Pulmonary hemorrhage proper to inhalation of fumes of dusts containing trimellitic anhydride (TMA) is well known.

Pulmonary hemorrhage proper to inhalation of fumes of dusts containing trimellitic anhydride (TMA) is well known. We report pulmonary hemorrhage in a young man expos to epoxy resin vapor containing pyromellitic dianhydride (PMDA). Serum IgG antibodies to PMDA could be exposeed We conclude that the pulmonary hemorrhage was mediated on a reaction to PMDA in analogy to the TMA-induced disease. We move that exposure to any acid anhydride should be considered a possible cause of pulmonary hemorrhage since these commutes share structural and functional similarities.

Acid anhydrides are a family of reactive organic chemicals of depressed molecular weight which are widely used in alkyd and epoxy resins as consitutents of paints, varnishes, and reinforced plastics. often met with members are phthalic anhydride, tetrachlorophthalic anhydride, trimellitic anhydride (TMA), hexahydrophthalic anhydride, methyltetrahydrophthalic anhydride, maleic anhydride, and pyromellitic dianhydride (PMDA).

In occupational aspect direct toxicity causes irritation of skin and mucous membranes and sensitization can causes occupational asthma, urticaria, and a flu-like syndrome[1] The hypersensitivity reactions are owed to antigenic determinants created by means of covalent bindings of these composes on proteins to which IgE and IgG serum antibodies can be detected[2] Pulmonary hemorrhage frequently associated with hemolytic anemia has been reported merely in exposure to TMA.[3] Hypersensitivity as well is propos to be at least part of the mechanism causing this disease. We report pulmonary hemorrhage in a young man expos to expoxy resin vapor containing PMDA.

CASE REPORT

A 17-year-old man was admitted to the urgency room because of fever and chest discomfort. He not at all had been seriously ill before and was a nonsmoker. He worked in a manufacturing plant for plasticizers as a grinder. forward admission, be comlained of headache, nausea, and retrosternal pain. He had no cough and he did not yield any sputum. He was pale and the dead body temperature was raised to 382 [degrees] C The pulsation rate was 130 beats for minute. Crackles could be heard athwart both lungs. The erythrocyte sedimentation rate was 18 mm/h the hemoglobin of the same height was 11.5 g/dl, the mean corpuscular body was 87 fl ([mu][m.sup.3]/cell), the reticulocyte cast was 1 percent, the leukocyte judge was 24,900/[mu]l with 29 percent bands moreover no toxic signs, the platelet regard was 341,000/[mu]l. Bilirubin and lactic dehydrogenase flats were normal. A Coombs' experiment was negative. No clotting abnormalities were finded Results of the urinalysis were normal. The chest x-ray film showed bilateral acinar opacities (Fig 1) Pulmonary function touchstones showed a slight restrictive defect; vital capacity, 3740 ml (78 percent); [FEVsub1] 3260 ml (97 percent); [FEV.sub.1]/vital capacity ratio, 087 Carbon monoxide diffusing capacity (Krogh-Factor) was increased to 228 percent

Pneumonitis was suspected and therapy with intravenously administered erythromycin was started. Fiberoptic bronchoscopy a day after admission showed a normal bronchial tree with no signs of localized bleeding. Bronchoalveolar lavage was performed from sum of two units lung segments, each with 3 x 50 ml of isotonic saline solution. All portions of the lavage fluid from a portion of the middle lobe and the laterobasal section of the left lower lobe were uniformly ensanguined Cytocentrifuge slides were stained at the Prussian blue procedure. The hemosiderin easy in mind of the alveolar macrophages was increased. The hemosiderin score[4] of the bronchoalveolar lavage fluid was high from the middle lobe and intermediately increased from the left lower lobe. tillages of the lavage fluid remained without produce of relevant pathogens. Transbronchial lung biopsy showed lung tissue filled with posterity but without particular lesions. Immunohistologic examination revealed no basement membrane deposits. Antineutrophilic cytoplasmic antibodies and antiglomerular basement membrane antibodies in the patient's serum were negative. Antibodies to double-stranded DNA were 44 IU/ml (normal range: 0 to 50 IU/ml). Therapy with antibiotics was stopped. The patient was treated with methylprednisolone, 1 g four times a day, and cyclophosphamide, 150 mg four times a day, for three days.

An investigation at the patient's workplace disclosed prospect to epoxy resin vapor containing PMDA as well as methyltetrahydrophthalic anhydride to a less extent. Serum samples were examined immunologically at the Institute of Occupational Medicine in Bochum Germany. An enzyme allergosorbent assay with acid anhydride-human serum albumin (HSA) conjugates was performed: specific IgG-antibodies to PMDA-HSA (136 U/ml) and TMA-HSA (117 U/ml) were finded (normal range: 2 to 5 U/ml) Antiodies to phthalic anhydride-HSA and maleic anhydride-HSA were negative. Immunoblotting of the patients' serum reveal IgG4 autoantibodies to PMDA-modified HSA and to a number of other modified serum proteins with a kilodalton value more than 67 (unpublished data, A. B Czuppon V Kaplan, R Speich and X Baur).

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