Chapter One - Toxicology of Inorganic Carcinogens

Is The Toxicity Of Bipyridylium Herbicides Two-Fold?

Toxicology of aquatic pollution: Physiological, molecular and cellular approaches: Edited by E.W. Taylor; Society for Experimental Biology, Seminar Series 57; Cambridge University Press, Cambridge; 1996; 283 pp.; GBP 55.00, US$ 85.00; ISBN 0-521-45524-3

Progress of research on the toxicology of antibiotic pollution in aquatic organisms

Gene expression patterns in rainbow trout, Oncorhynchus mykiss, exposed to a suite of model toxicants

The mode of toxic action (MOA) is recognized as a key determinant of chemical toxicity and as an alternative to chemical class-based predictive toxicity modeling. However, MOA classification has never been standardized in ecotoxicology, and a comprehensive comparison of classification tools and approaches has never been reported. Here we critically evaluate three MOA classification methodologies using an aquatic toxicity data set of 3448 chemicals, compare the approaches, and assess utility and limitations in screening and early tier assessments. The comparisons focused on three commonly used tools: Verhaar prediction of toxicity MOA, the U.S. Environmental Protection Agency (EPA) ASsessment Tool for Evaluating Risk (ASTER) QSAR (quantitative structure activity relationship) application, and the EPA Mode of Action and Toxicity (MOAtox) database. Of the 3448 MOAs predicted using the Verhaar scheme, 1165 were classified by ASTER, and 802 were available in MOAtox. Of the subset of 432 chemicals with MOA assignments for each of the three schemes, 42% had complete concordance in MOA classification, and there was no agreement for 7% of the chemicals. The research shows the potential for large differences in MOA classification between the five broad groups of the Verhaar scheme and the more mechanism-based assignments of ASTER and MOAtox. Harmonization of classification schemes is needed to use MOA classification in chemical hazard and risk assessment more broadly.

Mercury exists naturally and as a man-made contaminant. The release of processed mercury can lead to a progressive increase in the amount of atmospheric mercury, which enters the atmospheric-soil-water distribution cycles where it can remain in circulation for years. Mercury poisoning is the result of exposure to mercury or mercury compounds resulting in various toxic effects depend on its chemical form and route of exposure. The major route of human exposure to methylmercury (MeHg) is largely through eating contaminated fish, seafood, and wildlife which have been exposed to mercury through ingestion of contaminated lower organisms. MeHg toxicity is associated with nervous system damage in adults and impaired neurological development in infants and children. Ingested mercury may undergo bioaccumulation leading to progressive increases in body burdens. This review addresses the systemic pathophysiology of individual organ systems associated with mercury poisoning. Mercury has profound cellular, cardiovascular, hematological, pulmonary, renal, immunological, neurological, endocrine, reproductive, and embryonic toxicological effects.

Results of a cyclosporin A ringstudy

Heavy metals show significant risks to both human health and the environment. The analysis of the toxic mechanisms of heavy metals and their toxic effects on humans has received increasing attention. For this reason, this comprehensive research explores the toxicology effects of heavy metals, delving into their common sources, mechanisms of toxicity, specific health effects, routes of human exposure, regulation and prevention strategies, and notable case studies. Each section provides in-depth insights, from the neurological impacts of lead to the potential link between lead exposure and Alzheimer's disease. The research underscores the importance of understanding heavy metal toxicity, its regulatory framework, and preventive measures. Ultimately, addressing heavy metal contamination requires global cooperation, stringent regulations, and ongoing research to protect individuals and ecosystems from the adverse effects of these toxic elements. In addition, this study also provides a new approach for the study of the impact of heavy metals on human health.

Acute toxicity studies are essential preliminaries to repeated‐dosing studies, but the former give limited information about organ‐specific toxicity. Many toxic effects are not detected in acute studies because of the need for cumulative toxicity to develop or because of a long latency to development of toxicity. Evaluation of repeated‐exposure toxicity requires that studies be conducted by an appropriate route for a sufficient number of exposures. The initial concentrations or doses chosen will be determined by findings from acute studies, when these permit the detection of toxicity. Short‐term repeated‐dose studies vary in length from a few (5‐9) days to 28 days, while subchronic studies are usually 90 days, and chronic studies 18 months or more, in rodents. The material to be tested should be of known purity. Most repeated‐exposure studies are conducted using rats or mice, with some regulatory agencies also requiring the use of a larger species (e.g. dog), for subchronic studies. The choice of species is heavily constrained by regulatory authorities and the requirement for normative data. Dosing may be by various routes, that chosen depending largely on the likely route of human exposure. Oral dosing can be gavage, or incorporation of test material into the diet or drinking water. In‐life observations include clinical observation, food and water consumption and body weight determinations. Standard haematology, clinical chemistry and urinalysis measurements are necessary in all studies. At termination, necropsy is carried out, selected organs are weighed and selected organs processed for histopathology.

Development of a neurotoxic equivalence scheme of relative potency for assessing the risk of PCB mixtures

PPARα and TCE: Keshava et al. Respond

Integrative assessment of mixture toxicity of household chemicals using the toxic unit approach and mode of action.

The medical effects of mold exposure

Ultra-trace measurement of Dechloranes to investigate food as a route of human exposure

How benthic diatoms within natural communities respond to eight common herbicides with different modes of action