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Biomedical subjects

D J Hendrick

Publications and source records attributed to D J Hendrick.

At least 91 records · Page 5Linked to original sources
PubMed1986

Modification of the methacholine inhalation test and its epidemiologic use in polyurethane workers.

The dosimeter method of administering doubling cumulative doses of methacholine to measure bronchial responsiveness was standardized to control for the effects of a number of potential influencing variables. The aerodynamic mass median diameter of the challenge aerosol produced from a DeVilbiss 646 nebulizer proved to be 1.2 mu, and the mean output per inhalation 8.9 microliters. Each challenge dose comprised 5 inhalations. Cumulative doses ranged from 0.3 methacholine inhalation units (1 unit = 1 inhalation of aerosol from a 1-mg/ml solution of methacholine, i.e., 8.9 micrograms methacholine) to a possible 640 units, the maximum that was considered reasonable to avoid the risk of unacceptable systemic effects. Responsiveness was expressed as the dose provoking a 20% decline (PD20) in FEV1. Modifications in this full protocol were introduced to facilitate epidemiologic investigations. Physician assessments coupled with baseline measurements of ventilatory function allowed starting at higher dosages for persons with low probability of hyperresponsiveness, thereby shortening the time required for testing to an average of 38 min. In a validation study of 20 persons using both the full and modified protocols, no significant differences were detected between measured PD20 values (geometric means Full versus Modified, 14.83 versus 14.88; r = 0.99). The modified protocol was used to measure bronchial responsiveness in 254 workers exposed to toluene diisocyanate. It proved to be safe and acceptable. Sixty-four workers (25.2%) were found to be reactors. The frequency distribution of the PD20 values exhibited a steadily increasing trend, consistent with a unimodal distribution.

Adult↗
PubMed1985

Mycobacterium malmoense in the north-east of England.

We report a 6 year experience (1979-1984) of isolating Mycobacterium malmoense in the north-east of England. Eleven subjects were involved of whom 10 had active infection--9 pulmonary, one cervical adenitis. The 11 new isolates represent 0.7% of all new mycobacterial isolates during this period and 10% of new non-tuberculous isolates. In all but 2 cases there was pre-existing pulmonary disease and/or a recognised predisposing factor to mycobacterial infection. The organisms were generally insensitive to isoniazid but sensitive to both rifampicin and ethionamide. The results of chemotherapy are described.

Adult↗
PubMed1985

Time course of the increase in airway responsiveness associated with late asthmatic reactions to toluene diisocyanate in sensitized subjects.

To understand better the mechanism of the increase in airway responsiveness associated with late asthmatic reactions, we determined the time course of toluene diisocyanate (TDI) effect on airway responsiveness in six sensitized subjects who exhibited a late asthmatic response after TDI exposure (0.018 +/- 0.005 ppm, 30 min) in the laboratory. Airway responsiveness was assessed before TDI exposure and then at 8 hr, 1 day, 1 wk, and 1 mo after TDI exposure. To assess responsiveness we determined the provocative dose of methacholine causing a decrease in FEV1 of 20% (PD20FEV1). The methacholine PD20 decreased from 0.50 mg geometric standard error of the mean (GSEM = 1.54) to 0.06 mg (GSEM = 1.55) (p less than 0.001) at 8 hr after exposure to TDI, was still decreased to 0.15 mg (GSEM = 1.93) (p less than 0.05) at 1 day, returned to 0.26 mg (GSEM = 1.91) (p greater than 0.05) at 1 wk, and returned to 0.43 mg (GSEM = 1.71) at 1 mo, indicating that full recovery occurred within 1 to 4 wk. These results demonstrate that TDI-induced late asthmatic response is associated with a reversible increase in airway responsiveness to methacholine and suggest that the TDI effect is linked to an acute inflammatory response in the airways.

Adolescent↗
PubMed1984

Occupational asthma. Update on a proliferating problem.

The list of agents known or suspected to cause occupational asthma is increasing almost daily. Potency, dose, and size of the population exposed determine the magnitude of the problem in any given industry. Investigation involves determining whether asthma is present, whether it is occupational, and what agent is responsible. Management of occupational asthma must be approached on an individual basis and at an industry-wide level.

Asthma↗
PubMed1984

Comparison of ultrasonically nebulized distilled water and hyperventilation with cold air in asthma.

To assess the potential value of brief non-pharmacologic challenge tests in the measurement of bronchial responsiveness and to investigate whether the responses are induced by similar mechanisms, we carried out comparative five-minute inhalation challenges with ultrasonically nebulized distilled water and cold air hyperventilation in nine asthmatic subjects. Decrements in FEV1 following both challenges were closely correlated (r = 0.885) and ranged from 8% to 59% of baseline following challenge with the former and from 6% to 59% following the latter. Each method was therefore equally effective in demonstrating bronchial hyperresponsiveness. Moreover, the strong correlation between the responses to both challenges coupled with previous observations suggests that the two stimuli may act by similar mechanisms.

Administration, Intranasal↗
PubMed1983

Effect of atropine on the bronchial response of asthmatic subjects to the inhalation of ultrasonically nebulized distilled water.

To determine whether atropine provides protection against the bronchoconstriction that develops in asthmatic subjects after inhalation of ultrasonically nebulized distilled water, we exposed six asthmatic patients to this stimulus with and without pretreatment with atropine (0.04 mg/kg). The mean FEV1 decreased from 3.32 to 2.39 L (-28%) without and from 3.49 to 3.18 L (-9%) with atropine. This protective effect was statistically significant (p less than 0.05), suggesting that cholinergic pathways are involved in the obstructive response to the inhalation of ultrasonically nebulized distilled water.

