Absence of lung tumor promotion with reduced tumor size in mice after inhalation of copper welding fumes.

Welding fumes are a Group 1 (carcinogenic to humans) carcinogen as classified by the International Agency for Research on Cancer. The process of welding creates inhalable fumes rich in iron (Fe) that may also contain known carcinogenic metals such as chromium (Cr) and nickel (Ni). Epidemiological evidence has shown that both mild steel (Fe-rich) and stainless steel (Fe-rich + Cr + Ni) welding fume exposure increases lung cancer risk, and experimental animal data support these findings.

Evaluation of Cystic Endometrial Hyperplasia and the Normal Estrous Cycle in Longitudinal Sections of Uterus from Female Harlan Sprague-Dawley Rats.

The National Toxicology Program (NTP) has recently introduced the practice of examining longitudinal histological sections of the female rodent uterus to improve the identification of non-neoplastic lesions, preneoplastic lesions, and uterine tumors. This practice has created a need for reference material that includes normal histology, spontaneous lesions, and inducible lesions in longitudinal as well as transverse sections of the body of the uterus, uterine horns, cervix and vagina. Using 3 archived NTP reproductive and developmental toxicity studies, the authors reviewed longitudinal and transverse sections of uteri from female Hsd:Sprague Dawley SD® (Hsd:SD) rats for cystic endometrial hyperplasia (CEH).

Toward a molecular equivalent dose: use of the medaka model in comparative risk assessment.

Recent changes in the risk assessment landscape underscore the need to be able to compare the results of toxicity and dose-response testing between a growing list of animal models and, quite possibly, an array of in vitro screening assays. How do we compare test results for a given compound between vastly different species? For example, what dose level in the ambient water of a small fish model would be equivalent to 10 ppm of a given compound in the rat's drinking water? Where do we begin? To initially address these questions, and in order to compare dose-response tests in a standard rodent model with a fish model, we used the concept of molecular dose. Assays that quantify types of DNA damage that are directly relevant to carcinogenesis integrate the factors such as chemical exposure, uptake, distribution, metabolism, etc.