Inhalation exposure system

The main criteria for the design and operation of any dynamic (as opposed to static) inhalation exposure system are the following... 

Figure 21.1 An inhalation exposure system (Modified from Adkins, B. et al. Am. Int. Hyg. Assoc. J. 41 494, 1980.)...

Adkins, B., O Conner, R.W., Dement, J.M. (1987). Inhalation exposure system used for acute and repeated-dose methyl isocyanate exposure of laboratory animals. Environ. Health Perspect. 72 45-51. 

Higgins, C.E., T.M. Gayle, and J.R. Stokely Sensor for detection of tobacco smoke particulates in inhalation exposure systems Beitr. Tabakforsch. Int. 9 (1978) 185-189. 

GI Tract May cause gastrointestinal irritation with nausea, vomiting, and diarrhea. May cause effects similar to those for inhalation exposure. Systemic Effects May cause central nervous system depression. Metabolism may release cyanide, which may result in headache, dizziness, weakness, collapse, unconsciousness, and possible death. May be metabolized to cyanide, which in turn acts by inhibiting cytochrome oxidase, impairing cellular respiration. May cause tissue anoxia, characterized by weakness, headache, dizziness, confusion, cyanosis (bluish discoloration of skin due to deficient oxygenation of the blood), weak and irregular heart beat, collapse, unconsciousness, convulsions, coma, and death. 

B. A. Wong, Inhalation exposure systems design, methods and operation, Toxicol. Pathol, 2007,35(1), 3-14. 

Cheng Y-S, Moss OR. Inhalation exposure systems. In McClellan RO, Henderson RF, eds. Concepts in Inhalation Toxicology. Washington, DC Taylor and Francis, 1995 25-66. 

Previous particle exposure studies have not used real ambient particles to investigate particle toxicity or develop dose-response relationships. Our laboratory has developed and evaluated a technique that can be used to separate and concentrate respirable particles from ambient air before their delivery to an inhalation exposure system (14,15). With this approach, particles are airborne throughout the... 

Inhalation exposure to high concentrations of ethylene oxide has been reported to result in respiratory system irritation and edema (236). 

Ocular Effects. One study reported that seven children exposed to methyl parathion by inhalation, oral, and possibly dermal routes exhibited pinpoint pupils (miosis) (Dean et al. 1984). This effect is a consequence of the effects on the autonomic nervous system. No other studies were located regarding ocular effects in humans or animals after inhalation exposure to methyl parathion. 

Irregular respiration was observed in both male and female rats after a 4-hour nose-only inhalation exposure to aerosolized endosulfan (Hoechst 1983a). In both male and female rats, dyspnea was observed at the lowest concentrations tested (12.3 and 3.6 mg/m for males and females, respectively). Autopsies of the rats that died revealed dark-red, pinhead-sized foci on the lungs. It is unclear whether these effects represent direct effects of inhaled endosulfan on respiratory tissues or whether they are secondary to central nervous system effects on respiratory function. No treatment-related effects were... 

EPA s Integrated Risk Information System (IRIS) lists an oral reference dose (RfD) of 0.006 mg/kg/day for endosulfan (IRIS 2000). No reference concentration (RfC) for chronic inhalation exposures to endosulfan was reported. 

Musculoskeletal Effects. No studies were located regarding musculoskeletal effects in humans after inhalation exposure to trichloroethylene. Trichloroethylene exposure can result in nervous system effects that result in secondary effects on muscle strength, especially in the face (Leandri et al. 1995). See Section 2.2.1.4 for further discussion of nervous system effects following trichloroethylene exposure. 

Route Dependent Toxicity. The toxicity of trichloroethylene does not seem to be heavily dependent upon its route of entry. Inhalation and ingestion are the primary exposure routes, and the liver, heart, and central nervous system are the primary targets for both routes (Candura and Faustman 1991). Renal toxicity results principally from oral exposure, and dermal exposure generally confines its toxic effects to the skin, although broad systemic effects can be induced imder conditions of high exposure (Bauer and Rabens 1974). Attributing such effects solely to dermal exposure, however, is difficult because inhalation exposure is often a factor in these cases as well. 

In the past, trichloroethylene was used as a human anesthetic. Trichloroethylene has also been used by individuals who intentionally inhale it for its narcotic properties. Therefore, most of the information regarding the effects of trichloroethylene in humans comes from case studies and experiments describing effects of trichloroethylene after inhalation exposure. These studies indicate that the primary effect of exposure to trichloroethylene is on the central nervous system. Effects include headache, vertigo, fatigue, short-term memory loss, decreased word associations, central nervous system depression, and anesthesia. 

Some members of a community that were exposed to trichloroethylene along with a variety of other solvents in their drinking water complained of respiratory disorders, but the complaints could not be attributed specifically to trichloroethylene (Byers et al. 1988). This effect may have been due to immune system impairment resulting in increased susceptibility to infection. A study in mice in which inhalation exposure to trichloroethylene increased the susceptibility to pulmonary infection with Streptococcus zooepidemicus (Aranyi et al. 1986) provides evidence that trichloroethylene may result in adverse respiratory effects through effects on the immune system. 

Gastrointestinal Effects. Case reports indicate that acute inhalation exposure to trichloroethylene results in nausea and vomiting (Buxton and Hayward 1967 Clearfield 1970 David et al. 1989 DeFalque 1961 Gutch et al. 1965 Milby 1968). Anorexia, nausea, vomiting, and intolerance to fatty foods have also been reported after chronic occupational exposure to trichloroethylene (El Ghawabi et al. 1973 Schattner and Malnick 1990 Smith 1966). Trichloroethylene-induced efiects on the autonomic nervous system may contribute to these effects (Grandjean et al. 1955). Some of the people exposed to trichloroethylene and other chlorinated... 

Exposure of organisms to pesticides occurs through contact or inhalation. Inhalation exposure can be assessed using some of the active samplers discussed in the previous section, for example air samplers mimicking respiratory systems. Contact exposure can be assessed using samplers that represent collection by horizontal or vertical surfaces, or combinations of these orientations. This article addresses only the first part of this process, i.e., consideration of techniques for sampling sprays in the environment. 

Mewhinney JA, Griffith WC, Muggenburg BA. 1980. Proposed retention model for human inhalation exposure to 241Am02. In International Radiation Protection Society, ed. Radiation protection A systemic approach to safety Proceedings of the 5th Congress of the International Radiation Protection Society, Jerusalem, March 1980. New York Pergamon Press, 615-618. 

Troop exposure to these materials could result from leaking DF containers, accidents that disrupt packaging, spills at production or storage facilities, or accidents during transport. Because DF and DC are relatively volatile compounds, the primary route of exposure is expected to be the respiratory system. However, ingestion also results from inhalation exposures in animals and could occur in humans. DF and DC vapors have a pungent odor and may cause severe and painful irritation of the eyes, nose, throat, and lungs. Data provided are for DF only, DC has similar properties. 

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