Current ecotoxicity testing needs among selected U.S. federal agencies.

U.S. regulatory and research agencies use ecotoxicity test data to assess the hazards associated with substances that may be released into the environment, including but not limited to industrial chemicals, pharmaceuticals, pesticides, food additives, and color additives. These data are used to conduct hazard assessments and evaluate potential risks to aquatic life (e.g., invertebrates, fish), birds, wildlife species, or the environment. To identify opportunities for regulatory uses of non-animal replacements for ecotoxicity tests, the needs and uses for data from tests utilizing animals must first be clarified. Accordingly, the objective of this review was to identify the ecotoxicity test data relied upon by U.S. federal agencies. The standards, test guidelines, guidance documents, and/or endpoints that are used to address each of the agencies' regulatory and research needs regarding ecotoxicity testing are described in the context of their application to decision-making. Testing and information use, needs, and/or requirements relevant to the regulatory or programmatic mandates of the agencies taking part in the Interagency Coordinating Committee on the Validation of Alternative Methods Ecotoxicology Workgroup are captured. This information will be useful for coordinating efforts to develop and implement alternative test methods to reduce, refine, or replace animal use in chemical safety evaluations.

Pediatric Environmental Health: Using Data on Toxic Chemical Emissions in Practice.

Children's unique behavioral and physiological characteristics can increase their exposure and susceptibility to environmental chemicals. The link between exposure to environmental chemicals and specific health outcomes, however, is often uncertain. This article introduces several resources to help health practitioners identify potential environmental exposures and risks related to toxic chemicals. It focuses on the U.S. Environmental Protection Agency's (EPA's) free and public environmental data, including the Toxics Release Inventory (TRI) data that contain information about toxics released to the environment. Three hypothetical case studies are presented to demonstrate how these data can help answer environmental exposure questions. The first case study illustrates a scenario where multiple patients in an area exhibit the same symptoms with a suspected link to environmental chemicals. The second case study illustrates a scenario where a patient with a confirmed exposure to a toxic chemical needs assistance with identifying potential environmental sources. And the third case study illustrates a scenario where a patient is concerned about the potential for future exposure to an environmental contaminant in a particular geographic area. Each case study includes contacts for follow-up questions, including the Pediatric Environmental Health Specialty Units (PEHSUs), EPA regional staff, state environmental agencies, and local health departments. These resources can help practitioners access and interpret environmental data, answer questions about potential exposures, and inform next steps if necessary.

Comparative chronic liver toxicity of benzo[a]pyrene in two populations of the atlantic killifish (Fundulus heteroclitus) with different exposure histories.

BACKGROUND: The Atlantic Wood Industries Superfund site on the Elizabeth River (ER) in Portsmouth, Virginia, is contaminated with polycyclic aromatic hydrocarbons (PAHs) derived from creosote. Embryos and larvae of ER killifish (Fundulus heteroclitus) are refractory to the induction of enzymes regulated by the aryl hydrocarbon receptor including cytochrome P4501A (CYP1A) and are resistant to PAH-induced lethality and teratogenicity. However, adult ER killifish show a greater prevalence of hepatic and pancreatic tumors compared with those from reference sites. OBJECTIVES: We used controlled laboratory studies to determine if ER killifish are more or less sensitive to PAH-induced chronic hepatic toxicity than killifish from an uncontaminated site. METHODS: Larvae from the ER and a reference site on King's Creek (KC) were subjected to two 24-hr aqueous exposures of benzo[a]pyrene (BaP; 0-400 µg/L). At various time points, larvae were analyzed for CYP1A activity, BaP concentrations, nuclear and mitochondrial DNA damage, and liver pathology. RESULTS: CYP1A activity was induced by BaP in KC but not ER larvae, and KC larvae demonstrated a greater reduction in whole-body concentrations of BaP over time. Mitochondrial and nuclear DNA lesion frequency increased significantly in BaP-exposed KC larvae, but not in ER larvae. Nine months postexposure, KC juveniles exhibited significantly more hepatic foci of cellular alteration and only KC juveniles developed hepatocellular carcinomas. CONCLUSIONS: In addition to acquiring the heritable resistance to the acute teratogenic effects of PAHs, ER fish appear to have concomitantly developed resistance to chronic effects, including cancer.