Exposure, human

Of all the uncertainties surrounding the hypothesis that environmental chemicals with endocrine disrupting properties are responsible for the observed effects in humans and wildlife, one of the major unknowns relates to exposure. Humans and wildlife can be, and sometimes are, exposed to these substances in the environment but our knowledge of the levels, routes and timing of exposure is poor. 

Reproductive Effects. Operating room nurses exposed to trichloroethylene have been reported to have an increased incidence of miscarriages, but they were exposed to many other anesthetics as well (Corbett et al. 1974). Survey results of 1,926 women who had spontaneous abortions revealed a greater risk of abortion associated with trichloroethylene exposure (Windham et al. 1991). This study is limited by multiple chemical exposure. Humans exposed to trichloroethylene in the drinking water in certain areas of the country have not shown adverse reproductive effects (Byers et al. 1988 Freni and Bloomer 1988 Lagakos et al. 1986a). 

Polyalphaolefin Hydraulic Fluids. No acute exposure human studies were located. 

Evans HL New York University Medical Center, New York, NY Behavioral and biochemical markers of human lead exposures (human, rat) National Institute of Environmental Health Sciences... 

Exposure Human breathing rate m3/(person day) 18 GLOBOX... 

Novelli, E.L.B., N.L. Rodrigues, and B.O. Ribas. 1995. Superoxide radical and toxicity of environmental nickel exposure. Human Exper. Toxicol. 14 248-251. 

Syrian hamster, Cricetus sp. 0.12-2 Gy, single acute exposure Human, Homo sapiens Genes modifying cytoskeletal development adversely affected at all doses within 3 h by both high LET (neutrons) and low LET (gamma rays, X-rays) radiations 11... 

Cyanide is rapidly absorbed (within seconds) following inhalation exposure. Humans retained 58% of hydrogen cyanide in the lungs after inhaling the gas through normal breathing (Landahl and Herrmann 1950). 

Keywords Emerging contaminants, Flame retardants, Human exposure, Human health. Personal care products, Phthalates, Review... 

Exposure is considered as single events, or series of repeated events, or as continuous exposure. The duration and frequency of exposure, the routes of exposure, human habits and practices, as well as the technological processes need to be considered. Furthermore, the spatial scale of the exposure (e.g., personal/local/regional level) has to be taken into account. 

Arsine is the most acutely toxic form of arsenic. It binds with oxidized hemoglobin, causing profound hemolysis of sudden onset. Inhalation of 250ppm may be fatal within 30 minutes, whereas 10-50 ppm may cause anemia and death with more prolonged exposure. Human experience has indicated that there is usually a delay of 2-24 hours after exposure before the onset of headache, malaise, weakness, dizziness, and dyspnea, with abdominal pain, nausea, and vomiting. Dark red urine is frequently noted 4—6 hours after exposure. This often progresses to brown urine, with jaundice appearing at 24-48 hours after exposure. 

Vol. 1 Exposure, Human Responses and Building Investigations, Helsinki, Finland, pp. 53-62. 

No other systemic effects were reported for humans exposed via inhalation or dermal (nonbum) exposure, humans burned with white phosphorus, or animals dermally (nonbum) exposed. 

Ebert E, Price P, Keenan R. 1996. Estimating exposures to dioxin-like compounds for subsistence anglers in North American. In Human exposure, human health risk assessment, and organohalogen compounds, 16th Symposium on Chlorinated Dioxins and Related Compounds, Amsterdam Holland, volume 30, 66-69. 

Research should determine systemic exposure from the various relevant modes of exposure. Toxicological studies have been done for gavage and inhalation of aerosolized fuel and vapors. Data are not available to determine the comparability of exposure by these routes and modes of exposure. Humans are exposed dermally as well as by inhalation. The contribution to the internal dose from exposure of the skin to JP-8 or its vapors is not known. Measurements of jet-fuel components in blood of exposed workers would permit comparisons to similar data... 

A major study (Cronkite 1986 Cronkite et al. 1984, 1985) provides a basis for a reproducible animal model. In this study, mice were exposed to 300 ppm benzene by inhalation 6 hours per day, 5 days per week for 16 weeks. This exposure regimen was selected because the authors thought it most closely paralleled likely human exposure. Human epidemiological studies in the literature reported that workers were exposed for about 15% of their life span 16 weeks represent 15% of the life span of mice. 

Exposure human acute toxicity 2005-2010) have demonstrated that it is... 

The rcspiratoiy tract, especially the upper respiratory tract, is a critical target of the toxicity of airborne formaldehyde as shown by acute controlled exposure human studies, by studies of humans exposed acutely or repeatedly under occupational or residential conditions, and by studies of animals (including primates) exposed by inhalation for acute, intermediate, and chronic durations. 

Acute Controlled Exposure Human Studies. More than 15 published studies of respiratory function and/or irritation of the nose, eyes, and throat are available involving acute controlled exposure of volunteers, generally at formaldehyde concentrations 3 ppm. Recent reviews of these studies include those by ACGIH (1992), Krivanek and Imbus (1992), and Paustenbach et al. (1997). 

Repeated-Exposure Human Studies. Studies of formaldehyde-exposed humans with repeated exposure under occupational or residential conditions provide confirmatory evidence that formaldehyde can be irritating to the upper respiratory tract (Boysen et al. 1990 Edling et al. 1988 Garry et al. 1980 ... 

Epidemiological and Human Dosimetry Studies. Results from many acute controlled-exposure human studies and cross-sectional studies of groups of persons repeatedly exposed to airborne formaldehyde provide strong evidence that the upper respiratory tract is the critical target of airborne formaldehyde for any duration of exposure, allow reasonable estimates to be made of minimal risk levels for acute and chronic durations of exposure, and provide strong support for deriving intermediate-duration minimal risk levels from animal exposure-response data. There is considerable confidence that adherence to these values will protect persons living near formaldehyde-contaminated hazardous waste... 

Tire Anderson and Molhave (1983) study identified an apparent effect level (0.2 ppm), based on subjective reports of irritation that is lower than the effect levels (0.35-0.4 ppm) in the studies by Pazdrak et al. (1993), Krakowiak et al. (1998), and Bender et al. (1993), which used more objective measures of acute irritation (eosinophil counts and protein concentrations in nasal lavage fluid or time to first reporting of irritation see section 2.2.1.2 Systemic Effects - Respiratory Effects Acute Controlled Exposure Human Studies.) Because of the use of objective measures of toxicity and the general weight of the available data indicating that some people will not experience eye or upper respiratoiy tract irritation from formaldehyde even at 1 ppm (see Day et al. 1984 Kulle et al. 1987, Weber Tschopp et al. 1977, and Witek et al. 1986), the Pazdrak et al. (1993) LOAEL of 0.4 ppm was considered a minimal LOAEL in a group of potentially sensitive individuals (some subjects had dennal hypersensitivity to fonnaldehyde) and selected as the basis of the acute MRL. 

Abnormal fetal development during to toxic exposure (humans, rats, mice)... 

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