Lethal sublethal

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. 

A total of 45 different species were employed, but authors did not always specify their choice of species. Ideally, bioassays should have some basic characteristics, as defined by Giesy and Hoke (1989). An adequate battery of bioassays needs in principle to measure various types (acute, chronic, genotoxic) and levels (lethal, sublethal) of ecotoxicity, without any redundancy, with test species belonging to different trophic levels or characterized by different ecological and biological traits (Ducrot et al., 2005). Another important aspect in the selection of bioassays for a test... 

Peripheral nerve lesions at lethal sublethal doses. 

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. 

TNE- a also protects mice against the lethal effects of radiation (164). TNE- a given before sublethal kradiation reduces the decline of neutrophils and total blood counts and accelerates the recovery of peripheral blood cells (190). TNE- a also alters the radiosensitivity of murine G1 progenitors (191). 

Acute toxicity studies are often dominated by consideration of lethaUty, including calculation of the median lethal dose. By routes other than inhalation, this is expressed as the LD q with 95% confidence limits. For inhalation experiments, it is convenient to calculate the atmospheric concentration of test material producing a 50% mortaUty over a specified period of time, usually 4 h ie, the 4-h LC q. It is desirable to know the nature, time to onset, dose—related severity, and reversibiUty of sublethal toxic effects. 

Toxicity. A 1% concn of the gas in air is lethal to rats in 1 hour, its effect being similar to C monoxide the LD50 in rats when injected intra-peritoneally is 8.2ml/kg (Ref 16). Earlier workers assumed that the toxicity of N trifluoride would be similar to H fluoride and that the latter would be formed by hydrolysis in body tissues (Ref 1). This has recently been shown to be erroneous, and that it is stable under physiological conds. The toxic effect is due to its ability to complex with the hemoglobin of the blood causing anoxia. This effect is reversible, and animals receiving a sublethal dose recover rapidly upon removal from contact with N trifluoride (Ref 14)... 

Diarrhea was observed in rats exposed for 5 days, 6 hours/day to both lethal and sublethal doses of P-endosulfan ( 250 mg/kg/day for males and i6 mg/kg/day for females) (Hoechst 1989b). Autopsy of animals from this study revealed that the mesenteric blood vessels of one of the surviving females exposed to 16 mg/kg/day were distended with blood, and that the small intestines of animals dying as a result of exposure were filled with a reddish fluid (500 mg/kg/day for males and 31.25 for mg/kg/day females). In contrast, no treatment-related effects were revealed by routine gross and histopathological examination of gastrointestinal tissues (stomach, small and large intestines, and pancreas) from rats exposed to doses of 27 mg/kg/day (females) and 81 mg/kg/day (males) for 30 days, 6 hours/day,... 

Neurotoxic compounds can have behavioral effects in the field (see Chapters 5, 9, and 15), and these may reduce the breeding or feeding snccess of animals and their ability to avoid predation. A number of the examples that follow are of sub-lethal effects of pollutants. The occurrence of sublethal effects in natural populations is intimately connected with the question of persistence. Chemicals with long biological half-lives present a particular risk. The maintenance of substantial levels in individuals, and along food chains, over long periods of time maximizes the risk of sublethal effects. Risks are less with less persistent compounds, which are rapidly... 

From an ecotoxicological point of view, it has often been suspected that sublethal effects, such as those described here, can be more important than lethal ones. Both p,p -DDT and p,p -DDD are persistent neurotoxins, and may very well have caused behavioral effects in the field. This issue was not resolved when DDT was widely used, and remains a matter for speculation. More is known, however, about eggshell thinning caused by p,p -DDE and its effects upon reproduction, which will be discussed in Section 5.2.5.I. 

FIGURE 5.6 Dieldrin intoxication in hnmans and its relationship to blood levels. The hatched area represents the sublethal effects seen at 15-30% of lethal threshold concentration in blood (after Jager 1970). 

Experimental animals exposed to sublethal doses of cyclodienes show a similar picture, with changes in EEG patterns, disorientation, loss of muscular coordination and vomiting, as well as convulsions, the latter becoming more severe with increasing doses (Hayes and Laws 1991). It is clear from these wide-ranging studies that a number of neurotoxic effects can be caused by cyclodienes at levels well below those that are lethal. In the human studies described here, subclinical symptoms were frequently reported when dieldrin blood levels were in the range 50-100 pg/L, an order of magnitude below those associated with lethal intoxication. 

The inhibition of brain cholinesterase is a biomarker assay for organophosphorous (OP) and carbamate insecticides (Chapter 10, Section 10.2.4). OPs inhibit the enzyme by forming covalent bonds with a serine residue at the active center. Inhibition is, at best, slowly reversible. The degree of toxic effect depends upon the extent of cholinesterase inhibition caused by one or more OP and/or carbamate insecticides. In the case of OPs administered to vertebrates, a typical scenario is as follows sublethal symptoms begin to appear at 40-50% inhibition of cholinesterase, lethal toxicity above 70% inhibition. 

It is very clear, therefore, that there have been many examples of neurotoxic effects, both lethal and sublethal, caused by pesticides in the field over a long period of time. Far less clear, despite certain well-documented cases, is to what extent these effects, especially sublethal ones, have had consequent effects at the population level and above. Interest in this question remains because neurotoxic pesticides such as pyre-throids, neonicotinoids, OPs, and carbamates continue to be used, and questions continue to be asked about their side effects, for example, on fish (Sandahl et al. 2005), and on bees and other beneficial insects (see, for example, Barnett et al. 2007). 

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