Sublethal levels toxicity

Selenium, in the form of selenate or selenite, is toxic to D. desulfuricans (Tomei et al. 1995) and Wolinella succinogenes (Tomei et al. 1992) at elevated levels. At sublethal levels of 0.1-1. OmM selenite or 10 mM selenate, minimal levels of growth is observed with both D. desulfuricans and Wolinella succinogenes. With both selenate and selenite, colloidal elemental selenium (Se°) is produced inside the cell and released into the culture fluid after cell death. This reduction of Se(VI) and Se(IV) by these anaerobes is not coupled to growth and proceeds by mechanisms that have not yet been identified. Selenite and selenate reduction with formation of elemental selenium by these nonrespiratory processes serve to detoxify the environment for future bacteria and may be important for the geochemical cycle of selenium. 

The pT-index allows the assessment and comparison of the toxic potential of sediments and dredged material. It is one example of an integrated bioassay-battery approach developed for the purpose of environmental management. This sediment assessment index relies on the use of an appropriate battery of bioassays at different trophic levels (decomposers, primary producers, and consumers) allowing the measurement of various types (acute, chronic) and levels (lethal, sublethal) of toxicity. 

Toxicity is an important biological test and is also a signpost that other types of activity will be noted for the toxic compound at sublethal levels. 

Researchers were also able to establish the link between declines of other predatory species such as the European sparrowhawk and the use of organo-chlorine pesticides other than DDT. For instance, the cyclodiene insecticides aldrin, dieldrin, and he-ptachlor used as seed treatments caused massive mortality of both seed-eating species and their predators. All of the insecticides had the following points in common they were highly soluble in fats and refractory to metabolism. The impacts on the predatory species typically take place in periods of food stress when fat soluble residues are released from fat stores and returned into general circulation. In a food-stressed individual, the brain remains as the most lipid rich tissue and this is where contaminants move to. Toxicity results when threshold values in brain tissue are exceeded. At sublethal levels, documented effects of cyclodiene insecticides in birds have included changes in their reproductive, social, and avoidance behaviors. 

In general, a greater proportion of aquatic organisms are exposed to sublethal concentrations of toxics compared to acutely lethal concentrations. There is general acceptance that chronic exposure of fish to sublethal levels of toxics makes them more prone to disease states. Although scientifically controversial, intuitively one can grasp how individual responses such as growth, reproduction rates, and survival probability, as a function of age, could relate to population level responses. 

The second category of toxicity studies involves experiments designed to evaluate specific kinds of toxicity in detail. The tests may be designed, for example, to study the tendency of a toxicant to cause abnormal fetal development (teratogenic tests), to affect the reproductive capacity of an organism, to cause mutations, to produce tumors, to cause cancer, to affect the photosynthetic rates of plants, and so forth. These specific tests are necessary because mar r of the important effects of toxicants on organisms, particularly at the sublethal level, do not become apparent in standard tests to evaluate overall effects. 

Lead-contaminated environments have resulted in comparable increases in organism and human lead burdens, as indicated by a recent estimate of the natural level of lead in blood of preindustrial humans (0.016 fxg/dL or 0.8 nM). This estimate has important public health implications because it suggests that blood lead levels that are now considered acceptable in children (i.e., < 10 ug/dL or <480 nM) are nearly 600-fold greater than estimated natural levels, while they are only 10-fold lower than levels ( 100 fig.dL or 4800 n that may cause encephalopathy and death in many individuals of a population. Understanding of the extent of sublethal lead toxicity in humans may benefit from studies that consider control populations possessing natural (i.e., preindustrial) lead burdens. 

It is apparent that the extent of sublethal lead toxicity in humans may be best addressed by studies that consider control populations possessing natural (i.e., preindustrial) lead burdens, as well as state-of-the-art, trace-metal-clean techniques and advanced instrumentation. Trace-metal-clean techniques are required to prevent the inadvertent lead contamination of samples, which has plagued many previous analyses of environmental and human lead levels. Advanced instrumentation is required to provide the sentivity, accuracy, and precision that are needed to quantify the sublethal effects of lead concentrations at environmental levels of exposure. Fortunately, methodologies utilizing these advancements are now capable of addressing many of the important issues (e.g., lead biomolecular speciation, low exposure effects) in environmental and human lead toxicology. 

Toxicity. Lethality is the primary ha2ard of phosphine exposure. Phosphine may be fatal if inhaled, swallowed, or absorbed through skin. AH phosphine-related effects seen at sublethal inhalation exposure concentrations are relatively small and completely reversible. The symptoms of sublethal phosphine inhalation exposure include headache, weakness, fatigue, di22iness, and tightness of the chest. Convulsions may be observed prior to death in response to high levels of phosphine inhalation. Some data are given in Table 2. 

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