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1.  Lung volumes and flow rates in black and white subjects 
Thorax  1974;29(2):185-188.
Lapp, N. L., Amandus, H. E., Hall, R., and Morgan, W. K. C. (1974).Thorax, 29, 185-188. Lung volumes and flow rates in black and white subjects. It has been known for some time that the vital capacity and forced expiratory volume in one second of black subjects are about 12% lower than those of whites of the same age and height. In the present study, total lung capacity and residual volume were also shown to be decreased by about the same percentage. Expiratory flow rates were similarly decreased, but when the difference in lung size was evened out by matching black and white subjects of the same total lung capacity, no significant differences in flow rates were observed.
PMCID: PMC470126  PMID: 4831524
2.  Urinary hydroxyproline excretion in coalworkers' pneumoconiosis 
Resnick, H., Lapp, N. L., and Morgan, W. K. C. (1969).Brit. J. industr. Med.,26, 135-138. Urinary hydroxyproline excretion in coalworkers' pneumoconiosis. As there is an increased formation of one or all the fibrous proteins in coalworkers' pneumoconiosis, it was felt that a study of the turnover rate of these proteins might shed some light on the pathogenesis of the disease. Urinary hydroxyproline excretion was therefore studied in a group of miners, of whom 19 had simple pneumoconiosis and five had progressive massive fibrosis. No significant deviation from the normal was found.
PMCID: PMC1008907  PMID: 5780105
3.  Airways obstruction, coal mining, and disability. 
It has recently been suggested that the inhalation of coal in the absence of complicated coal workers' pneumoconiosis (CWP) or smoking can lead to disabling airways obstruction. The cause of such obstruction has been variously attributed to emphysema or bronchitis. The frequency of significant airways obstruction in a group of United States coal miners seeking compensation for occupationally induced pulmonary impairment was therefore determined. In a sample of 611 "Black Lung" claimants there was only one subject who was a non-smoker and who in the absence of other non-occupationally related diseases,--for example, asthma and bronchiectasis--had sufficient airways obstruction to render it difficult for him to carry out hard labour. An alternative explanation for his reduced ventilatory capacity other than coal dust or smoking may be available. If the inhalation of coal dust in the absence of smoking and complicated CWP ever induces sufficient ventilatory impairment to preclude a miner from working, it is indeed rare.
PMCID: PMC1127953  PMID: 8199664
4.  Pilot study of closing volume in byssinosis. 
A study of the relative sensitivities of forced expiratory volume in one second (FEV1), maximal mid-expiratory flow (MMF), and closing volume (CV) in the detection of subjects with byssinosis was carried out in a North Carolina cotton mill. Altogether 35 workers participated in the study. Of these, nine showed a decline in FEV1 of 10% or more during the first work shift that followed the weekend break. Twelve subjects showed a decrease in MMF of 15% or more. In contrast only six workers exhibited a 10% increase in closing capacity, while ten showed a 10% increase in CV. Recent evidence of the magnitude of variability in closing volume manoeuvres suggests that our chosen level of change was too low, A 40% change in CV would have identified only five subjects. CV is a more complex manoeuvre for the subject being tested and for the technician to perform, is more time consuming, and is subject to greater variation. To have any advantage over spirometry, CV would have to be appreciably more sensitive. Our study suggests that it is not. However, the MMF may prove to be more sensitive than the FEV1 in the detection of byssinosis.
PMCID: PMC1008065  PMID: 1156572
6.  The “Cochrane Collaboration” 
Thorax  1995;50(3):293.
PMCID: PMC1021196
9.  Prevalence of small opacities in chest radiographs of nickel sinter plant workers. 
Radiographs from 745 nickel sinter plant workers were taken and classified by five readers using the International Labour Office (1980) protocol. Each reader worked independently and the films were randomly mixed with films from a non-dust exposed office population and also with films from subjects known to have silicosis or asbestosis. The prevalence of small irregular opacities was selected as the outcome of interest. In the sinter workers this was within the range identified in cigarette smokers or in workers exposed to dusts of low fibrogenicity. Only minimal evidence of small round opacities was noted. There was no evidence from the chest radiographs that exposures to high concentrations of dusts containing compounds of nickel caused an inflammatory or fibrogenic response in the lungs of the exposed population.
PMCID: PMC1012161  PMID: 8507595
12.  Mesothelioma and exposure to asbestos. 
BMJ : British Medical Journal  1991;302(6785):1153.
PMCID: PMC1669818  PMID: 2043801
14.  Inhaled particle deposition and body habitus. 
As a result of the intrapleural pressure gradient that exists in the human lung, both ventilation and particle deposition increase from apex to base. Since the intrapleural gradient varies with the height of the subject, it was decided to compare regional particle deposition in tall, short, and obese subjects to ascertain whether it was influenced by height and weight. Surprisingly, deposition in the vertical plane was not significantly influenced by the height of the subject when corrected for ventilated lung volume. In addition, it was shown that in obese subjects there was increased deposition in the middle zones relative to the apices and bases. This finding persisted after correction for ventilated lung volume and differential attenuation resulting from non-uniform thickness of the fat layer in the obese subject's chest. In the tall and short groups there was a consistent pattern in the concentric deposition of particles with there being a gradient from the central or hilar region to the periphery of the lungs, with the latter showing the most deposition.
PMCID: PMC1035092  PMID: 2310705
18.  Chest diseases 
PMCID: PMC1875901
21.  Industrial bronchitis. 
For many years there has been much argument whether workers in the dusty trades are prone to chronic bronchitis. In 1966 the Medical Research Council issued a report of a Select Committee which concluded that occupationally induced bronchitis did not play a significant part in the aetiology of airways obstruction in dust-exposed men. Since then epidemiological studies have demonstrated that the prolonged inhalation of dust leads to an increase in prevalence of cough and sputum. Furthermore, new physiological techniques have demonstrated a slight decrement in ventilatory capacity as a result of industrial bronchitis, and which is related to lifetime dust exposure. Unlike bronchitis induced by cigarette smoke, the predominant effect of industrial bronchitis is on large rather than small airways and the condition is not accompanied by emphysema.
PMCID: PMC1008445  PMID: 367424
22.  An accurate and rapid radiographic method of determining total lung capacity 
Thorax  1972;27(2):163-168.
The accuracy and reliability of Barnhard's radiographic method of determining total lung capacity have been confirmed by several groups of investigators. Despite its simplicity and general reliability, it has several shortcomings, especially when used in large-scale epidemiological surveys. Of these, the most serious is related to film technique; thus, when the cardiac and diaphragmatic shadows are poorly defined, the appropriate measurements cannot be made accurately. A further drawback involves the time needed to measure the segments and to perform the necessary calculations.
We therefore set out to develop an abbreviated and simpler radiographic method for determining total lung capacity. This uses a step-wise multiple regression model which allows total lung capacity to be derived as follows: posteroanterior and lateral films are divided into the standard sections as described in the text, the width, depth, and height of sections 1 and 4 are measured in centimetres, finally the necessary derivations and substitutions are made and applied to the formula Ŷ = −1·41148 + (0·00479 X1) + (0·00097 X4), where Ŷ is the total lung capacity. In our hands this method has provided a simple, rapid, and acceptable method of determining total lung capacity.
PMCID: PMC472515  PMID: 5034594
23.  Respiratory Failure 
British Medical Journal  1965;2(5460):534.
PMCID: PMC1845609
25.  Rheumatoid Pneumoconiosis in Association with Asbestosis 
Thorax  1964;19(5):433-435.
PMCID: PMC1018856  PMID: 14216972

Results 1-25 (51)