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Human exposure inhalation

Accidental dermal exposure is the most common route for human exposure inhalation and ingestion are also possible. Occupational sources include the manufacture of chemicals, photographic film, solvents, and plastics. [Pg.1353]

Toxicity. Sulfur tetrafluoride has an inhalation toxicity comparable to phosgene. The current OSHA standard maximum allowable concentration for human exposure in air is 0.4 mg/m (TWA) (54). On exposure to moisture, eg, on the surface of skin, sulfur tetrafluoride Hberates hydrofluoric acid and care must be taken to avoid bums. One case of accidental exposure of electrical workers to decomposed SF gas containing SF has been cited (108). [Pg.244]

Human incidents have been reported in workers involved in the production or uses of PCNs. In the United States as well as in Germany and Austraha, the severity of the PCN-induced toxicosis was higher after exposure to the higher chlorinated PCN mixtures. In humans the inhalation of hot vapors was the most important route of exposure and resulted in symptoms including rashes or chloracne, jaundice, weight loss, yellow atrophy of the hver, and in extreme cases, death (75,77—79). [Pg.67]

Sufficient evidence is available to indicate that atmospheric pollution in vaiying degrees does affect health adversely. [Amdur, Melvin, and Drinker, Effec t of Inhalation of Sulfur Dioxide by Man, Lancet, 2, 758 (1953) Barton, Corn, Gee, VassaUo, and Thomas, Response of Healthy Men to Inhaled Low Concentrations of Gas-Aerosol Mixtures, Arch. Lnviron. Health, 18, 681 (1969) Bates, Bell, Burnham, Hazucha, and Mantha, Problems in Studies of Human Exposure to Air Pollutants, Can. Med. A.s.soc. J., 103, 833 (1970) Ciocco and... [Pg.2178]

Health Hazards Information - Recommended Personal Protective Equipment Dust mask goggles or face shield protective gloves Symptoms Following Exposure Inhalation of dust irritates nose and throat. Contact with eyes causes irritation General Treatment for Exposure INHALATION move to fresh air. EYES flush immediately with physiological saline or water get medical care if irritation persists. SKIN flush with water Toxicity by Inhalation (Thresholdlimit Value) Data not available Short-Term Exposure Limits Data not available Toxicity by Ingestion Grade 1 oral LDjq 11.7 g/kg (rat) Late Toxicity Chronic effects in humans are unknown Vapor (Gas) Irritant Characteristics Not pertinent liqidd or Solid Irritant Characteristics Data not available Odor Threshold Data not available. [Pg.87]

The toxic action of bromine is similar to that of chlorine and can cause physiological damage to humans through inhalation and oral routes. It is an irritant to the mucous membranes of the eyes and upper respiratory tract. Severe exposures may result in pulmonary edema. Chronic exposure is similar to therapeutic ingestion of excessive bromides. [Pg.476]

Utell, M. J. (1985). Effects of inhaled acid aerosols on lung mechanics an analysis of human exposure studies. Environmental Health Perspect. 63, 39-44. [Pg.233]

Implications to Humans. Acidic precipitation has not been observed with concentrations that pose a concern to human exposure. The acidic airborne pollutants in the particulate or gaseous forms such as the oxides of sulphur and of nitrogen, and the associated photochemical oxidant ozone, are inhaled. This may lead to the irritation of the respiratory tract, and subsequently to impaired lung function, aggravated asthma and bronchitis. [Pg.56]

Stewart RD, Fisher TN, Hosko MJ, et al Experimental human exposure to methylene chloride. Arch Environ Health 25 342-348, 1972 Substance Abuse and Mental Health Services Administration Preliminary Estimates from the 1995 National Household Survey on Drug Abuse. Rockville, MD, U.S. Department of Health and Human Services, 1996 Tenenbein M, PillayN Sensory evoked potentials in inhalant (volatile solvent) abuse. J Paediatr Child Health 29 206-208, 1993... [Pg.312]

