Exposure, acute

Acute exposure generally refers to single-dose, high-concentration exposures over short periods. Some of the chemicals used in the polyurethane industry can cause acute health problems and have an immediate effect on the health of people exposed to it. The most prominent of the chemicals are the isocyanates. People with bronchial problems can have an immediate attack. It is often suggested that all employees be screened for lung function and for potential problems. Isocyanates also have the potential to sensitize people, and they can develop problems in the future. 

If mercuric catalysts are used, they must be handled with great care. They can cause burns to the skin that will develop over the next 12 hours subsequent to handling. 

Treatment of acute arsenic poisoning includes removal from the exposure source, supportive measures for loss of fluids, and chelation therapy (Ibrahim et al., 2006). Chelators that can be used include dimercaprol or 2,3-dimercaptosuccinic acid. In cases of renal failure, hemodialysis should be considered. 

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The third of the major hazards and the one with the greatest disaster potential is the release of toxic chemicals. The hazard posed by toxic release depends not only on the chemical species but also on the conditions of exposure. The high disaster potential from toxic release arises in situations where large numbers of people are briefly exposed to high concentrations of toxic material, i.e., acute exposure. However, the long-term health risks associated with prolonged exposure at low concentrations, i.e., chronic exposure, also present serious hazards. 

Hydraziae is toxic and readily absorbed by oral, dermal, or inhalation routes of exposure. Contact with hydraziae irritates the skin, eyes, and respiratory tract. Liquid splashed iato the eyes may cause permanent damage to the cornea. At high doses it can cause convulsions, but even low doses may result ia ceatral aervous system depressioa. Death from acute exposure results from coavulsioas, respiratory arrest, and cardiovascular coUapse. Repeated exposure may affect the lungs, Hver, and kidneys. Of the hydraziae derivatives studied, 1,1-dimethylhydrazine (UDMH) appears to be the least hepatotoxic monomethyl-hydrazine (MMH) seems to be more toxic to the kidneys. Evidence is limited as to the effect of hydraziae oa reproductioa and/or development however, animal studies demonstrate that only doses that produce toxicity ia pregaant rats result ia embryotoxicity (164). 

Acute exposures involve a single exposure to the test chemical in order to determine if this is effective in producing immediate, delayed, or persistent... 

Cumulative effects are those where there is progressive injury and worsening of the toxic effect as a result of repeated-exposure conditions. Each exposure produces a further increment of injury a dding to that already existing. Many materials known to induce a particular type of toxic effect by acute exposure can also eUcit the same effect by a cumulative procedure from repetitive exposure to a dose less than that causing threshold injury by acute exposure. 

Acute benzene poisoning results in CNS depression and is characterized by an initial euphoria followed by staggered gait, stupor, coma, and convulsions. Exposure to approximately 4000 ppm benzene results in complete loss of consciousness. Insomnia, agitation, headache, nausea, and drowsiness may persist for weeks after exposure (126). Continued inhalation of benzene to the point of euphoria has caused irreversible encephalopathy with tremulousness, emotional lability, and diffuse cerebral atrophy (125). In deaths arising from acute exposure, respiratory tract infection, hypo- and hyperplasia of sternal bone marrow, congested kidneys, and cerebral edema have been found at autopsy. 

Treatment for acute exposure to benzene vapor involves removing the subject from the affected area, followed by artificial respiration with oxygen intubation and cardiac monitors may be necessary for severe acute exposures (125,127). Because of its low surface tension, benzene poses a significant aspiration hazard if the liquid enters the lungs. Emesis is indicated in alert patients if more than 1 mL of benzene per kg of body weight has been ingested and less than two hours have passed between ingestion and treatment (127). 

Trichloroethane is much more toxic than 1,1,2-trichloroethane in acute exposure studies (108). The 1991 ACGIH recommended TWA value for... 

The vapors of aHyl chloride are very irritating to the eyes, nose, and throat. Lung injury may be delayed in onset. Liver and kidney injury can result from exposure to vapors kidney injury is expected to be most severe in acute exposures. High concentrations of vapor can be lethal. FoHowing chronic exposures to the vapors, Hver injury would be expected to occur first (23). 

This is a brief summary of NFPA 704 which addresses hazards that maybe caused by shoii-term, acute exposure to a material during handling under conditions of fire, spill, or similar emergencies. This standard provides a simple, easily recognized, easily understood system of markings. The objective is to provide on-the-spot identification of hazardous materials. 

Hydrogen cyanide (prussic acid) is a liquid with a boiling point of 26°C. Its vapour is flammable and extremely toxic. The effects of acute exposure are given in Table 5.34. This material is a basic building block for the manufacture of a range of chemical products such as sodium, iron or potassium cyanide, methyl methacrylate, adiponitrile, triazines, chelates. 

