1,2-Dichlorobenzene (1,2-DCB) is in various industries as solvents in herbicides, pesticides, and wax, and as degreasers or in the production of dyes. Studies on the hazards and risks of 1,2-DCB showed that this substance can cause skin corrosion, skin irritability, respiratory irritability, and certain target organ toxicity. Industrial workers are exposed to 1,2-DCB by inhalation or skin exposure and there is a lack of information on human hazards even though they can be exposed to organic compounds such as benzene or other DCB complexes rather than a single substance. In this study, we investigated the specific organ toxicity of 1,2- DCB and sex differences using whole-body inhalation in laboratory mice. Male and female mice were exposed to 0–120 ppm of the test substance for 13 weeks. After euthanization, the organs were collected, histopathological assessments and immunohistochemistry (IHC) were performed, and lipid peroxidation was analyzed. Macro and microscopic lesions were observed in the livers of male mice exposed to the test substance, and microscopic alterations were observed in the nasal cavities of male and female mice. IHC analysis of the liver confirmed a greater increase in cytochrome P450 induction in males than in female mice, and malondialdehyde and 4-hydroxynonenal were increased in both sexes by 1,2-DCB inhalation. Based on the relevant literature and experimental results, 1,2-DCB is believed to cause specific organ toxicity in the livers of male mice and the nasal cavities of both sexes of mice, which is supposed to be related to sex differences in cytochrome P450 induction and changes in lipid and oxidative products associated with the early metabolites of the test substance.

This case report describes the pathological features of pulmonary alveolar proteinosis(PAP) in mouse. Grossly, multiple irregular yellow-grey patches were observed on the lung surface of a C57BL/6 mouse. Histopathologically, the alveolar walls were thickened by type II cell hyperplasia and cellular infiltrates, and the bronchioles and alveolar lumens were filled with amorphous eosinophilic lipoproteinaceous material. This material was positive for Periodic acid-Schiff stain. Gomori methenamine silver staining was negative. Immunohistochemical staining showed that cells in the alveolar wall and lumen were positive for surfactant protein B, chitinase-like protein-3, and CD68. As a result, PAP was diagnosed. This is a rare case of spontaneous PAP in mice, and we report the histopathological characteristics along with the literature.

The surfactant, 2-{2-[2-(4-nonylphenoxy)ethoxy]ethoxy}ethan-1-ol, is used in detergents, pesticides, cosmetics, and disinfectants. Since it is found in products that can be inhaled, we evaluated its toxicity to humans upon exposure. A total of 18 rats were exposed to nasal inhalation for 4 hr to determine the acute inhalation toxicity of 2-{2-[2-(4-nonylphenoxy) ethoxy]ethoxy}ethan-1-ol; the exposure concentrations were 5.0, 1.0, and 0.5 mg/L, with three males and three females at each concentration. After the end of the exposure, mortality, general symptoms, and weight changes were observed for 14 days, and autopsy findings were confirmed. The actual concentrations of the test substance in the chamber during the exposure were measured as 3.29, 1.03, and 0.52 mg/L, respectively. The delivered dose was 552.72, 173.04, and 87.36 mg/kg/day for males, and 829.08, 259.56, and 131.04 mg/kg/day for females. As a result of the test in the OECD Test Guideline 436, all animals exposed to a concentration of 3.29 mg/L died; three males and one female died out of six exposed to the 1.0 mg/L concentration. In addition, one died out of six males exposed to a 0.5 mg/L concentration. As a result, 2-{2-[2-(4-nonylphenoxy)ethoxy]ethoxy}ethan-1-ol was considered to be Globally Harmonized System of Classification and Labelling of Chemicals Category 2 (> 0.5–1 mg/L).