Search PubMed⌕ Search

Biomedical subjects

S M Brooks

Publications and source records attributed to S M Brooks.

At least 37 records · Page 2Linked to original sources
PubMed1986

Delayed anaphylactoid reaction in a worker exposed to chromium.

A 29-year-old male welder reported systemic reactions after exposure to chromium. Inhalation challenge testing to 29 micrograms/m3 of sodium chromate aerosol resulted in late appearing systemic urticaria, angioedema, and severe bronchospasm that occurred at the same time as a threefold rise in plasma histamine. A direct leukocyte inhibitory factor test to 5.5 X 10(-6)mol/L Na2CrO4 was positive. Although the mechanism of this reaction is unknown, the positive leukocyte inhibitory factor and the general acceptance of hexavalent chromium as a contact skin sensitizer suggest that cell-mediated mechanisms could be involved.

Adult↗
PubMed1986

Toluene diisocyanate-induced airway hyperreactivity and pathology in the guinea pig.

We assessed the nature and progression of airway mucosal disease and histaminic reactivity in English short-haired guinea pigs at 2, 24, 72, 168, and 504 hours after toluene diisocyanate (TDI) exposure (4 hours of 3 ppm of TDI for 5 consecutive days). To also determine whether TDI-specific, IgE-like antibodies developed in TDI-exposed animals, passive cutaneous anaphylaxis testing was done 28 days after TDI. Bronchial reactivity was determined serially by measuring specific airway conductance as a function of increasing doses of aerosolized histamine in six exposed and three control animals studied intact and unanesthetized. The remaining 10 exposed and 10 control guinea pigs were sacrificed in groups of two at each time point to obtain airway tissue for light microscopic examination. We found that airway hyperreactivity to histamine occurred after TDI in all animals tested. It was maximal 2 hours after the 5-day exposure and remitted by 72 hours. In addition, marked airway obstruction occurred after TDI that persisted for at least 168 hours. There were dramatic signs of airway mucosal damage associated with the bronchial hyperreactivity that included substantial decreases in epithelial cilia, mucin content, and mast cells, as well as squamous metaplasia, numerous mitotic figures, and a prominent polymorphonuclear leukocytic infiltrate. Passive cutaneous anaphylaxis tests in exposed animals were negative. Our results suggest that TDI-induced bronchial hyperreactivity may be related to airway mucosal injury and inflammation.

Airway Resistance↗
PubMed1986

Persistent airways disease caused by toluene diisocyanate.

The natural history of isocyanate-induced asthma is not well documented. We evaluated a patient who developed persistent shortness of breath, wheezing, and cough after a massive exposure to toluene diisocyanate (TDI). Despite no further occupational exposures to isocyanates, he continued to have symptoms of asthma and variable airway obstruction 12 yr later. A methacholine inhalation challenge test was markedly positive, and a bronchial challenge test to TDI produced a dual asthmatic response. This report demonstrates that sensitivity to TDI can persist for many years in the absence of further occupational exposure and suggests that some patients with TDI-induced asthma do not recover from their disease after being removed from isocyanate exposure.

Asthma↗
PubMed1986

Chronic asthma due to toluene diisocyanate.

Twelve subjects were studied with inhalation challenge testing to toluene diisocyanate (TDI) because of suspected TDI asthma based on a consistent clinical and occupational history. In seven cases, TDI asthma was documented by a positive inhalation challenge to low levels of TDI. Six of the seven TDI reactors had persistent respiratory symptoms and required daily treatment even though they had been removed from isocyanate exposure for intervals as long as 12 years (mean 4.5 years). These six TDI reactors had either dual (four cases) or late bronchospasm (two cases) to less than 20 ppb TDI, and all had a positive methacholine or cold air challenge prior to study. The one TDI reactor with a negative methacholine challenge had a positive (immediate) bronchospastic response to a TDI challenge performed one week after removal from isocyanate exposure. Five workers had a negative TDI challenge, two of whom had persistent respiratory symptoms and positive methacholine challenges at the time of TDI inhalation testing. We conclude that respiratory symptoms may persist following long-term removal from occupational exposure to TDI and are associated with nonspecific bronchial hyperreactivity. The TDI sensitivity may also persist for a long time even in the absence of any additional occupational exposure. Long-term prospective studies of symptomatic isocyanate workers are needed to fully define the extent of this problem.

Adult↗
PubMed1986

Morphology of tracheal and bronchial epithelium and type II cells of the peripheral lung of the guinea pig after inhalation of toluene diisocyanate vapors.

Toluene diisocyanate (TDI), a polymerizing agent used in production of plastics, can cause airways disease in some exposed individuals. Using guinea pigs as a model, the response of the airways and the type II cells of the peripheral lung was monitored morphologically and morphometrically after exposure to TDI vapors at 30 ppb, 260 ppb, and 3100 ppb. The two low doses of TDI caused little change in airways epithelium. There was no gross inflammatory cell infiltrate, however, surface infoldings and intracellular ciliated cysts increased in numbers. Animals exposed to 3100 ppb TDI 4 h/day for 5 days, sustained considerable damage to the epithelium, and stratified nonkeratinizing cells lined the airways until one week after exposure. Polymorphonuclear leukocytes were present in the early period after exposure. Increased numbers of eosinophils were present between one and two weeks following exposure. Mitoses in the epithelium were common during recovery. In the peripheral lung, though a modest subjective increase in the number of type II cells was seen after 3100 ppb TDI, the volume density of type II cells, and organellar components (lamellar bodies, mitochondria, cisternal bodies) did not change significantly after any exposure level of TDI.