Although a number of studies have reported the effects of inhalation exposure to methyl parathion in humans, no inhalation MRLs were derived based on human data because of the lack of adequate quantitative exposure information. Animal data were also insufficient to support the derivation of an acute-, intermediate-, or chronic-duration inhalation MRL. [Pg.37]

Estimates of exposure levels posing minimal risk to humans (Minimal Risk Levels or MRLs) have been made for methyl parathion. An MRL is defined as an estimate of daily human exposure to a substance that is likely to be without an appreciable risk of adverse effects (noncarcinogenic) over a specified duration of exposure. MRLs are derived when reliable and sufficient data exist to identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration within a given route of exposure. MRLs are based on noncancerous health effects only and do not consider carcinogenic effects. MRLs can be derived for acute, intermediate, and chronic duration exposures for inhalation and oral routes. Appropriate methodology does not exist to develop MRLs for dermal exposure. [Pg.40]

Although methods have been established to derive these levels (Barnes and Dourson 1988 EPA 1990c), uncertainties are associated with these techniques. Furthermore, ATSDR acknowledges additional uncertainties inherent in the application of the procedures to derive less than lifetime MRLs. As an example, acute inhalation MRLs may not be protective for health effects that are delayed in development or are acquired following repeated acute insults, such as h q)ersensitivity reactions, asthma, or chronic bronchitis. As these kinds of health effects data become available and methods to assess levels of significant human exposure improve, these MRLs will be revised. [Pg.40]

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]

Absorption, Distribution, Metabolism, and Excretion. Evidence of absorption comes from the occurrence of toxic effects following exposure to methyl parathion by all three routes (Fazekas 1971 Miyamoto et al. 1963b Nemec et al. 1968 Skiimer and Kilgore 1982b). These data indicate that the compound is absorbed by both humans and animals. No information is available to assess the relative rates and extent of absorption following inhalation and dermal exposure in humans or inhalation in animals. A dermal study in rats indicates that methyl parathion is rapidly absorbed through the skin (Abu-Qare et al. 2000). Additional data further indicate that methyl parathion is absorbed extensively and rapidly in humans and animals via oral and dermal routes of exposure (Braeckman et al. 1983 Flollingworth et al. 1967 Ware et al. 1973). However, additional toxicokinetic studies are needed to elucidate or further examine the efficiency and kinetics of absorption by all three exposure routes. [Pg.128]

No studies were located regarding excretion of methyl parathion in humans following inhalation exposure. The limited information available from human case studies indicates that the chemical s metabolites are rapidly excreted primarily in the urine in humans following oral (Morgan et al. 1977) or dermal (Ware et al. 1974, 1975) exposure and in animals following oral (Hollingworth et al. 1973) or dermal (Abu-Qare et al. 2000) exposure. [Pg.129]

Respiratory Effects. No studies were located regarding respiratory effects in humans after inhalation exposure to endosulfan. [Pg.36]

Cardiovascular Effects. No studies were located regarding cardiovascular effects in humans after inhalation exposure to endosulfan. Routine gross and histopathologic examination of the heart and aorta of rats exposed (nose-only) to concentrations of endosulfan of up to 2 mg/m for 6 hours/day,... [Pg.41]


See other pages where Human exposure inhalation is mentioned: [Pg.67]    [Pg.285]    [Pg.50]    [Pg.67]    [Pg.285]    [Pg.50]    [Pg.136]    [Pg.352]    [Pg.4]    [Pg.6]    [Pg.30]    [Pg.113]    [Pg.121]    [Pg.165]    [Pg.325]    [Pg.372]    [Pg.87]    [Pg.130]    [Pg.35]    [Pg.35]    [Pg.41]    [Pg.43]    [Pg.118]    [Pg.147]    [Pg.189]    [Pg.195]   
See also in sourсe #XX -- [ Pg.16 , Pg.226 , Pg.227 , Pg.228 ]




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