Exposure to sulfur dioxide in the ambient air has been associated with reduced lung function, increased incidence of respiratory symptoms and diseases, irritation of the eyes, nose, and throat, and premature mortality. Children, the elderly, and those already suffering from respiratory ailments, such as asthmatics, are especially at risk. Health impacts appear to be linked especially to brief exposures to ambient concentrations above 1,000 ixg/in (acute exposures measured over 10 minutes). Some epidemiologic studies, however, have shown an association between relatively low annual mean levels and excess mortality. It is not clear whether long-... 

Chronic Health Effect A chronic health effect is an adverse health effect resulting from long-term exposure to a substance. The effects could be a skin rash, bronchitis, cancer, or any other medical condition. An example would be liver cancer from inhaling low levels of benzene at your workplace over several years. The term is also applied to a persistent (months, years, or permanent) adverse health effect resulting from a short-term (acute) exposure. Chronic effects from long-term exposure to chemicals are fairly common. Recognize the PEL (permissible exposure level) for each substance in your workplace and minimize your exposure whenever possible. 

Acute effects Symptoms of injury or other physical manifestations that follow an acute exposure. 

Acute exposure Exposure to a high level or concentration of a pollutant for a relatively short time. 

The hazard index for acute exposure to the emissions near tlie pumps is ... 

Finally, die reader should note that liaznrd risk assessments (HZRA) are examined for acute rather dian clironic exposures. For purposes of diis book, acute exposures are considered to occur for a short period of time. Materitd on clironic liealdi exposures (HRA) is available in Part III of die book. However, it should also be noted that HRA is often mi integral part of HZRA, particularly with any (and in particular) accidental chemical release. 

Table 1 Summary of metal concentrations (in )ig of total metal concentration) causing toxicity on fluvial biofilms (in terms of effective concentrations EC50) after acute exposure (of few hours of exposure) and chronic exposure (of several weeks of exposure)...

When spills and releases of hazardous gases or liquids occur, the concentration of the hazardous material in the vicinity of the release is often the greatest concern, since potential health effects on those nearby will be determined by the concentration of the substance at the time of the acute exposure. There are many models of routine continuous discharges (e.g., discharges arising from leaky valves in chemical plants), but these carmot be applied to single episodic events. Research on the ambient behavior of short-term environmental releases and the development of models for concentration profiles in episodic releases are cmcial if we are to plan appropriate safety and abatement measures. 

Ocular Effects. Pinpoint pupils (miosis) have been observed in individuals following acute exposure to methyl parathion. Electroretinographic changes have been reported in mice following intraperitoneal injection of 1.5 mg of methyl parathion. These changes were a direct effect of methyl parathion on... 

For methyl parathion, most of the information on health effects in humans is derived from cases of acute exposure to relatively high concentrations of the pesticide. Such reports have not addressed the issue of the potential endocrine-disrupting capacity of methyl parathion in humans. An added complication in determining whether methyl parathion has endocrine-disrupting capabilities in humans is the fact that humans are seldom exposed to a single pesticide. 

The most specific biomarker of exposure to methyl parathion is the presence of the compound in serum or tissue. This is an especially good biomarker for detection shortly after acute exposure. For example, methyl parathion levels were detected in the sera of five men who were exposed for 5 hours in a cotton field 12 hours after it was sprayed with methyl parathion. The route of exposure was dermal, through unprotected hands. Serum levels averaged 156 ppb after 3 hours of the 5-hour exposure, and averaged 101.4 and 2.4 ppb at 7 and 24 hours postexposure, respectively (Ware et al. 1975). 

The database for the health effects of methyl parathion after ingestion in experimental animals is substantial. However, as can be seen in Figure 3-5, only limited information is available on the effects of inhalation and dermal exposure to methyl parathion in animals. Furthermore, the health effects such as death and neurotoxicity resulting from acute exposure in animals are more fully studied than systemic and immunotoxic effects associated with acute exposure. 

Neurotoxicity. Information in both humans and animals indicates that the nervous system is the major target of methyl parathion-induced toxicity following acute exposure by any route (Daly 1989 Dean et al. 1984 EPA 1978e Fazekas 1971 Gupta et al. 1985 Nemec et al. 1968 Roberts et al. 1988 Suba 1984 Yamamoto et al. 1982 Youssef et al. 1987). The most prominent signs of acute exposure to methyl... 

Practically all toxicokinetic properties reported are based on the results from acute exposure studies. Generally, no information was available regarding intermediate or chronic exposure to methyl parathion. Because methyl parathion is an enzyme inhibitor, the kinetics of metabolism during chronic exposure could differ from those seen during acute exposure. Similarly, excretion kinetics may differ with time. Thus, additional studies on the distribution, metabolism, and excretion of methyl parathion and its toxic metabolite, methyl paraoxon, during intermediate and chronic exposure are needed to assess the potential for toxicity following longer-duration exposures. 

Methods of Reducing Toxic Effects. There is good information on the procedures used to limit absorption and to interfere with the mechanism of action of methyl parathion after acute exposures (Aaron and Howland 1998 Bronstein and Currance 1988 EPA 1989b Proctor et al. 1988 Stutz and Janusz 1988). However, no information is available on dealing with long-term, low-level exposures. 

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