Subchronic inhalation toxicity of 3.5-microm diameter carbon fibers in rats.

No effects were seen when rats were exposed for 6 h day(-1), 5 days per week, for 16 weeks to an atmosphere of 20 mg m(-3) of carbon fibers (25 x 10(6) fibers m(-3)) and small amounts of fiber particulate resulting from preparation of the ultimate test material. The carbon fibers were made from polyacrylonitrile fiber. They were 3.

Thyroid function and thyroid tumors in toxaphene-treated rats.

Historically, a direct and irreversible genotoxic reaction of a xenobiotic with DNA has been considered to be a universal and obligatory initiating event in the etiology of neoplasia, and it was assumed therefore that (1) there was no threshold other than zero exposure for cancer initiation, and (2) like radiation, exposure was additive over a lifetime. Human exposure to xenobiotics causing neoplasia in laboratory rodents has been regulated in many countries on that basis. In the last decade evidence has accumulated indicating that some neoplasia in laboratory rodents may not be caused by a direct and irreversible interaction of xenobiotics with DNA.

Monochloroacetic acid toxicity in the mouse associated with blood-brain barrier damage.

Monochloroacetic acid (MCA) causes front paw rigidity in 10% of mice surviving a single oral toxic dose (320-380 mg/kg). Mice exhibiting front paw rigidity were killed at various times after MCA treatment and their brains were prepared for histological examination. As early as 48 hr post-treatment, RBCs were found outside capillaries in several brain regions, especially the cerebellum.

Pulmonary response and transmigration of inorganic fibers by inhalation exposure.

Rats, hamsters, and guinea pigs were exposed by inhalation to different concentrations of potassium octatitanate fibers. Following 3 months of exposure, the animals were sacrificed between the 15th and 24th month. The exposed animals showed dose-related dust deposition and pulmonary fibrosis mainly in the respiratory bronchiolar region.