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Water: Microbial

Thesaurus of Terms Used in Microbial Risk Assessment: 5.12 Chemical Risk Assessment Terms

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baseline condition

A phase conducted during an experiment where the independent variable, an event or variable manipulated by a researcher, is absent. A baseline is used for comparison when the independent variable is subsequently introduced. (RRTC-PBS 2003)

bioassay

An assay for determining the potency (or concentration) of a substance that causes a biological change in experimental animals. (EPA 2003)
A test conducted in living organisms (in vivo) or with living cells (in vitro) to determine the hazard or potency of a chemical by its effect on animals, isolated tissues, or microorganisms. (OAQPS 1989)
A test to determine the relative strength of a substance by comparing its effect on a test organism with that of a standard preparation. (EPA 2005b)
A method of testing a material’s effects on living organisms. (EPA 2005e)
Using living organisms to measure the effect of a substance, factor, or condition. (SRA 2004)

bioavailability
  1. The degree to which a substance becomes available to the target tissue after administration or exposure. (EPA 2003)
  2. The ability to be absorbed and available to interact with the metabolic processes of an organism. (EPA 2004)
  3. A measure of the degree to which a dose of a substance becomes physiologically available to the body tissues depending upon adsorption, distribution, metabolism, and excretion rates. (OAQPS 1989)
  4. The rate and extent to which an agent can be absorbed by an organism and is available for metabolism or interaction with biologically significant receptors. Bioavailability involves both release from a medium (if present) and absorption by an organism. (IPCS 2004)
biological half-life

The time required for a biological system (such as a human or animal) to eliminate, by natural processes, half the amount of a substance (such as a radioactive material) that has been absorbed into that system. (RAIS 2004, SRA 2004)

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chronic toxicity
  1. The capacity of a substance to cause adverse human health effects as a result of chronic exposure. (EPA 2003)
  2. The effects of long term or repeated low level exposures to a toxic substance (cancer, liver damage, reproductive disorders, etc.). (EPA 2005e)
frank effect level (ACRONYM: FEL)
  1. A level of exposure or dose which produces irreversible, adverse effects at a statistically or biologically significant increase in frequency or severity between those exposed and those not exposed. (EPA 2003)
  2. Exposure level which produces unmistakable adverse effects, such as irreversible functional impairment or mortality, at a statistically or biologically significant increase in frequency or severity between an exposed population and its appropriate control. (RAIS 2004)
half-life (ACRONYM: t½ )
  1. The time it takes for half the original amount of a substance to disappear. In the environment, the half-life is the time it takes for half the original amount of a substance to disappear when it is changed to another chemical by bacteria, fungi, sunlight, or other chemical processes. In the human body, the half-life is the time it takes for half the original amount of the substance to disappear, either by being changed to another substance or by leaving the body. In the case of radioactive material, the half life is the amount of time necessary for one half the initial number of radioactive atoms to change or transform into another atom (that is normally not radioactive). After two half lives, 25% of the original number of radioactive atoms remain. (ATSDR 2004)
  2. (a) The time required for a pollutant to lose one-half of its original concentration. For example, the biochemical half-life of DDT in the environment is 15 years. (b) The time required for half of the atoms of a radioactive element to undergo self-transmutation or decay (half-life of radium is 1620 years). (c) The time required for the elimination of half a total dose from the body. (EPA 2005b)
hazard index (ACRONYM: HI)
  1. The sum of more than one hazard quotient for multiple substances and/or multiple exposure pathways. The HI is calculated separately for chronic, subchronic, and shorter-term duration exposures. (EPA 2004)
  2. Potential noncarcinogenic (systemic) effects are characterized by comparing projected intakes of chemicals to toxicity values (i.e, reference doses). The numerical risk or hazard quotient estimate that results is a ratio. The ratio of the intake over the reference dose (hazard index) is compared to unity (1.0). If the quotient is less than 1, then the systemic effects are assumed not to be of concern; if the hazard quotient is greater than 1, then the systemic effects are assumed to be of concern. The hazard index is the sum of hazard quotients. (RAIS 2004)

