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C R Zeiss

Publications and source records attributed to C R Zeiss.

At least 37 records · Page 2Linked to original sources
PubMed1988

A serial immunologic and histopathologic study of lung injury induced by trimellitic anhydride.

Trimellitic anhydride (TMA) can induce immunologic lung disease in exposed workers. We have developed a rat model of TMA lung injury characterized by lung hemorrhage and an immune response to trimellityl (TM) haptenized lung proteins. The model is similar to the pulmonary disease-anemia syndrome (PDA) seen in workers exposed to TMA fumes. Sprague-Dawley rats, 15 per exposure period, inhaled micronized TMA powder, 100 micrograms/m3, 6 h/day, for 2,6, or 10 days and were sacrificed. At each time period, total, IgG, IgA, and IgM antibody to TM-rat serum albumin (TM-RSA) were measured by radiolabeled antigen binding and enzyme-linked immunosorbent assay (ELISA) in serum and bronchoalveolar lavage fluid (BAL). Hemorrhagic lung foci, weight, and displacement volume were determined, and lungs were examined by light and electron microscopy. There was no lung injury or antibody response at 2 days. There was minimal lung injury at 6 days with low levels of antibody in BAL and serum. At 10 days, there was a marked increase in hemorrhagic foci and in BAL and serum antibody levels. BAL antibody levels at 6 and 10 days had higher correlations with measures of lung injury than corresponding serum levels. There was minimal ultrastructural change at 6 days. By Day 10, there was marked intraalveolar hemorrhage, alveolar septal inflammatory nodules, abundant alveolar macrophages, and evidence of endothelial and epithelial cell injury. These results indicate that the immune response to inhaled TMA occurs parallel with the development of lung lesions, and antibody levels in BAL and serum are highly correlated with lung injury.

Animals↗
PubMed1987

The pathologic and immunologic response to inhaled trimellitic anhydride in rats.

Trimellitic anhydride (TMA) is a chemical intermediate used in the paint and plastics industry. Inhalation of TMA can induce four types of syndromes in TMA workers; three are immunologically based whereas the fourth, an irritant syndrome, is nonimmunologic. To evaluate the potential inhalation hazard of TMA under controlled conditions, Sprague-Dawley rats were exposed 6 hr/day via inhalation to target concentrations of 0, 10, 30, 100, and 300 micrograms/m3 for varying durations. Two sets of rats received either 5 or 10 exposures and were terminated. A third set received 10 exposures, and was held 12 days and terminated. A fourth set received 10 exposures, and was held 12 days, challenged with a single 6-hr exposure, and terminated. A fifth set received 10 exposures, and was held 12 weeks and terminated. There were no effects after 5 exposures; however, after 10 exposures the following parameters were increased in a concentration-related manner: absolute and relative lung weights, external hemorrhagic lung foci, alveolar macrophage accumulation, alveolar hemorrhage, pneumonitis, and lung and mediastinal lymph node nonspecific IgG and complement (C3). The rats exposed and rested 12 days were nearly recovered from these effects; however, rats rested 12 days and subsequently challenged exhibited lesions similar to those seen immediately following exposure. Exposed rats rested 12 weeks were completely normal in all of the above parameters. The timing and nature of the lung lesions, along with the presence of lung IgG and complement, are consistent with some of the known aspects of TMA-induced lesions in humans, and are reflective of results obtained from other hypersensitivity pneumonitis models.

Administration, Inhalation↗
PubMed1987

Levels and specificity of antibody in bronchoalveolar lavage (BAL) and serum in an animal model of trimellitic anhydride-induced lung injury.

A study was undertaken to characterize the antibody response in rats exposed to trimellitic anhydride (TMA) by inhalation. Total antibody levels directed to trimellitic rat serum albumin (TM-RSA) from TMA-exposed rats were assayed by an ammonium sulfate technique. Total antibody levels in bronchoalveolar lavage (BAL) and the matched serum were compared by correction for the albumin content of each. An ELISA was developed to detect IgG, IgA, and IgM directed toward TM-RSA in BAL and serum and to compare class-specific antibody levels in BAL and serum by normalizing for albumin content. The specificity of the rat IgG response was determined by ELISA inhibition with TM-RSA and TM-human serum albumin (TM-HSA) and compared with reciprocal inhibition studies with serum from TMA-exposed workers. The levels of total antibody in BAL were three to 15 times greater than the levels found in the matched serum pair. IgG, IgA, and IgM antibodies were detected in the BAL and the serum of TMA-exposed rats but not in control rats. In each of the four rats tested, all antibody classes were present in equal or greater amounts in the BAL than in the serum. Complete inhibition of the rat IgG binding in ELISA was observed when TM-RSA or TM-HSA were added as inhibitors. Human IgG was inhibited in ELISA only by TM-HSA. In an animal model of human lung disease, the levels of total antibody as well as class-specific antibodies directed against TM-RSA were greater in BAL than in serum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

A model of immunologic lung injury induced by trimellitic anhydride inhalation: antibody response.

