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Inhalation route

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). [Pg.288]

Explain why the inhalation route for lead is considered an important hazard when it accounts for only about 20% of the potential allowable body burden. [Pg.109]

Very few data are available on the effects of organotins in humans. Of the reported unintentional occupational exposures, none has an estimate of exposure concentration. Exposure was largely via the inhalation route, with some possibility of dermal exposure. Neurological effects were the most commonly reported, and these can persist for long periods. [Pg.5]

Chromosome aberrations were detected in lymphocytes of individuals acutely intoxicated by methyl parathion by the inhalation route (Van Bao et al. 1974). Blood samples were taken 3-6 days after exposure and again at 30 and 380 days. A temporary but significant (p<0.05) increase was noted in the frequency of stable chromosomal aberrations in the exposed individuals. The study limitations include small sample size, absence of a control group, lack of quantification of exposure levels, and a possible concomitant exposure to other substances via the dermal route. [Pg.81]

Figure 3-5 graphically depicts the information that currently exists on the health effects of methyl parathion in humans and animals by various routes of exposure. The available literature reviewed concerning the health effects of methyl parathion in humans described case reports of longer-term studies of pesticide workers and case reports of accidental or intentional ingestion of methyl parathion. The occupational exposure is believed to be via the dermal and inhalation routes. The information on human exposure is limited in that the possibility of concurrent exposure to other pesticides or other toxic substances cannot be quantified. [Pg.120]

MRLs are derived for hazardous substances using the no-observed-adverse-effect level/uncertainty factor approach. They are below levels that might cause adverse health effects in the people most sensitive to such chemical-induced effects. MRLs are derived for acute (1-14 days), intermediate (15-364 days), and chronic (365 days and longer) durations and for the oral and inhalation routes of exposure. Currently, MRLs for the dermal route of exposure are not derived because ATSDR has not yet identified a method suitable for this route of exposure. MRLs are generally based on the most sensitive chemical-induced end point considered to be of relevance to humans. Serious health effects (such as irreparable damage to the liver or kidneys, or birth defects) are not used as a basis for establishing MRLs. Exposure to a level above the MRL does not mean that adverse health effects will occur. [Pg.247]

In occupational settings, exposure to endosulfan is mainly via the dermal and inhalation routes. Although workers involved in the manufacture and formulation of pesticide products containing endosulfan are potentially exposed to high concentrations of the compound, actual exposure is probably limited by the use of engineering controls and personal protection equipment. The highest documented dermal and inhalation exposures have been reported for agricultural workers involved in the spray... [Pg.236]

MRLs are derived for hazardous substances using the no-observed-adverse-effect level/uncertainty factor approach. They are below levels that might cause adverse health effects in the people most sensitive to such chemical-induced effects. MRLs are derived for acute (1-14 days), intermediate (15-364 days), and chronic (365 days and longer) durations and for the oral and inhalation routes of exposure. [Pg.328]

P2-Agonists cause airway smooth muscle relaxation by stimulating adenyl cyclase to increase the formation of cyclic adenosine monophosphate (cAMP). Other non-bronchodilator effects have been observed, such as improvement in mucociliary transport, but their significance is uncertain.11 P2-Agonists are available in inhalation, oral, and parenteral dosage forms the inhalation route is preferred because of fewer adverse effects. [Pg.236]

Absorbed Dose, Chemical—The amount of a substance that is either absorbed into the body or placed in contact with the skin. For oral or inhalation routes, this is normally the product of the intake quantity and the uptake fraction divided by the body weight and, if appropriate, the time, expressed as mg/kg for a single intake or mg/kg/day for multiple intakes. For dermal exposure, this is the amount of material applied to the skin, and is normally divided by the body mass and expressed as mg/kg. [Pg.268]

L/min, and 43 L/min, respectively.4 Therefore, the amount of chlorpyrifos absorbed via the inhalation route for the female and male was calculated as ... [Pg.57]

Table 4 summarizes the results of using physical techniques to estimate total chlorpyrifos doses of adults following activity on treated grass. Total doses ranged from 3.03 pg/kg to 5.04 pg/kg (mean, 3.88 pg/kg). Approximately 85% of the chlorpyrifos dose came from the whole body dermal route. About 15% came from the inhalation route. Hand exposure was insignificant. [Pg.58]

If only ingestion experiments have been performed, it may be necessary to assume similar responses via the inhalation route, with appropriate dose scaling. [Pg.300]

As discussed in the introduction to Section 2.2, the bulk of the human data on the health effects of lead are expressed in terms of internal exposure, or PbB levels, rather than external exposure levels (i.e., mg/m3 or mg/kg/day). For the general population, exposure to lead occurs primarily via the oral route with some contribution from the inhalation route, whereas occupational exposure is primarily by inhalation with some oral. Therefore, it is difficult to distinguish specific routes and levels of exposure. For this reason, the human health effects data for lead will be presented in terms of PbB levels in this section. Health effects associated with human exposures to lead and internal lead doses are shown in Table 2-1. [Pg.37]

In most of these studies, prenatal exposure was generally estimated through maternal and/or cord blood lead concentrations. Exposure of the mothers can be assumed to have been primarily through the oral route, but with contribution from the inhalation route as well. The most relevant studies are discussed below, along with results from a few investigations of different markers for lead exposure. [Pg.113]

Deaths associated with occupational exposure to inorganic lead (which is predominantly by the inhalation route of exposure) are discussed in Section 2.2.1.1. No studies were located regarding death in animals after inhalation exposure to inorganic lead. [Pg.130]

Exposure pathway describes how the substances enter into the human body. All possible pathways are not considered for all substances and emission scenarios, only the ones that are relevant for a specific substance and emission scenario are included. For example in the case of substances that are not present in the air, the inhalation route is not taken into account. [Pg.95]

Roberts et al. 1989). Studies indicate that the metabolism of acrylonitrile in animals proceeds by the same pathways whether exposure is by the oral (Ahmed et al. 1983 Langvardt et al. 1980 Pilon et al. 1988a) or the inhalation route (Gutetal. 1985 Muller et al. 1987 Tardif et al. 1987). No data were located regarding the metabolism of acrylonitrile following dermal exposure. [Pg.53]


See other pages where Inhalation route is mentioned: [Pg.255]    [Pg.263]    [Pg.231]    [Pg.393]    [Pg.427]    [Pg.66]    [Pg.286]    [Pg.364]    [Pg.35]    [Pg.92]    [Pg.122]    [Pg.123]    [Pg.124]    [Pg.191]    [Pg.150]    [Pg.180]    [Pg.188]    [Pg.217]    [Pg.236]    [Pg.308]    [Pg.94]    [Pg.93]    [Pg.144]    [Pg.400]    [Pg.35]   


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