Toxicant, population response

The type of measurement made, and hence the type of data treatment, depends on the requirements of the test. Thus, measurement of the percent response at the molecular level may be important mechanistically and more precisely measured. However, for the assessment of toxicity, measurement of the population response may be more appropriate. 

Potential protective effect of selenium in fish. Selenium is known to bioconcentrate in fish, and selenium has been observed to correlate with mercury levels in the blood of fish consumed (Grandjean et al. 1992). Furthermore, there is evidence suggesting that consumption of methylmercury from fish, in conjunction with other beneficial constituents in fish (e.g., omega-3 fatty acids) may not result in the same toxicity dose-response relationship observed with methylmercury exposure from consumption of contaminated grain (as in the Iraqi population) (Davidson et al. 1998). 

Van Kirk RW, Hill SL. 2007. Demographic model predicts trout population response to selenium based on individual-level toxicity. Ecol Model 206 407 -20. 

A critique of this issue is beyond the scope of this book but not irrelevant to its goals. It is valid and useful to ask whether class-stratified lead exposures in ancient cultures and societies defined macroscale dose—population responses for toxic endpoints and to define such endpoints at the higher end of the entire dose—response spectrum. Lead-associated impairments of function at executive and other levels would be consistent with, if not the sole basis of, the political and anthropological histories of the Imperial era. One can also argue that even a contributory role for lead reproductive and other systemic toxicity as a risk factor in the survival of lead-exposed populations merits consideration. At minimum, lead would be a serious risk factor for multiple reproductive, developmental neurotoxic, immunotoxic, and endocrinological effects. 

The term dose—response in environmental epidemiology is typically understood to mean that quantitative relationship in which adverse effect severity and multiplicity increase in proportion to the intensity of exposure or dose indexed externally (intake/uptake quantities) or internally (exposure biomarkers). In the case of experimental animal exposures, reference is often to the administered dose, but biomarkers can also be available. Dose—response has also been employed to denote impacts at some selected effect level of a toxicant in terms of increasing affected fractions of some population as exposure increases. In this case, a dose—population response label is more precise. 

A second topic of importance to low-level Pb effects is that of dose—population response relationships, relationships where the endpoint is the prevalence or incidence of some sentinel or index effect, rather than the typically understood dose—toxic response relationship. The former is statistical, while the latter is toxicological. As PbB increases across a target population, the firaction of exposed individuals presenting with some adverse effect at a defined level increases. 

Equation 1 (TABLE 2) is the toxicity QSAR for this data set a slope of essentially negative one and r of 0.99 is achieved. Equation 2 is generated using equation 1 and the bioconcentration/Kow relationship of Halfon (1985). It indicates that a whole-body toxicant concentration of approximately 6,500 yumol L or 0.0065 mol L (or mol Kg when the density is about 1.0) is associated with an acutely toxic lethal response in half the exposed population of fathead minnows at essentially infinite time, i.e., threshold. 

Dose—response evaluation is used in describing the quantitative relationship between the amount of exposure to a substance and the extent of toxic injury or disease. Data may be derived from animal studies or from studies in exposed human populations. Dose—response toxicity relationship for a substance varies under different exposure conditions. The risk of a substance can not be ascertained with any degree of confidence unless... 

In addition to the effect of biological variabihty in group response for a given exposure dose, the magnitude of the dose for any given individual also determines the severity of the toxic injury. In general, the considerations for dose—response relationship with respect to both the proportion of a population responding and the severity of the response are similar for local and systemic effects. However, if metabohc activation is a factor in toxicity, then a saturation level may be reached. 

Dose-Response Evaluation The process of quantitatively evaluating toxicity information and characterizing the relationship between the dose a contaminant administered or received, and the incidence of adverse health effects in the exposed population. From a quantitative dose-respoiise relationship, toxicity values can be derived that are used in the risk characterization step to estimate the likelihood of adverse effects occurring in humans at different exposure levels. 

Median Effective Concentration (EC) The concentration of toxicant or intensity of other stimulus which produces some selected response in one half of a test population. 

A susceptible population will exhibit a different or enhanced response to methyl parathion than will most persons exposed to the same level of methyl parathion in the environment. Reasons may include genetic makeup, age, health and nutritional status, and exposure to other toxic substances (e g., cigarette smoke). These parameters result in reduced detoxification or excretion of methyl parathion, or compromised fimction of organs affected by methyl parathion. Populations who are at greater risk due to their imusually high exposure to methyl parathion are discussed in Section 6.7 Populations With Potentially High Exposures. 

Unusually susceptible populations are those groups of individuals who respond more quickly or at lower exposure levels than the general population to the toxic effects of methyl parathion. These responses may be genetic in origin or may be due to differences in development or life style factors such as nutrition or behavior, or due to preexisting disease states. 

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