Acute exposure, defined

In humans, acute exposure to acrylonitrile results in characteristics of cyanide-type toxicity. Symptoms in humans associated with acrylonitrile poisoning include limb weakness, labored and irregular breathing, dizziness and impaired judgment, cyanosis, nausea, collapse, and convulsions (Baxter 1979). However, the doses that produce these effects were not clearly defined. Workers exposed to 16 to 100 ppm for 20 to 45 minutes complained of headaches and nausea, apprehension and nervous irritation (Wilson et al. 1948). The workers exposed to acrylonitrile vapors fully recovered. In a study with human volunteers exposed to acrylonitrile at doses of 2.3 and 4.6 ppm, no symptoms attributable to effects on the nervous system were observed (Jakubowski et al. 1987). 

Stochastic radiation effects are typically associated with those that occur over many months or years (i.e., are typically chronic instead of acute). Chronic doses are typically on the order of background doses (0.3 rem [0.003 Sv] or less) and are not necessarily associated with larger doses that could result from a terrorist attack with radiological weapons. However, stochastic health effects are defined here as effects that occur many years after chronic or acute exposure to radiological contaminants. Stochastic effects are categorized as cancers and hereditary effects. Because no case of hereditary effects (e.g., mutation of future generations) has been documented, this discussion focuses on cancer risk. 

In some circumstances such as may be encountered after a terrorist attack, acute doses may be more important than potential chronic effects. More specifically, high doses of radiation may be immediately dangerous to life and health and could lead to severe injury including sickness, irreparable tissue damage, and death, although the more severe effects would likely only be observed after a nuclear explosion. For the purpose of this discussion, acute exposures are defined as those that occur in a relatively short time (over several days or less) and result in a dose of at least 25-35 rad (0.25-0.35 Gy).6-7... 

Immunotoxicity. No information on immunotoxicity after exposure to 1,3,5-TNB by any of the three routes is available in humans or animals. Therefore, animal studies following acute, intermediate, and chronic exposure to 1,3,5-TNB via all three routes would help in estimating the potential immunotoxic effects in humans. Spleen enlargement was reported in acute-(Blackburn et al. 1988) and intermediate-duration (Cody et al. 1981 Linder et al. 1986) studies in animals. These effects, however, were secondary to adverse hematological effects. Studies in laboratory animals following acute exposure to 1,3-DNB by the oral route would help define possible effects on antibody production and cellular immunity. This information could be used to determine populations sensitive to possible exposure to 1,3-DNB at locations close to ammunition plants or in specific workplaces. 

All of the previously mentioned exposure methods can be used to estimate either chronic exposure (over a period of years) or acute exposure (single day) for the United States population and population subgroups. Both chronic and acute assessments are usually based on a no observed adverse effect level (NOAEL) in an animal species. Acute exposure is defined relative to an acute (single dose) toxicological endpoint (usually a NOAEL) and may be expressed as a margin of exposure (MOE) or as a percentage of an acute reference dose that is based on a NOAEL and an uncertainty factor (see below). 

A central tool in ATSDR assessment of public health impacts is the minimal risk level (MRL) health guidance value. MRLs have been developed by ATSDR for many hazardous waste constituents, though no new MRLs have been developed for TPH. A limited number of existing MRLs can be applied to TPH assessment. Most are MRLs for individual TPH components (e.g., benzene) however, a few MRLs are available for whole petroleum products. MRLs for substances that represent the fractions defined by the ATSDR approach to assessing TPH health impacts are provided and discussed in this profile. In recognition of the likelihood that even acute exposures to fresh releases will be to fractions of a product, the information on pertinent fractions of TPH should also be consulted (particularly Sections 2.3, 6.1, 6.2 and 6.6). 

Additional animal studies to investigate the acute effects of hydrazines after inhalation, oral, and dermal exposures would better define the threshold dose for adverse health effects. Such studies would be useful in predicting adverse health effects in humans following acute exposures. 

It is common practice for toxicologists to differentiate exposure to chemicals based on the dose and the duration of exposure. Lour timeframes have been used to define duration of exposures acute, subacute, subchronic, and chronic. It is useful in light of today s interest in long-term, low-levef exposures to clarify these terms. Acute exposure is defined as exposure to a chemical for less than 24 h. Subacute exposure refers to an exposure of 1 month or less, subchronic for 1 to 3 months, and chronic for more than 3 months. These exposures can be by any route for most chemicals it is the oral route with the chemical given in the diet. However, the limited animal studies using nerve agents have usually employed parenteral administration... 

Sidell and Hurst have described the long-term effects produced from acute symptomatic clinical dose exposure to mustard, but less is known about the clinical effects from chronic, sometimes symptomatic, low-dose exposure. Acute is defined here as an exposure lasting less than 24 h. The term chronic refers to an exposure lasting for days, weeks, months, and even years. Clinical means producing a recognizable illness directly related to mustard exposure. Symptomatic means having either the acute or chronic clinical illness produced by sulfur mustard. Asymptomatic, of course, is without symptoms at all. 

Acute Exposure Acute exposure is defined as a single exposure or smaller multiple exposures occurring over 24 hours or less. 

With regard to human health effects of MBOCA, the few available studies were either case reports of acute occupational exposure or involved intermediate or chronic epidemiological studies. Acute exposures to MBOCA were by the inhalation, oral, or dermal routes, although in some studies it was difficult to clearly define the exposure route. Intermediate exposures were by either inhalation and/or dermal contact no intermediate oral exposure studies were located. Chronic exposure in humans occurred by inhalation and/or dermal contact no chronic oral studies were located. No information is available regarding immunological, neurologic, reproductive, developmental, or genotoxic effect in humans by any route of exposure. Studies on cancer incidence in humans after inhalation and/or dermal exposure to MBOCA were located. 

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