Hdb Env Chem Vol. 5, Part N (2006): 71–150 DOI 10.1007/698_5_040 © Springer-Verlag Berlin Heidelberg 2005 Published online: 2 December 2005 Polychlorinated Dibenzo-p-dioxins and Dibenzofurans in the Great Lakes Ross J. Norstrom Centre for Analytical and Environmental Chemistry, Department of Chemistry, Carleton University, Ottawa, ON K1S 5B6, Canada [email protected] 1Introduction................................... 73 2 Occurrence and Geographical Distribution .................. 75 2.1 Air........................................ 75 2.1.1ConcentrationsinAir.............................. 75 2.1.2AirDepositionModels............................. 78 2.2 Water....................................... 83 2.2.1SaginawRiver.................................. 83 2.2.2DetroitRiver................................... 84 2.2.3NiagaraRiver.................................. 85 2.3 LakeSediments................................. 86 2.4 RiverandBaySediments............................ 91 2.4.1 Fox River/GreenBaySediments........................ 91 2.4.2LakeSuperiorBaySediments.......................... 91 2.4.3 Saginaw River/SaginawBaySediments.................... 92 2.4.4DetroitRiverSediments............................. 94 2.4.5NiagaraRiverSediments............................ 95 2.5 Fish........................................ 97 2.5.1 Surveys of 2378-TeCDD and 2378-TeCDF . ................ 98 2.5.2ComprehensiveSurveys............................. 103 2.6 SeabirdsandSnappingTurtleEggs...................... 107 2.6.1HerringGullEggs................................ 107 2.6.2Double-CrestedCormorantEggs........................ 111 2.6.3CaspianandForster’sTernEggs........................ 115 2.6.4SnappingTurtleEggs.............................. 118 2.7 HumanSerum.................................. 120 3 Temporal Trends ................................ 122 3.1 SedimentCores................................. 122 3.2 Fish........................................ 124 3.3 HerringGullEggs................................ 125 4Sources...................................... 128 4.1 Combustion................................... 128 4.2 EvidencefromHerringGullEggsandLakeTrout.............. 129 4.3 SaginawRiver.................................. 130 4.4 NiagaraRiver.................................. 131 72 R.J. Norstrom 5Effects...................................... 134 5.1 LakeTrout.................................... 135 5.2 HerringGulls.................................. 139 5.3 OtherSeabirdsandSnappingTurtles..................... 140 5.4 Humans..................................... 142 6Conclusions................................... 144 References ....................................... 146 Abstract The history of “dioxin”, PCDD/F, contamination in the Great Lakes is reviewed. Occurrence, geographical distribution, and temporal trends in air, water, sediments, fish, seabirds, snapping turtles, and humans are presented, and eco/human toxicological im- plications reviewed. Patterns and concentrations in sediment indicate that atmospheric input dominated in Lake Superior, lower Lake Michigan, and Lake Erie. Inputs from the Saginaw River to Lake Huron and Fox River to upper Lake Michigan added some PCDD/F loading to these lakes above atmospheric deposition. Lake Ontario was heavily impacted by input of PCDD/Fs, particularly 2378-TeCDD, from the Niagara River. Sediment core and biomonitoring data revealed that PCDD/F contamination peaked in most lakes in the late 1960s to early 1970s, followed by rapid, order of magnitude declines in the mid- to late 1970s. The downward trend stalled in some lakes in the 1980s, but seems to have continued after the late 1990s, probably in response to various remediation efforts and reductions in PCDD/F emissions to the atmosphere. During the height of contamination, effects attributed in whole or in part to PCDD/F contamination included reproductive failure in lake trout and herring gulls in Lake Ontario. AHR-mediated sublethal effects may still be occurring in seabirds and fish, but much of this is thought to be due to dioxin-like PCBs rather than PCDD/Fs. Keywords Dioxins · Effects · Furans · Levels · Sources · Trends Abbreviations AHR Aryl hydrocarbon receptor AHR-congeners PCDD/Fs with chlorine at the 2,3,7,8-positions, PCBs with chlorine at the 3,34,4-positions, not more than one chlorine at 2,2,6,6-positions BMF Biomagnification factor BSAF Biota-sediment bioaccumulation factor Congener Any member of a compound class, e.g., PCDDs, PCDFs or PCBs EROD Ethoxyresorufin-o-deethylase Homolog Group of isomers with the same carbon skeleton and number of chlorines, e.g., TeCDDs H4IIE Rat hepatoma cell line PCBs Polychlorinated biphenyls PCDD Polychlorinated dibenzo-p-dioxin PCDF Polychlorinated dibenzofuran PCDD/F Polychlorinated