decreases in airflow, and (4) clinically significant decreases in peak flow were often preceded by large increases in perceived stress. A laboratory study found: (1) exposure of asthmatics to specific passive and asthma-related stressors resulted in decreased airflow and that these decreases are associated with a concurrent increase in vagal (parasympathetic) tone, (2) an active stressor that resulted in increased sympathetic arousal did not result in decreased airflow, (3) relaxation resulted in parasympathetic arousal and decreased airflow, and (4) asthma self-efficacy was associated with parasympathetic reactivity. In sum, the program of research has generated findings that help explain how stress, coping and self-efficacy contribute to asthma control led to concrete suggestions to improve c

The purpose of this study was to determine if exercise-induced asthma (EIA) could be prevented in an outdoor environment in asthmatic children attending a summer camp 3 hours after their usual dose of medication. Most studies that test for ETA are done in a controlled environment which may make results not applicable to asthmatic children who spend a lot of their time outside. The relationship of aerobic fitness and level of activity to the severity of EIA were also examined. A total of 25 subjects (10.9+0.9 yrs, M±SD) were tested. Subjects were instructed to run around a grass field circular course (0.1 mile) for 5 minutes. The subjects could stop at any time. Baseline measurements of heart rate, respiratory rate and peak flow were determined before the test and at 1, 5, and 10 minutes following the end of the run. A fall in peak flow of >10% from baseline was considered positive for EIA. A total of 14 subjects experienced EIA following the run. There were no significant differences between the group who experienced EIA and those who did not in terms of heart rate, respiratory rate, or distance run. There was a significant difference between peak flow recordings as expected. Aerobic fitness and physical activity were not related to the severity of EIA. The results of this study suggests that additional medications may be needed to prevent EIA in these children in order to allow participation in activities which may produce EIA. Moreover, 3 hours may be beyond the protection time limit for some asthmatic children. / School of Physical Education

Work-related asthma surveillance is needed to improve management of occupational exposures, clinical recognition/diagnosis, and worker compensation policies. This work investigated asthma in relation to work by evaluating the utility of existing Canadian surveillance data in providing useful information about the burden of work-related asthma; estimating the burden of work-related asthma among Canada's adult population; and evaluating the effect of job risk on asthma after considering other potential risk factors for asthma. The working population formed samples from two Statistics Canada surveillance programs: Canadian Community Health Survey (CCHS), 2002/03 Cycle 2.1 and National Population Health Survey (NPHS), Longitudinal Component (1994/95-2002/03). Both surveys enquired about health professional-diagnosed asthma; NPHS additionally asked age at time of diagnosis, so adult-onset versus childhood-onset asthma was determined. Both surveys enquired about current job held; corresponding job codes were linked to an asthma-specific job exposure matrix to judge job risk for occupational asthma. CCHS only provided current job information, in contrast, NPHS longitudinal data was used to determine job held at time of asthma-onset. Statistical measures for asthma in relation to job risk were estimated. CCHS results were likely biased by the healthy worker effect, as it showed the opposite effect of job risk on asthma than the NPHS; higher asthma prevalence was shown for NPHS men and women in high risk jobs. NPHS results indicated a large burden of adult-onset asthma among men (19,000) and childhood-onset asthma among women (17,000) attributed to working in high risk jobs for occupational asthma. Using NPHS, adjusted and crude prevalence odds ratio estimates were compared to further assess effect of job risk on asthma. For adult-onset asthma, there was no difference between estimates (men: 1.8, women: 1.1); for childhood-onset asthma, adjusted estimates were larger than crude, respectively (men: 1.3 v 1.2, women: 2.0 v 1.7). Age of asthma-onset and job held at time of asthma-onset is necessary surveillance information for estimating work-related asthma. There may be increased risk of work" caused" asthma among men and work "exacerbated" asthma among women in high risk jobs. Considering other risk factors for asthma did not reduce effect of job risk on asthma.

[Truncated abstract] Asthma affects millions of people worldwide and places a substantial burden on the healthcare system. Despite advances in our understanding of disease mechanisms and the role of respiratory viruses in asthma exacerbations, there is little known regarding the role of the epithelium in commonly observed structural changes in the airway wall. The epithelium of the airways provides an essential protective barrier between the environment and underlying structures and is responsible for the secretion of diverse compounds. Since it is likely that dysregulated epithelial characteristics and function in childhood asthma are critical determinants of disease progression in adults, it is pertinent to investigate the cellular mechanisms involved in paediatric asthma. However, full comprehension of paediatric respiratory diseases and the childhood antecedents of adult respiratory disease are currently hampered by the difficulty in obtaining relevant target organ tissue and most of the data to date have been generated from studies involving adults or commercially derived cell lines. This laboratory has successfully developed methodologies of obtaining and studying samples of paediatric primary airway epithelial cells (pAECs) and has identified significant biochemical and functional differences between healthy non-atopic (pAECHNA) and atopic asthmatic (pAECAA) airway cells, which have assisted in the identification of potential mechanisms responsible for abnormal epithelial function. Stevens 2009 ... Exposure of pAECs with RV resulted in elevated PAI-1 mRNA expression and reduced MMP-9 release in both pAECAA and pAECHNA samples. Collectively, the data presented indicate that RV exposure induces a pronounced antiproliferative and retardative repair effect in pAECAA and that the presence of virus may have a role in the PAI-1 and MMP expression witnessed in these cells. In conclusion, this investigation has further characterised the essential role the airway epithelium plays in childhood asthma by demonstrating for the first time that pAECs from asthmatic children lack the ability to successfully repair mechanically induced wounds. This investigation also showed that PAI-1 is elevated in pAECAA and has a functional role in the pAEC proliferative and regenerative processes. It was demonstrated that MMP-2 and MMP-9 activities and the MMP-9/TIMP-1 as well as MMP2/TIMP2 ratios were significantly reduced in pAECAA thereby providing additional evidence that there is a dysregulation in the mechanisms that monitor the turnover of the ECM in childhood asthma. Furthermore, this study has shown for the first time that pAECs from untreated mild atopic-asthmatic children are more sensitive to the pathogenic effects of RV than healthy control cells and that RV exposure delays cellular proliferation and repair. Ultimately, these findings support the hypothesis postulated and provide evidence that indeed the dysregulated epithelial functional characteristics seen in childhood mild asthma may be a critical determinant of disease progression in adults.

Doctor of Philosophy / Asthma can be a chronic disorder requiring regular medications if the symptoms are persistent. The regimen is often complex, involving a number of drugs and a variety or routes of administration. Although drug therapy may not alter the natural history of asthma it can improve lung function enabling those with asthma to lead as near a normal life as possible. Thus medication compliance is an important factor in the managemnt of asthma. (Note : Special enclosures (Publication reprints) at end of thesis have been removed for digital submission, with permission of author)

Thesis (M.A.)--Northern Kentucky University, 2007. / Made available through ProQuest. Publication number: AAT 1447775. ProQuest document ID: 1472164161. Includes bibliographical references (p. 48-51)