Category - Part 12
Airways Obstruction From Asbestos Exposure: Categories
Each posteroanterior radiograph was scored for profusion category on the expanded ILO scale from 0/0 to 3/3. One experienced reader read all radiographs for consistency of interpretation. Periodically during the study, at intervals of 500 chest films, blinded sets of 100 chest films were reread for intrareader variation. Variation was confined to ILO profusion categories of 0/1, 1/0, and 1/1, was randomly above or below original readings, and never exceeded and testing their significance and the proportion of the variance each explained.
All pulmonary function values were adjusted for height and age of workers and expressed as means percent predicted. Because 81 percent of these men had smoked cigarettes for 1 year or longer, for current and ex-smokers, FEVi, flows, and TLC were adjusted for duration of smoking. These regression equations gave equivalent values to those of Morris et al in nonsmokers.
Airways Obstruction From Asbestos Exposure: History
One medical team gave questionnaires to these workers and did chest physical examinations, chest radiographs, spirometry, and measured alveolar carbon monoxide to validate smoking histories. The questionnaire was completed by trained interviewers. Occupational history included proximity to and duration of exposure to asbestos, medical, pulmonary, and cardiovascular histories, including criteria to define chronic bronchitis and asthma based on the Epidemiology Standardization Project, DLD-78.
Spirometry was done on rolling seal spirometers (Ohio 820, Sensor Medics, Anaheim, Calif) with the subjects standing using a nose clip and otherwise followed the American Thoracic Society (ATS) Snowbird recommendations. Spirometer calibrations were checked for volume and clock speed repeatedly at each site. Care was taken to ensure complete expiration, that is a plateau or a duration of at least 10 s. Alveolar carbon monoxide was measured after a 20-s breath hold with a fuel cell analyzer. buy ventolin inhaler
Airways Obstruction From Asbestos Exposure: Methods
The men with asbestosis and the age-matched asbestos-exposed comparison men were from 8,720 workers studied at 47 sites across the United States from California to Florida. The asbestos exposed men (ILO profusion 0/0 and 0/1) were individually matched for age to men with asbestosis (ILO profusion 1 /0 to 3/3) in each smoking category using a computer algorithm. A few current and ex-smokers, older than 65 years, were matched to the next youngest or oldest individual if the match pool for their identical age was exhausted. Most of the men with asbestosis had ILO profusions of 1/0 to 1/2, 3 percent had profusions of 2/1 to 2/3, and only 0.3 percent had profusions of 3/2 or greater.
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Airways Obstruction From Asbestos Exposure: Data
Another possibility, that volume has been replaced by fibrosis in normal-sized lungs, would increase the postmortem weight of lungs. Weight is not increased in asbestosis nor are alveoli filled by nonradiodense material as in alveolar lipoproteinosis.
Alternately there would be “apparent restrictive impairment” if obstruction continued through advancement of asbestosis causing air trapping and progressive reduction of FVC within a normal TLC. The ideal demonstration of the time course of functional impairment of asbestosis would be by periodic pulmonary function measurements during a life-long study of an asbestos-exposed population accompanied by morphometric studies of the lungs of decedents. Lacking the luxuries of 20 years and funding for follow-up from these baselines, another approach is to assume that the profusion of irregular opacities approximates the structural abnormality and construct the time course using cross-sectional data.
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Airways Obstruction From Asbestos Exposure
Workers with clinical asbestosis have been characterized as having “restrictive” disease because of reduced vital capacity (VC) and in some cases reduced total lung capacity (TLC). This is thought to occur despite airway obstruction and increased TLC due to cigarette smoking. The TLC was decreased when functional residual capacities (FRC) were measured by gas dilution using the closed circuit helium method, which underestimates residual volume when there is air trapping. Only a few FRCs in asbestosis were measured by body plethysmography. Two other factors, incomplete expirations (early termination) which undermeasure VC and the use of pneumotachygraphs for spirometry which do not yield accurate volumes at low flows may have underestimated VC, and TLC when VC was added to RV there asthma inhaler. Despite these problems, a 1970 study of asbestos exposure in miners and millers found reduced FEVi, that is, airways obstruction and reduced FVC before there was visible radiographic asbestosis. Subsequently, FEF75-85 and/or FEF25-75 were shown to be reduced before FEVi and FVC were decreased.” This physiologic obstruction has been attributed to peribronchiolar infiltrates and fibrosis as observed originally by Gloyne in 1933 and described subsequently by Wright and Churg.
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Bronchial Responsiveness in Children Exposed to Atmospheric Pollution in Hong Kong: Conclusion
Other factors that may have accounted for the differences between districts include the variation in respiratory symptoms in the two groups of children. Our subsets sampled for histamine were comparable, and only one of the 13 symptoms, wheezing, was significantly higher in the KDT sample. A history of asthma and wheezing was associated with increased BR, but the district effect remained when the asthmatic and wheezing patients were excluded.
The mechanism by which atmospheric pollution increases BR is not entirely clear. Several experimental studies have shown that O311,31,32 and NO2 exposure cause an increase in BR in atopic and nonatopic subjects. Ozone levels are much higher in KDT than SDT, but comparable figures for 19891990 were not available. Sulfur dioxide has also been found to cause a decrease in pulmonary function in allergic subjects. Although there are other studies that have not shown any increase in BR after exposure to pollutants, epidemiologic evidence does support a higher prevalence of BHR and higher BR in subjects exposed to atmospheric pollution Moreover, findings of impaired delayed hypersensitivity and a significantly lower helper/suppressor T cell ratio in exposed children suggests an immune-mediated pathogenetic mechanism.
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Bronchial Responsiveness in Children Exposed to Atmospheric Pollution in Hong Kong: Discussion
The crude prevalence of BHR was 25.5 percent (95 percent CI=21.4 to 29.7 percent). A comparison of the distribution of BHR, categorized by degree of severity between the two districts, is shown in Table 4. There was a higher prevalence of BHR in children from KDT (x2=7.74, df=3, p=0.052) mainly attributable to more mild hyperreactivity in KDT. The district difference was accounted for by a higher prevalence of BHR in boys (x2= 11.28, df=3, p=0.010) but not in girls (x2=6.24, df=3, p=0.100). When those children who had a history of wheezing and/or who were diagnosed asthmatic were excluded, a difference in prevalence of BHR between the two districts was still observed (x2=8.93, df=3, p=0.030) (Table 4).
Mean (SD) PD20 among those cases with a PD20<7.80 дто1 was 4.65 дто1 (2.24) for SDT (n=50) and 3.93 fimol (2.33) for KDT (n=58) (t=1.63, df=105, p=0.107).
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