Animals↗
PubMed1985

Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures.

Ten individuals developed an asthma-like illness after a single exposure to high levels of an irritating vapor, fume, or smoke. In most instances, the high level exposure was the result of an accident occurring in the workplace or a situation where there was poor ventilation and limited air exchange in the area. In all cases, symptoms developed within a few hours and often minutes after exposure. We have designated the illness as reactive airway dysfunction syndrome (RADS) because a consistent physiologic accompaniment was airways hyperreactivity. When tested, all subjects showed positive methacholine challenge tests. No documented preexisting respiratory illness was identified nor did subjects relate past respiratory complaints. In two subjects, atopy was documented, but in all others, no evidence of allergy was identified. In the majority of the cases, there was persistence of respiratory symptoms and continuation of airways hyperreactivity for more than one year and often several years after the incident. The incriminated etiologic agent varied, but all shared a common characteristic of being irritant in nature. In two cases, bronchial biopsy specimens were available, and an airways inflammatory response was noted. This investigation suggests acute high level, uncontrolled irritant exposures may cause an asthma-like syndrome in some individuals which is different from typical occupational asthma. It can lead to long-term sequelae and chronic airways disease. Nonimmunologic mechanisms seem operative in the pathogenesis of this syndrome.

Adult↗
PubMed1985

Asthma and rhinitis due to ethylcyanoacrylate instant glue.

A 32-year-old man developed asthma due to a cyanoacrylate ester instant glue used in building remote control model airplanes. Typical asthma and rhinitis symptoms developed after 1 year using the adhesive. Delayed onset of symptoms was consistently related to the application of the glue to balsa wood. Bronchial provocation to the glue vapors in a manner simulating his home exposure resulted in a late asthmatic response with rhinorrhea and lacrimation. Increased bronchial hyperreactivity to methacholine occurred after bronchial challenge and persisted for several weeks. Complete resolution of the patient's asthma symptoms occurred with avoidance of the glue. Reversion to a negative methacholine challenge test occurred after 6 months of continued avoidance.

Adhesives↗
PubMed1985

Reactive airways dysfunction syndrome. Case reports of persistent airways hyperreactivity following high-level irritant exposures.

Two individuals developed an asthma-like illness after a single exposure to high levels of an irritating aerosol, vapor, fume, or smoke. Symptoms developed within a few hours. A consistent physiologic accompaniment was airways hyperreactivity, with the two subjects showing positive methacholine challenge tests. No documented preexisting respiratory illness was identified, nor did subjects relate past respiratory complaints. Respiratory symptoms and airways hyperreactivity persisted for at least four years after the incident. The incriminated etiologic agents all shared a common characteristic of being irritant in nature. Bronchial biopsy specimens showed an airways inflammatory response. This report suggests that acute high-level irritant exposures may produce an asthma-like syndrome in some individuals, with long-term sequelae and chronic airways disease. Nonimmunologic mechanisms seems to be operative in the pathogenesis of this syndrome.

Adult↗
PubMed1984

Failure of enzyme encapsulation to prevent sensitization of workers in the dry bleach industry.

BDE added to dry bleach have been associated with immunologic sensitization and development of clinical allergic disease in detergent workers and occasionally in consumers. However, improved dust control and modification of the manufacturing process through encapsulation of enzyme were believed to have reduced or eliminated these problems. To determine whether or not immunologic sensitization could still develop in the detergent industry, we studied employees of a dry bleach manufacturing plant that incorporated encapsulated BDE into a consumer product. We performed air sampling for enzyme dust and total particulates, administered questionnaires, conducted physical examinations, and spirometry in 13 currently exposed, two previously exposed and nine nonexposed, employees. To assess sensitization status, RAST and ELISA were performed. Air concentrations of enzyme dust ranged from 0.002 to 1.57 micrograms/m3; all of these levels were below the TLV of 3.9 micrograms/m3. Positive BDE-specific RAST results (3.4%, 4.4%, and 8.0% binding) were obtained in three of 12 currently exposed workers. Results of personal breathing-zone air sampling indicated that these workers had high dust-exposure levels. Specificity of RAST was verified by RAST inhibition with BDE. BDE-RAST binding was not significantly elevated in the nonworkers (range: 0.6% to 1.4% binding). Positive results for specific IgG by ELISA were obtained in four of 12 currently exposed and in one of two previously exposed workers but in none of the nonexposed workers. We conclude that immunologic sensitization can develop after occupational exposure to encapsulated BDE in the dry bleach industry. We have not proved, however, that this immunologic reactivity is related to clinical sensitivity.

Adult↗
PubMed1984

Pulmonary changes after exposure to vermiculite contaminated with fibrous tremolite.

