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PCDDs , toxicity

Chlorobenzenes are stable compounds and decompose slowly only under excess heating at high temperatures to release some HCl gas and traces of phosgene. It is possible, under certain limited conditions of incomplete combustion or pyrolysis, to form polychlorinated dibenzo-/)-dioxins (PCDDs) and dibenzofurans (PCDFs) from chlorobenzenes (Cm OROCARBONS and cm OROHYDROCARBONS, toxic aromatics). [Pg.48]

In addition to their endocrine disrupting properties, it must be appreciated that many of the chemicals in question possess more general toxic properties, which may be potentiated by metabolism by the organism. Several PAHs, PCBs and PCDDs are carcinogenic, while certain phthalate esters can enhance the excretion of zinc, potentially leading to zinc deficiency. Zinc, an essential element, plays a vital role in spermatogenesis and mature T-cell production. Deficiency may result in abnormalities of the male reproductive system, depletion of spermatogenesis and suppression of the immune system. [Pg.77]

These results show the fate of aromatic bromine compounds during municipal waste incineration bromine is exchanged by chlorine on the surface of fly ash at the electrostatic precipitator at 250-3(X)°C. But the toxic potential at brominated dibenzodioxins and furans is not reduced by these transformations. The increase of PCDD/F concentration in MWI by adding bromine compounds has been pointed out by Lahl and coworkers (ref. 26). [Pg.380]

Because of the concern over hnman health hazards associated with PCDDs, many toxicity tests have been performed on rodents. Some toxicity data are given for 2,3,7,8-TCDD as follows ... [Pg.158]

Both PCDDs and PCDEs are refractory lipophilic pollutants formed by the interaction of chlorophenols. They enter the environment as a consequence of their presence as impurities in pesticides, following certain industrial accidents, in effluents from pulp mills, and because of the incomplete combustion of PCB residues in furnaces. Although present at very low levels in the environment, some of them (e.g., 2,3,7,8-TCDD) are highly toxic and undergo biomagnification in food chains. [Pg.160]

PCDDs and PCDEs, together with coplanar PCBs, can express Ah-receptor-mediated toxicity. TCDD (dioxin) is used as a reference compound in the determination of TEFs, which can be used to estimate TEQs (toxic equivalents) for residues of PHAHs found in wildlife samples. Biomarker assays for Ah-receptor-mediated toxicity have been based on the induction of P450 lAl. TEQs measured in field samples have sometimes been related to toxic effects upon individuals and associated ecological effects (e.g., reproductive success). [Pg.160]

Coplanar PCBs, PCDDs, and PCDFs express Ah-receptor-mediated toxicity (Chapter 6, Section 6.2.4). Binding to the receptor leads to induction of cytochrome P4501 and a number of associated toxic effects. Again, toxic effects are related to the extent of binding to this receptor and appear to be additive, even with complex mixtures of planar polychlorinated compounds. Induction of P4501A1/2 has been widely used as the basis of a biomarker assay. Residue data can be used to estimate TEQs for dioxin (see Chapter 7, Section 7.2.4). [Pg.246]

Ah-receptor-mediated toxicity Toxic effects associated with the binding of polychlorinated aromatic componnds snch as coplanar PCBs and PCDDs to the Ah receptor. [Pg.331]

Safe, S. (1990). PCBs, PCDDs, PCDFs and related compounds Environmental and mechanistic considerations which support the development of toxic equivalency figures. CRC Critical Reviews in Toxicology 24, 1-63. [Pg.366]

The evaluation of risk has underlined the possible adverse effects both on human health after the exposure to drinking water contaminated by landfill leachate and on small rodents and aquatic species at the hypothesized condition for humans, the estimated toxic effects of the raw leachate are mainly due to the levels of ammonia and cadmium and carcinogenic effects are induced by arsenic first and then by PCBs and PCDD/Fs while ecological potential risk is mainly attributable to the concentration of inorganic compounds, in particular ammonia for small rodents, cadmium, ammonia, and heavy metals for fishes. [Pg.178]

In addition, the concern about e-waste not only focuses on its vast quantity generated daily, but also more on the need to handle the toxic chemicals embedded in it. It is well known that e-waste contains lead, beryllium, mercury, cadmium (Cd), and brominated flame retardants (BFRs) among other chemical materials [3]. Furthermore, highly toxic chemicals such as polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and polybrominated dibenzo-p-dioxins and dibenzo-furans (PBDD/Fs) can be formed during the recycling process [4]. [Pg.281]

