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Biomarkers of Effect

Effect. Biomarkers of effects are not available for trichloroethylene. There is no clinical disease state that is unique to trichloroethylene exposure. Interpretation of the behavioral observations in humans is complicated by many factors, such as possible irritant effects of the odor and nonspecific effects on the nervous system (e.g., fatigue). Further studies in this area would be useful in determining the exposure levels that may be... [Pg.189]

Subcategories of bioindicators at suboiganismal levels are generally referred to as biomarkers. Biomarkers may reflect either exposure, effect, or susceptibility of these, biomarkers of effect are both more valuable and more difficult to find. An ideal biomarker of mercury effect would be ... [Pg.151]

No biomarkers have been identified to characterize the effects associated with exposure to diisopropyl methylphosphonate. At high doses in animals, diisopropyl methylphosphonate affects RBC and the nervous system. However, because the effects are not unique to diisopropyl methylphosphonate, they would not serve as useful biomarkers of effects. No clinical signs or symptoms in humans have been positively linked to diisopropyl methylphosphonate exposure. [Pg.99]

Effect. No biomarkers of effect were identified that were specific to diisopropyl methylphosphonate. No specific target organs of diisopropyl methylphosphonate are known, and no toxic effects in humans can be positively linked to diisopropyl methylphosphonate exposure. [Pg.139]

Mineral Oil Hydraulic Fluid. Data were insufficient to indicate biomarkers of effects caused by mineral oil hydraulic fluids. [Pg.226]

Mineral Oil Hydraulic Fluids and Polyalphaolefin Hydraulic Fluids. The data bases of the toxicity of mineral oil and polyalphaolefin hydraulic fluids are very limited. Further toxicity testing may elucidate biomarkers of effect for these classes of hydraulic fluids. [Pg.248]

Organophosphate Ester Hydraulic Fluids. The biomarkers of effects after exposure to organophosphate ester hydraulic fluids are well established in cases of delayed neuropathy (clinical signs of peripheral neuropathy). Further study would be helpful to determine whether certain effects (such as diarrhea after oral exposure) are due to direct action of the toxic agent on the target organ or to inhibition of acetylcholinesterase at the acetylcholine nerve receptor site on the organ. [Pg.248]

Effect. Potential biomarkers of the subclinical effects of hydrogen sulfide are decreases in the activities of the heme synthesis enzymes, ALA-S and Haem-S (Jappinen and Tenhunen 1990). These effects have nothing to do with the mechanism of toxicity, however. Neurological indices are also used as biomarkers of effect for hydrogen sulfide (Gaitonde et al. 1987 Kilbum 1993 Stine et al. 1976 Tvedt et al. 1991b). [Pg.128]

Because hexachlorobenzene can interfere with porphyrin metabolism and produce chemical porphyria, the evaluation of the urinary porphyrin pattern has been proposed as an early biomarker of effect (San Martin et al., 1977 Schmid, I960, 1966 Wray et al., 1962). However, apart from an outbreak of chemical porphyria which occurred in Turkey in the 1950s following ingestion of hexachlorobenzene-contaminated food, cases of chemical porphyria among... [Pg.13]

There is no clinical disease state that is pathognomonic for lead exposure. The neurotoxic effects and hematopoietic effects of lead are well recognized. The primary biomarkers of effect for lead are EP, ALAD, basophilic stippling and premature erythrocyte hemolysis, and presence of intranuclear lead inclusion bodies in the kidneys. Of these, activity of ALAD is a sensitive indicator of lead exposure (Hemberg et al. 1970 Morris et al. 1988 Somashekaraiah et al. 1990 Tola et al. 1973), but the assay can not distinguish between moderate and severe exposure (Graziano 1994). Sensitive, reliable, well-established methods exist to monitor for these biomarkers however, they are not specific for lead exposure. Therefore, there is a need to develop more specific biomarkers of effect for lead. Recent data... [Pg.351]

Biomarkers are broadly defined as indicators signaling events in biologic systems or samples. They have been classified as biomarkers of exposure, biomarkers of effect, and biomarkers of susceptibility (NAS/NRC 1989). [Pg.65]

They also may not be directly adverse, but can indicate potential health impairment (e.g., DNA adducts). Biomarkers of effects caused by acrylonitrile are discussed in Section 2.5.2. [Pg.65]

Studies using radioactivity-labeled acrylonitrile indicate that acrylonitrile or its metabolites form covalent adducts with cellular macromolecules in most tissues. Studies to develop chemical or immunological methods for measuring these adducts would be especially valuable in detecting and perhaps even quantifying human exposure to acrylonitrile. Adverse health effects demonstrated following exposure to acrylonitrile, particularly acute exposures, were characteristic of cyanide toxicity. Because these effects are also indicative of exposure to many other toxicants, additional methods are needed for more specific biomarkers of effects of acrylonitrile exposure. [Pg.96]

Rickwood, C. and Galloway, T. S., Acetylcholinesterase as a biomarker of effect A study of the mussel Mytilus edulis exposed to the priority pollutant chlorfenvinphos, Aquatic Toxicol., 67, 45, 2004. [Pg.381]

The formation of hyaline droplets is unique in male rats and is not indicative of the toxic effect of hexachloroethane. Therefore, they are not useful as biomarkers of effect. There is a need to identify compound-specific biomarkers for the effects of hexachloroethane exposure at this time. [Pg.143]

The neurotoxic effects of -hexane have been associated with the pyrrolidation of protein (Graham et al. 1995) by 2,5-hexanedione. Therefore, the development of analytical methods to determine this potential biomarker of effect of -hexane in hair and the subsequent crosslinking of the blood proteins, spectrin and hemoglobin, would be useful. [Pg.216]

No biomarkers of effects caused by di-w-octylphthalate have been identified in humans or animals. [Pg.68]

Effect Since exposure to di-u-octylphthalatc does not produce a unique clinical disease state, no biomarkers of effect have been identified. Additional information on the potential health effects of di-n-octylphthalate is needed to identify biomarkers of exposure to this compound. [Pg.77]


See other pages where Biomarkers of Effect is mentioned: [Pg.112]    [Pg.128]    [Pg.177]    [Pg.177]    [Pg.180]    [Pg.196]    [Pg.196]    [Pg.167]    [Pg.241]    [Pg.113]    [Pg.98]    [Pg.223]    [Pg.226]    [Pg.113]    [Pg.310]    [Pg.312]    [Pg.319]    [Pg.65]    [Pg.96]    [Pg.110]    [Pg.150]    [Pg.152]    [Pg.168]    [Pg.83]    [Pg.110]    [Pg.128]    [Pg.143]    [Pg.163]    [Pg.67]    [Pg.120]   


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