Mink Contaminant Exposure Data

I.

Organochlorine Contaminants

1.

During the 1970-71 fur season, 35 mink were collected from the central Iowa counties of Story, Boone, and Hamilton (Franson et al., 1974). Adipose tissue was analyzed for all samples, and brain and liver analyzed for five of these samples. Residues of DDE were <5.40 µg/g wet weight in adipose tissue, <0.08 µg/g in the brain, and <0.11 µg/g in the liver. DDD was <1.54 µg/g adipose, <0.05 µg/g brain, and <0.03 µg/g liver. DDT was <1.85 µg/g adipose, not detected in the brain, and detected in two mink livers at 0.01 µg/g. o,p’-DDT was <1.22 µg/g adipose, not detected in the brain, and detected in one mink liver at 0.01 µg/g. Dieldrin was <4.90 µg/g adipose, <0.04 µg/g brain, and <0.07 µg/g liver. Heptachlor epoxide was detected in 20 mink in the adipose tissue at levels <0.20 µg/g. Lindane was detected in the brain at <0.04 µg/g and not detected in the liver. ß-BHC was detected in 7 mink in adipose tissue at <0.11 µg/g, detected in the brain at <0.08 µg/g, and not detected in the liver. Organochlorine residues did not differ among various age classes.

2.

Mink collected in 1973-74 from the county of Simcoe in southern Ontario were analyzed for organochlorine residues (Frank et al., 1979). Average concentration of organochlorines detected in the muscle were 0.054 µg/g wet weight DDE, 0.0036 µg/g TDE, 0.0053 µg/g dieldrin, and 0.27 µg/g PCB. Concentrations in fat were 4.2 µg/g DDE+TDE, 0.76 µg/g dieldrin and 32 µg/g PCB.

3.

Mink from areas of Alabama and Georgia treated with mirex between 1973 and 1976 were collected six months, one year, and two years after cessation of treatment and quantified for organochlorine contaminants (Hill and Dent, 1985.) Mean residues in muscle samples showed a gradual increase from 0.14 µg/g wet weight, to 0.28 µg/g, to 0.53 µg/g, respectively. Liver levels were 0.10 µg/g, 0.41 µg/g, and 0.05 µg/g, respectively.

4.

During 1978-79, brain, liver, and muscle tissues were analyzed from 32 mink collected in rural western Maryland (O’Shea et al., 1981). Livers of 4 of 10 females from Frederick and Carroll Counties contained detectable levels of PCBs, with an arithmetic mean of 1.17 µg/g wet weight. Three of twelve males from these counties also contained detectable PCB levels in the liver at 1.1, 1.4, and 2.0 µg/g. The highest concentration detected was 2.4 µg/g PCBs from a female in Harford County. PCBs were not detected in other tissues, with the exception of two Frederick County individuals. One male contained 0.44 µg/g and 0.60 µg/g in brain and muscle, respectively, and 0.99 µg/g was detected in the brain of a female. Other contaminants were detected at low concentrations including oxychlordane (<2.2 µg/g), DDE (<0.50 µg/g), dieldrin (<0.07 µg/g), heptachlor epoxide (<0.20 µg/g), DDT (0.17 µg/g) and trans-nonachlor (0.17 µg/g).

5.

From 1978 to 1979, 59 mink carcasses were collected from five locations in Oregon: Lower Columbia River, northwest coastal rivers region, the Blue and Wallowa Mountains, Upper Klamath Lake, and Klamath River (Henny et al., 1981). DDE, oxychlordane, and PCBs were analyzed in the liver. With only 2 exceptions, DDE from all location were <1 µg/g wet weight. One male collected from the northwest coastal rivers and one from the Blue and Wallowa Mountains each contained DDE residues of 1.2 µg/g. Oxychlordane was detected at <1 µg/g in all mink examined. PCBs were detected at a high of 3.5 µg/g in a male from the NW Coastal Rivers. In addition to the liver, the leg muscle was also analyzed for DDE and PCBs. DDE in the leg muscle was detected at <1 µg/g at all locations sampled. PCBs were detected at highs of 1.6 and 1.5 µg/g in males from the Lower Columbia River and the northwest coastal rivers, respectively.

6.

In 1978 to 1979, 55 wild mink from five regions in lake Erie were analyzed for PCB and organochlorine residues (Proulx et al., 1987). PCB geometric means for Mersea, Dunn-Rainham, Walsingham, Wainfleet, and Tuscarora Townships were 1.32 µg/g wet weight, 1.71 µg/g, 0.51 µg/g, 0.29 µg/g, and 0.08 µg/g, respectively. DDE concentrations were 0.22 µg/g, 0.14 µg/g, 0.26 µg/g, 0.05 µg/g, and 0.07 µg/g, respectively. HCB values were <0.01 µg/g for all townships. Oxychlordane, ß-HCH, DDD, and dieldrin levels were detected at <0.03 µg/g for all townships. DDT was detected at a level of 0.02 µg/g in one mink in each of Mersea and Walsingham townships. Mirex was not detected in this study. PCB lipid weights were 29.17 µg/g, 26.12 µg/g, 10.74 µg/g, 6.08 µg/g, and 1.81 µg/g, respectively. DDE lipid weights were 4.83 µg/g, 2.08 µg/g, 5.48 µg/g, 1.16 µg/g, and 1.62 µg/g, respectively.

7.

Mink trapped from eight locations in New York state between 1982 and 1984 were analyzed for organochlorine contaminants in the fat and liver (Foley et al., 1988). Geometric mean PCB (Aroclor 1254/1260) concentrations in the eight locations ranged from 0.8-4.4 µg/g wet weight in the fat and 0.1-0.6 µg/g in liver. Mean DDE concentrations ranged from 0.12-0.74 µg/g in fat and 0.01-0.04 µg/g in liver. Lowest values of both compounds occurred on the West Appalachian Platueau and highest were on the North Hudson River for PCB and the West Adirondack Mountains for DDE.

8.

Adipose and liver tissues were analyzed from 109 mink collected between 1983 and 1985 from six samples sites in New York State: the eastern lake plains, west Adirondack Mountains, northeast Adirondack Mountains, the Hudson River Valley (HR), the Appalachian Plateau, and from within 8 km of Lake Ontario (LO) (Foley et al., 1991). Geometric means of liver residues were 0.3 µg/g wet weight PCB, 0.03 µg/g DDE, 0.002 µg/g HCB, and 0.032 µg/g dieldrin. PCBs ranged from 0.1-37.6 µg/g, and were significantly higher in LO and HR compared to other sites. Also detected at low levels were mirex and photomirex (LO only), and oxychlordane.

9.

Mink found dead in Wisconsin from 1986-1987 were analyzed for PCB residues in muscle (Meyer and Hurley, 1991). Two groups of mink collected from the Oconto River had mean PCB levels of 1.9 and 2.3 µg/g wet weight. Two mink found near the Sheboygan River had concentrations of 5.4 and 1.9 µg/g, and one found near Buffalo had a level of 0.3 µg/g. A total of five carcasses from sites that did not have PCB-contaminated fish (backwaters of the Mississippi River and Langlade, Jackson, Columbia, and Green Lake Counties) had PCB levels at or below the detection level (0.20 µg/g). Dieldrin and DDE were detected in the Oconto County carcasses only (<0.5 µg/g).

10.

Mink carcasses were collected between 1987-89 from 24 watersheds in Connecticut and 9 in Massachusetts (Major and Carr, 1991). Mean chlordane concentrations for watersheds ranged from 0.19-1.50 µg/g wet weight in Connecticut and 0.05-0.56 µg/g in Massachusetts. Mean DDT concentrations ranged from 0.10-0.49 µg/g in Connecticut and 0.03-0.17 µg/g in Massachusetts. Mean PCB concentrations ranged from 0.94-10.0 µg/g in Connecticut and 0.44-4.1 µg/g in Massachusetts. Mean dieldrin concentrations ranged from 0.040-0.13 µg/g in Connecticut and 0.005-0.115 µg/g in Massachusetts. Concentrations of endrin and mirex were <0.05 µg/g for both states. Values of chlordane, DDT, and PCB were significantly higher in Connecticut than Massachusetts.

11.

A total of 79 mink were collected from trappers in1988 and 1989 from fifteen townships in central or southern Ontario (Haffner et al., 1988).  Maximum mean concentrations of PCB congeners were 1.2 ng/g wet weight PCB 52, 7.2 ng/g PCB 101, 1.9 ng/g PCB118, 73 ng/g PCB 153, 4.7 ng/g PCB 105, 131 ng/g PCB 138, 144 ng/g PCB 180, 13 ng/g PCB 203, 1.1 ng/g PCB 77, 1.6 ng/g PCB 126, and 0.29 ng/g PCB 169.  TEQs ranged from 3.4-171 pg/g, and were comprised of over 90% PCBs 126 and 118.  Mean concentrations of α-HCH, HCB, oxychlordane, DDE, DDD, photo-mirex, mirex, heptachlor epoxide, and dieldrin were <0.2 ug/g.

