Chronic dioxin

Table 8 Calculated annual input of TEQ in the Dutch coastal zone from the rivers, atmospheric emission and disposal of dredged material (period 1999-2005). For the TEQ-lev-els in sediment, the ecotoxicological risk is estimated as % Potentially Affected Fraction of species (PAF) and calculated based on the SSD for chronic dioxin-toxicity (Figure 6). 

The major, clinically apparent symptom of chronic dioxin intoxication is a phthisis-like loss in body constitution, the causes of which are inflammation of the gastroin-... 

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. 

Although the effects of chronic exposure of humans to low levels of POPs are difficult to predict, some biological effects have been described. For example, exposure of children to PCBs and PCDD/Fs may be linked to an elevated risk for infectious diseases. Exposure of pregnant women to PCDD/Fs may cause lower fertility in their male offspring. The adverse effects to human health of acute and chronic exposure of high concentrations of POPs, especially among industrial workers exposed to daily intakes of chemicals, are more evident. Elevated concentrations of DDE and TCDD have been associated with the development of cancers such as breast cancer, leukaemia and thyroid cancer. Dioxin exposure may also be associated with immunotoxicity, reproductive diseases and neurotoxicity. Extreme exposure to chlorinated compounds has resulted in death [101]. 

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). 

Viluksela M et al Subchronic/chronic toxicity of a mixture of four chlorinated dibenzo- -dioxins in rats. I. Design, general observations, hematology, and liver concentrations. Toxicol Appl Pharmacol 151 57, 1998... 

Chronic exposure is associated with an increased prevalence of conjunctivitis, chronic sinusitis, bronchitis, polyneuritis, and dermatitis. Chloracne has been reported and is probably the result of dioxin contaminants in commercial-grade pentachlorophenol. On the skin, solutions of pentachlorophenol as dilute as 1 % may cause irritation if contact is repeated or prolonged. 

Table 7 Example application of process in Box B to evaluate the risk of dioxins in Dutch sediments. No observed effect (NOEC) concentrations for chronic toxicity of dioxins in vertebrates (immune, reproductive and developmental toxicity) expressed as internal concentration (ng TEQ/g Iw). The sediment to fish bioconcentration factor is set at 4 (ng TEQ/g Organic Carbon to ng/g lipid weight in fish) based on Traas et al. (2001). Based on a species-specific biomagnification factor (BMP) from fish to animal (ng TEQ/g Iw) the internal NOEC is extrapolated to a NOEC in sediment. These data are used to construct the SSDs in Figures 5 and 6.

Cantoni, L., M. Salmons, and M. Rizzardini. 1981. Porphyrogenic effect of chronic treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin in female rats. Dose-effect relationship following urinary excretion of porphyrins. Toxicol. Appl. Pharmacol. 57 156-163. 

R. J. Kociba et al., Results of a 2-Year Chronic Toxicity and Oncogenicity Study of 2,3,7,8- Tetrachlorodibenzo-p-dioxin (TCDD) in Rats, Toxicol. Appl. Pharmacol. 46 (1978) 279-505. 

Calvert GM, Sweeney MH, Morris JA, et al. 1991. Evaluation of chronic bronchitis, chronic obstructive pulmonary disease, and ventilatory function among workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Am Rev Resp Dis 144 1302-1306. 

Goldstein JA, Linko P, Bergman H. 1982. Induction of porphyria in the rat by chronic versus acute exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Biochem Pharmacol 31 1607-1613. 

Kociba RJ, Keyes DG, Beyer JE, et al. 1978a. Results of a two-year chronic toxicity and oncogenicity study of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats. Toxicol Appl Pharmacol 46 279-303. 

Pazderova-Vejlupkova J, Nemcova M, Pickova J, et al. 1981. The development and prognosis of chronic intoxication by tetrachlorodibenzo-p-dioxin in men. Arch Environ Health 36 5-11. 

Peper M, Klett M, Frcntzcl-Bcymc R, et al. 1993. Neuropsychological effects of chronic exposure to environmental dioxins and fiirans. Environ Res 60 124-135. 

Rozman K, Roth WL, Greim H, et al. 1993. Relative potency of chlorinated dibenzo-p-dioxins (CDDs) in acute, subchronic and chronic (carcinogenicity) toxicity studies Implications for risk assessment of chemical mixtures. Toxicology 77(l-2) 39-50. 

Schantz SL, Barsotti DA, Allen JR. 1979. Toxicological effects produced in nonhuman primates chronically exposed to fifty parts-per-trillion 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Toxicol Appl Pharmacol 48 A180. 

Sewall CH, Flager N, Van den Heuvel JP, et al. 1995. Alterations in thyroid function in female Sprague-Dawley rats following chronic treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicol Appl Pharmacol 132 237-244. 

Tritscher AM, Goldstein JA, Portier CJ, et al. 1992. Dose-response relationships for chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin in a rat tumor promotion model Quantification and immuno-localization of CYP1A1 and CYP1A2 in the liver. Cancer Res 52 3436-3442. 

Van den Berg M, Van Greevenbroek M, Olie K, et al. 1986c. Bioavailability of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans on fly ash after semi-chronic oral ingestion by the rat. Chemosphere 15 509-518. 

Action level for dioxin and dioxin-like compounds in soil. Action levels are concentrations of chemicals at which consideration of action to interdict exposure occurs 1 ppb TCDD in residential soil was identified by Kimbrough et al. (1984) as a "level of concern" and recommended as "a reasonable level to begin consideration of action to limit exposure." The conclusions of Kimbrough et al. (1984) were derived in part from an evaluation of the carcinogenic potential of TCDD, based on a 2-year oral chronic toxicity and oncogenicity study in rats (Kociba et al. 1978). With the advancement of knowledge about dioxin-like chemicals and their assumed common mechanism of toxicity, the TEQs were introduced into the risk assessment process. Since then, 1 ppb of total dioxins (expressed as TEQs) in soil has been used as an action level by ATSDR. 

Coincident with the development of sampling procedures were the constant iterative improvements in extraction, separation, identification and quantitation of organic compounds. Special emphasis was placed on selected compound classes such as the polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), chlorinated benzenes, and chlorinated dibenzo-p-dioxins (dioxins). The best available procedures were used to determine these components because they have known acute or chronic effects and previous studies suggested that they might be present in effluents from the combustion of coal alone and combination coal/RDF. 

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