Dioxin treatment

Dioxin-containing wastes are prohibited from land disposal (dioxins) Treatment standards constituent concentration in waste extract (dioxins) Yes <1 ppb 401 KAR 37 030 NREPC 1988 401 KAR 37 040 NREPC 1988... 

Kelling CK, Menahan LA, Peterson RE. 1987. Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment on mechanical function of the rat heart. Toxicol Appl Pharmacol 91 497-501. 

Lundgren K, Andries M, Thompson C, et al. 1986. Dioxin treatment of rats results in increased in vitro induction of sister chromatid exchanges by -naphthoflavone An animal model for human exposure to halogenated aromatics. Toxicol Appl Pharmacol 85 189-195. 

U.S. Congress 1991. Dioxin treatment technologies background paper. Office of Technology Assessment. OTA-BP-O-93. Washington, DC U.S. Government Printing Office. November 1991. 

Unwillingness by commercial waste disposers to accept dioxin-contaminated waste, a decision which led to testing of many novel dioxin treatment schemes. 

Most carbon adsorption units use granular activated carbon (GAC). The powdered form of activated carbon (PAC) typically is less than 100 microns in diameter and may be used to reduce dioxins in incinerator emissions (2) and in the treatment of drinking water and wastewater treatment (see the section on "Activated Sludge"). 

Optimized modern dry scrubbing systems for incinerator gas cleaning are much more effective (and expensive) than their counterparts used so far for utility boiler flue gas cleaning. Brinckman and Maresca [ASME Med. Waste Symp. (1992)] describe the use of dry hydrated lime or sodium bicarbonate injection followed by membrane filtration as preferred treatment technology for control of acid gas and particulate matter emissions from modular medical waste incinerators, which have especially high dioxin emissions. 

Baird is the 20-acre site of a former chemical mixing and batching company. Poor waste disposal practices resulted in the contamination of groundwater, soil, the municipal water supply, and a brook adjacent to the site. Over one hundred contaminants, including chlorinated and nonchlorinated volatile organics, heavy metals, pesticides, herbicides, and dioxins, had been identified in site soil and groundwater. Remediation activities included soil excavation and incineration, and groundwater treatment (the audit focused on the soil excavation and incineration... 

Use of some biomass feedstocks can increase potential environmental risks. Municipal solid waste can contain toxic materials that can produce dioxins and other poisons in the flue gas, and these should not be burned without special emission controls. Demolition wood can contain lead from paint, other heavy metals, creosote, and halides used in presen a-tive treatments. Sewage sludge has a high amount of sulfur, and sulfur dioxide emission can increase if sewage sludge is used as a feedstock. 

Pathological changes observed in animals treated with chlorodibenzo-dioxins were inconsistent from animal to animal and species to species. Hepatic lesions were observed consistently, but the nature, degree, and distribution of the lesions were variable. Changes in organs other than the liver were sporadic and unpredictable. Gross and microscopic examination of tissues after chlorodibenzodioxin treatment did not reveal the cause of death. An in-depth evaluation of the toxicity associated with chronic exposure to the chlorodibenzodioxins is needed. 

The postnatal effects of maternal treatment with 2,7-dichlorodibenzo-p-dioxin are summarized in Table VII. No significant changes were found. The progeny on becoming adult were mated within the treatment groups. No effects on male or female fertility, embryonic viability, and total implantation/corpora lutea ratio were observed. 

Oral treatment of pregnant dams with 0.25 /xg (or more) /kg/day of 2,3,7,8-tetrachlorodibenzo-p-dioxin for 10 days during gestation resulted in adverse effects on rat development. No adverse effects were seen at the 0.125 ju,g/kg/day. When C-2,3,7,8-tetrachlorodibenzo-p-dioxin (2.99 fjLc/mg) was given at 2 /xg/kg/day there was activity, primarily in liver and to a lesser extent, in fat and brain. When a single oral dose of 200 /Ag/kg was administered on gestation days 16, 17, or 18 and was followed 6 hours later with tissue sampling, the label was also observed in the fetus and placenta. Placenta had approximately twice as much label as the fetus. 

Tetrachlorodibenzo-p-dioxin elicited no apparent prenatal or postnatal effects when doses of up to 800 /xg/kg/day were given orally for 10 days of gestation. Treatment with 250-2000 /xg/kg/day of 2,7-di-chlorodibenzo-p-dioxin (99% purity) had no significant effect on prenatal and postnatal measures of toxicity but caused a low incidence of cardiac lesions. 2,3-Dichlorodibenzo-p-dioxin and 2-chlorodibenzo-p-dioxin up to 2000 /xg/kg/day had no adverse effect on survival, average weight, and skeleton of term fetuses. 