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hazard quotient (ACRONYM: HQ)
  1. The ratio of a single substance exposure level over a specified time period (e.g., chronic) to a reference value (e.g., an RfC) for that substance derived from a similar exposure period. (EPA 2004)
  2. The ratio of estimated site-specific exposure to a single chemical from a site over a specified period to the estimated daily exposure level, at which no adverse health effects are likely to occur. (EPA 2005b)
hazard ratio

A term used to compare an animal’s daily dietary intake of a pesticide to its LD 50 value. A ratio greater than 1.0 indicates that the animal is likely to consume a dose amount which would kill 50 percent of animals of the same species. (EPA 2005b)

human equivalent concentration (ACRONYM: HEC)
  1. The human concentration (for inhalation exposure) of an agent that is believed to induce the same magnitude of toxic effect as the experimental animal species concentration or dose. This adjustment may incorporate toxicokinetic information on the particular agent, if available, or use a default procedure, such as assuming that daily oral doses experienced for a lifetime are proportional to body weight raised to the 0.75 power. (EPA 2003)
  2. Exposure concentration for humans that has been adjusted for dosimetric differences between experimental animal species and humans to be equivalent to the exposure concentration associated with observed effects in the experimental animal species. If occupational human exposures are used for extrapolation, the human equivalent concentration represents the equivalent human exposure concentration adjusted to a continuous basis. (RAIS 2004)
    RELATED TERMS: human equivalent dose
human equivalent dose (ACRONYM: HED)

A dose which, when administered to humans, produces an effect equal to that produced by a dose in animals. (EPA 2005b, RAIS 2004)
RELATED TERMS: human equivalent concentration

interspecies dose conversion

The process of extrapolating from animal doses to human equivalent doses. (EPA 2003)

key event

A “key event” is an empirically observable precursor step that is itself a necessary element of the mode of action or is a biologically based marker for such an element. (EPA 2005a)

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lethal concentration-50 (ACRONYM: LC50 )
  1. Median level concentration, a standard measure of toxicity. It tells how much of a substance is needed to kill half of a group of experimental organisms in a given time. (EPA 2005b)
  2. A concentration of a pollutant or effluent at which 50% of the test organisms die; a common measure of acute toxicity. (EPA 2005e)
    RELATED TERMS: lethal dose, lethal dose-50
linearized multistage procedure

A modification of the multistage model, used for estimating carcinogenic risk, that incorporates a linear upper bound on extra risk for exposures below the experimental range. (EPA 2003)
RELATED TERMS: multistage model

lower limit on effective dose-10 (ACRONYM: LED10 )

The 95% lower confidence limit of the dose of a chemical needed to produce an adverse effect in 10 percent of those exposed to the chemical, relative to control. (EPA 2003)

lowest observed adverse effect level (ACRONYM: LOAEL)
  1. The lowest level of a stressor evaluated in a test that causes statistically significant differences from the controls. (EPA 1998a)
  2. The lowest exposure level at which there are biologically significant increases in frequency or severity of adverse effects between the exposed population and its appropriate control group. (EPA 2003)
  3. The lowest exposure level in a study or group of studies at which there are statistically or biologically significant increases in frequency or severity of adverse effects between the exposed population and its appropriate control group. Also referred to as lowest-effect level (LEL).(EPA 2004)
  4. The lowest level of a stressor that causes statistically and biologically significant differences in test samples as compared to other samples subjected to no stressor. (EPA 2005b)
  5. The lowest dose in a toxicity study resulting in adverse health effects. (EPA 2005e)
  6. The lowest tested dose of a substance that has been reported to cause harmful (adverse) health effects in people or animals. (ATSDR 2004)

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lowest-observed effect level (ACRONYM: LOEL or LEL)