12.

A decline in coastal mink populations in Georgia, North Carolina, and South Carolina prompted the 1989 to 1991 collection of 141 mink from the three states to examine levels of 17 substances (Osowski et al., 1995). Coastal individuals were compared with samples from the piedmont, mountain, and foothill areas. Two substances had significantly higher concentrations in coastal regions: PCB, detected in 97% of mink with a median concentration of 0.211 µg/g wet weight, and dieldrin, found in 64% with a median of 0.0865 µg/g. Also detected in coastal mink in all three states was DDE at 0.105 µg/g. Aldrin was found at 0.272 µg/g in South Carolina, trace levels in Georgia, and was not detected in North Carolina. DDD levels were 0.15 µg/g in Georgia, trace amounts in North Carolina and not detectable in South Carolina. DDT was found in North Carolina mink only at levels of 0.018 µg/g and chlordane was found at trace levels in Georgia alone. Not detected in any of the coastal populations were endrin and -BHC.

13.

A total of 213 wild mink were collected in Minnesota during the 1989 and 1990 trapping seasons (Ensor et al., 1993). Elevated organochlorine levels detected were at 0.029 µg/g wet weight DDT, 0.398 µg/g DDE, 0.035 µg/g dieldrin, 0.4438 µg/g total DDT, 0.569 µg/g Aroclor 1254, 1.238 µg/g Aroclor 1260, and 1.807 µg/g total PCBs.

14.

During the winters of 1990-1992, trappers submitted samples collected within 10 meters of the river bank, including 11 mink from the upper reaches of the Fraser River and 19 mink from along the Columbia River (Elliott et al., 1999).  Four mink were also collected from a reference site, Malheur National Wildlife Refuge.  Hepatic concentrations of organochlorines, pooled from each of 13 collection sites, were generally low (<0.10 ug/g wet weight) at all sites, with the exception of DDE (means ranged from 0.0013 - 2.400 ug/g), and PCBs (ND-0.380 ug/g).  Concentrations of PCDDs and PCDFs were generally low (<0.1 pg/g), with the exception of OCDD, for which means ranged from ND-0.842 pg/g.  Concentrations of PCB congeners ranged from ND-0.112 pg/g 37, ND-0.0051 pg/g 81, 0.0031 - 0.014 77, 0.0029-0.220 pg/g 126, ND-0.018 pg/g 169, ND-6.600 pg/g 105, ND-31.400 pg/g 118, and ND-0.0087 pg/g 189.  TEQs were generally higher on the upper Columbia River compared to other sites, with values reaching 0.031 pg/g.

15.

A total of 1025 mink carcasses were collected from seven locations in the western Northwest Territories in Canada during winters 1991-92 to 1994-95 (Poole et al., 1998). Contaminant concentrations (ng/g wet weight) were determined in liver for each location and means ranged as follows: 1.19-9.52 total DDT, 0.03-0.20 total HCH, 0.05-0.67 HCB, 0.87-3.48 total chlordane, 0.08-0.74 dieldrin, 0.08-0.39 total mirex, and 7.02-73.07 total PCB. DDE was detected in 96.7% of livers and comprised 99% of residues in total DDT. The majority of PCB congeners detected contained more than five chlorine atoms. Concentrations of total HCH and HCB were significantly higher in females than males. TEQs of liver tissue were generally low, reaching a maximum of 0.28 pg/g wet weight at one location.

16.

A total of 26 skinned mink carcasses were collected from commercial trappers during the winters of 1994-1995 and 1995-1996 from four locations in British Columbia: Fraser River near Prince George and Chilliwack, Fraser Valley near the terminus of the Fraser River, Kootenay River near Creston and Cranbrook, and Columbia River between Revelstoke and Trail (Harding et al., 1999).  Hepatic concentrations of PCBs, dieldrin, and DDT-related compounds (primarily DDE) were 0.08 µg/g wet weight in mink from the Lower Fraser River (N=8) and the Upper Fraser River (N=12).  At Kootenay River (N=4) and Lower Fraser Valley (N=2), respectively, hepatic concentrations were 16 and 18 ng/g total PCBs, 11 and 8.8 pg/g PCB-77, and 24 and 62 pg/g PCB-126.  Concentrations of PCB-169, PCDDs, and PCDFs were below the limit of detection at both sites.  These concentrations were similar to those from an earlier collection of mink (1990-1991) from the Columbia River and Fraser Valley.  There was no difference in contaminant concentrations between males and females at any site.  A significant correlation existed between age and total pesticide contamination. 

17.

From 1993-1994, captive mink at Michigan State University Experimental Fur Farm were housed in individual outdoor cages and fed fish from Poplar Creek in the Oak Ridge Reservation (ORR), Tennessee, as well as from two reference sites, Clinch River above the ORR, and the Atlantic Ocean (Halbrook et al. 1999). Five groups of 8 female and 2 male mink were fed diets with the following combination of fish mixed with mink chow: 75% ocean fish (diet A),  75% Clinch River fish (diet B),  25% Poplar Creek fish and 50% ocean fish (diet C), 50% Poplar Creek fish and 25% ocean fish (diet D), and 75% Poplar Creek fish (diet E).  Mean concentrations (ng/g wet weight) of arochlor 1260 in adult female mink fat tissues were 3,169 for diet A, 61,250 for diet B, diet C was not quantified, 105,860 for diet D, and 128,630 for diet E.  Mean concentrations (ng/g wet weight) of arochlor 1260 in adult female mink liver tissue were <5 on all diets, except for diet E, where it was 7,250.  Mean concentrations (ng/g wet weight) of arochlor 1260 in 6-week-old kit liver tissue were 99 for diet A, 785 for diet B, NQ for diets C and D, nad 5,396 for diet E.  Mean concentrations (ng/g wet weight) of arochlor 1260 in 6-week-old kit whole body (minus liver) were: 82 for diet A, 1,791 for diet B, NQ for diets C and D, and 6,260 for diet E.  Female fat and kit liver and whole body arochlor 1260 concentrations were significantly lower on diet B than E (p values ranged from 0.003 to <0.001).

During the winters of 1998/1999-2002/2003, 83 carcasses were collected from mink trapped from near the Canadian shores of Lakes St. Clair and Erie (Martin et al. 2006).  Mink from the western Lake Erie sites had higher concentrations of PCBs than those from inland sites or Lake St. Clair.  Contaminants in were detected at the following levels (ng/g wet weight): 2.5-23.6 total PCBs, 0.40-3.69 DDE, 0.27-0.66 DDT, nd-0.069 DDD, 0.066-2.629 oxychlordane,  nd-1.036 dieldrin, nd-0.061 heptachlor epoxide, nd-0.264 mirex, nd-0.092 octachlorostyrene. 

II.

Cholinesterase-Inhibiting Pesticides

No direct exposure data available

III.

Trace Elements, Metals, and Metalloids

1.

Mink collected along the Wisconsin River watershed in 1972-1975 were analyzed for Hg in the fur (7.71 µg/g wet weight), liver (2.08 µg/g), kidney (2.33 µg/g), muscle (1.26 µg/g), and brain (0.46 µg/g) (Sheffy and St. Amant, 1982). Mercury concentrations in the mink were generally greater than in other furbearers that were collected (beaver, muskrat, red fox, and raccoon) with the exception of the river otter.

2.

Hair samples from mink collected from the piedmont and lower coastal plain of Georgia in 1973 contained a mean Hg concentration of 10.7 µg/g dry weight (Cumbie, 1975).

3.

Mink collected in 1973-1974 from the county of Simcoe in southern Ontario contained a mean of 0.71 µg/g wet weight Hg residue in the muscle (Frank et al., 1979).

4.

A wild female mink found in 1975 in the proximity of the South Saskatchewan River near the city of Saskatoon was diagnosed with Hg poisoning (Wobeser and Swift, 1976). Mercury concentrations detected were 58.2 µg/g in the liver, 31.9 µg/g in the kidney, 15.2 µg/g in the muscle, 13.4 µg/g in the brain, and 34.9 µg/g in the fur.

5.