We studied lung injury induced in Sprague-Dawley rats by trimellitic anhydride (TMA) inhalation. Groups of 40 male and 20 female rats were exposed to TMA by inhalation at target concentrations of 0, 10, 30, 100, and 300 micrograms/m3, 6 hours per day, 5 days per week, for 2 weeks. Rats in each exposure group were sacrificed after 10 exposures or rested for 12 days and either sacrificed or received a 6-hour TMA challenge at their initial exposure levels and sacrificed at 24 hours. At each sacrifice, serum antibody to radiolabeled trimellityl rat serum albumin (RSA-TM) was measured by an ammonium sulfate technique, and lung pathology was determined. After 10 days of exposure, external hemorrhagic lung foci were directly related to the exposure concentration of TMA. Serum antibody binding of RSA-TM correlated with exposure concentration, hemorrhagic lung foci, and lung weight. There was healing of lung lesions 12 days after exposure with a return of lung lesions only 18 hours after the 6-hour inhalation challenge. A correlation between serum antibody to RSA-TM, hemorrhagic foci, and lung weight existed after challenge. This model clarifies two clinical entities observed in exposed workers, the late respiratory systemic and the pulmonary disease-anemia syndromes.

Administration, Inhalation↗
PubMed1985

Specific bronchoalveolar lavage IgG antibody in hypersensitivity pneumonitis from diphenylmethane diisocyanate.

We evaluated a patient for dyspnea, fever, malaise, and hypoxemia that developed after exposure to diphenylmethane diisocyanate (MDI). Specific inhalation challenge with MDI caused fever, leukocytosis, a restrictive decline in forced vital capacity, and a decrease in Pao2 several hours after challenge. Bronchoalveolar lavage 24 h after challenge showed lymphocytic alveolitis. Specific IgG antibodies to MDI human serum albumin (MDI-HSA) conjugate were demonstrated in serum and bronchial lavage fluid using the enzyme-linked immunoabsorbent (ELISA) technique. These findings suggest participation of both humoral and cellular immunity in the pathogenesis of hypersensitivity pneumonitis from isocyanate exposure.

Alveolitis, Extrinsic Allergic↗
PubMed1985

Serologic survey of rotavirus, Norwalk agent and Prototheca wickerhamii in wastewater workers.

Analysis of paired sera from 48 wastewater workers and controls who reported gastrointestinal illness did not reveal any excess of seroconversions to Norwalk agent or to rotavirus. Inexperienced wastewater-exposed workers had higher levels of antibody to Norwalk agent than did experienced and control workers and those with high and medium aerosol exposure had higher titres than those in the low aerosol category. Analysis for Prototheca antibody titres was essentially negative.

Adult↗
PubMed1985

Creating an indoor environmental problem from a nonproblem: a need for cautious evaluation of antibodies against hapten-protein complexes.

An epidemic of illness in three schools in New York State occurred in early 1983. An epidemiological review of the problem led to the conclusion that some of the symptoms could have been explained by irritant reactions to boiler exhaust gases but that a major factor was likely public concern about environmental contamination and heightened awareness of common minor symptoms and of exacerbations of chronic illnesses. Diphenylmethane diisocyanate (MDI) from polyurethane insulation had previously been suspected as a potential cause. An earlier investigation had found low levels of anti MDI-human serum albumin in a small number of subjects who did not have typical symptoms of identified MDI or other hypersensitivity syndromes. Similar antibodies were found in two of nine unaffected children in Chicago, who served as a comparison group. The identification of these antibodies, however, was inappropriately used to support the idea of a school contaminated with MDI in spite of the absence of detectable MDI in the environment. The availability of highly sensitive immunoassays should not be inappropriately used to accelerate the fear of environmental toxins when there is no clinical correlation.

Air Pollutants↗
PubMed1984

IgG antibody to purified protein derivative by enzyme-linked immunosorbent assay in the diagnosis of pulmonary tuberculosis.

