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Biomedical subjects

C R Zeiss

Publications and source records attributed to C R Zeiss.

At least 19 recordsLinked to original sources
PubMed2000

Human leucocyte antigens (HLA) and trimellitic anhydride (TMA) immunological lung disease.

Occupational immunological lung disease, due to low molecular weight, reactive chemicals such as trimellitic anhydride (TMA), is an emerging health problem. If there were a marker that was highly predictive of the ability of the immune system to recognize TMA as an allergen, better prevention strategies could be employed with at risk individuals. The purpose of this study is to evaluate whether human leucocyte antigen (HLA) class specificity is associated with the development of late respiratory systemic syndrome (LRSS) or asthma due to immunological sensitivity to trimellitic anhydride (TMA). This is a case control study of 17 individuals with LRSS, 12 with asthma and 22 TMA similarly exposed individuals who did not develop LRSS or asthma. Comparing the sensitized individuals (LRSS or asthma) with the non-sensitized individuals (controls), we found no difference in frequency of any HLA antigen. In summary, the lack of association of HLA antigens with LRSS or asthma due to TMA suggests that these will not be useful markers to identify at risk individuals.

Adult↗
PubMed1996

Bean bag allergy revisited: a case of allergy to inhaled soybean dust.

BACKGROUND: Soybean is a common food allergen. It can cause Type 1 allergy (IgE-mediated) symptoms from its ingestion, as well as from inhalation of its dust. OBJECTIVE: To report a case of allergy in a child from the inhalation of soybean dust from a bean bag and the course of this allergy over time. METHODS: Case report; routine skin testing and laboratory tests; bean bag challenge studies; special studies with saline extracts of the bean bag soybeans. RESULTS: A 6-year-old boy with a 1-year history of allergic rhinitis noted symptoms of urticaria, eyelid angioedema, and mild respiratory distress while at school playing with a bean bag containing soybeans. Skin tests revealed positive reactions to commercial soybean extract and bean bag soybean extracts. Bean bag challenge was also positive. The patient's serum was able to transfer this sensitivity by the Prausnitz-Küstner (P-K) reaction. RAST and polystyrene tube radioimmunoassay techniques, however, did not detect specific IgE to soybean allergens. During follow-up, the patient developed allergy symptoms with ingestion of other beans. This latter allergy lasted for only 2 years, but the bean bag allergy was still present 4 years later (bean bag challenge). The patient returned at age 19 for recurrence of his allergic rhinitis and de novo asthma. Repeat bean bag challenge at age 24 was negative. CONCLUSIONS: To the best of our knowledge, this is the first reported childhood case of IgE-mediated allergy from soybean dust during play with a bean bag containing dry soybeans. Over time, despite the loss of this sensitivity, he developed asthma, another IgE-mediated illness.

Administration, Inhalation↗
PubMed1994

Induction of type I hypersensitivity in guinea pigs after inhalation of phthalic anhydride.

Guinea pigs were exposed through inhalation to phthalic anhydride (PA) dust at 0.5, 1.0, and 5.0 mg/m3, 3 hours/day for 5 consecutive days. Inhalation challenge with aerosolized phthalic anhydride-guinea pig serum albumin (PA-GPSA) conjugate elicited immediate-onset respiratory reactions in animals exposed to all three levels of dust. Inhalation challenge of a subgroup of animals with phthalic anhydride dust did not elicit an immediate response, as measured by changes in respiratory frequency and plethysmograph pressure. Serologic studies showed that these animals had allergic IgG1a antibody to PA-GPSA. There was a dose-dependent increase in specific IgG antibody activity, as measured by ELISA. Animals exposed to and challenged with 5.0 mg/m3 PA dust had significant numbers of hemorrhagic lung foci. Those animals with the greatest number of foci had high IgG antibody activity to PA, as measured by ELISA. This study showed that exposure to levels of PA dust as low as 0.5 mg/m3, below the current threshold limit value of 6.0 mg/m3, can sensitize animals to produce allergic antibody.

Administration, Inhalation↗
PubMed1993

Isocyanate induced lung disease.

A review of the pathogenesis of isocyanate induced lung disease is given with an emphasis on immunologic mechanisms of disease.

Cyanates↗
PubMed1993

A clinical and immunologic study of workers with trimellitic-anhydride-induced immunologic lung disease after transfer to low exposure jobs.