In a study, the lowest dose or exposure level at which a statistically or biologically significant effect is observed in the exposed population compared with an appropriate unexposed control group. (EPA 2003)

non-cancer risk

The potential or probability to incur a noncancer health effect (e.g., lead poisoning, neurological disorders, liver disease) due to exposure to hazardous substances. (TAFBERP 2005)

non-threshold toxicant

A chemical for which there is no exposure level below which an adverse health outcome is not expected to occur. Such substances are considered to pose some risk of harm at any level of exposure. (EPA 2004)

no-observed-adverse-effect level (ACRONYM: NOAEL)
  1. The highest exposure level at which there are no biologically significant increases in the frequency or severity of adverse effect between the exposed population and its appropriate control; some effects may be produced at this level, but they are not considered adverse or precursors of adverse effects. (EPA 2003)
  2. An highest exposure level at which there are no statistically or biologically significant increases in the frequency or severity of adverse effect between the exposed population and its appropriate control; some effects may be produced at this level, but they are not considered adverse, nor precursors to adverse effects. (EPA 2004)
  3. An exposure level at which there are no statistically or biologically significant increases in the frequency or severity of adverse effects between the exposed population and its appropriate control; some effects may be produced at this level, but they are not considered as adverse, or as precursors to adverse effects. In an experiment with several NOAELs, the regulatory focus is primarily on the highest one, leading to the common usage of the term NOAEL as the highest exposure without adverse effects. (EPA 2005b)
  4. The highest tested dose of a substance that has been reported to have no harmful (adverse) health effects on people or animals. (ATSDR 2004)

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no-observed-effect level (ACRONYM: NOEL)
  1. The highest level of a stressor evaluated in a test that does not cause statistically significant differences from the controls. (EPA 1998a)
  2. An exposure level at which there are no statistically or biologically significant increases in the frequency or severity of any effect between the exposed population and its appropriate control. (EPA 2003, EPA 2005b)
pharmacokinetic model

A model that can be used to predict the time course of absorption, distribution, metabolism, and excretion of a foreign substance in an organism’s body (e.g., pesticide). (EPA 1998b)

pharmacokinetics
  1. The study of the time course of absorption, distribution, metabolism, and excretion of a foreign substance (e.g., a drug or pollutant) in an organism’s body. (EPA 1992)
  2. The field of study concerned with defining, through measurement or modeling, the absorption, distribution, metabolism, and excretion of drugs or chemicals in a biological system as a function of time. (EPA 1995b)
  3. The study of the way that drugs move through the body after they are swallowed or injected. (EPA 2005b)
physiologically based pharmacoki (ACRONYM: PBPK model)
  1. A model that estimates the dose to a target tissue or organ by taking into account the rate of absorption into the body, distribution among target organs and tissues, metabolism, and excretion. (EPA 2003)
  2. A computer model that describes what happens to a chemical in the body. This model describes how the chemical gets into the body, where it goes in the body, how it is changed by the body, and how it leaves the body. (ATSDR 2004)
reference concentration (ACRONYM: RfC)

An estimate (with uncertainty spanning perhaps an order of magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. It can be derived from a NOAEL, LOAEL, or benchmark concentration, with uncertainty factors generally applied to reflect limitations of the data used. Generally used in EPA’s noncancer health assessments. (EPA 2003)

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reference dose (ACRONYM: RfD)
  1. An estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. It can be derived from a NOAEL, LOAEL, or benchmark dose, with uncertainty factors generally applied to reflect limitations of the data used. Generally used in EPA’s noncancer health assessments. (EPA 2003)
  2. The RfD is a numerical estimate of a daily oral exposure to the human population, including sensitive subgroups such as children, that is not likely to cause harmful effects during a lifetime. RfDs are generally used for health effects that are thought to have a threshold or low dose limit for producing effects. (EPA 2005b)
  3. An EPA estimate, with uncertainty or safety factors built in, of the daily lifetime dose of a substance that is unlikely to cause harm in humans. (ATSDR 2004)
  4. An estimate of the daily exposure dose that is likely to be without deleterious effect even if continued exposure occurs over a lifetime. (IPCS/OECD 2004)
    RELATED TERMS: acceptable daily intake
reference value (ACRONYM: RfV)