Carcasses of 173 mink were collected from 1979 to 1981 from five Manitoba drainage basins: Duck Mountain (control), Wekusko, Whiteshell, Burntwood, and Winnepeg River (Kucera, 1982). Mean Hg levels for males and females of each area found in the liver were, respectively, 1.05 and 3.44 µg/g dry weight, 2.35 and 4.68 µg/g, 3.38 and 4.87 µg/g, 4.13 and 7.31 µg/g, and 7.45 and 12.31 µg/g. Mean Hg kidney levels were 1.02 and 2.32 µg/g, 2.33 and 2.31 µg/g, 3.18 and 3.44 µg/g, 2.40 and 7.02 µg/g, and 6.08 and 8.05 µg/g. Mean Hg brain concentrations were 0.36 and 0.93 µg/g, 0.75 and 1.78 µg/g, 1.05 and 1.51 µg/g, 1.23 and 5.28 µg/g, and 2.66 and 3.36 µg/g. When values for males and females were combined, samples from Burntwood and Winnipeg were both significantly higher than the control location.

6.

Mink carcasses collected from Virginia trappers during the 1981-82 and 1982-83 seasons were analyzed for metals (Ogle et al., 1985). Concentrations of Pb ranged from 0.00-21.15 µg/g dry weight in the bone, 0.00-5.22 µg/g in the kidney, and 0.00-12.74 µg/g in the liver. Zinc values ranged from 54.01-215.74 µg/g in the bone, 48.24-173.40 µg/g in the kidney, and 54.68-304.17 µg/g in the liver. Concentrations of Cu were 0.00-29.74 µg/g in the bone, 6.65-196.67 µg/g in the kidney, and 10.84-193.56 µg/g in the liver. Cadmium, measured only in the kidney and liver, ranged from 0.11-15.99 µg/g and 10.84-193.56 µg/g, respectively.

7.

From 1981 to 1983, mink samples were collected from Okanogan county, Washington, and the North Fork and main channel of the Coeur d’Alene river in Idaho (Blus et al., 1987). Lead was highest in liver samples collected from the main channel (geometric mean 4.1 µg/g wet weight). The geometric mean for Cu ranged from 3.2 µg/g in the North Fork to 7.9 µg/g in the main Channel. Zinc values were lowest in the North Fork (geometric mean 14.4 µg/g) and highest in Washington (28.0 µg/g). Mercury concentration was highest in Washington (geometric mean 1.26 µg/g), and Cd, which was analyzed in the kidney samples, was highest at the main channel (0.57 µg/g).

8.

Mink trapped from eight locations in New York state between 1982 and 1984 were analyzed for Hg contamination in liver (Foley et al., 1988). Geometric mean concentrations in the eight locations ranged from 0.94-2.87 µg/g wet weight. Lowest values were detected at Lake Ontario and highest values at the Northeast Adirondack Mountains.

9.

During the 1983-1984 and 1984-1985 trapping seasons, 94 mink were collected from five study sites in Ontario for Hg analysis (Wren et al., 1986). The sites included the English River system (contaminated with Hg from chlor-alkali plant between 1962 and 1970), the Turkey Lakes (relatively pristine), the Muskoka lakes (reduced pH from acid precipitation), Sudbury (subject to acid and metal deposition from smelter emissions since 1885), and Cambridge (reference site). At the contaminated sites, liver and kidney had greater Hg concentrations than muscle and brain; liver and kidney concentrations were 2.55 and 2.08, 2.36 and 1.86, 2.17 and 2.49, 0.56 and 0.59 µg/g wet weight; at the reference site liver Hg concentration was 0.14, and kidney samples were apparently not analyzed.

10.

Adipose and liver tissue were analyzed from 109 mink collected between 1983 and 1985 from six samples sites in New York State: the eastern lake plains, west Adirondack Mountains, northeast Adirondack Mountains, the Hudson River Valley, the Appalachian Plateau, and from within 8 km of Lake Ontario (Foley et al., 1991). Geometric mean concentrations of metals detected were 1.85 µg/g wet weight Hg, 0.16 µg/g Cd, and 0.27 µg/g Pb.

11.

From 1984-89, 29 mink were trapped in north-central Illinois (Halbrook et al., 1996). Fourteen elements were detected in at least 75% of the samples. For example, kidney, liver, and muscle samples contained (µg/g wet weight): 6.51, 4.52, 7.85 Al; 4.30, 6.76, 3.07 Cu; 20.47, 24.06, 37.28 Zn; and 0.14, 0.21, 0.21 Hg. Mean concentrations of other elements detected in fewer than 75% of the samples were: 2.30, 1.67, 2.16 As; 0.06, 0.06, 0.06 Be; 0.32, 0.18, 0.08 Cd; 2.16, 1.72, 1.80 Cr; 0.33, 0.27, 0.20 Mo; and 1.07, 0.85, 0.67 Ni. Vanadium was quantified in the kidney and liver only, at mean concentrations of 2.63 and 2.08. Lead was measured in the liver and muscle only, at means of 0.90 and 0.73. Mean concentrations of Se and Sn, measured only in the kidney were 1.75 and 0.84, and Sb, measured only in the liver, was 0.92.

12.

Mink found dead in Wisconsin from 1986-1987 were analyzed for concentrations of Hg in liver (Meyer and Hurley, 1991). Two groups of mink collected from the Oconto River had mean total Hg levels of 0.43 and 0.88 µg/g wet weight. Two mink found near the Sheboygan River had concentrations of 0.63 and 0.08 µg/g. A total of four carcasses from Langlade, Jackson, Columbia, and Buffalo Counties had Hg levels of 0.88, 1.60, 0.21, and 0.23 µg/g, respectively.

13.

Mink carcasses were collected between 1987-89 from 24 watersheds in Connecticut and 9 in Massachusetts for determination of contaminant levels (Major and Carr, 1991). Mean Hg concentrations for watersheds ranged from 1.1-8.47 µg/g wet weight in Connecticut and 0.008-1.92 µg/g in Massachusetts. Overall Hg values were significantly higher in Connecticut.

14.

A total of 213 mink occurring throughout Minnesota were collected during the 1989 and 1990 trapping seasons (Ensor et al., 1993). Metals detected included Hg (1.94 µg/g), Se (0.95 µg/g), Pb (0.61 µg/g), and Cd (0.29 µg/g).

15.

A decline in coastal mink populations in Georgia, North Carolina, and South Carolina prompted the 1989 to 1991 collection of 141 mink from the three states to determine of concentrations of 17 substances (Osowski et al., 1995). Coastal individuals were compared with samples from the piedmont, mountain, and foothill areas. Mercury was found in significantly higher concentrations in coastal regions, with a 2.244 µg/g wet weight median concentration. Also detected in coastal mink in all three states was Cu at 0.224 µg/g.

16.

Mink carcasses collected from commercial trappers in British Columbia from 1990-1995 were analyzed for exposure to 20 metals (Harding et al., 1998).  With the exception of Cd, which was elevated in mink from the Kootenay River, concentrations in both tissues were considered low and within the normal range for this species.  Renal concentrations in samples collected from the Kootenay River and the Lower Fraser River, respectively, were 3.25 and 7.18 µg/g dry weight Al, 0.29 and 0.15 µg/g Ba, 3.61 and 0.73 Cd, 494 and 381 µg/g Ca, <0.4 and 0.25 µg/g Co, 0.98 and 1.68 µg/g Cr, 12.13 and 12.4 µg/g Cu, 715 and 456 µg/g Fe, 1.13 and 0.59 µg/g Pb, 433 and 533 µg/g Mg, 2.4 and 3.56 µg/g Mn, 3.37 and 3.13 µg/g Hg, <0.8 and 0.48 µg/g Mo, 7010 and 8680 µg/g K, 4.0 and <4 µg/g Se, 4360 and 4710 µg/g Na, 0.52 and 0.45 µg/g Sr, 6.25 and 5.5 µg/g Sn, 0.13 and 0.41 µg/g Ti, and 67 and 65 µg/g Zn.  Hepatic concentrations in samples collected from the Lower and Upper Fraser River, respectively, were 3.63 and 3.5 µg/g Al, 0.06 and 0.08 µg/g Ba, 0.26 and 0.10 Cd, 380 and 551 µg/g Ca, 0.23 and 0.33 µg/g Co, 1.16 and 1.98 µg/g Cr, 23 and 24 µg/g Cu, 1050 and 982 µg/g Fe, 0.45 and 0.21 µg/g Pb, 634 and 580 µg/g Mg, 8.98 and 8.53 µg/g Mn, 4.62 and 4.05 µg/g Hg, 1.5 and 0.98 µg/g Mo, 7470 and 8110 µg/g K, 2.06 and 2.42 µg/g Se, 5050 and 4490 µg/g Na, 0.45 and 0.32 µg/g Sr, 5.53 and 5.17 µg/g Sn, <0.2 and <0.2 µg/g Ti, and 95 and 95 µg/g Zn. 

17.

