And baseline toxicity

Sorption II Partitioning to Living Media -Bioaccumulation and Baseline Toxicity... 

R.L. Lipnick (1990). Narcosis Fundamental and Baseline Toxicity Mechanism for Nonelectrolyte Organic Chemicals. In W. Karcher and J. Devillers (eds.) Practical Applications of Quantitative Structure-Activity Relationships (QSAR) in Environmental Chemistry and Toxicology, Kluwer Academic Publishers, Dordrecht, The Netherlands, pp. 129-144... 

Lipnick RL. Narcosis Fundamental and baseline toxicity mechanism for nonelectrolyte organic chemicals. In Karcher W, Devillers J, editors, Practical applications of quantitative structure-activity relationships (QSAR) in environmental chemistry and toxicology. Dordrecht Kluwer Academic, 1990. p. 281-93. 

If the parent compound is specifically acting (TR > 10) and no toxicity data are available for the metabolite (case II), we assume that the true toxicity of the metabolite lies between exhibiting the same specific moa as the parent compound and baseline toxicity. In that case we compute a range of RP, as depicted in Fig. 2b. Possible RP range between RPmin,i (Eq. 6) for the assumption of baseline toxicity and RPmax,i (Eq. 7) for the assumption that the metabolite exhibits the same moa as the parent compound. Note that Eq. 7 will result in the same value as Eq. 5. 

As a conclusion one can say that the distinction of islands of specific activity from within a sea of baseline toxicity, with each island representing a local chemical biological mechanism domain, is still a challenge to be solved by scientists working both experimentally and computationally. 

To optimize chemotherapy administration, the clinician must identify, monitor, treat, and prevent or minimize treatment-related toxicity. Pertinent laboratory data and other procedures should be reviewed to establish a baseline for monitoring purposes. Major organ and system toxicities to be monitored include hematologic, neurologic, skin, pulmonary, GI, renal, and cardiac. 

Oherg, T. (2004) A QSAR for baseline toxicity validation, domain of application, and prediction. Chem. Res. Toxicol.,... 

Lipnick, R.L. (1993) Baseline toxicity QSAR models a means to assess mechanism of toxicity for aquatic organisms and mammals, in... 

You are interested in the well-being of Ampelisca abdita, living in a harbor whose sediments are contaminated with 4-nonylphenol. You remember that the lethal volume fraction of narcotic chemicals in membranes is about 0.01 L compound L I lipid. If the sediment contains 2% organic carbon by weight, and the amphipod is assumed to accumulate body burdens up to equilibrium with the sediments on which it lives, what sediment concentration of 4-nonylphenol should be deemed acceptable with respect to baseline toxicity Assume a log ,lipsw = 5.5 for 4-nonylphenol. Use Eq. 9-26c (alkylated and chlorinated benzenes ) for estimating Kioc. Compare your result with the findings of Fay et al. (2000), who observed a die-off of half the amphipods when they were exposed to about 0.16 g 4-nonylphenol - kg-1 sediment. 

Based on the activities that were initially conducted for the enabling activity project (Bravante and Medina, 2004), it was reported that little is known about POPs in the country and that even the users have minimal understanding of their hazards. As no comprehensive data on POPs is available for use as baseline information, a more comprehensive inventory is needed for the Philippines to have an actual measure of the risks that must be managed and addressed in the NIP. The Initial National Inventory conducted showed that POPs have already been banned in the country except HCB and mirex, which have no recorded use, importation or production in the country. Significant amounts of PCBs mainly come from electric transformers and capacitors. Dioxins and Source Inventory by DOST showed that there are numerous sources of dioxins and furans in the country, which emit significant quantities of dioxins and furans into the environment. No treatment facility in the country that deals with the destruction of POPs and other toxic hazardous wastes are present in the country (Bravante and Moreno, 2005). 

Leslie, H.A., J.L.M. Hermens, and M.H.S. Kraak. 2004. Baseline toxicity of a chlorobenzene mixture and total body residues measured and estimated with solid-phase microextraction. Environ. Toxicol. Chem. 23 2017-2021. 

The CAFC also commented on the absence of a reasonable expectation of success. In this particular instant, the CAFC rejected Danbury s reasoning that an expectation of success merely required an expectation of minimal activity. Rather, the CAFC held that the success of discovering famotidine was not the expectation of discovering one of the tens of thousands of compounds that exhibit baseline H2 antagonist activity but was the finding of a compound that had high activity, few side effects, and lacked toxicity. ... 

Two protocols are presented, the first for baseline toxicity, and the second for groups of compounds with the same assumed primary mode of action. The protocols are more broadly explained in De Zwart and Posthuma (2005). Example spreadsheet calculations can be found in Box 5.2. 

Lipnick RL. 1993. Baseline toxicity (Q)SAR models a means to assess mechanism of toxicity for aquatic organisms and mammals. In La Point TW, editor. Environmental toxicology and risk assessment STP 1216. Volume 2. Philadelphia (PA) American Society for Testing and Materials, p 610-619. 

Albanese, S., Cicchella, D., De Vivo, B., and Lima, A. (2006). Geochemical background and baseline values of toxic elements in stream sediments of Campania region (Italy). J. Geochem. Explor. 93, 21-34. doi 10.1016/j.gexplo.2006.07.006. 

Common unspecific mode of action of all organic compounds has been taken up in quantitative structure-activity relationships (QSARs see Chapter 5) as the concept of baseline toxicity and in toxicokinetics as the body burden concept (see Chapter 2). Baseline toxicity refers to the idea that a minimum toxicity expectation may be formulated for any given organic compound based on considerations of a compound s partition properties between hydrophilic and lipophilic chemicals (e.g., between water and octanol). Commonly, this is expressed in terms of the octanol-water partition coefficient (K0,J of a chemical. The partition coefficient allows estimations of a local concentration or body burden for each individual chemical in the mixture. Assuming that this produces the same toxic effect (disturbances of cell membranes), it is then possible to anticipate joint narcotic action by adding together the respective local concentrations or body burdens for each individual mixture component. 

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