dibenzo-p-dioxin and -furan TeCDD (F) Tet rachloro dibenzo-p-dioxin (-furan) PnCDD (F) Pentachlorodibenzo-p-dioxin (-furan) HxCDD (F) Hexachlorodibenzo-p-dioxin (-furan) HpCDD (F) Heptachlorodibenzo-p-dioxin (-furan) Polychlorinated Dibenzo-p-dioxinsandDibenzofuransintheGreatLakes 73 OCDD (F) Octachlorodibenzo-p-dioxin (-furan) 2378-TeCDD (and similar) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (commas are left out of all formulae for brevity) SPMD Semi-permeable membrane device - Total concentration of congeners in the group 2,4,5-T 2,4,5-Trichlorophenoxyacetic acid TEQ 2,3,7,8-TeCDD toxic equivalent concentration TEF 2,3,7,8-TeCDD toxic equivalent factor (relative toxicity/potency to 2,3,7,8-TeCDD) WHO World Health Organization 1 Introduction The history of “dioxins”, polychlorinated dibenzo-p-dioxins (PCDDs), and polychlorinated dibenzofurans (PCDFs) in the Great Lakes really begins in 1978 when 2378-TeCDD was reported to be in fish from the Tittabawassee River in Michigan downstream from a large DOW chemical complex in Mid- land [1], and in Lake Ontario fish. The Michigan findings were subsequently confirmed by Harless and Lewis [2, 3]. PCDD/Fs had been widely recognized as an important class of environmental contaminants when this news broke. Early concern about PCDD/Fs had been primarily about industrial accidents, chemical manufacturing waste, the fungicide pentachlorophenol and the her- bicide, 2,4,5-T. This herbicide, and its production wastes, were known to con- tain 2378-TeCDD as a byproduct from condensation of 2,4,5-trichlorophenol during its production [4]. TeCDD was a subject of considerable interest in the USA because of exposure of servicemen and women to Agent Orange, a de- foliant used in the Viet Nam war, which contained 2,4,5-T as one of the main ingredients. It was also known that a wide range of PCDD/Fs were emitted by municipal waste incinerators and other combustion processes when a source of chlorine was present [5], and that commercial PCB mixtures contained avarietyofPCDFs[6].Itwasnotuntilmuchlaterthatbleachedkraftpulp mills were identified as a specific source of 2378-TeCDD and 2378-TeCDF [7]. The finding of 2378-TeCDD in Great Lakes fish caused the scientific commu- nity to take notice. The Love Canal waste dumpsite issue was gaining wide coverage in the press about the same time [8], so stories about “the most toxic chemical known to man” created immediate consternation in the Great Lakes community, which put pressure on government agencies in both the USA and Canada to address the issue. The result was a flurry of activities in the mid- to late-1980s to survey concentrations of 2378-TeCDD in a variety of fish, birds, and sediments from around the Great Lakes, and to scope the implications to health of fish, wildlife, and humans. Among these was a preliminary investigation in 1980 of 2378-TeCDD in herring gull eggs, which found concentrations in eggs from Saginaw Bay, 74 R.J. Norstrom Lake Huron and Lake Ontario to be four to six times higher than in Lakes Michigan, Huron (main body), and Erie [9]. Although the data were semi- quantitative, they provided early evidence that Saginaw Bay and Lake Ontario were the areas of most concern. Herring gull eggs from Lake Ontario, 1981, were reanalyzed using improved methods and found to have 132 ng kg–1 of 2378-TeCDD [10]. This study also provided the first evidence of the presence of 12378-PnCDD and HxCDDs in the Great Lakes. Immediate suspicion fell on effluent and waste disposal from the large number of chlorine-based chem- ical industries in the Niagara Falls, NY area, especially Love Canal and other dumpsites along the Niagara River. Herring gull eggs collected in 1971 and archived in the Canadian Wildlife Service Specimen Bank were also analyzed and found to be contaminated with 1225 ng kg–1 of 2378-TeCDD [11]. This concentration was well above the –1 LD50 of 2378-TeCDD in chicken embryos, 250 ng kg [12].Atthetime,there were no data on the toxicity of 2378-TeCDD in wild birds. When these early 1970s Lake Ontario herring gull egg concentrations were lined up against the complete failure of herring gull eggs to hatch in the same period, due pri- marily to early death of embryos [13, 14], it was assumed that the chemical culprit had been apprehended. The story turned out to be more complicated than that, as usual. We now know that the herring gull is about 50 times less sensitive than the chicken to 2378-TeCDD toxicity [15]. However, these early surveys provided considerable ammunition to begin comprehensive studies on PCDD/F contamination in the Great Lakes. In the 25 years since dioxin concerns began in the Great Lakes, an enor- mous amount of information has been generated on sources, deposition, concentrations in sediments and biota, and temporal