A total of 1025 mink carcasses were collected from seven locations in the western Northwest Territories in Canada during winters 1991-92 to 1994-95 (Poole et al., 1998). Heavy metal concentrations (µg/g dry weight), excluding Hg, were determined in kidney for each location and included the following ranged of means: 2.34-9.49 Al, 0.16-1.12 Cd, 14.29-20.82 Cu, 0.19-1.89 Ni, and 0.10-0.99 Pb. Mercury, analyzed in the liver, ranged from means of 0.91-3.30 µg/g wet weight among locations.

18.

Of eight mink collected between 1993 and 1994 near a Hg mine in Clear Lake, California, only one Hg concentration value approached toxicity thresholds for wildlife species and was found in the brain of an individual mink (Wolfe and Norman, 1998).  Mercury concentrations in tissues for that mink (in mg/g wet weight) were as follows: 7.10 in brain, 9.25 in liver, 21.5 in fur, 0.18 in blood, and 34.1 in claws.  The other seven mink collected were all below the following Hg tissue concentrations (in mg/g): 0.40 in brain, 10.1 in liver, 7.99 in fur, 0.63 in blood, 1.13 in muscle, 1.30 in kidney, and 11.9 in claws.

19.

Wild mink were collected during two trapping seasons (1993-1994 and 1994-1995) from James Bay Territory, Québec, Canada (Fortin et al., 2001).  For the 1993-1994 trapping season, mean total Hg concentrations (N=39) in tissues ranged from 0.96 mg/g wet weight in brain to 30.1 mg/g in fur. Mean (range) total Hg concentration (N=316) in liver was 3.71 (0.07-44.1) mg/g when both trapping seasons were pooled. Log liver total Hg concentrations increased with age and were greatest in areas with moraine deposits and closest to local industrial centers.  Log liver total Hg concentrations were low in areas with rich clay deposits and areas furthest from local industrial centers.

20.

In 1994, 19 mink were selected from 800 collected in Ontario, Canada (Evans et al., 2000).  Mean (standard deviation) total Hg concentrations were 0.34 (0.24) mg/g wet weight in brain, 1.01 (0.92) mg/g in kidney, 1.53 (1.24) mg/g in liver, and 17.26 (12.50) mg/g in fur. Mean (standard deviation) MeHg concentrations were 0.26 (0.19) mg/g wet weight in brain, 0.94 (0.86) mg/g in kidney, 1.21 (0.85) mg/g in liver, and 11.25 (8.01) mg/g in fur.

21.

Mercury was detected in hair samples taken from the abdominal and caudal regions of all 12 adult mink collected from four sites at the Oak Ridge Reservation, Tennessee (Stevens et al., 1997). Mean concentrations were 104.0, 11.0, and 8.80 µg/g dry weight at the contaminated sites and 5.15 µg/g at reference sites.

IV.

Petroleum

No residue data available

V.

Other

1.

In 1974 and 1975, farm mink, ages 10 to 12 weeks were put in groups of 2 males and 8 females and fed 0, 1, 2.5, 6.25, or 15.625 ppm polybrominated biphenyls (PBBs) mixed into mink feed, or 1.54 or 11.98 ppm PBB obtained from mixing PBB contaminated poultry or beef, respectively, into mink feed(Aulerich and Ringer 1979).  PBB was found at 60 times the dietary concentration in the adipose tissue.  Average PBB residues in brain, skeletal muscle and adipose tissue of control minks were 0.14, 0.73, and 8.14 ppm.  Range of average PBB residues in brain, skeletal muscle, and adipose tissue of treated minks was 1.5-94.6, 7.3-71.6, and 91.2-986 ppm.   

Mink Contaminant Response Data

I.

Organochlorine Contaminants

1.

Fish seined from the Southwest Miramichi River in New Brunswick in 1967 were incorporated into commercial mink diets, resulting in DDE levels of 0.58 and 0.42 ppm (in feed) for two experimental groups (Gilbert, 1969). Mink fed this diet exhibited higher levels of DDE in liver and adipose tissue than controls. Experimental animals also had reduced erythrocyte and leukocyte counts, hemoglobin and hematocrit, and a higher pH of the blood. Adrenal, spleen and testes weights were all elevated, and females had significantly greater embryonic loss. Sex ratio of litters was weighted in favor of females in treated groups.

2.

Male and female mink were fed diets containing fish from Lake Michigan and Lake Erie prior to and throughout breeding (Aulerich et al., 1971). All females fed Lake Michigan coho salmon experienced complete reproductive failure, and all mink died by the end of the whelping period. Those fed Lake Michigan bloater chub, Lake Michigan yellow perch, and Lake Erie coho also exhibited reduced numbers whelping, decreased kit weight, and poor kit survival. Pesticide levels appeared to be related to degree of reproductive decline or mortality. Total DDT levels of Lake Michigan coho, Lake Michigan chub, Lake Michigan perch, and Lake Erie coho were 18.23 µg/g, 8.81 µg/g, 3.34 µg/g, and 2.76 µg/g, respectively, and dieldrin concentrations were 0.118 µg/g, 0.149 µg/g, 0.061 µg/g, and 0.031 µg/g, respectively.

3.

The effect of DDT on reproduction in mink was studied (Duby et al., 1971). o,p'-DDT was confirmed to be uterotrophic. When injected with either o,p'-DDT, p,p'-DDT or technical DDT, there were no indications of any effect on either fertility or fecundity.

4.

In order to examine the effect of PCBs on reproduction, mink were assigned to a control group and fed a basal high protein meat diet, or fed the basal diet containing coho salmon from Lake Michigan, or fed the basal diet plus a supplement containing 10 ppm of the following PCB aroclors: 1242, 1248, and 1254 (Ringer et al., 1972). All of the mink fed diets supplemented with Aroclors died prior to whelping. Six of the 15 fed the coho salmon died prior to the end of the experiment, but none of the control died. Tissue analysis revealed that the PCBs were most concentrated in the brain at a mean of approximately 11 µg/g. In a second experiment, mink were fed PCBs at either 5 or 10 ppm and in combination with either 10 ppm of DDT or 0.5 ppm of dieldrin. All treatment groups gained less weight and had a higher percent mortality than the control group. Mortality was 100% in mink feed 10 ppm of PCB plus 0.5 ppm of dieldrin.

5.

Prior to and during breeding, mink were fed a diet containing either 0.64 or 3.57 ppm Aroclor 1254 derived, in part, from cows injected with the PCB (Platonow and Karstad, 1973). Reproductive failure occurred in all females, and death occurred in all mink fed the 3.57 ppm diet. Gross lesions observed were yellowish discoloration of the liver and hemorrhage into the abdominal cavity or gastrointestinal tract. Microscopic lesions included nephrosis, fatty degeneration and necrosis of the liver, brain edema, disseminated intravascular coagulation and fibrosis of coronary arteries.

6.

A significant decrease in reproductive success was observed when mink were fed coho salmon collected from Lake Michigan in 1968 (Aulerich et al., 1973). Out of 14 control mink that were fed ocean perch and mated, 13 whelped. In the treatment group fed coho salmon, no whelping occurred in 8 mink that mated. No decrease in whelping occurred when the mink were fed coho salmon from the west coast. Kit mortality greater than 50% was observed when mink were fed fish from the Great Lakes. Mink fed fish from the Great Lakes exhibited signs of toxicity similar to those whose diet contained PCBs. The mink fed a diet containing 30% coho salmon from Lake Michigan acculumated PCBs in tissues, with greatest residues in brain (11.07 µg/g).

7.

Feeding studies conducted to investigate reproductive effects of PCB to mink, including those reported in Aulerich et al, 1971 and 1973, are further described (Aulerich and Ringer, 1977). In 1971-72, a study was initiated to examine long-term effects of PCBs interacting with dieldrin and DDT. Results indicated that 10 ppm Aroclor 1254 depressed weight gain in young mink. All mink fed Aroclor 1254 plus 0.5 ppm dieldrin died by the end of the experiment, only one of six survived the diet of Aroclor alone, and 4 of 6 survived of those fed Aroclor plus 10 ppm DDT. All mink failed to produce offspring. Enlargement of the liver, kidneys, and heart was observed. In the 1972-73 study, four Aroclors (1016, 1221, 1242, 1254) were fed to mink throughout the breeding season, but only Aroclor 1254 resulted in an adverse reproductive effects (0.3 kits whelped per female). Acute toxicity (LD₅₀) was estimated for Aroclors 1221, 1242, and 1254, and was found to vary inversely with chlorine content of the Aroclors. In a final study, females fed PCBs or Lake Michigan salmon that failed to whelp young were placed on control diets; they were found to successfully produce offspring in the following breeding season.

8.

Female mink exposed to 3.3 ppm PCB plus 3.3 ppm DDT, 11 ppm PCB alone, or 0.05 ppm PCB ("controls") for 66 days were mated with untreated males (Jensen et al., 1977). Liver weights were higher in treated groups compared to controls. The number of implantation sites in breeding females was not different among groups, but the number of delivering females and the number of kits born per female significantly decreased in the 3.3 ppm group. No kits were delivered in the 11 ppm group. Concentrations of hepatic cytochrome P450 were significantly higher for both treatment groups.

