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5.0 3.4 Dose (log) LD05 (b) LD50
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Figure 11.3 The dose-response relationship. (a) Five segments of the sigmoidal dose-response curve as described in the text. (b) Linearized dose-response relationship through log (dose)-probit (effect) transformations. Locations of the LD50 and LD05 are depicted.
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NONCONVENTIONAL DOSE-RESPONSE RELATIONSHIPS
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The dose-response line also can be used to estimate the threshold dose. The threshold dose is de ned as the lowest dose of the chemical that would be expected to elicit a response under conditions at which the assay was performed. The threshold dose is often empirically estimated as being a dose less that the lowest dose at which an effect was measured but higher than the greatest dose at which no effect was detected. Conceptually, the threshold dose is de ned as the intercept of segments I and II of the dose-response curve (Figure 11.3a). Statistically, the threshold dose can be estimated from the linearized dose-response curve as the LC05. This value will closely approximate the threshold dose and can be statistically derived from the entire data set (i.e., the dose-response line). However, con dence in this value is greatly compromised, since it is derived from one end of the line (Figure 11.3b).
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11.4 NONCONVENTIONAL DOSE-RESPONSE RELATIONSHIPS
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The low-level effects of chemicals have received attention among pharmacologists for over 100 years. A current resurgence in interest among pharmacologists in low-level effects stems from use of homeopathic approaches to treating disease. Proponents of homeopathy maintain that low levels of toxic materials stimulate physiological responses that can target disease without eliciting adverse effects in the individual undergoing treatment. Homeopathic principles may have application in toxicology based on the premise that exposure to some chemicals at subthreshold levels, as de ned by standard acute toxicity evaluations, can elicit toxicological as well as pharmacological effects. Both pharmacological and toxicological homeopathy may be the consequence of hormesis. Hormesis is de ned as an overcompensatory response to some disruption in homeostasis. Thus hormesis is typically evident at low doses of a chemical at which gross disruptions in homeostasis do not mask the hormetic response. Further, hormesis typically presents as an effect opposite to that elicited at higher levels of the chemical. For example, a chemical that stimulates corticosteroid secretion at high dosages resulting in hyperadrenocorticism might elicit a hormetic response at low dosages resulting in corticosteroid de ciency. A hypothetical nonconventional dose-response relationship resulting from such interactions is depicted in Figure 11.4. At the true threshold dose,
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Figure 11.4 Nonconventional dose-response relationship involving low-dose effects and compensation. (I) True initiation of the response followed by a compensatory response that returns the effects to the 0% level. (II) A negative response due to overcompensation (hormesis) followed by recovery to the 0% effect level. (III) The standard sigmoidal dose-response relationship.
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ACUTE TOXICITY
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the organisms begin to exhibit increased stimulation in corticosteroid secretion. However, at slightly higher doses, a compensatory response occurs whereby corticosteroid secretion is decreased in order to maintain homeostasis within the organism. Overcompensation may actually result in a decrease in corticosteroid secretion at certain toxicant dosages. Finally the compensatory abilities of the organism are overcome by the high doses of the toxicant at the pseudo threshold dose, above which the standard dose-response relationship occurs. Nonconventional dose-response relationships have been observed with respect to both acute and chronic toxicity and are particularly relevant to the risk assessment process when establishing levels of exposure that are anticipated to pose no harm.
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MECHANISMS OF ACUTE TOXICITY
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An exhaustive review of the mechanisms by which chemicals cause acute toxicity is beyond the scope of this chapter. However, certain mechanisms of toxicity are relevant since they are common to many important classes of toxicants. Some of these mechanisms of acute toxicity are discussed.
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