Effect of inhaled aerosol of 1-chloroacetophenone (CN) and Dibenz (b,f)-1,4 oxazepine (CR) on lung mechanics and pulmonary surfactants in rats.

Inhalation toxicity following exposure to 1-Chloroacetophenone (CN) and Dibenz(b,f)-1,4 oxazepine (CR) aerosols for 60 min at sublethal concentrations were studied in rats. The dynamic surface tension (gamma max and stability ratio) of lung homogenate increased significantly on CN exposure. The lung mechanics studies revealed a significant increase in compliance in CN exposed rats. CR, on the other hand did not influence any of the above variables except for a decrease in compliance. Total lung phospholipids and sphingomyelin contents decreased significantly following exposure to CN, while CR exposure produced an increase in sphingomyelin, reduction in phosphatidylcholine and ethanolamine, with no change in total phospholipid contents. Histomorphological observations indicated cellular degeneration in the epithelium of the bronchiole and alveolar septal-wall thickening due to the presence of an increased number of mononuclear cells in CN exposed rats. However, CR induced inflammatory reaction and enlargement of respiratory air spaces. It is concluded that of the two sensory irritants (tear gases) examined, CN is potentially more toxic compared to CR in rats.

Time dependent histomorphological assessment of lung damage induced by inhaled dibenz(b,f)-1-4-oxazepine (CR) and 1-chloroacetophenone (CN) in rats.

Lung damage caused by inhalation (single exposure for 60 min) of sublethal concentration of pure aerosols of dibenz(b,f)-1,4-oxazepine (CR) and 1-chloroacetophenone (CN) have been examined at different time intervals in rats. The damage was not severe with CR (2830 mg.m-3) but in the case of CN (60.26 mg.m-3) it was evident up to 30th day post exposure. Necrobiosis, attenuation of bronchiolar epithelium, edema in the air ways and also in the lumen of alveoli leading to substantial changes in the histoarchitecture of the lung were observed during CN exposure. On the other hand CR caused degenerative changes which disappeared on 30th day.

Blastic OKT6-positive proliferation preceding malignant histiocytosis.

A 45-year old male presented latero-cervical lymphoadenopathy. Biopsy revealed a malignant proliferation of immature "lymphoid" cells bearing T6 antigen and HLA-DR but negative for other lymphoid markers, suggesting a phenotype similar to Langerhans cells. The patient did not receive any therapy and six months later developed a histologically typical malignant histiocytosis, involving spleen and liver. Other reported cases of lymphoid malignancies (two bearing the T6 antigen on blast cells) preceding malignant histiocytosis were found and compared with ours. Most of these cases were characterized by the pediatric age of the patients and were presented as acute leukemias exhibiting, in at least some of them, reliable T-cell markers. Our case appears to represent, on the other hand, a blastic proliferation of precursors of both histiocytes and Langerhans dendritic cells which eventually progressed to malignant histiocytosis. The relevance of this observation in the debate on the origin of Langerhans cells and the relationships existing between macrophages and dendritic cells is discussed.

[Corneal damage caused by chloracetophenone]. / Hornhauttrübungen durch Chloracetophenon.

Chloracetophenone solubilized in 1,1,1-trichlorethan was applied in different concentrations to the rabbit cornea. Applications were made to the centre of the cornea as well as to the limbal area and also in an experiment with centrallimbal burning. The ensuing stromal scarring was related to the absolute quantity of applied chloracetophenone, and burning of the limbal area seemed to be more effective than central applications.

The comparative acute mammalian toxicity of 1-chloroacetophenone (CN) and 2-chlorobenzylidene malononitrile (CS).

The comparative acute toxicity of two peripheral sensory irritant materials, 1-chloroacetophenone (CN) and 2-chlorobenzylidene malononitrile (CS), has been investigated in several species of small mammal using solutions in polyethylene glycol 300 for intravenous, intraperitoneal and oral administration, and as pure aerosols for inhalation exposure. Additionally, the comparative potency for inducing primary contact dermatitis was studied. CN and CS were found to be about equitoxic by intravenous and intraperitoneal injection, but CS was significantly less toxic by the oral and inhalation routes and less likely to cause non-lethal tissue damage than CN.