9.

Mink fed a diet of 11 ppm PCB (Clophen A50 and A60) for 66 days were analyzed for Cd and Hg concentrations (Olsson et al., 1979). Concentrations of Cd in PCB-treated animals were higher than those found in the control. Concentrations of Hg showed no significant difference between groups.

10.

Mink were divided into treatment groups and fed either 0, 5, 10, 20, or 40 ppm Aroclor 1242 or 20 ppm Aroclor 1016 prior to and throughout the breeding season (Bleavins et al., 1980). Total mortality occurred in 20 and 40 ppm Aroclor 1242 groups, and in 66.7% of the 10 ppm group. Aroclor 1016 produced mortality in 25% of individuals. Mink fed all levels of Aroclor 1242 exhibited total reproductive failure with no mink whelping. Mink fed Aroclor 1016 had a 44.4% whelping rate and kits had a significantly lower body weight at 4 weeks.

11.

Male and female mink were either placed in a control group, or fed 20 ppm of Aroclor 1016 or 1242 for 28 days (Shull et al., 1982). Liver weight tended to be 5-15% greater in both males and females fed 1016 or 1242 compared to control mink. Cytochrome P450 was significantly greater in mink fed Aroclor 1242 compared to controls. In another experiment, mink received intraperitoneal injections of Aroclor 1242; hepatic cytochrome P450 and benzo(a)pyrene activity increased compared to controls.

12.

On three consecutive days mink were injected with either phenobarbital (PB) or 3-methylcholanthrene (MC) (Shull et al., 1983). After each injection with PB, mink were lethargic and the amount of time they slept was greater on day 3 compared to the first day. An increase of 36% in liver weight and 29% in lung weight was observed. After injection with MC, food consumption decreased and decreases in body weight (11%) and liver weight (21%) were observed. There was no difference in microsomal protein or in NADPH-cytochrome P450 reductase between control mink and those injected with PB or MC. A significant increase in cytochrome P450 (448) was observed for the PB- and MC-injected mink. There was no difference in Cytochrome b₅ for the PB-injected mink but an increase was observed for the MC injected mink. When examining specific hepatic microsomal MFO activity, it was found that aminopyrine N-demethylase activity increased significantly over controls for the PB-treated mink, and benzo(a)pyrene hydroxylase and ethoxyresorufin-O-deethylase activities increased significantly in the MC-injected mink compared to controls.

13.

One group of female mink was fed a diet supplemented with 0, 1, 5, or 25 ppm HCB and tested for mitogenic lymphocyte blastogenesis response, and a second group was fed a diet of 0, 1, or 5 ppm HCB and mated (Bleavins et al., 1983). Mink fed the 25 ppm diet showed no physical signs of distress or toxicity, but exhibited reduced blastogenic response to the Concanavalin A mitogen. Kits born to and nursed by mink at both the 1 and 5 ppm level and fed non-HCB-supplemented feed also exhibited a reduced T-cell response to the Concanavalin A mitogen.

14.

Kits born to male and female mink exposed to concentrations of 0, 1, and 5 ppm HCB were sacrificed at 16-17 weeks and examined (Rush et al., 1983). Kit mortality to weaning increased from 8.2% in control to 44.1 and 77.4% in the 1 and 5 ppm groups, respectively. Surviving kits showed no change in body weight, liver weight or kidney weight. None of the kits had altered cytochrome b₅ levels, but those from the 5 ppm group had elevated hepatic cytochrome P450 concentration and ethoxyresorufin-O-deethylase activity. No changes were observed in ethoxycoumarin-O-deethylase, benzphetamine-N-deethylase, NADH cytochrome-c reductase, or in vitro renal function. No hepatic damage was observed. Tetraethylammonium accumulation was significantly decreased in 5 ppm kidneys. HCB was detected primarily in the fat at a mean concentration of 0.63 µg/g for the 5 ppm group, but also detected in the brain, liver, kidney, and muscle.

15.

In a study conducted from 1979-80, mink were divided into 6 dietary groups and fed fish from the Great Lakes (carp, white sucker, perch, whitefish, or alewife) or a control diet of Atlantic cod, haddock, and flounder (Hornshaw et al., 1983). No difference in weight gain was observed between the control groups and any of the treatment groups. None of the kits were whelped alive in the group fed carp. The percent kit survival from birth to four weeks tended to be lower in all treatment groups compared to the control, though there were no significant differences found in reproduction. In the second year, two groups of minks were studied: those fed a standard mink diet of marine fish and those fed a mix of perch scraps and sucker from the Great Lakes. A significant drop in the number live whelps was seen for the Great Lakes-fed group when compared to controls. PCB residues (as Aroclor 1254), measured in both studies, accumulated in subcutaneous body fat as much as 38 times the dietary level, with individual congeners accumulating up to 200 times. The half-life of PCB in adipose tissue was found to be 98 days.

16.

Adult mink were fed HCB in concentrations of 1, 5, or 25 ppm for 47 weeks (Bleavins et al., 1984). Adult mink in all dosage groups showed significantly elevated levels of hypothalamic seratonin, with no effect on regional brain norepinephrine or dopamine concentrations. Young mink exposed to HCB in utero and during lactation exhibited a significant decrease in hypothalamic dopamine levels at the 1 and 5 ppm concentrations, with no effect on regional brain concentrations of serotonin or norepinephrine.

17.

Adult female mink were fed diets supplemented with 2.5 ppm Aroclor 1254, 0.1 or 0.5 ppm PCB congener 169, 2.5 or 5.0 ppm PCB congener 153, or 2.5 or 5.0 ppm PCB congener 136 (Aulerich et al., 1985). Congener 169 caused total mortality within 60 days at 0.5 ppm, and 50% mortality within 90 days at the 0.1 ppm level. No adverse reproductive effects were seen in the congener 153 or 136 groups, while the Aroclor group resulted in a single stillborn kit whelped. Plasma progesterone concentrations showed a significant increase in the 0.1 ppm congener 169 group, and a significant decrease in those fed Aroclor. All mink, excluding those fed congener 136, showed a significant increase in hepatic cytochrome P450 concentration, the greatest occurring with Aroclor and congener 169. Benzo(a)pyrene hydroxylase activities increased significantly with Aroclor, congener 153 and 169. Ethoxyresorufin-O-deethylase activities increased significantly in those fed Aroclor. Norepinephrine concentrations were increased by Aroclor, congeners 136 and 153, and dopamine levels were effected by Aroclor and congener 169. Concentrations of 17ß-Estradiol were not significantly altered.

18.

At the Michigan State Experimental Fur Farm, in 1981 and 1982, HCB was added to mink food at 0, 1, 5, 25, 125, and 625 ppm and fed to groups consisting of 10 females and 3 males for each dose (Bleavins et al., 1984b). Mean number of kits whelped/number of alive kits for 0, 1, 5, 25, 125, and 625 ppm treatment groups, respectively, were 6.4/4.9, 5.3/4.3, 5.9/5.3, 3.4/1.9; the 25 ppm groups had significantly fewer total kits (p<0.05) and alive kits (p<0.01) than the control group.  Number of kits/mean kit body weight (g) at birth, 3 weeks, and 6 weeks, for the 0, 1, 5, and 25 ppm treatment groups, respectively, were: 49/9.0, 45/97, 45/245; 34/7.9, 23/87, 19/229; 53/8.1, 12/68, 12/173; and 15/7.6, 2/36, 2/71.  The 5ppm and 25 ppm groups had significantly lower body weight at all times measured than the control group, and the 1 ppm group had significantly lower weight at birth (p<0.01).  The 5 ppm group had significantly lower biomass than the control group (145g compared to 441g, p<0.05).  In the 125 and 625 ppm groups, all mink died.  Survival ranged from 18-79 days for males and 9-266 for females. 

In a concurrent experiment, mink were fed 0 or 2.5 ppm HCB; kits were cross-fostered between treatments.  Male kits born to control mink and fostered by HCB treated mink had significantly greater body weight at 6 weeks (340g compared to 297g in control mink, p<0.05).  Female kits in the HCB group raised by their own mother had significantly greater body weight at 3 weeks (105g compared to 94g in the control, p<0.05).  Kit mortality at 3 and 6 weeks ranged from 3.0% to 22.5%, but did not differ among groups. 

19.

