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Exposure routes Injection

Therefore, animal experiments show that selenium might be protective in terms of neurodevelopmental responses bnt this is not clear. The selenium dose, form, and exposure route (injection vs ingestion) might affect the tissne deposition profiles. Althongh seleninm appears to have a protective effect in animals, no association has been confirmed in humans. The mechanism by which seleninm inflnences the deposition of Hg is not established. Proposed mechanisms inclnde the formation of seleno-MeHg complexes, a seleninm-induced release of MeHg fiom sulfhydryl bonds in the blood, and tissue-specific mechanisms that inflnence intracellular uptake (Glyrm and Lind 1995). [Pg.98]

In assessing animal data, careful attention must be paid to the quality of the data, the incidence of spontaneous tumors in the control population, consistency if more than one study is available, and statistical validity. If the exposure route and experimental regimen employed do not agree with the most likely mode(s) of human exposure (e.g., intramuscular injection), the data must be interpreted cautiously. Consideration should be given to data on metabolism of the compound by the animal species tested, as compared with metabolism in humans if this information is known. If only in vitro data are available, only qualitative estimates may be possible because of uncertainties regarding the association between in vitro results and human or animal effects. The availability of associated pharmacokinetic data, however, may allow development of a rough quantitative estimate. [Pg.299]

C]taurine-labeled MWNTs were administered to mice by three different exposure routes (intravenous injection, gavage, and intratracheal instillation) and their biodistribution was monitored [134], After intravenous injection, [14C]taurine-labeled MWNTs accumulated in the liver, heart, and lung after gavage administration, [14C]taurine-labeled MWNTs was only detectable in the stomach, intestine, and feces. No [14C]taurine-labeled MWNTs were detected in the blood. Finally, [14C] taurine-labeled MWNTs were partly cleared from the lungs after intratracheal instillation. Since various cell and tissue types have demonstrated a high affinity for uptake of taurine, it should be noted that the label used in this investigation may have influenced the biodistribution of the MWNTs tested [101]. [Pg.196]

In the pharmaceutical industry, the two most common routes of administration are via diet and gavage (PMA, 1988). Some compounds are given by drinking water, topical (dermal) application, or injection, depending on the expected clinical exposure route, which is the primary criterion for determining the route of administration in carcinogenicity studies. When more than one clinical route is anticipated for a drug, the dietary route is often chosen for practical reasons. [Pg.306]

Exposure route is usually ingestion, inhalation, or dermal absorption, but sometimes includes more exotic means for a specified substance to enter the body (like injection). [Pg.496]

Two case studies of acute intrusion of barium sulfate into the peritoneal space during barium enema examination of four men showed barium sulfate caused an acute inflammatory tissue response (Kay 1954 Yamamura et al. 1985), and in one case resulted in formation of a fibrous granuloma (Kay 1954). This is an extremely rare mode of entry and not of significant concern for individuals exposed at a hazardous waste site. Increased fluid accumulation in the intestinal lumen of rats was observed after intraperitoneal injection of barium chloride (Hardcastle et al. 1983b, 1985) however, this observation is not significant for individuals exposed at hazardous waste sites because of the route of exposure and because there has been no documentation of this effect occurring in humans following normal exposure routes. [Pg.44]

Acute Toxicity Measure Acute toxicity of a chemical may be measured through different routes and by systemic exposures by injections such as subcutaneous, intravenous, intramuscular, and intratracheal, which are all used in experimental and medical support. Appropriate knowledge about measures and acute toxicity warnings of chemicals are necessary to contain chemical hazards vis-a-vis to achieve chemical safety and human health. [Pg.38]

What are the likely routes of exposure to the worker Typical incidents should also be considered here, for example, needle stick-related exposure when injecting the material into a chromatograph, inhalation when charging a tablet press, etc. [Pg.388]

The nature of the exposure, route (e.g., skin, oral, intraperitoneal injection), and duration (exposure vs. time profile) may also be important. The overall fate may be primarily determined by the stability and reactivity of the drug within the biological environments encountered. [Pg.226]

Exposure route The avenue by which a chemical comes into contact with an organism, e.g. inhalation, ingestion, dermal contact, injection, etc. (USEPA, 1997b). [Pg.396]

