Individual toxic level

Primary biomarkers of exposure are the presence of 1,2-dibromoethane in blood or exhaled breath or excretion of specific metabolites in urine. In humans exposed to toxic levels of 1,2- dibromoethane (Letz et al. 1984), the parent compound was not measured in blood samples collected before death. However, two exposed individuals had elevated levels of serum bromide ions. This elevation is likely to have resulted from debromination of 1,2-dibromoethane during its metabolism. Elevated serum bromide is not specific to 1,2-dibromoethane exposure, but, rather, it is indicative of exposure to classes of brominated chemicals. 

The biological half-life in humans for methyl mercury is about 70 days because elimination is slow, irregular, and individualized, there is a considerable risk of an accumulation of mercury to toxic levels. A precise relationship between atmospheric levels of alkyl mercury and concentrations of mercury in blood or urine has not been shown. Clinical observations indicate that concentrations of 50-100pg mercury/lOOml of whole blood may be associated with symptoms of intoxication concentrations around 10-20pg mercury/ 100 ml are not associated with symptoms. In a study of 20 workers engaged in the manufacture of organic mercurials and exposed for 6 years to mercury concentrations in air between 0.01 and O.lmg/m, there was no evidence of physical impairment or clinical laboratory abnormalities. Low levels of methyl mercury in the blood do not seem to affect the results of behavioral performance tests. ... 

Individual chapters deal with the determination of metals, non-metals, organic compounds and organometallic compounds in soil and in plants that grow in soil. A separate chapter deals with sampling procedures. A relationship between toxicant levels in soil and plants that grow in that soil has been established and is the subject of the concluding chapter. 

In single-species risk prediction for individual toxicants and toxicant mixtures, the effect is expressed as the proportion of an exposed population that is likely to be somehow affected by toxic action (quantal responses), or as a reduction in performance parameters such as growth, clutch size, and juvenile period (continuous responses). Both concentration addition- and response addition-based methods are commonly applied for both response types. Assemblage-level risk prediction has only been introduced more recently (e.g., De Zwart and Posthuma 2005) and is founded on similar principles while focusing on the fraction of species that are likely affected by mixture exposure. 

The procedure to set up such an experimental design is as follows. Once the EC50s of the individual toxicants are established, the chemical concentrations can be expressed in terms of these EC50 as toxic units (c / EC50). Choose the toxic unit levels that need to be tested, for instance, 0, 0.25, 0.5, 1, 2, and 4 toxic units. Choose the ratios to be tested, for instance, 1 0, 213 1/3, l/2 l/2, 1/3 213, 0 1. Calculate the... 

Clearly, in the normal individual, iron levels are under extremely tight control and there is little opportunity for iron-catalysed free radical generating reactions to occur. However, there are situations when the iron status can change, either locally, as in ischaemic tissue, or systematically, as with idiopathic haemochromatosis or transfusion-induced iron overload. In such circumstances, abnormal levels of iron can induce toxic symptoms. 

The presence of systemic disease can alter the way an individual detoxifies or excretes a drug. Liver and kidney disease, in particular, can markedly influence drug response by allowing the drug to accumulate to toxic levels. The rate of excretion of digoxin, for example, is reduced considerably in patients with renal impairment, thus causing an increased risk of alterations in color vision in these patients. 

CNS depression is the most frequently reported clinical effect. The typical overdose patient may present with extreme somnolence that may progress to frank coma. Miosis is usually present unless the individual is acidotic or has suffered hypoxic brain injury. Respiratory depression can occur and may progress to respiratory arrest. Pulmonary edema may be seen. Bradycardia, hypotension, and hyperthermia can develop. Hydrocodone is often combined in products with acetaminophen therefore, patients should be evaluated for hepatotoxicity secondary to acetaminophen overdose. Available opiate immunoassays cross-react unreliably with hydrocodone. Peak therapeutic serum levels are 0.024 mg 1 toxic levels have been reported to reach 0.1-1.3 pgml , but are of little prognostic or therapeutic value. 

As the individual toxicity threshold of BAs has not been defined exactly, varying significantly between individuals, histamine levels above 500-1000 mg/kg must be considered of potential risk to human health (Taylor, 1985). In some European Countries tolerance levels for histamine in food and beverages have been defined. The maximum level of tolerance of histamine in wine has been established in Switzerland at lOmg/L, in France at 8mg/L, in Belgium at 5-6 mg/L, and in Germany at 2 mg/L, however the level for histamine-free wines should be lower than 0.5 mg/L (Bauza et al., 1995 Lehtonen, 1996). 

The biogeochemistry of organic pollutants in marine systems is of enormous economic and environmental Impact. The environmental behavior of polychlorinated biphenyls (PCB s) has been studied rather extensively because of their detrimental effects on human health and on living marine resources (30-32). As discussed in the chapters by J.W. Farrington et, due to recent advances in gas capillary chromotographic methods, it is now possible to study the biogeochemistry of individual PCB s rather than that of combined industrial mixtures of PCB s (33-36). In order to realistically assess the risks to animal health, it is important to be able to work with individual PCB levels rather than with unresolved mixtures because individual PCB s can vary greatly in terms of toxicity (37). 

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