Two LC₅₀ trials were conducted to assess primary and secondary toxicity of Aroclor 1254 in mink (Aulerich et al., 1986). Primary toxicity tests (Aroclor 1254 mixed into feed) yielded LC₅₀ estimates of 79.0 ppm and 48.5 ppm for 28- and 35-day tests, respectively. The 35-day test included a 7-day withdrawal period. LC₅₀ values for individuals fed the metabolized PCB (i.e., secondary toxicity; Aroclor 1254 fed initially to rabbits, and then rabbit is incorporated into the diet of the mink) in concentrations equal to that of the unmetabolized PCB were 47.0 and 31.5 ppm for the two durations. Food consumption and body weight gain means were lower for minks in the secondary toxicity test. The findings indicate the potential for enhancement of toxicity upon metabolism of some halogenated hydrocarbon mixtures.

20.

Three 28-day dietary Aroclor 1254 trials were conducted to assess the effects of age, dietary compositions, and season/year on LC₅₀ estimates (Hornshaw et al., 1986a). Males and females in all groups exhibited increased weight loss with increased dietary concentrations of the PCB mixture. Males demonstrated significant weight loss at concentrations > 18.0 ppm and greater, and females at levels of >32.4 ppm. Little effect was found between the three tests of age, diet, and season/year. Dietary LC₅₀ values were 83, 84, and 79 ppm, respectively. After a 7-day withdrawal period (untreated diet substituted), mink continued to succumb and LC₅₀ estimates became 58, 47, and 49 ppm.

21.

Mink received three daily injections of either PCB congener 47 or congener 77, and were sacrificed after 7 days (Gillette et al., 1987). Those receiving the congener 77 showed a significant decrease in food consumption and body weight, and an increase in cytochrome P450 levels and microsomal epoxide hydrolase activity. No change in activity was exhibited by either group for cytochrome b₅, NAPDH cytochrome c reductase, ECOD, AHH, APND, or aldrin epoxidase. Mink fed congener 77 exhibited abnormalities of the small intestine. Liver concentration of congener 77 was 11.5% of body fat concentration. No effect was seen in organ weights of either group.

22.

Mink diets were supplemented for 135 days with either 0.01 or 0.05 ppm PCB congener 169 (Aulerich et al., 1987a). Exposure to 0.05 ppm resulted in 50% mortality, while no deaths occurred in the 0.01 ppm group. The 0.05 ppm group showed significant body weight loss after two months of feeding, as well as abnormal molt, deformed nails, anorexia, and bloody stools. Organ weights were significantly greater than controls for the brain, liver, kidneys, and adrenals in the 0.05 ppm group, and for the liver alone in the 0.01 ppm group. Free and total T₃ concentrations were significantly decreased in both groups, and T₄ levels were reduced in the 0.05 ppm group.

23.

Eighty-four ranch-bred mink were separated into four treatment groups and one control group, and fed commercial mink food supplemented with one of the following treatments: 1.0 ppm PCB (Aroclor 1254), 1.0 ppm MeHg, 1.0 ppm PCB plus 1.0 ppm MeHg, 0.5 ppm PCB plus 0.5 ppm MeHg (½MeHg/PCB group), or no toxicant (Wren et al., 1987a). Liver PCB concentrations were consistently the highest for the PCB only group in adult mink. Levels in 5-week-old kits were highest in the ½Hg/PCB group (<2.42 µg/g) as compared to the PCB only group (<1.82 µg/g) and approximated levels of adult mink fed the experimental diets for over 7 months. No significant differences were found of the test groups in examination of the thyroid gland, pituitary gland, adrenal gland, or serum T4 or T3 levels.

24.

Eighty-four ranch-bred mink were separated into four treatment groups and one control group and fed commercial mink food supplemented with one of the following treatments: 1.0 ppm PCB (Aroclor 1254), 1.0 ppm MeHg, 1.0 ppm PCB plus 1.0 ppm MeHg, 0.5 ppm PCB plus 0.5 ppm MeHg (½MeHg/PCB group), or no supplement (Wren et al., 1987b). Kits nursed by mothers exposed to 1.0 ppm PCB had significantly reduced growth rates. Kits with mothers in the PCB/MeHg group had a significantly lower rate of survival to weaning. There was no significant difference in female fertility, percentage of females whelped, or number of kits born.

25.

Newborn mink were separated into six groups and administered daily 0.1 µg TCDD/kg body weight, 1 µg TCDD/kg body weight, 10 µg epidermal growth factor (EGF)/kg body weight, 50 µg EGF/kg body weight, a 1:9 acetone/corn oil mixture (TCDD vehicle), or 0.85% sodium chloride (EGF vehicle) for twelve consecutive days (Aulerich et al., 1988). Doses of 1 µg TCDD/kg body weight were lethal to all test subjects within two weeks. Those treated with 0.1 µg TCDD/kg body weight showed significant body weight reduction by two weeks for males and three weeks for females. Mortality in this group continued after dosing and was 62% by the 19^th week. Significant weight reductions first occurred in both EGF groups in the second week in both males and females. Mortality occurred mainly during the dosing period in these groups. Days to eyelid opening was significantly reduced from a mean of 34.2 days in control to 27.4 days in the 10 µg EGF group and 15.1 days in the 50 µg EGF group. Eyelid opening was not significantly different in the TCDD groups, nor was incisor or premolar eruption for any of the test groups.

26.

Sixteen adult mink were administered a single oral dose of TCDD in concentrations of 0, 2.5, 5.0, or 7.5 µg/kg body weight (Hochstein et al., 1988). A 28-day LD₅₀ value of 4.2 µg/kg body weight was determined. Food consumption decreased significantly in the first week for the 5.0 and 7.5 µg/kg groups, increasing in the third week for survivors. Body weight was significantly lower in the survivors of the 2.5 µg/kg group and individuals that died in the 5.0 and 7.5 µg/kg groups. A significant increase in weight occurred in the kidneys and brains of 5.0 and 7.5 µg/kg dosed mink, in the heart of the 5.0 µg/kg animals, in the thyroid glands of the 7.5 µg/kg group, and in the adrenal glands of all test groups. No significant weight increase occurred in the liver or spleen, though gross necropsy revealed mottling and discoloration of these organs as well as the kidney.

27.

Female mink were exposed to 1 ppm Aroclor 1254 from two weeks after breeding until whelping, for a period totaling approximately 45 days (Hunter, 1991). This exposure resulted in reduction of the cervical apocrine gland in kits, with greatest effect in the first two weeks of life, and reduction of the area of epithelial cell cytoplasm.

28.

To evaluate potential biomarkers of contaminant exposure, mink were divided into five groups and fed the following diets: 40% ocean fish, 10% Saginaw Bay fish (SBC), 20% SBC, or 40% SBC (Melancon et al., 1992). EROD, ECOD, AHH, and cytochrome P450 IA activity were found to significantly increase over the control values. PROD was found to significantly decrease over control values.

29.

Mink fed daily doses of PCBs or PCB fractions during mating and gestation had higher urinary cortisol excretion at the time of embryonic implantation than controls (Madej et al., 1992). Urinary excretion of estrone sulfate increased later in test groups than control, yet occurred at higher levels at the time of parturition.

30.

Reproductive outcomes of female mink receiving daily doses of commercial PCBs or PCB fractions were studied (Kihlström et al., 1992). Litter size and number of live whelps were decreased with administration of Clophen A50 or Aroclor 1254, in daily doses of 2 mg and 1.64 mg, respectively. Implantation rate did not decrease. The frequency of interrupted pregnancies, as well as liver weights increased. Similar results occurred with mink given combinations of two or more CB fractions, yet not for mink exposed to single fractions separately. Individuals given the single fraction containing the bi- and tricyclic contaminants polychlorinated naphthalene and PCDF showed significantly higher number of live whelps and an increased survival rate.

31.

Adult mink fed daily doses of Clophen A50, PCB fractions containing 0- or 1-ortho-CBs, or the synthetic mixture of congeners 77, 126 and 169 exhibited EROD activities that were increased two- to threefold compared to controls (Brunström 1992). Studies of Aroclor 1254 and mixtures of four fractions prepared from Aroclor 1254 also revealed an approximate twofold increase of AHH activity in adult mink. Kits born to females exposed to the 0- or 1-ortho-CBs showed a 30-fold increase of EROD levels. In a third study, EROD, AHH, and APND activities were increased 1.6 to 2.7 times in females fed Aroclor 1254 daily one month before mating.

32.

Mink fed PCB and PCB fractions were examined for evidence of change in Vitamin A concentration in the liver, kidney, and lungs (Håkansson et al., 1992). Exposure to Clophen A50 and Clophen fractions containing non- or 1-ortho-CBs resulted in a 48 to 67% decrease in hepatic and pulmonary Vitamin A content, but no observable renal decrease. Aroclor 1254 induced no change in Vitamin A tissue levels, however fractions containing 2 to 4- and 1-ortho-CBs showed a significant reduction in pulmonary levels.

33.