No chronic animal toxicity studies have been conducted on VX however, there are two subchronic studies which can be used for developing an RfD. In one study, rats were dosed by s.c. injection 5 days per week for 90 days (Goldman et al., 1988). In the second study, sheep received daily doses of VX in feed for 56 days (Rice et al., 1971). Both of these studies identify blood cholinesterase as the most sensitive endpoint. Data are available indicating that sheep are more sensitive than rats to the toxic effects of VX. Ivanov et al. (1993) reported that the oral LD50 in sheep is 6 figfkg whereas that for rats is 66 //g/kg. In addition, Ivanov et al. (1993) suggested that this increased susceptibihty in sheep may be due, in part, to the lower concentration of catalytic sites for serum ChE in sheep (7.098 x lO mol/L vs. 1.704 x 10 mol/L in rats). The Rice et al. (1971) study is selected here for deriving an oral RfD because it utilized an exposure route that is more relevant for an oral RfD, and also because the experimental evidence indicates that sheep are the more sensitive of the species tested. [Pg.235]

Inhalation is the exposure route for humans. Animal studies have used inhalation exposures and intrapleural or intraperitoneal injections. Current potential occupational exposure to erionite appears to be as the result of mining and producing other natural zeolites, some of which may contain erionite fibers. Environmental and residential exposure can occur via dusts containing erionite. [Pg.1050]

EXPOSURE ROUTES ingestion skin contact inhalation subsurface ground injection as an insecticide manufacture, formulation, application of insecticide mothers milk cows milk commercially prepared baby foods... [Pg.325]

Although exposure by injection routes in humans is not likely, data from distribution studies in laboratory animals provides insight into the toxicokinetics of plutonium in the body. In dogs, once plutonium entered the blood stream, it was bound to transferrin, a serum transport protein (Stevens et al. 1968). Plutonium competed with iron for the transferrin in the blood. If transferrin was saturated with iron, then more plutonium would deposit in the liver and not in the bone (Ragan 1977). Similar binding of plutonium to transferrin was observed in human blood serum (Stover et al. [Pg.62]

Chronic Toxicity. No studies were found in the available literature concerning the chronic toxicity of HN2 in animals or humans by the oral exposure route. In a 50-wk study in which 20 mice were injected subcutaneously with 1 mg HN2 kg wk", 3 of 10 animals surviving for at least 250 d exhibited chronic lymphocytopenia (Boyland and Homing 1949). [Pg.52]

Agent GA (Tabun). RfDe = 4 x 10 mg kg d" . A NOAEL was identified in a 90-d study in rats. A total uncertainty factor of 3000 was applied to account for protection of sensitive subpopulations (10), animal-to-human extrapolation (10), extrapolation from a subchronic to chronic exposure (3), and incomplete data base (3). An uncertainty factor of 3 was used to extrapolate from a subchronic to chronic exposure because of the unlikelihood that the LOAEL would have been substantially lower if the exposure had been chronic. A LOAEL-to-NOAEL uncertainty factor was not needed because a NOAEL was used in the derivation. The data base for GA lacks a multigeneration reproductive toxicity study, but because the available evidence indicates that organophosphate cholinesterase inhibitors such as GA are not likely to be reproductive toxins, the missing study was not considered critical. Therefore, a UFd of 3, not the default value of 10, was applied. A Modifying Factor of 3 was applied because the key study involved a nonoral exposure route (intraperitoneal injections). [Pg.150]

Routes of exposure are the pathways by which chemicals may reach or enter the body. To cause toxic effects in a living organism or body, a chemical must find a way to come in contact with and enter the body. To prevent exposure to harmful chemicals, it is only necessary to prevent entry or exposure to the body. If you know the potential routes of exposure and you seek to prevent chemicals from entering by those pathways, you will effectively prevent exposure to those chemicals and will be protecting yourself from harm. There are four routes of entry or exposure ingestion, inhalation, skin and eye exposure, and injection. [Pg.117]

The model is capable of simulating exposure from three routes intravenous, subcutaneous and dermal. Although the intravenous route may not be a very probable real world exposure route, data from intravenous dosing allow for the estimation of unknown parameters without the uncertainty of route specific kinetics such as permeability or absorption. Intravenous exposures are modeled as injections directly into the venous blood supply over a short period of time. [Pg.217]

Other minor routes of exposure include through the eye (ocular contact). Direct injection is also a route of exposure, but this route is typically used for medicines to maximize their efficacy (e.g., insulin). Each of the three main environmental exposure routes and examples are discussed below. [Pg.27]

In order to induce a toxic effect, local or systemic, the causative material must first come into contact with an exposed body surface these are the routes of exposure. In normal circumstances, and depending on the nature of the material, the practical routes of exposure are by swallowing, inhalation, and skin and eye contact. In addition, and for therapeutic purposes, it may be necessary to consider intramuscular, intravenous, and subcutaneous injections as routes of adininistration. [Pg.229]


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Exposure routes

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