Next, we attempted to deal with translocation of foliar-applied TCDD. Labeled dioxins were applied to the center leaflet of the first trifoliate leaf of 3-week-old soybean plants and the first leaf blade of 12-day-old oat plants. All compounds were applied in an aqueous surfactant solution (Tween 80) to enhance leaf adsorption and to keep the water insoluble dioxins in solution. Plants were harvested 2, 7, 14, and 21 days after treatment, dissected into treated and untreated parts, and analyzed separately. Neither dioxin nor chlorophenol was translocated from the treated leaf. A rapid loss of the dichlorodioxin and dichlorophenol occurred from the leaf surface. This loss may have resulted from volatilization. Very little TCDD was lost from soybean leaves while a gradual loss (38% in 21 days) did occur from oat leaves. 

Treatment of l,2,3,4-tetrachlorodibenzo[l,4]dioxin on Ca-based sorbents at temperatures of 160-300°C resulted in its conversion into products with molecular masses of... 

Gullett BK, DF Natschke, KRE Bruce (1997) Thermal treatment of 1,2,3,4-tetrachlorodibenzo-p-dioxin by reaction with Ca-based sorbents at 23-300°C. Environ Sci Technol 31 1855-1862. 

TCDF and possibly 2,3,7,8-TCDD may still be formed. Dioxin and furan are not effectively degraded during wastewater treatment they partition to the sludge (and may be discharged with TSS into receiving waters untreated). 

On the other hand, sludge samples showed a slight increase (two- to threefold) of dioxin-like activity after the fungal treatment, reaching values above the mg/L BNF equivalent mark. This data can be interpreted as an indicator for bio-activation of some compounds, other than UV filters, present in the sludge by the treatment with T. versicolor. These results emphasize the need of a broad screening of biological assays tests, as they differ in their capacity to detect specific hazardous effects. 

In Scheme 6.230, the multistep synthesis of 2,3-dihydro-4-pyridones is highlighted [411]. The pathway described by Panunzio and coworkers starts from a dioxin-4-one precursor, which is readed with 2 equivalents of benzyl alcohol under solvent-free microwave conditions to furnish the corresponding /1-diketo benzyl esters. Subsequent treatment with 1 equivalent of N,N-dimethylformamide dimethyl acetal (DMFDMA), again under solvent-free conditions, produces an enamine, which is then cyclized with an amine building block (1.1 equivalents) to produce the desired 4-pyridinone produds. All microwave protocols were conducted under open-vessel conditions using power control. 

The application of flavonoids for the treatment of various diseases associated with free radical overproduction is considered in Chapter 29. However, it seems useful to discuss here some studies describing the activity of flavonoids under certain pathophysiological conditions. Oral pretreatment with rutin of rats, in which gastric lesions were induced by the administration of 100% ethanol, resulted in the reduction of the area of gastric lesions [157]. Rutin was found to be an effective inhibitor of TBAR products in the gastric mucosa induced by 50%i ethanol [158]. Rutin and quercetin were active in the reduction of azoxymethanol-induced colonic neoplasma and focal area of dysplasia in the mice [159], Chemopreventive effects of quercetin and rutin were also shown in normal and azoxymethane-treated mouse colon [160]. Flavonoids exhibited radioprotective effect on 7-ray irradiated mice [161], which was correlated with their antioxidative activity. Dietary flavones and flavonols protected against the toxicity of the environmental contaminant dioxin [162], Rutin inhibited ovariectomy-induced osteopenia in rats [163],... 

In mammals, phenobarbital and phenytoin increase serum ceruloplasmin concentrations (Aaseth and Norseth 1986). Chronic copper poisoning in sheep is exacerbated when diets contain heliotrope plants (Heliotropium sp., Echium spp., Senecio sp.). Aggravated effects of the heliotrope plants include reduced survival and a twofold to threefold increase in liver and kidney copper concentrations when compared to control animals fed copper without heliotropes (Howell et al. 1991). Rats given acutely toxic doses of 2,3,7,8-tetrachlorodibenzo-para-dioxin had elevated concentrations of copper in liver and kidney because of impaired biliary excretion of copper (Elsenhans et al. 1991). Morphine increases copper concentrations in the central nervous system of rats, and dithiocarbam-ates inhibit biliary excretion (Aaseth and Norseth 1986). In human patients, urinary excretion of copper is increased after treatment with D-penicillamine, calcium disodium EDTA, or calcium trisodium diethylenetriamine penta acetic acid (Flora 1991). 

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