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Biomedical subjects

B T Butcher

Publications and source records attributed to B T Butcher.

11 recordsLinked to original sources
PubMed1979

Inhalation challenge and pharmacologic studies of toluene diisocyanate (TDI)-sensitive workers.

Workers with "sensitivity" to toluene diisocyanate (TDI) studied in depth in an attempt to determine mechanisms of bronchial hyperreactivity. Tests included provocative inhalation challenge (PIC) with TDI and methacholine challenge. Blood samples obtained prior to and at various times after PIC were used to measure complement and split products of complement and plasma histamine levels and to determine dose-response slopes of lymphocyte cyclic adenosine monophosphate (cAMP) following stimulation with agonists. TDI-reactive individuals were all reactive to methacholine and responded to PIC with TDI by immediate, delayed, or dual bronchospastic reactions. No change in plasma histamine, total complement levels, or split products of complement were measurable. TDI reactors gave decreased lymphocyte cAMP dose response slopes to stimulation with isoproterenol, prostaglandin E1, and TDI, which suggests that impairment of adrenergic receptors may play an important role in TDI reactivity.

Aerosols↗
PubMed1977

The in vitro effect of toluene diisocyanate on lymphocyte cyclic adenosine monophosphate production by isoproterenol, prostaglandin, and histamine: a possible mode of action.

Toluene diisocyanate (TDI) significantly inhibits the rise in intracellular cyclic 3',5'-adenosine monophosphate (cAMP) that follows in vitro incubation of human lymphocytes with 6.7 x 10(-3) M isoproterenol and 1 x 10(-6) M prostagladin E1 (p less than 0.05). TDI has no significant effect on th production of lymphocyte cAMP following incubation with histamine (1 x 10(-3) M). The inhibitory action of TDI is greatest at a concentration of 3.3 x 10(-4) M and diminishes as the TDI concentration is increased or decreased. TDI also caused four- to fivefold stimulation of lymphocyte cAMP, an effect that is maximal at 1 x 10(-3) M, a concentration which has no significant inhibitory effect on stimulation of cAMP by isoproterenol or prostagladin E1. Conversely, 3.3 x 10(-4) M TDI, which inhibits cAMP production by isoproterenol and prostaglandin, has little stimulatory effect itself on cAMP production. This evidence suggests that TDI might induce obstructive airways disease through pharmacologic mechanisms and that TDI may be acting as a partial agonist.

Asthma↗
PubMed1977

Toluene diisocyanate pulmonary disease: immunopharmacologic and mecholyl challenge studies.

Selected workers exhibiting clinical "sensitivity" to toluene diiosocyanate (TDI) (wheezing, cough, and dyspnea upon entering a TDI-containing area) were studied for : (1) in vitro TDI-induced leukocyte histamine release; (2) determination of cyclic 3',5' adenosine monophosphate (cAMP) levels of lymphocytes exposed to TDI; (3) effect of TDI on the isoproterenol-induced increase of lymphocyte cAMP levels: and (4) acetyl-beta-methylcholine (mecholyl) inhalation challenge. TDI did not induce histamine release from leukocytes of "sensitive" or "nonsensitive" individuals, nor were lymphocyte cAMP levels affected by in vitro TDI exposure, TDI did, however, diminish in vitro stimulation of cAMP by isoproterenol. This effect, seen with cells of "sensitive" and "nonsensitive" individuals, appeared to be dose-dependent; there were no significant differences between the two groups. When challenged with mecholyl, 7 of 10 "sensitive" but only 1 of 10 "nonsensitive" individuals showed a greater than 20% decrease in FEV1. These results suggest that TDI-induced obstructive airways disorders may be associated with altered beta-adrenergic function.

Administration, Intranasal↗
PubMed1977

Longitudinal study of workers employed in the manufacture of toluene-diisocyanate.

Workers at a toluene-diisocyanate manufacturing plant were studied longitudinally to determine the effects of the chemical on their health. Studies included health questionnaire, pulmonary function, environmental monitoring, and immunologic testing. Workers reporting increased lower respiratory symptoms were from the nonsmoker group. Environmental monitoring showed frequent excursions of toluene-diisocyanate concentrations above the threshold limiting value. There was poor correlation between area and personal exposure levels. No exposure-related decline of pulmonary function was demonstrable. Immunologic studies showed development of a positive skin test to a toluene-diisocyanate-human serum albumin conjugate by some persons and an increasing incidence of toluene-diisocyanate-specific IgE antibodies as measured by a radioallergosorbent test. Toluene-diisocyanate did not induce histamine release from leukocytes in vitro but did diminish the in vitro stimulation of cyclic adenosine monophosphate by isoproterenol. Most of the clinically sensitive persons demonstrated adverse bronchial response when challenged by inhalation of toluene-diisocyanate. This response was dose dependent in some persons. When challenged with Mecholyl, clinically sensitive persons showed greater reactivity of airways than nonsensitive persons.

Antibodies↗
PubMed1976

Toluene diisocyanate (TDI) pulmonary disease: immunologic and inhalation challenge studies.

Clinical and serologic effects of TDI exposure were studied in 112 occupationally exposed plant workers. Sera were obtained before and after commencement of TDI production. All subjects were skin-tested with common inhalant allergens and a TDI-HSA conjugate. Total eosinophil counts, immunoglobulin quantitations, and specific antibody assays by PCA, P-K, and radioimmunoassay were performed. Clinically "sensitive" individuals were tested by provocative inhalation challenge with from 0.005 ppm to the threshold limit value of 0.02 ppm TDI. No TDI-induced immunologic changes were noted with the exception of 3 individuals who demonstrated small positive wheal-and-erythema reactions to TDI-HSA but not to HSA alone. Inhalation challenge with TDI vapor produced airways obstruction, as measured by FEF (25-75). These responses were of the immediate, delayed, and dual type, and were provoked in some cases with levels as low as 0.005 ppm TDI.

Airway Obstruction↗
PubMed1975

Secretory and humoral immunologic response of atopic and non-atopic individuals to intranasally administered antigen.

Groups of twelve asymptomatic atopic and fourteen non-atopic individuals were immunized with tetanus toxoid 7.5 Lf units X 2 by means of nasal droplets. Serum and nasal secretion samples were collected on days 1, 15 and 36. Protein content of dialysed secretions was determined by the Lowry method and 1.0 mg/ml samples used for specific antibody assays by passive haemagglutination (PHA) and radioimmunosorption (RISA) employing cyanogen bromide activated Sephadex G-25. IgG, IgA, IgM, and IgD were quantitated by single radial diffusion (SRD), and IgE by the RISA technique. Mean PHA secretion titres rose significantly in both groups during the course of the study. Serum and nasal secretion RISA IgA anti-toxoid levels were higher in the non-atopic group throughout the course of immunization but both groups showed a significant increase in mean levels following immunization (P less than 0.05). Conversely nasal secretion IgE-anti-toxoid levels were significantly higher in the atopic group throughout the course of immunization although no quantitative increase in levels was noted. Total IgG, IgD, IgE, and IgM levels in serum and secretions did not rise during the course of immunization but nasal wash IgA levels rose in both groups. IgD levels were significantly higher in serum and nasal secretions of the atopic group. Our results suggest that atopic and non-atopic individuals differ quantitatively in Ig class specific antibody production following topical mucous membrane immunization.

Antibody Formation↗