Dioxins in freshwater and marine water

​​Toxicant default guideline values for protecting aquatic ecosystems

October 2000

Description of chemical

Polychlorinated dibenzo-p-dioxins (PCDDs) are formed from various synthetic or pyrolytic reactions. PCDDs are known to exist in a variety of chemicals, including pesticides, the wood preservative pentachlorophenol, and chlorinated phenols (CCREM 1987). They can be formed by combustion processes, including the burning of fossil fuels, wood and garbage. PCDDs are a group of chemicals composed of 75 chemically related compounds.

In general, little information is available on the fate of PCDDs in the aquatic environment. Most of the available data refer to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). TCDD is a symmetrical, almost planar, molecule with formula C₁₂H₄Cl₄O₂ and molecular weight of 321.9. It is relatively insoluble in water (0.2 µg/L) and its Log K_ow is around 6.2 (USEPA 1984a). It is the most toxic dioxin congener.

Concentrations of dioxins and related furans have been found at cleaner sites at between 1 and 5 pg/L (10^-12 g/L) and at up to 100 pg/L at more contaminated sites (Sijm & Opperhuizen 1996). Dioxins are more readily associated with sediment and the average concentration in Lake Ontario sediments prior to 1990 was 68 ng/kg (Sijm & Opperhuizen 1996). TCDD is usually less than 15% of total dioxins. The surface sediments in Homebush Bay, near historical industrial contamination, contained around 3 µg/kg of 2,3,7,8-TCDD wet weight (Thompson et al. 1992), resulting in imposition of a fish ban in the bay.

TCDD can cause delayed mortality in juvenile fish, decreased food consumption and body weight and histological lesions (Sijm & Opperhuizen 1996). Early life stage mortality from TCDD has been found at residue levels between 0.065 and 0.4 µg/kg for eggs of two species of freshwater trout (Sijm & Opperhuizen 1996). The lowest LOEC for inhibition of growth from eggs of Oncorhynchus mykiss is less than 0.1 ng/L, corresponding to a body burden of 0.0003 µg/kg of egg. Growth in juvenile fish may be affected at 1 ng/L (Sijm & Opperhuizen 1996). Food and sediment are likely to be more important sources of dioxin than water.

Jarvinen and Ankley (1999) report data on tissue residues and effects for 2,3,7,8-TCDD for 12 freshwater species and one marine species. It is not possible to summarise the data here but readers are referred to that publication for more information.

Elonen et al. (1998) reported NOEC figures for seven freshwater fish species based on TCDD concentration in eggs that caused significant decreases in survival or growth of juveniles. No observed effect concentrations (NOECs) were between 175 and 1190 µg/kg and lowest observed effect concentrations (LOECs) were between 270 and 2000 µg/kg. Lake herring, Coregonus artedii, were most sensitive but even these were around than eight times less sensitive than lake trout (40 µg/kg Salvelinus namaycush) (Spitzbergen et al. 1991).

Aquatic toxicology

TCDD exhibits a delayed biological response in many species, and is highly lethal at low concentrations to aquatic organisms (USEPA 1984a). The available information indicates that acute effects for some freshwater animal species exposed to TCDD occur at concentrations greater than 1.0 µg/L. Chronic concentrations are less than 0.01 µg/L, with a chronic concentration for rainbow trout of less than 0.001 µg/L (USEPA 1984a). Predicted bioaccumulation factors for TCDD ranged from 3000 to 900,000 but measured bioaccumulation factors ranged from 390 to 13,000 (USEPA 1984a). Elevated dioxin levels have been found in fish, shellfish and sediments in some localised urban and industrial areas in Australia (Thompson et al. 1992) and overseas (USEPA 1984a, CCREM 1987, Palmer et al. 1988).

The toxicity data, reviewed by USEPA (1984a), were not in a suitable form to derive guideline values for aquatic life. USEPA (1984a) did not derive a guideline figure but considered that water concentrations > 0.00001 µg/L TCDD could lead to excessive levels of dioxin in fish and shellfish for human consumption, assuming a bioconcentration factor (BF) >5000.

References

ANZECC & ARMCANZ 2000. Australian and New Zealand Guidelines for Fresh and Marine Water Quality, Australian and New Zealand Environment and Conservation Council and Agriculture and Resource Management Council of Australia and New Zealand, Canberra.

CCREM 1987. Canadian water quality guidelines. Canadian Council of Resource and Environment Ministers, Ontario.

Elonen GE, Spehar RL, Holcombe GW, Johnson RD, Fernandez JD, Erickson RJ, Tietge JE & Cook PM 1998. Comparative toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin to seven freshwater fish species during early life-stage development. Environmental Toxicology and Chemistry 17, 472–483.

Jarvinen A W & Ankley G T 1999. Linkage of effects to tissue residues: Development of a comprehensive database for aquatic organisms exposed to inorganic and organic chemicals. SETAC Technical Publication Series, SETAC Press, Pensacola FL.

Palmer FH, Sapudar RA, Heath JA, Richard NJ & Bowes GW 1988. Chlorinated dibenzo-p-dioxin and dibenzofuran contamination in California from chlorophenol wood preservative use. Report No. 88-5WQ, Division of Water Quality, California State Water Resources Control Board.

Sijm DTHM & Opperhuizen A 1996. Dioxins: An environmental risk to fish? Chapter 8 in Environmental contaminants in wildlife: Interpreting tissue concentrations, eds WN Beyer, GH Heinz & AW Redmon-Norwood. SETAC Special Publication Series. CRC Press, Lewis Publishers, B

oca Raton.

Spitzbergen JM, Walker MK, Olson JR & Peterson RE 1991. Pathological alterations in early life stages of lake trout, Salvelinus namaycush, exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin as fertilised eggs. Aquatic Toxicology 9, 41–72.

Thompson GB, Chapman JC & Richardson BJ 1992. Disposal of hazardous wastes in Australia: Implications for marine pollution. Marine Pollution Bulletin 25, 155-162.

USEPA 1984a. Ambient water quality criteria for 2,3,7,8-tetrachlorodibenzo-p-dioxin, EPA, Washington DC.