Workers exposed to vermiculite contaminated with fibrous tremolite were surveyed for the presence of respiratory symptoms by questionnaire, and for pneumoconiosis by chest radiograph. Pulmonary function was measured by spirometry and single-breath carbon monoxide diffusing capacity ( DLCOsb ). Fiber exposure indexes, expressed as fiber/ml-yr, were derived for each worker from available industrial hygiene data and work histories. The estimated cumulative exposure for the work force ranged from 0.01 to 39 fiber/ml-yr. Discriminant analysis demonstrated significant correlates with shortness of breath and pleuritic chest pain to cumulative fiber exposure. The radiographic changes were limited to pleural changes and involved 4.4% of the population. Parametric and discriminant analysis demonstrated a significant correlation with radiographic changes and cumulative fiber exposure. There were no correlations between spirometry or DLCOsb and fiber exposure. Exposure to vermiculite contaminated with fibrous tremolite can cause pleural changes in occupationally exposed workers. This is supported by the previously identified 12 cases of benign pleural effusions in this working population and the association of pleural radiographic changes and pleuritic chest symptoms with cumulative fiber exposure. The lack of significant parenchymal radiographic, spirometric, and DLCOsb changes most likely reflects the low cumulative fiber exposure.

Adult↗
PubMed1984

Hyperreactive airway smooth muscle responsiveness after inhalation of toluene diisocyanate vapors.

Guinea pigs were exposed to 29 parts per billion of toluene diisocyanate (TDI) vapors 5 h per day for 20 consecutive days. Control animal exposure was to filtered air, with similar length of exposure, air flow, heat load, humidity, and other factors. Animals were killed 20 h after the last exposure, and tracheal smooth muscle relaxation and contraction responses to agonists were determined. There was no difference in beta-adrenergic responsiveness between the 2 groups; the mean -log ED50 (concentration of agonist corresponding to 50% of maximal effect) for isoproterenol-induced responses was similar (9.73 +/- 0.06 SE for exposed animals and 9.56 +/- 0.13 for control animals, p = 0.29). Significant differences in carbachol-produced contractility were observed. The dose-effect curve from carbachol-stimulated strips was shifted upward and to the left for TDI-exposed animals. Beginning with the lowest dose of carbachol, significant differences were observed between exposure groups; these differences became even more pronounced as the concentration of carbachol was increased. The mean -log ED50 of carbachol-treated strips from TDI-exposed animals was 6.44 + 0.04 SE, which was significantly lower than that of the control strips, 6.23 + 0.04 (p = 0.01). The maximal smooth muscle tension was also greater in TDI-exposed animals. The observed increase in maximal tension and the shift of the dose-effect curve for TDI-exposed animals suggest a direct effect of TDI on tracheal smooth muscle.

Animals↗
PubMed1983

Effect of toluene diisocyanate on beta adrenergic receptor function. Biochemical and physiologic studies.

The effects of toluene diisocyanate (TDI) on beta adrenergic receptor function was investigated using 2 different experimental model systems: (1) a biochemical model measured beta adrenergic adenylate cyclase activity of frog erythrocytes and (2) guinea pig tracheal smooth muscle responsiveness after in vivo exposure was used to assess physiologic function. The TDI inhibited isoproterenol-stimulated erythrocyte adenylate cyclase activity in a dose-dependent manner. Similar results were obtained with fluoride-ion-stimulated activity, suggesting that TDI caused a nonspecific inhibition of adenylate cyclase activity. No difference in tracheal smooth muscle responsiveness, measured as the concentration of isoproterenol corresponding to 50% of maximal relaxation (ED50), was observed in TDI-exposed (9.36 +/- 0.11 SE) guinea pigs when compared with control (9.38 +/- 0.06 SE) animals, nor was there a difference in the degree of maximal relaxation induced by isoproterenol. The differences between the in vitro cell studies and the tracheal smooth muscle investigations suggest that mechanisms other than direct beta adrenergic blockade should be considered in TDI-induced asthma.

Adenylyl Cyclases↗
PubMed1982

The evaluation of occupational airways disease in the laboratory and workplace.

Occupational immunologic lung disease can be identified both in the individual patient under laboratory conditions and in a population of workers in industry. Occupational airways disorder is the most common occupational immunologic pulmonary process and is a disease of the airways caused by the inhalation of a substance or material that the worker manufactures or uses directly or that is incidentally present at the worksite. There are several occupational airways disorders, including industrial bronchitis, occupational asthma, and reactive airways disease syndrome, the latter two of which will be discussed more thoroughly. Occupational asthma can be appropriately identified when the following are present (1) typical symptoms, i.e., wheeze, cough, shortness of breath, and/or chest tightness; (2) specific identification of the offending agent; (3) documentation that the agent can cause asthma; (4) wheezes on physical examination; (5) pulmonary function changes; (6) immunologic abnormalities; (7) airway hyperreactivity; and (8) positive bronchial challenge with specific material. The diagnosis of occupational airways disorder requires a comprehensive approach, including clinical history, physiologic measurements, immunologic testing, and identification of airway hyperreactivity. By this approach both individual subjects and working populations can be studied.

Asthma↗