Exposure routes health effect functions

The animal database on the health effects of DEHP is more complete, especially for studies using the oral route (Figure 3-6). Most studies have been conducted in rodent species, particularly rats and mice, using acute, intermediate, and chronic exposure durations. However, results are available from monkey studies as well. Systemic investigations have focused on the liver. There are limited data for the kidney, thyroid, and pancreas. There are limited data from in vivo studies of immune function or neurotoxicity. On the other hand, there are a number of studies that have evaluated the developmental and reproductive effects of DEHP. There is also adequate information to demonstrate that DEHP is not genotoxic in any conventional in vivo or in vitro studies of genotoxicity. The hepatic carcinogenic potential of DEHP has been clearly demonstrated in rodents. 

In the RPF method (eqn (1)), the user must identify the constraints of the application of a set of RPFs. For example, the health effect, dose range of component doses, route(s) of exposure, and dura-tion(s) of exposure for which the RPFs can be applied must be specified (e.g., a set of RPFs may be constrained to oral exposures and not be used for exposures to the same mixture through the inhalation route). To apply the method, an RPF is estimated for each mixture component the RPF estimates the toxicity of the component relative to that of the IC. RPFs commonly are estimated from a ratio of equally toxic doses of the individual dose-response functions for the component and the IC. For example, the quotient of the effective dose at which ten percent of a test population exhibits an effect (EDio) of the IC and the component could serve as a value for the component s RPF obviously, the RPF for the IC equals 1. The index chemical equivalent dose of an individual component is the product of the component dose and the RPF of the component. These equivalent doses are summed across all components. The risk posed by the mixture is estimated by comparing the summed index chemical equivalent doses of the mixture to the dose-response function of the IC ... 

To maintain its primary function as an organ of gas exchange, the mammalian respiratory system must be able to defend itself from constant assault of hazardous agents that enter the body by this route of exposure. When these normal pulmonary defenses are compromised, inhaled toxic substances have the potential for initiating or aggravating existing lung disease. The health effects associated with airborne... 

Strontium is fairly reactive and therefore is rarely found in its pure form in the earth s crust. Examples of common strontium compounds include strontium carbonate, strontium chloride, strontium hydroxide, strontium nitrate, strontium oxide, and strontium titanate. The most toxic strontium compound is strontium chromate, which is used in the production of pigments and can cause cancer by the inhalation route. Strontium chromate is not included in the Levels of Significant Exposure (LSE) tables for strontium since the carcinogenic effects of the compound are a function of the concentration of hexavalent chromium, and strontium only contributes to solubility. The Toxicological Profile for Chromium (ATSDR 2000) should be consulted for additional information on the health effects of strontium chromate. 

Coal Tar Products. Elevated red and white cell counts in urine were noted in 6-8% (29-34 of 452) of the employees examined in an industrial health survey in nine coal tar plants in which coal tar creosote and coal tar were the main treatments used (TOMA 1981). Some of these cell count elevations were attributed to urinary tract infections resulting from inadequate personal hygiene, and not to industrial exposure to toxic chemicals. However, some of the workers with elevated red and white cell counts in urine had cellular and granular casts and traces of protein, suggesting abnormal renal function. These individuals were referred to their physicians for diagnosis. No determination of exposure was made at the nine coal tar plants (TOMA 1981). Moreover, no clear relationship could be established because exposure routes in addition to inhalation (e.g., oral and dermal) were likely. Also, the ability to relate renal effects to coal tar creosote and coal tar exposure was further confounded by the possibility that the subjects were also exposed to other chemicals and cigarette smoke. Additional limitations of the study included seasonal and geographical variation in plant locations, past employment history, voluntary participation in the study that could have biased it in favor of healthy workers, lack of statistical analyses, lack of adequate controls, and use of only current employees. 

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