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Perchlorate is an important oxidizer used in propellants, pyrotechnics, and as a gas generator in commercial airbags, fireworks, and roadside flares. It is highly water soluble, interferes with thyroidal iodide uptake and is an environmental contaminant. By changing the reaction chemistry, 5-aminotetrazole (5-AT) and nitrates replace perchlorate in some propellants. The short term toxicity of 5-AT was evaluated. Using a modified Ames assay, 5-AT was not mutagenic with or without S9 metabolic activation. 5-AT was considered “slightly toxic” with an EC50 of 28.8 mg 5-AT/L for a 15 min exposure in Aliivibrio fischeri. In the in vitro sodium iodide symporter test, 5-AT did not inhibit the uptake of iodine. In the acute rat oral test, no adverse effects and no mortalities were observed at the limit dose of 2000 mg 5-AT/kg. In the 14-day sub-acute study, there were no clinical signs of toxicity or morbidity up to 623 mg 5-AT/kg-day; the highest dose tested. No differences were observed in hematology, clinical chemistry, organ weight, body weight, food consumption, histopathology, or DNA damage (peripheral blood micronucleus assay) of treatments compared with controls. The No Observed Adverse Effect Level (NOAEL) was 623 mg 5-AT/kg-day, the highest dose in the subacute oral bioassay.

This chapter presents the wildlife toxicity assessment for nitroguanidine (NQ), a stable explosive compound used as a propellant in cartridges. This wildlife toxicity assessment addresses only toxicity to mammals, as data for amphibians, reptiles, and birds were lacking. Acute, chronic, and reproductive studies represented three mammalian species (rats, mice, and rabbits) in two orders, and showed limited toxicity of NQ to mammals. Water consumption was the most consistent effect. At high doses (1,000 mg/kg/day) other affects included death, reduced body weight gain, and reduced food consumption, which were attributed to decreased palatability and interference with digestion at 1,000 mg/kg/day. In developmental/reproduction studies, reduced fetal body weight and increased incidence of minor developmental alterations were noted. Thus, in mammals, the no and low observed adverse effect levels (NOAEL and LOAEL) for NQ were estimated to be 316 mg/kg/day and 1,000 mg/kg/day, respectively.

Biomedical, toxicological, and ecological databases were searched for reports and studies about the toxicology of the pesticide aldrin on wildlife (mammals, birds, reptiles, and amphibians). Citations were evaluated for biologically relevant endpoints such as reproduction, development, behavior, growth, and survival. Valid citations were used to develop toxicity reference values. Ingestion toxicity reference values were developed for mammals, birds, and amphibians. A paucity of available studies precluded the creation of ingestion toxicity reference values for reptiles. Inhalation and dermal contact toxicity reference values could not be developed for birds, reptiles, and amphibians due to a paucity of available studies.

This chapter presents the wildlife toxicity assessment (WTA) for chlordane, an organochlorine pesticide that was widely used in the U.S. from 1947 to 1978. Its use was curtailed following an increased concern about its cancer-causing effects, and it was entirely banned for use in 1988. It is highly persistent in the environment, causing a concern for wildlife toxicity. This WTA addresses chlordane’s toxicity to mammals, birds, and reptiles as there were no sufficient data on amphibian toxicity. The studies utilized indicate a moderate toxicity of chlordane, with effects on reproduction in mammals, birds, and reptiles. Based upon the available data in the mammalian studies, a chronic no observed adverse effect level (NOAEL) and low observed adverse effect level (LOAEL) were determined to be 2.1 and 21 milligrams per kilogram per day (mg/kg/day), respectively.

The treatment of chronic myelogenous leukemia (CML) with specific tyrosine kinase inhibitors typically results in clinical success, although therapeutic failure frequently occurs. In order to investigate the biological consequences of treating CML cells with such drugs, we previously reported that the antioxidant selenoprotein glutathione peroxidase-1 (GPx-1) was induced by imatinib in both patient samples and cultured cells. Here, we extend these findings to demonstrate that the treatment of CML cell lines, but not non-CML cells, results in an approximately four-fold increase in the levels of another important antioxidant protein, manganese superoxide dismutase (MnSOD), without altering the steady state levels of the corresponding transcript.