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Toxicity table

Articles made from polypropylene have good electrical and chemical resistance and low water absorption. Its other useful characteristics are its light weight (lowest thermoplastic polymer density), high abrasion resistance, dimensional stability, high impact strength, and no toxicity. Table 12-3 shows the properties of polypropylene. [Pg.332]

Pyrethroids show very marked selective toxicity (Table 12.2). They are highly toxic to terrestrial and aquatic arthropods and to fish, but only moderately toxic to rodents, and less toxic still to birds. The selectivity ratio between bees and rodents is 10,000- to 100,000-fold with topical application of the insecticides. They therefore appear to be environmentally safe so far as terrestrial vertebrates are concerned. There are, inevitably, concerns about their possible side effects in aquatic systems, especially on invertebrates. [Pg.236]

Less than 0.5 percent of the black children at the Dixie site were found to have lead toxicity (Table XX). As previously noted, the three non-black children (6.6 percent of non-black children) found to have lead toxicity were siblings In a household where the father had an occupational exposure to lead. [Pg.63]

Until recently, there was little evidence that the response or survival benefit from one endocrine therapy was clearly superior to that achieved with other therapies. Given this equality in efficacy, the choice of a particular endocrine therapy was based primarily on toxicity (Table 86-8). Based on these criteria, tamoxifen is the preferred initial agent when metastases are present. An exception to this occurs when the patient is receiving adjuvant tamoxifen at the time or within 1 year of occurrence of metastatic disease. [Pg.1316]

There are a number of different mechanisms by which microorganisms resist metal toxicity (Table 11.1). Five mechanisms that microbes use to mediate metal toxicity have been proposed and they include (1) formation of a permeability barrier,21-24 (2) active transport,25-29 (3) sequestration,30-32 (4) enzymatic detoxification,33 34 and (5) reduction in sensitivity.35,36 Microbes may use one or more of these mechanisms to exclude nonessential metals and regulate internal concentrations of essential metals. [Pg.410]

Monohalogenated Benzenes and Naphthalenes Trends in aromatic toxicities (Table IV) are somewhat obscured in these two series by the toxicities of the individual substituents (2). Fluorine and chlorine substituents are reasonably inert however, the bromine and iodine atoms, particularly the latter, are extremely toxic. In the case of inert substituents (F, Cl) the results resemble those of the alkylbenzenes in terms of steric hindrance to adsorption. [Pg.108]

A number of 3-day inhalation studies (Feron et al. 1995a, Cassee et al. 1996, 1998) were carried out in male rats with formaldehyde, acetaldehyde, and acrolein and mixtures of two or three of these toxicants (Table 10.10). They aU produce the same type of adverse effect (nasal cytotoxicity) but with different target sites (different regions of the nasal mucosa). The nasal changes seen after... [Pg.404]

There are a number of key features essential for a cell-based model to be effectively predictive of toxicity (Table 14.3). First, as indicated above, it must be sensitive enough to reflect early, sublethal injury and not merely cell death. [Pg.331]

The occurrence and timing of effects on intracellular ionized calcium concentration, lysosomal mass, oxidative stress or plasma membrane permeability frequently provide additional information indicative of mechanism of toxicity (Table 14.5). [Pg.335]

CR is a potent peripheral sensory Irritant of low toxicity by the usual routes of administration.3 It appears safer than CS, which replaced CN and DM in turn as riot-control agent because of greater effectiveness and lower toxicity. Table 4-20 shows comparative toxi-citles of these compounds in several species.2... [Pg.189]

The effects of digitalis on the electrical properties of the heart are a mixture of direct and autonomic actions. Direct actions on the membranes of cardiac cells follow a well-defined progression an early, brief prolongation of the action potential, followed by shortening (especially the plateau phase). The decrease in action potential duration is probably the result of increased potassium conductance that is caused by increased intracellular calcium (see Chapter 14). All these effects can be observed at therapeutic concentrations in the absence of overt toxicity (Table 13-2). [Pg.308]

