Biomedical subjects
Publications and source records attributed to G J Beck.
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The acute respiratory effects of exposure to low-level, short-term sulfur dioxide (SO2) were studied in ten asthmatic and ten healthy subjects. Subjects were exposed in an environmental chamber in a double-blind, random sequence to SO2) levels of 0.00, 0.25, 0.50, 0.75, and 1.00 ppm for 40 min. During the first 10 min subjects exercised on a cycloergometer at a level of 450 kpm/min. On separate days, subjects were exposed to 0 and 1.0 ppm SO2 in the absence of exercise. In exercising asthmatic subjects, breathing 1 ppm SO2 resulted in significant changes from baseline in airway resistance (Raw), forced expiratory volume in 1 sec (FEV1.0), maximal expiratory flow at 60% of the vital capacity (VC) below total lung capacity on the partial flow volume curve [MEF40% (P)] as well as reductions in flows at 50% of VC (Vmax50%). None of these parameters showed significant changes for exposures to 0.5 ppm or less, with the exception of small decreases (i.e., less than 0.2 L/sec) in Vmax50% at 0.25 and 0.5 ppm. Ten minutes after the end of exercise, there were no statistically significant differences from baseline, even though SO2 was still present in the chamber atmosphere. For asthmatic subjects, the average changes in Raw, FEV1.0, MEF40%(P), and Vmax50% increased as SO2 levels increased, suggestive of a dose-response relationship with a consistent effect first seen at 0.75 ppm. In individual exercising asthmatics, responses may occur at levels of SO2 below 0.75 ppm. No changes were seen in healthy individuals on any day, or in asthmatic subjects at rest.(ABSTRACT TRUNCATED AT 250 WORDS)
Formaldehyde (FA) is a common indoor air pollutant with irritative properties. It has been suggested that FA may produce physiologic alterations of the respiratory system. To study such responses, 15 nonsmoking, healthy subjects were exposed in a double blind, random manner to 0 and 2 ppm FA for 40 min in an environmental chamber. In addition, the same exposures were repeated on a separate day with the subjects performing moderate exercise (450 kpm/min) for 10 min. Exposures were carried out under controlled environmental conditions (temperature = 23 degrees C, relative humidity = 50%). Pulmonary function was measured before, during, and after exposures using partial and maximal flow-volume curves and airway resistance. Symptom diaries were given to the subjects; upper and lower airway symptoms were recorded for up to 24 hr following exposures. No significant bronchoconstriction was noted in this group. In 3 subjects, sequential measurements of peak flow over a 24-hr period following FA exposure failed to reveal any delayed airway response. On a separate day, 6 healthy subjects failed to demonstrate changes from their baseline responsiveness to methacholine after exposure to 2 ppm FA. Respiratory symptoms were, in general, confined to the upper airways and were mild to moderate in severity. We conclude that short exposures to 2 ppm FA do not result in acute or subacute changes in lung function among healthy individuals either at rest or with exercise. Subjective complaints following such exposures are confined to irritative phenomena of the upper airways.
Tantalum an experimental bronchographic material, may be retained in the lungs for a prolonged period following bronchography. The alveolar macrophage (AM) is a cell with potential for clearing tantalum particles from the airways. We studied the in vitro effects of tantalum oxide and two other particles, silca and latex, on rabbit AM viability and lysozyme release over 30 hours. Results indicate: 1) tantalum oxide, silica, and latex particles are ingested by rabbit AM in culture; 2) tantalum oxide and silica are both toxic to AM in vitro; and 3) tantalum oxide exerts its toxic effects less rapidly on AM than does silica. On the basis of these in vitro culture results we conclude that tantalum oxide may be toxic to alveolar macrophages in vivo. Delayed lung clearance of tantalum oxide particles may be due in part to their toxic effects on alveolar macrophages.
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The major limitation of coronary angioplasty is recurrent stenosis. Patient, clinical, and procedural factors at the time of angioplasty were correlated with the presence or absence of angiographically documented recurrent stenosis or continued patency. Patients with single-vessel, multilesion disease had a lower incidence of recurrence than those with single-vessel, single-lesion disease (22.2% v 37.3%). Patients with multivessel disease had the highest rate of recurrent stenosis (45%). Sex and age did not predict recurrence. Patients with more severe symptoms, patients without prior myocardial infarction (MI), and insulin-dependent diabetic patients were more likely to have recurrent stenosis. Of the lesion variables, a severe stenosis or a low gradient before angioplasty, the absence of an intimal tear after angioplasty, and left anterior descending artery lesions correlated with a higher recurrence rate. Inflation times greater than or equal to 30 seconds and a greater total number of inflations correlated with a higher recurrence rate. Multivariate analysis showed the following variables to be important predictors of recurrence: Canadian Heart Class, history of myocardial infarction, gradient before angioplasty, artery dilated, number of inflations, severity of stenosis before angioplasty, and insulin-dependent diabetes mellitus.
Fifteen asthmatic volunteers were exposed in a double-blind, random manner to room air and 2.0 ppm formaldehyde for 40 min in an environmental chamber. These exposures were repeated on a separate day during moderate exercise (450 kpm/min) for 10 min. Ambient and dew point temperatures were 23.0 +/- 0.0 degrees C and 11.5 +/- 1.0 degrees C, respectively. No significant airway obstruction as measured by flow-volume parameters and airway resistance was noted in this group during or immediately after exposure. Furthermore, sequential measurements of peak flow for 24 hr following formaldehyde exposure revealed no delayed airway response. In contrast, in comparison to the baseline methacholine inhalation challenge (MIC) test on the screening day, 8 of 12 asthmatics demonstrated a lower threshold to MIC following 2.0 ppm exposure for 40 min; however, the mean and median decrements of threshold in methacholine concentration of 10.4 mg/ml and 24.3 mg/ml were not significant (p = .12). Bad odor, sore throat, and eye irritation were common during exposure but symptoms were infrequent afterward.
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