The objective of the study was to determine the clinical and immunologic status of trimellitic anhydride (TMA) workers who have had immunologic lung diseases and who have been moved to lower exposure jobs. Twenty-nine consecutive workers with TMA-induced immunologic lung diseases who had been moved to low exposure jobs for more than 1 yr were studied retrospectively. Pulmonary symptoms were obtained by physician-administered questionnaire. Immunologic studies were performed using radioimmunoassay. Spirometry and chest film were obtained. Workers with late asthma (LA) (n = 3), late respiratory systemic syndrome (LRSS) (n = 8), or both LRSS and asthma rhinitis (A/R) (n = 6) had improved symptoms, improved pulmonary functions, and lower total antibody against TM-HSA. Five of the 12 workers with A/R had improved symptoms, improved pulmonary functions, and lower IgE against TM-HSA, whereas seven continued to have moderate to severe symptoms, abnormal pulmonary functions, and elevated IgE against TM-HSA. There were no chest film findings in any group that were definitely attributed to TMA. Although TMA workers with LA or LRSS improve when moved to lower exposure jobs, only half of workers with A/R improve; elevated IgE against TM-HSA appears to be a marker for the subpopulation of workers with A/R that does not improve.

Adult↗
PubMed1992

Localization of inhaled trimellitic anhydride to lung with a respiratory lymph node antibody secreting cell response.

Male Sprague-Dawley rats were exposed to trimellitic anhydride (TMA) by inhalation (500 micrograms/m3), 4 hours a day, for 1 to 10 days. TMA was localized to lung cells by immunoelectron microscopy. Enzyme-linked immunosorbent assay (ELISA) and Western blot analysis were used in an attempt to localize TMA to lung lavage proteins. The lung-associated lymph node (LALN) B-lymphocyte response was measured by quantitation of immunoglobulin (Ig)G, IgA, and IgM antibody secreting cells specific for TMA rat serum albumin (TM-RSA) by use of the enzyme-linked immunospot assay (ELISPOT) method. The IgG, IgM, and IgA antibody response to TM-RSA in serum and lavage fluid was quantitated by ELISA. Lung injury was assessed by the number of external lung hemorrhagic foci and lung weight. Immunoelectron microscopy localized TMA to alveolar and bronchial cells on all exposure days. ELISA detected trace amounts of TMA haptenized lavage proteins that could not be detected by Western blot analysis. A marked increase occurred in lung injury from day 7 to 10. The LALN IgG, IgA, and IgM antibody secreting cell response to TM-RSA paralleled measures of lung injury. IgG, IgM, and IgA serum and lavage antibody to TM-RSA were correlated with lung injury measures. Lavage and serum IgG antibody levels had the highest correlation with lung injury.

Administration, Inhalation↗
PubMed1990

Immunoblot analysis of sera from patients with allergic bronchopulmonary aspergillosis: correlation with disease activity.

Immunoblot analysis was used to evaluate the IgG, IgE, and IgA responses to Aspergillus fumigatus antigen with the sera of five patients with allergic bronchopulmonary aspergillosis (ABPA) before, during, and after suspected exacerbation of their disease. The results revealed a heterogenous antibody response, unique for each patient, to specific Aspergillus fumigatus antigens that correlated with the molecular weights of previously well-characterized antigens of importance in the immunopathogenesis of ABPA. A rating scale was devised for measuring band intensity that allowed the patient's antibody responses to be reproducibly semiquantitated. Immunoblot analysis demonstrated qualitative and semiquantitative information that is not available with other in vitro assays used in the study of patients with ABPA, such as ELISA. These initial results emphasize the need for additional evaluation of this technique to assess its potential clinical application in this disease.

Antigens, Fungal↗
PubMed1989

Lung injury induced by short-term intermittent trimellitic anhydride (TMA) inhalation.

We have developed a rat model of lung injury with interstitial pneumonitis, lung hemorrhage, and a systemic and pulmonary immune response to trimellitic anhydride (TMA)-haptenized proteins induced by TMA inhalation for 10 days. The present studies explored the induction of lung injury induced by short-term intermittent TMA inhalation, a model more likely to simulate short-term industrial exposures during inadvertent spills of TMA. Sprague-Dawley rats inhaled TMA powder (500 micrograms/m3) on days 1, 5, and 10, and were necropsied on day 30, 18 hours after a 6-hour TMA-inhalation challenge on day 29. Rats were bled every second day and at necropsy. Serum IgG, IgA, and IgM antibody to trimellityl rat serum albumin was measured by ELISA. There was a rise in IgM and IgA antibody to trimellityl rat serum albumin starting at day 5 that peaked at day 20 with a decline in IgM by day 30. IgG antibody rose at day 7, peaked at day 20, and plateaued. The IgG antibody level was 10 times higher than the IgA or IgM level. In a second experiment, 18 rats were administered TMA-inhalation exposure on days 1, 5, and 10, and a TMA challenge on day 22. The number of hemorrhagic foci, lung weights, and lung-displacement volumes at necropsy on day 23 were highly correlated with IgG, IgA, and IgM serum-antibody levels. In a final experiment, rats developed a mean of 112 hemorrhagic foci per lung on day 30 after receiving only two TMA-inhalation exposures on days 1 and 5 with a rechallenge on day 29. (ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1989

Immunologic tolerance in rats during 13 weeks of inhalation exposure to trimellitic anhydride.