In tree bark from Luqiao of Taizhou (Fig. 1), the mean concentrations of PCDD/ Fs (List 4 of Appendix) and PCBs (List 8 of Appendix) were 0.1 and 6.5 pg/g lipid weight, respectively. Among all the target analytes, 2,3,4,7,8-PeCDF and PCB-126 were the dominant contributors to toxic equivalency (TEQ). The high levels of PCDD/Fs and PCBs in tree bark suggested the impact of e-waste recycling operations on the local environment [50]. [Pg.290]

TCP), and pentachlorophenol (PCP), in order of abundance. Minor amounts of other trichlorophenols and dichlorophenols may also be present, as well as recalcitrant polychlorinated phenoxyphenols (PCPPs) and PCDD/Fs as impurities [75, 76]. In Finland, approximately 30,000 tons of CP products were used between 1934 and 1988, when they were banned because of their potential toxicity to humans and the environment [77, 78]. The careless manufacturing and application of wood preservatives together with the lack of suitable waste disposal caused massive contamination of river sediments and sawmill sites. For example, the river Kymijoki in southern Finland was identified as the largest source of dioxins accumulating in fish in the entire Baltic area. Similar products were used in other European countries, especially Nordic countries with a large forestry industry, such as Sweden [79]. [Pg.12]

The Stockholm Convention on POPs lists 22 priority chemical substances that pose potential risks of causing adverse effects to human health and the environment. Since the convention was enacted in 2004, evidence for the toxic effects of POPs such as DDT, dichlorodiphenyldichloroethylene (DDE), PCBs, PCDD/Fs and other halogenated compounds has been demonstrated for both humans and wildlife. [Pg.15]

Acute toxicities of selected PCDD isomers to the guinea pig and the mouse... [Pg.27]

PCDDs are present as trace impurities in some commercial herbicides and chlorophenols. They can be formed as a result of photochemical and thermal reactions in fly ash and other incineration products. Their presence in manufactured chemicals and industrial wastes is neither intentional nor desired. The chemical and environmental stability of PCDDs, coupled with their potential to accumulate in fat, has resulted in their detection throughout the global ecosystem. The number of chlorine atoms in PCDDs can vary between one and eight to produce up to 75 positional isomers. Some of these isomers are extremely toxic, while others are believed to be relatively innocuous. [Pg.1023]

Data on the bioavailability of PCDDs are limited. It is known that PCDDs incorporated into wood as a result of chlorophenol (preservative) treatment are bioavailable. Swine and poultry using chlorophenol-treated wooden pens or litter have been found to be contaminated with PCDDs (NRCC 1981). Toxicities of individual PCDD isomers can vary by a factor of 1000 to 10,000 for isomers as closely related as 2,3,7,8-TCDD and 1,2,3,8-TCDD, or 1,2,3,7,8-penta-CDD and 1,2,4,7,8-penta-CDD (Rappe 1984). Isomers with the highest biological activity and acute toxicity have four to six chlorine atoms, and all lateral (i.e., 2,3,7, and 8) positions substituted with chlorine. On this basis, the most toxic PCDD isomers are 2,3,7,8-TCDD, 1,2,3,7,8-penta-CDD, 1,2,3,6,7,8-hexa-CDD, 1,2,3,7,8,9-hexa-CDD, and 1,2,3,4,7,8-hexa-CDD (Rappe 1984). Ishizuka et al. (1998) have assigned toxic equivalencies for various PCDDs, with 2,3,7,8-TCDD given a value of 1 (highest biological activity), followed by a value of 0.5 for 1,2,3,7,8-penta-CDD a value of 0.1 for three PCDD isomers (1,2,3,4,7,8-hexa-CDD, 1,2,3,4,7,8-hexa-CDD, 1,2,3,7,8,9-hexa-CDD), a value of 0.01 for 1,2,3,4,6,7,8-hepta-CDD and a value of 0.001 for 1,2,3,4,6,7,8,9-octa-CDD. [Pg.1026]


See other pages where PCDDs , toxicity is mentioned: [Pg.1055]    [Pg.1055]    [Pg.10]    [Pg.11]    [Pg.277]    [Pg.1055]    [Pg.1055]    [Pg.10]    [Pg.11]    [Pg.277]    [Pg.421]    [Pg.65]    [Pg.189]    [Pg.338]    [Pg.70]    [Pg.147]    [Pg.151]    [Pg.151]    [Pg.153]    [Pg.155]    [Pg.171]    [Pg.280]    [Pg.281]    [Pg.296]    [Pg.299]    [Pg.300]    [Pg.310]    [Pg.354]    [Pg.11]    [Pg.16]    [Pg.159]    [Pg.1024]    [Pg.1024]    [Pg.1025]    [Pg.1029]    [Pg.1030]    [Pg.1041]    [Pg.1042]   
See also in sourсe #XX -- [ Pg.184 , Pg.185 ]




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