The retention of CBs and the lipophilic MeSO₂-CB was studied in mink treated with a wide variety of PCBs and PCB fractions for three months during pregnancy (Bergman et al., 1992a). Concentrations determined from muscle showed a significant increase of the body burden of CBs and metabolites in animals exposed to CBs fractions containing 2-4-ortho CBs or 1-ortho CBs. The most efficiently retained CBs were those that contained 5 or more chlorine atoms and lacked vicinal hydrogens in 3,4-positions. Those most easily metabolized were CBs with chlorine atoms in 2,5-positions and unsubstituted 3,4-positions. The CBs/ MeSO₂-CBs ratio was calculated and determined to be slightly lower in the liver than in the muscle samples.

34.

Biochemical parameters in blood and urine were examined in mink fed commercial PCB and CB fractions for a total of 53-69 days during the periods before and after mating (Edqvist et al., 1992). Mink fed PCBs exhibited elevated alanine aminotransferase. Lowered alkaline phosphatase resulted from exposure to PCB or CB fractions. Mink exposed to PCB or 2-4-ortho+1-ortho+0-ortho and 2-4-othro+0-ortho showed lower serum bile acids. Some of the observed biochemical changes were counteracted by the presence of bi- and tricyclic contaminants. Urinary parameters exhibited no significant change.

35.

Liver histology was studied in female mink receiving daily doses of commercial PCBs or PCB fractions (Bergman et al., 1992b). Effects included fatty changes in hepatocytes, hemosiderosis of Kupffer cells, and increased frequency of polymorphonuclear and mononuclear cells in groups exposed to commercial PCBs, those in 3 and 4 combination fractions, and 2-4-ortho and 0-ortho CBs. Of those mink treated in combination, exposure to 2-4-ortho and 0-ortho CBs were least affected. No effects were observed in the group exposed to bi- and tricyclic contaminants.

36.

Female mink receiving daily doses of commercial PCBs or PCB fractions (1-ortho, 0-ortho, and 2-4-ortho CBs, and bi- and tricyclic contaminants) were examined for morphological changes of the reproductive organs (Bäcklin et al., 1992). High incidences of fetal death occurred among groups exposed to commercial PCBs and combinations of their fractions. Those exposed to single PCB fractions incurred no increase in fetal death. Females fed Clophen A50 had a high predominance of late fetal death and had ovaries containing corpora lutea. Mink exposed to Aroclor 1254 experienced a high frequency of early fetal death and had ovaries containing corpora albicantia.

37.

Mink were fed heptachlor at 0, 6.25, 12.5, or 25 ppm for 180 days (Crum et al., 1993). Mortality of the female mink was directly related to dose. No mink died in the control (0 ppm) group and 100% died in the 12.5 ppm group. Heptachlor at the 6.25 ppm concentration did not alter the litter size, the number of kits whelped or the percent of kits alive at birth compared to the control group, but there was a decline in these parameters in the 12.5 ppm group. Kit weight at 3 week and 6 weeks was significantly lower in the 6.25 and 12.5 ppm group when compared to the controls. Heptachlor at 6.25 and 12.5 ppm did not affect male reproduction.

38.

Beginning in 1992, mink in the lab were dosed three times a week for 18 months with either 0.7 mg Clophen A50 (0.3 mg/day PCB), 0.24 mg Clophen A50 (0.1 mg/day PCB, fraction of Clophen A50 containing 0-1-ortho-CBs and dicyclic aromatic contaminants, fraction of Clophen A50 containing 2-4-ortho-CBs, blubber extract containing organochlorine pollutants (0.064 mg total PCB and 0.021 mg total DDT/day), or 1 ml of fish oil (Brunström et al., 2001). 

In the first season, mink exposed to the 0.3 mg/day PCB dose had decreased birth weights of young and reduced viability of offspring. The 0.3 mg/day PCB and 0-1-ortho-CB dosed mink had decreased thymus weights. In the second season, 39% of the 0.3 mg/day PCB dosed females and 93% of the control group produced offspring. All offspring from the 0.3 mg/day PCB dosed females died within one day.  The 0.1 mg/day PCB group had decreased kit survival (only 36% survived to two weeks versus 73% in the control group) and decreased offspring body weights at 2 and 5 weeks of age.  In both seasons, abnormalities in stillborn kits were higher in the 0.3 mg/day PCB group compared to the control group.  The 0-1-ortho-CB fraction dosed group had fewer kits per female and a two-week survival rate of only 7%. Growth rate and kit production were not affected by the 2-4-ortho-CB fraction dose, but had a lower two-week survival than the control group.

Hepatic PROD and EROD activities increased with PCB dose. PROD induction also occurred in the 2-4-ortho-CB dose. Both fractions induced EROD. The blubber extract contaminants strongly induced PROD and slightly induced EROD.

39.

Sixty mink were fed diets consisting of 0, 10, 20, or 40% carp collected from Saginaw Bay, Michigan, prior to and throughout the reproductive period (Heaton et al., 1995). The resultant diets contained 0.015, 0.72, 1.53, and 2.56 mg PCB/kg diet or 1.03, 19.41, 40.02, and 80.76 ng TEQs/kg diet, respectively. Food consumption was inversely proportional to percentage of carp in the diet. Mink fed the 40% diet exhibited signs of PCB intoxication including parental inattentiveness in females. The 40% group resulted in a significantly lower number of kits whelping, with all born stillborn or dying within 24 hours. Kit weight and survival to weaning was inversely proportional to percent of carp in diet. A dose-related decrease was measured in relative organ weights of the liver, spleen, kidney, lung, adrenal gland, and heart in 6-week-old kits, with the 20% group showing significantly greater adrenal gland weights. Adult mink showed a general dose-dependant increase of all relative organ weights. Lowest observable adverse effect levels of 0.134 mg PCBs/kg body weight/day or 3.6 ng TEQs/kg body weight/day for adult female mink were determined.

40.

Sixty mink were fed diets consisting of 0, 10, 20, or 40% carp collected from Saginaw Bay, Michigan, prior to and throughout the reproductive period (Tillitt et al., 1996). The resultant diets contained 0.015, 0.72, 1.53, and 2.56 ppm PCB or 1.03, 19.41, 40.02, and 80.76 ng TEQs/kg diet, respectively. Examination of dietary or tissue-based exposure of the mink to TCDD showed that TCDD equivalents of the planar halogenated hydrocarbon mixtures followed an additive model of toxicity, as compared with the H4IIE bioassay. The 10% treatment group (19.4 pg H4IIE bioassay-derived TCDD-EQs/g) exhibited significant reproductive effects. Consumption-normalized mink liver biomagnification factors were 6.4-74.2 for PCDDs, <1-75.8 for PCDFs, <1-15.9 for PCBs, and generally increased with degree of chlorination in each class.

41.

Prior to and throughout the reproductive period, male and female mink were fed diets partially composed of Saginaw Bay (Lake Huron) carp formulated to provide 0 (control), 0.25, 0.5, or 1.0 ppm PCB (Restum et al., 1998). After whelping of offspring, half of the treated mink were switched to the control diet for the next reproductive cycle and half remained on their respective treated diets. All kits born in the first reproductive cycle were maintained on their parents’ diet through weaning, after which time half were switched to the control diet. Breeding performance of females was adversely affected with increased PCB dietary concentration as evidenced by reduced vulvar swelling and delay of mating. Kit body weights at birth for both generations were generally inversely proportional to concentration of PCB in the diet, and survival was significantly lower for those continually treated with 1.0 ppm PCB. In mink continually exposed to 1.0 ppm PCB, serum T₄ concentrations were significantly greater than controls for adults of both sexes and serum T₃ was greater in adult males and female kits. Organ weights were affected by continuous feeding at concentrations of 0.5 ppm or higher in adults and 0.25 ppm or greater in kits. Those continuously fed at the 1.0 ppm level had significant weight differences in the kidney, liver, brain, spleen, heart and thyroid glands. The percentage of livers in with periportal hepatocellular lipidosis and diffuse hepatocellular lipidosis tended to increase with increased exposure to PCBs.

42.

Prior to and throughout the reproductive period, male and female mink were fed diets partially composed of Saginaw Bay (Lake Huron) carp formulated to provide 0 (control), 0.25, 0.5, or 1.0 ppm PCB to determine its effect on hepatic cytochrome P-450 induction (Shipp et al., 1998a). After whelping of offspring, half of the treated mink were switched to the control diet for the next reproductive cycle and half remained on their respective treated diets. All kits born in the first reproductive cycle were maintained on their parents’ diet through weaning, after which time half were switched to the control diet. Adults were sacrificed after the second reproductive cycle and kits at six weeks of age. In general, hepatic EROD activity increased with increasing PCB consumption. Hepatic EROD activity was significantly higher in mink continuously fed diets containing PCBs, but activity in mink switched to control diets was not significantly different than controls.

