Exposure low-level

The assessment should be in writing except if the work involves low level exposure and is simple, so that the assessment can be easily repeated and explained. 

The threshold for toxic injury is not the same for everyone because sensitivity varies greatly among individuals. Most chemicals in consumer products remain untested for health effects, such as cancer, reproductive problems, and the impacts of long-term, low level exposure. How these substances affect women, children, and people with existing conditions is also little studied. Once a person s defenses have been broken down and he or she has become hypersensitive, a wide variety of common chemical exposures can trigger a reaction. Just what products and other chemicals which cause problems varies greatly among affected individuals. 

Brown, iVl. A., and Brix, K. A. (1998). Review of health consequences from high-, mtermedi ate- and low-level exposure to organophospborus nerve agents. /. Appl. Toxicol. 18, 393-4i)8. 

Ruff, R. [,., Petito, C. K., and Acheson, L. S. (1981). Neuropathy associated with chrome low level exposure to -hexane. Clin. Toxicol. 18, 515-519. 

Developmental Effects. Adverse effects of methyl parathion on hirman fetal development have not been reported. Based on studies in animals, such effects appear to be possible if pregnant women were exposed during the first trimester to high concentrations of methyl parathion that resulted in significant depression of cholinesterase levels, particularly if concomitant signs and symptoms of organophosphate intoxication occur. Such an exposure scenario may occur with occupational exposure, exposure in homes or offices illegally sprayed with methyl parathion, or accidental exposure to methyl parathion, but is less likely as a result of low-level exposure. 

Following exposure of humans to organophosphates, but not specifically methyl parathion, restoration of plasma cholinesterase occurs more rapidly than does restoration of erythrocyte cholinesterase (Grob et al. 1950 Midtling et al. 1985). These findings are supported by studies of methyl parathion in animals. Erythrocyte cholinesterase levels are representative of acetylcholinesterase levels in the nervous system, and, therefore, may be a more accurate biomarker of the neurological effects of chronic low level exposure of humans to methyl parathion (Midtling et al. 1985 NIOSH 1976). 

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. 

No treatment strategies were located for chronic low-level exposures to endosulfan. 

Rapid dermal absorption of trichloroethylene is evident from a study in which peak blood and exhaled air concentrations occurred within 5 minutes after a human subject immersed one hand in a solution of unspecified trichloroethylene concentration for 30 minutes (Sato and Nakajima 1978). Studies on dermal absorption of trichloroethylene in humans, as well as animals, are complicated by the fact that exposure in these studies is usually by direct contact of the skin with the undiluted chemical. Trichloroethylene is a lipophilic solvent that defats the skin and disrupts the stratum comeum, thereby enhancing its own absorption. Thus, the rate of absorption probably increases in a nonlinear fashion with greater epidermal disruption. Although the extent of absorption through the skin may be relatively modest with normal industrial use (Sato and Nakajima 1978 Stewart and Dodd 1964), there is insufficient information to evaluate the effects of chronic, low-level exposure in hiunans, especially when multiple routes may be involved. 

A limited study in animals also presents evidence for increased susceptibility to Streptococcus zooepidomicus (Aran d et al. 1986). Immune system effects observed in mice exposed orally to trichloroethylene included inhibition of cell-mediated immunity, delayed type hypersensitivity, and inhibition of antibody-mediated immunity (Sanders et al. 1982). Female mice appeared to be more sensitive than male mice. A study in which a susceptible strain of mice was treated with intraperitoneal injections of trichloroethylene suggests that trichloroethylene can accelerate the autoimmune response (Khan et al. 1995). The immune system may be a sensitive end point for toxic effects from low-level exposure to trichloroethylene however, no firm conclusions can be drawn from the available information. Additional human and animal studies are needed to better characterize this end point and determine the potential for immunological effects for people exposed to trichloroethylene at hazardous waste sites. 

Biological Effects of Low Level Exposures (BELLE). www.BeUeQuliae.com BLACKSTOCK w p and WEIR M p (1999) Proteomics quantitative and physical mapping of cellular proteins. TIBTECH 17 121-7. 

In a report comparing community responses to low-level exposure to a mixture of air pollutants from pulp mills, Jaakkola et al. (1990) reported significant differences in respiratory symptoms between polluted and unpolluted communities. The pollutant mixture associated with the pulp mills included particulates, sulfur dioxide, and a series of malodorous sulfur compounds. Major contributors in the latter mixture include hydrogen sulfide, methyl mercaptan, and methyl sulfides. In this study the responses of populations from three communities were compared, a nonpolluted community, a moderately polluted community, and a severely polluted community. Initial exposure estimates were derived from dispersion modeling these estimates were subsequently confirmed with measurements taken from monitoring stations located in the two polluted communities. These measurements indicated that both the mean and the maximum 4-hour concentrations of hydrogen sulfide were higher in the more severely polluted community (4 and 56 g/m3 2.9 and 40 ppb) than in the moderately polluted one (2 and 22 g/m3 1.4 and 16 ppb). Particulate measurements made concurrently, and sulfur dioxide measurements made subsequently, showed a similar difference in the concentrations of these two pollutants between the two polluted communities. 

Partti-Pellinen K, Martilla O, Vilkka V, et al. 1996. The South Karelia air pollution study Effects of low-level exposure to malodorous sulfur compounds on symptoms. Arch Environ Health 51 315-320. 

Although several figures in Table IV are significant, the estimates are probably accurate to the first digit at best. However, they do suggest that widespread but low-level exposures from automobiles and service stations provide the majority of benzene molecules that enter human bodies. Whether these are the most biologically significant emissions depends on the behavior of dose-response relationships at low dose levels. 

U.S. Environmental Protection Agency. Assessment of Health Effects of Benzene Germane to Low-level Exposure. Washington, D.C. Office of Research and Development, 1978, EPA-600/1-78-061. 

The results also showed that the age-related increase in serum creatinine was earlier and faster and more linear among subjects in the highest quartile than among those in the lowest quartile. Based on the results, Kim et al. (1996a) concluded that low-level exposure to lead may impair renal function in middle-aged and older men however, the biological significance of a 0.08 mg/dL increase in serum creatinine is unknown. 

Selected studies are discussed below and include reports on occupational exposure to lead for females and males followed by environmental (low level) exposure to lead in females and males. 

Pattillo RA Morehouse School of Medicine, Atlanta, GA Neurobehavioral effects of low-level exposure in human newborns ATSDR... 

In environmental health studies conducted near four NPL sites (plus a comparison area for each), ATSDR collected lead concentration data from both environmental media and human body fluids to estimate low-level exposure risk and to document the magnitude of human exposure to lead near those sites. Environmental samples collected at participants homes included drinking water, yard soil, house dust, and house paint body fluids collected from participants included venous blood and urine specimens. For the four sites, mean concentrations of lead in soil ranged from 317 to 529 mg/kg, and mean concentrations of lead in dust ranged from 206 to 469 mg/kg (ATSDR 1995). 

Cooney GH, Bell A, McBride W, et al. 1989a. Low-level exposures to lead The Sydney lead study. Dev Med Child Neurol 31 640-649. 

Haenninen H, Mantere P, Hemberg S, et al. 1979. Subjective symptoms in low-level exposure to lead. Neurotoxicology 1 333-347. 

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