We studied the diagnostic utility of an enzyme-linked immunosorbent assay (ELISA) in hospitalized patients with suspected pulmonary tuberculosis (TB). A positive culture for M. tuberculosis identified active disease, and 3 negative cultures and smears defined the negative group. IgG antibody activity was determined by adding a 1:1,000 dilution of serum to plates coated with PPD antigen. Alkaline phosphatase labeled anti-IgG was added, color developed, and an optical density index (ODI) was determined. Twenty-one patients with M. tuberculosis TB had a mean ODI of 0.27, which was higher than 99 patients without TB, ODI 0.10 (p less than 0.001). An ODI of 0.15 or greater was established as a positive ELISA test. For patients with M. tuberculosis TB, the ELISA had a sensitivity of 67 and a specificity of 79%. The first smear had a sensitivity of 57 and a specificity of 99%. With the first smear and the ELISA test results, a combined sensitivity of 86% was achieved. When both ELISA and the first smear were negative (101 cases), active TB caused by M. tuberculosis was found in only three patients (3.0%).

Adult↗
PubMed1984

Four-year evaluation of workers exposed to trimellitic anhydride. A brief report.

In a four-year clinical, immunologic, and environmental study of trimellitic anhydride (TMA) exposure in a single plant, 20 workers exposed to TMA powder were evaluated in 1979 and a total of 32 workers were evaluated from 1979 to 1983. Two distinct groups emerged before and after workplace control improvements were made in 1979. Seventeen of the original 20 workers were available for longitudinal study through 1983. Annual clinical evaluations and serum radioimmunoassays for total antibody binding and specific IgE binding to 125I TM-HSA (human serum albumin) were performed on all 32 workers. In 1979, six workers had antibody against TM-HSA, three had the late respiratory systemic syndrome, and two had TMA-induced allergic rhinitis or allergic rhinitis and asthma. One worker had antibody against TM-HSA without illness. Fifteen additional workers were evaluated longitudinally after institution of several workplace control measures. Four of these 15 workers had TMA exposure prior to environmental improvement and joined the study in 1982. The remaining 11 workers joined the study in 1982 and had at least two years of TMA exposure in the modified workplace. None of these 11 workers developed a TMA-induced immunologic syndrome or significant total or specific IgE antibody binding to 125I TM-HSA.

Adult↗
PubMed1983

Immunologic and respiratory responses to airway challenges of dogs with toluene diisocyanate.

Dogs received biweekly or monthly aerosol immunization with single doses of toluene diisocyanate (TDI) that were cumulative doses analogous to human chronic exposure at 0.02 ppm. The three dogs developed systemic immune responses to TDI-dog serum albumin (DSA). The immune responses included IgG, IgA, and IgM antibody responses and development of lymphocyte reactivity. IgA titers approached IgG titers and both were persistent, whereas IgM titers were low and of short duration. IgE antibody titers demonstrated by endpoint cutaneous titration appeared but fluctuated and became negative in spite of continued aerosol exposure of TDI. Immediate-type airway responses occurred after TDI aerosolization. Some limited responses that showed only abnormalities of selected pulmonary function parameters were clearly not immunologically mediated because they occurred with initial exposure. Other immediate-type airway responses occurred that qualitatively simulated IgE-mediated, antigen-induced airway responses in dogs. There was a statistically significant correlation (p = 0.0268) between these latter airway responses and immediate-type skin reactivity. This study demonstrates that this dog model simulates the complexity of airway responses to TDI in man but may provide a laboratory system for evaluation of immunologic or other proposed mechanisms of TDI asthma.

Animals↗
PubMed1983

Combined alveolitis and asthma due to hexamethylene diisocyanate (HDI), with demonstration of crossed respiratory and immunologic reactivities to diphenylmethane diisocyanate (MDI).

A worker exposed intermittently to hexamethylene diisocyanate (HDI) developed episodes of dyspnea, wheezing, and fever on working days. Complete lung function tests performed when the subject was asymptomatic were normal except for increased airway responsiveness to histamine, which significantly improved after a 3 wk period off work. At that time, specific inhalation challenges with HDI were carried out. After being exposed for 5 min, the subject developed general malaise, cough, fever, and leukocytosis, together with a mixed restrictive and obstructive breathing defect. We demonstrated a subsequent increase in airway hyperexcitability, which lasted for 2 mo. The subject was also challenged with diphenylmethane diisocyanate (MDI) for 15 min. A late obstructive reaction was documented. Increased levels of specific IgG antibodies against HDI-human serum albumin (HSA) and MDI-HSA were demonstrated.

Alveolitis, Extrinsic Allergic↗
PubMed1983

Antibodies against toluene diisocyanate protein conjugates. Three methods of measurement.

With the use of canine antisera against toluene diisocyanate (TDI)-dog serum albumin (DSA), techniques for measuring antibody against TDI-DSA were evaluated. The use of an ammonium sulfate precipitation assay showed suggestive evidence of antibody binding but high levels of TDI-DSA precipitation in the absence of antibody limit any usefulness of this technique. Double-antibody co-precipitation techniques will measure total antibody or Ig class antibody against 125I-TDI-DSA. These techniques are quantitative. The polystyrene tube radioimmunoassay is a highly sensitive method of detecting and quantitatively estimating IgG antibody. The enzyme linked immunosorbent assay is a rapidly adaptable method for the quantitative estimation of IgG, IgA, and IgM against TDI-homologous proteins. All these techniques were compared and results are demonstrated by using the same serum sample for analysis.

