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effect, enter into particular reactions, and so on. The goal of QSAR studies in toxicology is to develop procedures whereby the toxicity of a compound can be predicted from its chemical structure by analogy with the properties of other toxicants of known structure and toxic properties. reactive intermediates (reactive metabolites) Chemical compounds, produced during the metabolism of xenobiotics, that are more chemically reactive than is the parent compound. Although they are susceptible to detoxication by conjugation reactions, these metabolites, as a consequence of their increased reactivity, have a greater potential for adverse effects than does the parent compound. A well-known example is the metabolism of benzo(a)pyrene to its carcinogenic dihydrodiol epoxide derivative as a result of metabolism by cytochrome P450 and epoxide hydrolase. Reactive intermediates involved in toxic effects include epoxides, quinones, free radicals, reactive oxygen species, and a small number of unstable conjugation products. reference dose (RfD) See acceptable daily intake (ADI). resistance See adaptation to toxicants. Resource Conservation and Recovery Act (RCRA) Administered by the EPA, the RCRA is the most important act governing the disposal of hazardous wastes in the United States; it promulgates standards for identi cation of hazardous wastes, their transportation, and their disposal. Included in the last are siting and construction criteria for land lls and other disposal facilities as well as the regulation of owners and operators of such facilities. risk assessment (risk analysis) The process by which the potential adverse health effects of human exposure to chemicals are characterized; it includes the development of both qualitative and quantitative expression of risk. The process of risk assessment may be divided into four major components: hazard identi cation, doseresponse assessment (high-dose to low-dose extrapolation), exposure assessment, and risk characterization. risk, toxicologic The probability that some adverse effect will result from a given exposure to a chemical is known as the risk. It is the estimated frequency of occurrence of an event in a population and may be expressed in absolute terms (e.g., 1 in 1 million) or in terms of relative risk (i.e., the ratio of the risk in question to that in an equivalent unexposed population). safety factor (uncertainty factor) A number by which the no observed effect level (NOEL) is divided to derive the reference dose (RfD), the reference concentration (RfC) or minimum risk level (MRL) of a chemical from experimental data. The safety factor is intended to account for the uncertainties inherent in estimating the potential effects of a chemical on humans from results obtained with test species. The safety factor allows for possible difference insensitivity between the test species and humans, as well as for variations in the sensitivity within the human population. The size of safety factor (e.g., 100 1000) varies with con dence in the database and the nature of the adverse effects. Small safety factors indicate a high degree of con dence in the data, an extensive database, and/or the availability of human data. Large safety factors are indicative of an inadequate and uncertain database and/or the severity of the unexpected toxic effect. selectivity (selective toxicity) A characteristic of the relationship between toxic chemicals and living organisms whereby a particular chemical may be highly toxic to one species but relatively innocuous to another. The search for and study of selective
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GLOSSARY
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toxicants is an important aspect of comparative toxicology because chemicals toxic to target species but innocuous to nontarget species are extremely valuable in agriculture and medicine. The mechanisms involved vary from differential penetration rates through different metabolic pathways to differences in receptor molecules at the site of toxic action. solvents In toxicology this term usually refers to industrial solvents. These belong to many different chemical classes and a number of these are known to cause problems of toxicity to humans. They include aliphatic hydrocarbons (e.g., hexane), halogenated aliphatic hydrogens (e.g., methylene chloride), aliphatic alcohols (e.g., methanol), glycols and glycol ethers (e.g., propylene and propylene glycol), and aromatic hydrocarbons (e.g., toluene). subchronic toxicity Toxicity due to chronic exposure to quantities of a toxicant that do not cause any evident acute toxicity for a time period that is extended but is not so long as to constitute a signi cant part of the lifespan or the species in question. In subchronic toxicity tests using mammals, a 30- to 90-day period is considered appropriate. synergism and potentiation The terms synergism and potentiation have been variously used and de ned but in any case involve a toxicity that is greater when two compounds are given simultaneously or sequentially than would be expected from a consideration of the toxicities of the compounds given alone. In an attempt to make the use of these terms uniform, it is a suggested that, insofar as toxic effects are concerned, they be used as de ned as follows: both involve toxicity greater that would be expected from the toxicities of the compounds administered separately, but in the case of synergism one compound has little or no intrinsic toxicity administered alone, whereas in the case of potentiation both compounds have appreciable toxicity when administered alone. teratogenesis This term refers to the production of defects in the reproduction process resulting in either reduced productivity due to fetal or embryonic mortality or the birth of offspring with physical, mental, behavioral, or developmental defects. Compounds causing such defects are known as teratogens. therapy Poisoning therapy may be nonspeci c or speci c. Nonspeci c therapy is treatment for poisoning that is not related to the mode of action of the particular toxicant. It is designed to prevent further uptake of the toxicant and to maintain vital signs. Speci c therapy, however, is therapy related to the mode of action of the toxicant and not simply to the maintenance of vital signs by treatment of symptoms. Speci c therapy may be based on activation and detoxication reactions, on mode of action, or on elimination of the toxicant. In some cases more than one antidote, with different modes of action, is available for the same toxicant. threshold dose This is the dose of a toxicant below which no adverse effect occurs. The existence of such a threshold is based on the fundamental tenet of toxicology that, for any chemical, there exists a range of doses over which the severity of the observed effect is directly related to the dose, the threshold level representing the lower limit of this dose range. Although practical thresholds are considered to exist for most adverse effects, for regulatory purposes it is assumed that there is no threshold dose for carcinogens. threshold limit value (TLV) The upper permissive limit of airborne concentrations of substances represents conditions under which it is believed that nearly all workers may be exposed repeatedly, day after day, without adverse effect. Threshold
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