Adult↗
PubMed1983

Immunologic aberrations in asbestos cement workers: dissociation from asbestosis.

Immunoregulatory disorders have been implicated in the pathogenesis of asbestosis. We therefore compared the immunologic status of a well-characterized group of 31 current and former asbestos-cement workers with that of a group of 52 healthy controls, after adjustments had been made for the possible confounding effects of age, race, and smoking. The asbestos workers had significantly decreased percentages and numbers of both B and T lymphocytes in peripheral blood and a paradoxical IgG hypergammaglobulinemia. Analysis of T-lymphocyte subpopulations revealed that total T-cell numbers (OKT3+), helper-inducer T-cell numbers (OKT4+), and suppressor-cytotoxic T cell numbers (OKT8+) were decreased by similar proportions. These decreases were negatively correlated with time elapsing since the end of exposure to asbestos. In both workers and controls, lymphocyte proliferative responses to phytohemagglutinin (PHA) were correlated positively with the number of OKT4+ cells and negatively with age and serum IgG levels. When adjustments had been made for these confounding variables, no differences in PHA responses were noted between workers and controls. No relationship was detected in the workers between any of the immunologic aberrations noted and (1) radiographic category of pneumoconiosis, (2) estimates of cumulative asbestos exposure, or (3) abnormalities of pulmonary function. These data suggest that the immunologic perturbations we have noted in asbestos-exposed individuals are epiphenomena, unrelated to the pathogenesis of asbestosis itself.

Adult↗
PubMed1983

Effect of cromolyn on carbachol-induced bronchoconstriction.

The effect of premedication with cromolyn 40 mg on the bronchial response to inhaled carbachol was investigated in four atopic and four non-atopic subjects with mild asthma. Paired carbachol inhalation tests were carried out on consecutive days in a double-blind fashion following randomized premedication with cromolyn or placebo. Bronchial sensitivity was expressed as the log dose of carbachol provoking a 15% decrease in FEV1 (log PD15 FEV1) or a 30% decrease in FEF25-75 (log PD30 FEF25-75). The mean log PD15 FEV1 was significantly greater following cromolyn compared to placebo (2.34 +/- .22 vs 1.87 +/- .10; mean +/- SE; p less than 0.05) as was log PD30 FEF25-75 (2.30 +/- .16 vs 1.72 +/- .08; p less than 0.005). These results indicate that cromolyn interferes with cholinergic induced bronchoconstriction and support the suggestion that it has an effect at a more fundamental level than the inhibition of antigen induced mediator release from mast cells.

Adult↗
PubMed1983

Bronchopulmonary disease in the workplace. Challenge testing with occupational agents.

Inhalation challenge tests may be indicated in the investigation of occupational asthma and hypersensitivity pneumonitis when a worker's history is unconvincing or the precise etiologic agent is unclear. Challenge exposures may be conducted in either the workplace or the laboratory, and surveillance should extend for 24 hours unless the probability of late responses is negligible.

Alveolitis, Extrinsic Allergic↗
PubMed1982

Five-year longitudinal study of workers employed in a new toluene diisocyanate manufacturing plant.

The respiratory health of 277 workers in a new toluene diisocyanate (TDI) manufacturing plant was studied prospectively during 5 yr of exposure. Personal TDI monitors were used to continuously measure peak and 8-h time-weighted average (TWA) concentrations in over 2,000 samples. Longitudinal change in pulmonary function was assessed in 223 men in whom 3 or more data points allowed construction of individual slopes of annual change. Regression of annual change on smoking (pack-years), atopic status, and cumulative TDI exposure dichotomized at 68.2 parts per billion (ppb) months into low and high exposure groups showed significant effects of smoking on spirometric tests and lung volumes. After adjusting for pack-years of smoking, the 74 men in the high cumulative TDI exposure category had significantly larger declines in FEV1, %FEV, and FEF25--75% than did the 149 men in the low category. Annual change in FEV1 was then examined in 6 smoking-exposure categories: in never smokers, average annual decline was 38 ml/yr greater in those with higher cumulative TDI exposure. Current and previous cigarette smokers did not show this effect of cumulative TDI exposure. Analysis of FEV1 change by time above 20 ppb TDI yielded a similar result in never smokers, a 24 ml/yr excess average decline attributable to longer time above 20 ppb. In current cigarette smokers, those with longer time above 20 ppb had excess decline of 18 ml/yr (42 versus 24 ml/yr). our low and high cumulative exposure groups spent 2 and 15%, respectively, of their working time above 5 ppb TDI. The different health effects observed in these groups supports the NIOSH-recommended standard of 5 ppb TDI as an 8-h TWA.

Adult↗
PubMed1982

Formaldehyde asthma: challenge exposure levels and fate after five years.

Because of current concern regarding possible adverse health effects of formaldehyde, we have reinvestigated two renal dialysis unit nurses shown to have formaldehyde asthma by inhalation provocation tests in 1973 and 1975, respectively. Their original tests were repeated and the formaldehyde levels generated (previously unknown) were measured. One nurse had not worked with formaldehyde since 1976 and had had no further symptoms. Her 1981 test (15-minute exposure to 6 parts per million [ppm] formaldehyde) provoked no asthmatic response. The other nurse had continued to work with formaldehyde, though under much improved conditions, and mild intermittent attacks of asthma had continued. Her test (five-minute exposure to 3 ppm formaldehyde) provoked a late asthmatic reaction similar to that observed in 1975. We conclude that in sensitized subjects specific late asthmatic reactions may be provoked by brief exposures to formaldehyde at about the current Occupational Safety and Health Administration standard (3 ppm); and that while asthmatic responsiveness may persist with continuing low levels of intermittent exposure, it may be lost following complete cessation of exposure.

Adult↗