An estimation of an exposure for [a given duration] to the human population (including susceptible subgroups) that is likely to be without an appreciable risk of adverse effects over a lifetime. It is derived from a BMDL, a NOAEL, a LOAEL, or another suitable point of departure, with uncertainty/variability factors applied to reflect limitations of the data used. (EPA 2003)

slope factor

An upper bound, approximating a 95% confidence limit, on the increased cancer risk from a lifetime exposure to an agent. This estimate, usually expressed in units of proportion (of a population) affected per mg/kg/day, is generally reserved for use in the low-dose region of the dose-response relationship, that is, for exposures corresponding to risks less than 1 in 100. (EPA 2003)

subchronic study

A toxicity study designed to measure effects from subchronic exposure to a chemical. (EPA 2003)

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synergism

An interaction of two or more chemicals that results in an effect greater than the sum of their separate effects. (EPA 2005b)

synergistic effect
  1. A biologic response to multiple substances where one substance worsens the effect of another substance. The combined effect of the substances acting together is greater than the sum of the effects of the substances acting by themselves. (ATSDR 2004)
  2. Joint effects of two or more agents, such as drugs that increase each other’s effectiveness when taken together. (RAIS 2004, SRA 2004)
    RELATED TERMS: additive effect, antagonistic effect
threshold toxicant

A chemical for which there is an exposure level below which an adverse health outcome is not expected to occur. (EPA 2004)

toxic substance

A chemical, physical, or biological agent that may cause an adverse effect or effects to biological systems. (EPA 2003)

toxicant
  1. A harmful substance or agent that may injure an exposed organism. (EPA 2005b)
  2. A substance that kills or injures an organism through chemical or physical action or by altering the organism’s environment; for example, cyanides, phenols, pesticides, or heavy metals; especially used for insect control. (RAIS 2004, SRA 2004)
    RELATED TERMS: toxin

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toxicity
  1. Deleterious or adverse biological effects elicited by a chemical, physical, or biological agent. (EPA 2003)
  2. The degree to which a substance or mixture of substances can harm humans or environmental receptors. (EPA 2004, EPA 2005b)
  3. The quality or degree of being poisonous or harmful to plant, animal, or human life. (CRCWQT 2002)
  4. Inherent property of an agent to cause an adverse biological effect. (IPCS/OECD 2004)
  5. The degree of danger posed by a substance to animal or plant life. (RAIS 2004, SRA 2004) 
toxicity assessment

Characterization of the toxicological properties and effects of a chemical, with special emphasis on establishment of dose-response characteristics. (EPA 2004, EPA 2005b)

toxicity test

Biological testing (usually with an cell system, invertebrate, fish, or small mammal) to determine the adverse effects of a compound. (EPA 2004)

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toxicodynamics

The determination and quantification of the sequence of events at the cellular and molecular levels leading to a toxic response to an environmental agent (sometimes referred to as pharmacodynamics). (EPA 2003)

toxicokinetics
  1. The determination and quantification of the time course of absorption, distribution, biotransformation, and excretion of chemicals (sometimes referred to as pharmacokinetics). (EPA 2003)
  2. The terms “toxicokinetics” and “pharmacokinetics” describe the same processes; “pharmacokinetics” was derived in reference to drugs or other substances used for treatment, while “toxicokinetics” has more recently been used to refer to nonpharmaceutical toxic substances such as environmental pollutants. (IPCS 2001)
toxicology
  1. The study of harmful interactions between chemical, physical, or biological agents and biological systems. (EPA 2003)
  2. The study of harmful interactions between chemicals and biological systems. (EPA 2004)
  3. Study of poisons, their effects, antidotes and detection. (CRCWQT 2002)

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