Trimellitic anhydride (TMA) causes several immunologically based pulmonary syndromes in humans. We developed a rat model representative of some of those syndromes whereby rats exposed for 2 weeks to TMA by inhalation developed hemorrhagic lung foci and pneumonitis accompanied by the appearance of TMA-specific serum antibody. The purpose of the study reported here was to examine the long-term, low-dose effects of TMA inhalation. Rats were exposed to target concentrations of 0, 2, 15, or 50 micrograms/m3 TMA 6 hr/day, 5 days/week for 13 weeks. The study included an interim 6.5-week termination and two recovery periods of 3 and 38 weeks, each with and without a final TMA inhalation challenge. Additional rats were bled regularly throughout the study and monitored for the appearance of TMA-specific antibody; other rats were terminated periodically during the 13-week exposure and examined for lung lesions. These serially terminated rats showed that TMA-induced lung lesions reached a maximum after approximately 2 weeks of exposure, but began to diminish thereafter. Rats bled regularly showed increasing TMA-specific antibody titers through the first 6 weeks of exposure, after which antibody titers diminished. Serum antibody levels rose sharply after the 13-week exposure ended and tapered off throughout the recovery period. Rats terminated after 6.5 weeks of exposure showed a dose-dependent increase in lung lesions and serum antibody. However, rats exposed to TMA for 13 weeks showed greatly reduced lung lesions and antibody titers. Rats exposed for 13 weeks and allowed to recover for 3 weeks showed increased antibody titers but few lesions, even after a TMA challenge. Rats exposed for 13 weeks and allowed to recover 38 weeks had reduced but still significant antibody titers; however, no lung lesions were noted even after a TMA inhalation challenge prior to termination. These results indicated that rats became tolerant to TMA and that 13 weeks of exposure to TMA did not produce lesions of any type, even after 38 weeks of recovery.

Administration, Inhalation↗
PubMed1988

Antibody response to trimellityl hemoglobin in trimellitic anhydride-induced lung injury.

Sprague-Dawley rats were exposed to trimellitic anhydride by inhalation, and the antibody response to trimellityl (TM)-conjugated hemoglobin (HB) and TM rat serum albumin (RSA) was compared. Groups of rats were exposed to trimellitic anhydride by inhalation 6 hours per day for 2, 6, or 10 days at 100 micrograms/m3 and compared to a control group exposed to filtered air. The IgG antibody response to TM-HB in both serum and bronchoalveolar lavage (BAL) fluid was measured with ELISA. IgG antibody levels to TM-HB rose significantly throughout the exposure. A positive correlation was found between IgG to TM-HB in serum and BAL fluid. In addition, this response in both serum and BAL fluid correlated with the IgG antibody response to TM-RSA. Cross-inhibition studies indicated the existence of shared antigenic determinants on TM-RSA and TM-HB. The IgG antibody to both antigens was specific for new antigenic determinants and not for the TM hapten.

Animals↗
PubMed1988

Evidence of immunologic control of lung injury induced by trimellitic anhydride.

Trimellitic anhydride (TMA) is a chemical intermediate that has been shown to cause immunologically mediated respiratory syndromes in humans. We developed a rat model in which lung lesions accompanied by TMA-specific antibody resembled effects seen in humans. Two sets of experiments were undertaken to determine if TMA lung injury was primarily controlled by the immune system. Experiment 1: Rats were exposed to 95 micrograms/m3 of TMA 6 h/day, 5 days/wk for 2 wk during which time they received daily injections of either the immunosuppressant cyclophosphamide or saline. The TMA-exposed/saline control rats exhibited the usual TMA-induced lung lesions accompanied by TMA-specific antibody. However, the TMA-exposed/cyclophosphamide rats showed no lesions and no antibody. The spleen cells from all rats were subjected to lymphocyte blastogenesis assays using T- and B-cell mitogens. Results confirmed that cyclophosphamide-treated rats showed very little if any blastogenic response, whereas saline-treated rats gave the normal immune response. Thus, cyclophosphamide eliminated T- and B-cell function, which in turn prevented the occurrence of TMA lesions. Experiment 2: An initial passive transfer experiment showed that serum from TMA-sensitized rats could be adoptively transferred into naive recipient rats, which when given a single TMA inhalation challenge exhibited TMA-induced lesions. Similar attempts to transfer spleen cells or spleen cells plus serum did not predispose recipients for lesions. A second modified passive transfer of sensitized serum using a larger number of recipient rats, followed by a TMA challenge, resulted in lesions in 14 of the 16 rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