In contrast to the difficult search for receptors responsible for antipsychotic efficacy, the differences in receptor effects of various antipsychotics do explain many of their toxicities (Tables 29-1 and 29-2). In particular, extrapyramidal toxicity appears to be consistently associated with high D2 potency. [Pg.632]

Fluorinated alkenes tend to be pulmonary irritants, but most of the commercially important alkenes, such as tetrafluoroethene (TFE) and hexafluoropropene (FIFP), are only slightly toxic (Table 5). [Pg.39]

In addition to older literature (e.g., sec ref 5), only a few new fluorinated alcohols have been investigated since 1960 in detail with respect to toxicity (Table 8). [Pg.41]

Interest centers on fluoroacetic acid itself,54-55,56 115 but its monofluorinated homologs have been equally studied to attempt to verify the observation that only compounds CFH2(CH2)nC02H with n = 0 or even numbers, and their derivatives (esters, salts) show considerable toxicity (Table 11) in addition to that of their acid function. In the course of in vivo metabolism these fluorinated derivatives end up, like any fatty acid by /(-oxidation or hydrolysis, as the toxic fluoroacetic acid. With an uneven number of n, metabolism stops at the stage of the less toxic 2-fluoropropanoic acid (CFH2CH2C02H). [Pg.42]

According to a private communication of D. Bennett, USA, introduction of methyl groups into the silatrane skeleton of 1-phenylsilatrane reduces significantly its toxicity (Table 1, 3). [Pg.81]

Alkyl-, 1-vinyl-, and 1-ethynylsilatranes are practically non-toxic (Table 5)... [Pg.84]

Certain strains of cyanobacteria produce toxins. These cyanobacterial toxins can be classified according to their chemical structure or their toxicity. Table 16.1 summarises the characteristics of the main cyanobacterial toxins. Depending on the chemical structure, there are cyclic peptides, alkaloids and lipopolysaccharides. According to the toxic effects, they are classified as ... [Pg.331]

Several factors are involved in the sensitivity of the kidney to a number of toxicants (Table 15.1), although the high renal blood flow and the increased concentration of excretory products following reabsorption of water from the tubular fluid are clearly of major importance. Although the kidneys comprise less than 1% of the body mass, they receive around 25% of the cardiac output. Thus significant amounts of exogenous chemicals and/or their metabolites are delivered to the kidney. [Pg.274]

Metabolites may be either pharmacologically inactive or active. Active metabolites may exhibit a similar activity to the drug or a different activity or be toxic (Table 9.1). In addition, they may exhibit different side effects. [Pg.184]

Surface and tissue deposits proved about equally effective on 7. confusus emerging from pine bolts treated with 0.05% wettable powder of lindane (surface deposit) and the same concentration of diesel oil solution. The solution does not crystallize (tissue deposit) or show surface toxicity (Table V). [Pg.209]

A similar test with the mountain pine beetle [Dendroctonus pon-derosae (Hopkins)] showed tissue deposits to be about twice as toxic (Table VI). A possible explanation is that D. ponderosae emerged over a 54-day period, allowing the surface lindane to volatilize I. confusus emerged over a period of 15 days. [Pg.210]


See other pages where Toxicity table is mentioned: [Pg.501]    [Pg.351]    [Pg.78]    [Pg.162]    [Pg.1144]    [Pg.511]    [Pg.234]    [Pg.1117]    [Pg.340]    [Pg.1117]    [Pg.175]    [Pg.277]    [Pg.1109]    [Pg.1109]    [Pg.79]    [Pg.82]    [Pg.223]    [Pg.64]    [Pg.441]    [Pg.1182]    [Pg.1182]    [Pg.356]    [Pg.118]    [Pg.84]    [Pg.33]    [Pg.1655]    [Pg.1659]    [Pg.82]    [Pg.130]   
See also in sourсe #XX -- [ Pg.401 ]

See also in sourсe #XX -- [ Pg.401 ]




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Arsenic Table toxicity

Essentiality and Toxicity of Trace Elements (see Table

Tables classification of toxic action

Tables toxicities of acid chlorides

Tables toxicities of fluoroacetic esters

Tables toxicities of w-fluorocarboxylates

Toxicants PELs, table

Toxicity Hodge-Sterner table

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