Parenteral, routes of exposure

Cancer. There are a few reports of cancer in people who have been exposed to carbon tetrachloride, but these data per se are not adequate to show that carbon tetrachloride causes cancer in humans. However, there is convincing evidence from animal studies that oral exposure to carbon tetrachloride leads to hepatic tumors (see Section 2.2.1.8), which is supported by a number of other animal studies employing parenteral routes of exposure (Della Porta et al. 1961 Reuber and Glover 1967, 1970). Collectively, these data suggest that carbon tetrachloride is reasonably likely to be a human carcinogen. 

Strychnine is a compound of high acute toxicity. The oral LD value in rats is 15mgkg. Parenteral routes of exposure are more toxic LD50 values in laboratory rodents range from 1 to 4 mg kg... 

Summary of Carcinogenicity Studies with Polycyclic Aromatic Hydrocarbons Using Parenteral Routes of Exposure... 

In the derivation of an RfD, human exposure data are preferred however, the only available data for HN2 pertain to acute exposures. Available animal data include acute toxicity data and short-term toxicity studies by parenteral routes of exposure. Acute toxicity endpoints are generally not used for developing subchronic or chronic reference values because they do not provide information on the possibility of cumulative effects following prolonged exposures. Thus, inadequacies in the available data base prevent the derivation of an RfD for HN2. 

The chapter covers end points in the same order they appear within the Discussion of Health Effects by Route of Exposure section, by route (inhalation, oral, dermal) and within route by effect. Human data are presented first, then animal data. Both are organized by duration (acute, intermediate, chronic). In vitro data and data from parenteral routes (intramuscular, intravenous, subcutaneous, etc.) are also considered in this chapter. If data are located in the scientific literature, a table of genotoxicity information is included. 

The model is designed to simulate oral, inhalation, and parenteral (e.g., injection) exposures to americium and cannot be applied to other routes of exposure without modification. 

With respect to oral sensitization, attempts have been made to develop animal models of food allergy, which so far has proven to be complicated. One crucial point is the route of exposure experience indicates that it may not be possible to develop an animal model, which rnirnics the human sensitization via the oral route. Exposure via the diet or in drinking water appears in rodents to be more likely to cause immunological hyporesponsiveness (i.e., tolerance) than sensitization, and therefore it may be necessary to use parenteral induction in animal testing (Dearman and Kimber 2007). 

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