Acute exposure toxicity

Acute-Duration Exposure. Information is not available on the health effects of 1,2-diphenylhydrazine resulting from inhalation exposure in humans or animals. Because 1,2-diphenylhydrazine is a solid with a low vapor pressure at ambient temperatures, it is highly unlikely that inhalation exposure to this chemical in the vapor state would occur (Chapter 5). However, the possibility of inhalation exposure to dusts of 1,2- diphenylhydrazine either free or adsorbed to soil is conceivable. Therefore, acute studies of inhalation exposure to dusts of 1,2- diphenylhydrazine could be designed to provide information on possible toxic effects and exposure levels that cause effects. No studies were located regarding acute oral exposure in humans. The only pertinent acute exposure toxicity studies of... 

Acute exposure Short period of exposure (minutes, hours, or a few days) relative to the life span of the organism (usually set at < 10% of an organism s life span). See also Acute effect and Acute toxicity. Volume 1(1,2,3,5,10), Volume 2(5,8,11). For Selenastrum capricornutum, whose cell numbers double every 12 h at 24°C, a contact time of 1-4 h with a test sample would correspond to an acute exposure allowing for the determination of corresponding acute toxicity effects. Measuring esterase inhibition in S. capricornutum after a 1-h exposure to a test chemical is another example of an acute exposure toxicity bioassay (Snell et al., 1996). Volume 1(3). 

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. 

The Du Pont HaskeU Laboratory for Toxicology and Industrial Medicine has conducted a study to determine the acute inhalation toxicity of fumes evolved from Tefzel fluoropolymers when heated at elevated temperatures. Rats were exposed to decomposition products of Tefzel for 4 h at various temperatures. The approximate lethal temperature (ALT) for Tefzel resins was deterrnined to be 335—350°C. AH rats survived exposure to pyrolysis products from Tefzel heated to 300°C for this time period. At the ALT level, death was from pulmonary edema carbon monoxide poisoning was probably a contributing factor. Hydrolyzable fluoride was present in the pyrolysis products, with concentration dependent on temperature. 

Health and Safety Factors. VDE is a flammable gas its combustion products are toxic. Liquid VDE on contact with the skin can cause frostbite. Acute inhalation toxicity of VDE is low median lethal concentrations (LC q) for rats were 128,000 ppm after a single 4-h exposure (52) and 800,000 ppm after a 30-min exposure (53). Cumulative toxicity is low exposure of rats and mice at levels of up to 50,000 ppm for 90 days did not cause any... 

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). 

Toxicology. The nitroparaffins have minimal effects by way of actual contact. There were neither systemic effects nor irritation in dermal studies in rabbits. Human exposure of a prolonged or often-repeated nature has led to low grade irritation attributable to removal of oil from the skin, an effect produced by most organic solvents. Eye irritation potential of all four nitroparaffins has been deterrnined in rabbits. Other than a transient slight redness and some lachrymation, no effects were noted. The average Draize score was 0.0. The acute oral toxicity, LD q, of all four nitroparaffins has been deterrnined in the rat (Table 8). 

Health and Safety Factors. Terephthahc acid has a low order of toxicity. Inhalation by rats for 6 h/d, 5 d/wk for 4 wk produced no fatahties at a dust exposure level of 25 mg/m. The mean acute oral toxicity for rats is over 18 g/kg (86), and for mice over 6 g/kg (87). When terephthahc acid was fed as 3% of the diet to rats, urinary calcuh formed in 90 d, some of which led to cancer. High doses of terephthahc acid lead to formation of calcium terephthalate at levels exceeding its solubihty in urine. This insoluble material leads to the calcuh and provides a threshold below which cancer is not observed (88). Normal precautions used in handling industrial chemicals should be observed with terephthahc acid. If ventilation is inadequate, a toxic-dust respirator should be used to avoid prolonged exposure. 

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. 

Considerable caution is necessary in making quantitative comparisons between different materials, even when considering the same toxic end point. This can be conveniendy illustrated using, as an example, death in response to a single exposure, ie, acute lethal toxicity. Studies to determine acute lethal toxicity by a particular route are usually conducted as described below. 

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

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. 

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)...

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. 

Acute exposure to large amounts of endosulfan results in frank effects manifested as hyperactivity, muscle tremors, ataxia, and convulsions. Possible mechanisms of toxicity include (a) alteration of neurotransmitter levels in brain areas by affecting synthesis, degradation, and/or rates of release and reuptake, and/or (b) interference with the binding of those neurotransmitter to their receptors. 

The effects of endosulfan have not been studied in children, but they would likely experience the same health effects seen in adults exposed to endosulfan. Data in adults, mostly derived from cases of accidental or intentional acute exposure (ingestion) to large amounts of endosulfan, indicate that the primary target of endosulfan toxicity is the nervous system. The effects are manifested as hyperactivity and convulsions and in some cases have resulted in death (Aleksandrowicz 1979 Blanco-Coronado et al. 1992 Boereboom et al. 1998 Cable and Doherty 1999 Lo et al. 1995 Terziev et al. 1974). These effects have been reproduced in experimental animals. 

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