Ammonium Sulfate↗
PubMed1983

The relationship of airborne trimellitic anhydride concentrations to trimellitic anhydride--induced symptoms and immune responses.

Eighteen workers exposed to trimellitic anhydride (TMA) powder were evaluated in 1979. Twelve of these workers were available for longitudinal study until 1982. Annual clinical evaluations and serum radioimmunoassays for total antibody binding and specific IgE binding to 125I-TM-HSA were performed. In 1979, five workers had antibody against TM-HSA. Of these, three workers were diagnosed with the late respiratory systemic syndrome (LRSS) and one worker with TMA-induced allergic rhinitis. The LRSS workers had significantly elevated total antibody binding of 125I-TM-HSA and the worker with rhinitis had significantly elevated specific IgE binding of 125I-TM-HSA per milliliter of serum. Although TMA handling was intermittent throughout the year, average airborne dust concentrations from 1974 to 1978 at job stations of the two heaviest TMA-exposed occupations, operator and assistant operator, were 2.1 and 0.82 mg/m3, respectively. After local exhaust ventilation had been improved, average airborne dust concentrations of TMA at the two latter job stations fell to levels of 0.03 and 0.01 mg/m3, respectively, in 1982. The decrease in TMA exposure coincided with a gradual fall in total antibody binding of 125I-TM-HSA per milliliter in 1982 and symptomatic improvement in the three individuals with the LRSS. The continuous low-level exposure of the worker with TMA rhinitis was sufficient to elicit a rise in specific IgE against TM-HSA from 1.1 ng of 125I-TM-HSA bound per milliliter in 1979 to 2.12 in 1982.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollution↗
PubMed1983

The relationship of total serum IgE and blocking antibody in trimellitic anhydride--induced occupational asthma.

Clinical and immunologic evaluations were performed on workers who manufacture trimellitic anhydride (TMA), a chemical used widely in the plastics industry. Serum samples of 29 workers exposed to TMA dust and fumes were assayed for total IgE, as well as specific IgE and total antibody binding to radiolabeled trimellityl human serum albumin (TM-HSA). Fifteen workers were determined to have significant specific IgE to TM-HSA (greater than or equal to 1 ng of 125I-TM-HSA bound per milliliter). Of these 15 individuals, seven workers had immediate asthma and rhinitis and positive cutaneous prick tests and eight were nonasthmatic and skin test negative. Mean peak total serum IgE was significantly higher in the prick test positive group (p less than 0.02) and higher than in 12 exposed asymptomatic IgE antibody-negative workers (p less than 0.001). Total serum IgE followed rises and falls in TM-HSA--Specific IgE binding, correlating to the onset of allergic symptoms in all seven workers. Total antibody binding of 125I-TM-HSA, as determined by the ammonium sulfate precipitation technique, was higher in the skin test-negative group of eight (mean 12,062 ng per milliliter 125I-TM-HSA bound) than in the seven symptomatic skin test-positive workers (mean 2930, p less than 0.004). Determinations of total antibody divided by specific IgE (both in nanograms of 125I-TM-HSA bound per milliliter) or blocking ratios clearly discriminated the seven skin test-positive workers with TMA-induced asthma (range 10 to 666) from the eight skin test-negative workers (range 1580 to 16,000).(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies↗
PubMed1983

Use of an enzyme-linked immunosorbent assay technique in the differential diagnosis of active pulmonary tuberculosis in humans.

Sera from patients with active pulmonary tuberculosis and pulmonary diseases frequently mimicking tuberculosis were assayed for immunoglobulin G antibody activity to purified protein derivative (PPD) by an enzyme-linked immunosorbent assay. A method of standardization was developed to limit assay variation. Patients with active pulmonary tuberculosis had a significantly greater mean level of antibody than had patients with atypical tuberculosis (P = 0.005), sarcoidosis (P = 0.0001), histoplasmosis (P = 0.004), blastomycosis (P = 0.008), or cryptococcosis (P = 0.017), patients who had received bacille Calmette-Guérin vaccination (P = 0.003) or who had a history of treated tuberculosis (P = 0.003), and PPD skin test-positive and skin test-negative control subjects (P = 0.001). This technique may have potential use as a rapid diagnostic aid in evaluating patients with suspected active pulmonary tuberculosis.

Antibody Formation↗