43.

Prior to and throughout the reproductive period, male and female mink were fed diets partially composed of Saginaw Bay (Lake Huron) carp formulated to provide 0 (control), 0.25, 0.5, or 1.0 ppm PCB to determine its effects on the binding sites for ovarian steroid hormones (Shipp et al., 1998b). After whelping of offspring, half of the treated mink were switched to the control diet for the next reproductive cycle and half remained on their respective treated diets. All kits born in the first reproductive cycle were maintained on their parents’ diet through weaning, after which time half were switched to the control diet. In the parental mink, hepatic estrogen sites showed a dose-dependent decrease for mink continuously fed treated food, yet no significant difference from controls in those switched to the control diet. Kits produced in the first reproductive cycle showed no difference in hepatic estrogen sites whether the diet was continuously treated or switched. Kits produced in the second reproductive cycle from both the parental and first filial generation tended to show decreased hepatic estrogen sites with increasing PCB exposure on both continuous and switched diets, though the low number of surviving mink made statistical significance difficult to attain. Uterine estrogen binding sites and uterine progesterone receptor concentration was not significantly altered by inclusion of PCBs in the diet in any form.

44.

Female mink were given diets containing a low, high, or no dose of Clophen A and mated with unexposed males (Bäcklin et al., 1998).  Exposed females received 0.65 mg PCBs per day for 54 days (total exposure=35.1 mg) or 1.3 mg per day (total exposure=70.2 mg).  Uteri of treated mink exhibited a greater percentage of implantation sites that were degenerate or contained dead fetuses, in a dose-dependant manner.  In implanted mink, there was no difference between treated and control animals in the number of implantation sites, though there were fewer mink with implantation sites in PCB-exposed groups.  Fetal death was also markedly increased in treated groups.  Histological examination revealed effects of PCBs to maternal vasculature and degenerative changes in the trophoblast and fetal vessels.

45.

Juvenile mink (N=8) collected from four locations in British Columbia during the winters of 1994-1995 and 1995-1996 were found to have a significant negative correlation between baculum length and hepatic PCB concentrations (Harding et al., 1999). 

46.

Fatty acid composition was measured in adipose tissue surrounding the lymph nodes in male and female minks fed control diets of freshwater and marine fish and similar diets laced with 1 mg PCBs or 1 mg PCBs and 62 mg Cu/kg diet (Käkelä and Hyvärinen, 1999).  Exposure to PCBs caused alterations in fatty acid of phospholipids, especially in females fed freshwater fish.  Slight but statistically significant alterations in fatty acid composition triacylglycerols were noted in mink fed marine fish.  The magnitude of fatty acid changes in the PCB-Cu group was midway between the changes observed in the PCB and control groups.

47.

Vitamin levels were measured in liver, adipose tissue, and plasma in male and female mink fed control diets of freshwater and marine fish and similar diets laced with 1 mg PCBs or 1 mg PCBs and 62 mg Cu / kg diet (Käkelä et al., 1999).   Exposure to PCBs caused decreases in hepatic vitamin A₂ in both sexes on the freshwater diet, and decreases in hepatic vitamin E in males.  Exposure to PCBs increased levels of vitamin A₁ in adipose tissue of minks fed the freshwater diet, but decreased the level of A₁ in the adipose of minks fed the marine diet.  PCBs also lowered the level of vitamin E in the adipose of minks on the freshwater, but not marine, diet.  The combination PCB-Cu diet caused no effect in vitamin levels of liver or adipose in any group.  All treatment groups experienced a decrease in plasma vitamin A₁ and A₂ to 50% the control values. Thyroxine concentration in plasma was increased slightly by PCBs and by the PCB-Cu diet.

48.

For one year, mink were fed diets containing mixtures of methylsulfonyl-PCBs and 3-methylsulfonyl-DDE based upon concentrations found in blubber from adult unstarved female Baltic gray seals, and then mated (Lund et al., 1999).  Treated females exhibited no signs of toxicity or effect on overall body weight, though kidney weight decreased by 15%.  Hepatic PROD exhibited 11-fold induction and hepatic progesterone a 2-fold induction in treated females, which also experienced a 30-35% decrease in plasma TT₃ and TT₄ concentrations.  Treated females exhibited a 50% increase in litter size and number of liveborn kits, though birth weight was 20% lower than controls and 2-week survival was only 47% compared to 73% in controls.  Five-week-old kits did not show signs of toxicity, though hepatic PROD activity was induced fivefold.  The mean total concentration of PCB and DDE methyl sulfones in muscle of exposed adults was 18 µg/g lipid weight.

49.

From 1993-1994, captive mink at Michigan State University Experimental Fur Farm were fed fish from Poplar Creek in the Oak Ridge Reservation, Tennessee, as well as from two reference sites, Clinch River above the ORR, and the Atlantic Ocean (Halbrook et al. 1999). Five groups of 8 female and 2 male mink were housed outdoors in individual cages and fed diets with the following combination of fish mixed with mink chow: 75% ocean fish (diet A), 75% Clinch River fish (diet B), 25% Poplar Creek fish and 50% ocean fish (diet C), 50% Poplar Creek fish and 25% ocean fish (diet D), and 75% Poplar Creek fish (diet E).  Diet A contained the lowest amount of arochlor 1260 (0.0006 mg/kg body weight per day), increasing the highest amount in diet E (0.23 mg.kg body weight per day).  Females on diet E weighed 20% less than females on diet A at the end of the study.  EROD activity significantly increased in females on diets D and E.  No histological lesions or significant differences in organ weights were found in any of the groups.  Mink on diet E tended to have smaller little size, but litter size at weaning (6 weeks) was not significantly different between groups. 

50.

At Michigan State University Experimental Fur Farm, 19 twelve-week-old male mink kits were treated with 3.19 mg/kg wet weight Aroclor 1254 in food, and 15 control kits were given food without detectable levels of PCBs (Aulerich et al., 2000).  Body mass gain, baculum weight, and baculum length did not differ between control and treatment groups.

51.

Adult female mink from Michigan State University were fed a diet for 6 months; 2 mink were fed a control diet and 2 were fed the same food with the addition of 5.0 ppb TCDD (Render et al., 2000).  Maxillae and mandibles were collected after 6 months.  The treated mink were thin, lethargic and had hair loss compared to untreated mink.  Treated mink had proliferation of squamous epithelial cells – nests of squamous epithelium adjacent to teeth, some with cystic centers, which resulted in loss of alveolar bone.

52.

Female mink were put into groups of twelve and fed diets containing 0.0006, 0.016, 0.053, 0.180, and 1.40 ng/g TCDD for 131 to 132 days (Hochstein et al., 2001).  As the dose increased, the body weight of the mink decreased and the liver weigh increased.  The mink in the group fed 1.40 ng/g TCDD had alopecia and thickened, deformed, and elongated toenails as well as ascites, gastric ulcers, intestinal hemorrhages, decreased adipose tissue, and mottled and discolored livers, spleens, and kindeys.  Focal lymphocytic meningitis in the region of the olfactory bulb was found in 42% of the 1.40 ng/g TCDD group.  Two of the mink fed a diet with 1.40 ng/g TCDD died before the end of the study (on day 34 and day 99).  Reproduction was subnormal for all groups.

II.

Cholinesterase-Inhibiting Pesticides

1.

Mink were fed methyl parathion at 0, 30, 48, 78, 125, and 200 ppm in their feed, mixed directly into diet, or obtained by mixing mink feed with rabbits that were dosed by gavage with methyl parathion, then sacrificed and combined with mink feed to get the correct concentration (Aulerich et al., 1987b). The tests were discontinued after 12 days because mink rejected the dosed food and were diagnosed as dying of starvation.  Weight change over 12 days in males in the primary exposure test ranged from –9 to –568 g, and in females it ranged from +32 to –415 g; total methyl parathion consumption ranged from 0-47.53 mg in males and 0-50.25 mg in females; mortality for 0, 30, 48, 78, 125, and 200 ppm groups respectively was 0, 20, 40, 60, 50, and 40%.  In the secondary exposure, weight change in males ranged from +23 to –623 g, and in females it ranged from +16 to -333 g; methyl parathion consumption ranged from 0-45.65 mg in males and 0-42.14 mg in females; mortality for 0, 30, 48, 78, 125, and 200 ppm groups respectively was 0, 20, 70, 40, 40, and 50%. 

III.

Trace Elements, Metals, and Metalloids

1.

Male and female mink were fed diets containing fish from Lake Michigan and Lake Erie prior to and throughout breeding (Aulerich et al., 1971). All females fed Lake Michigan coho salmon experienced complete reproductive failure and died by the end of the whelping period. Those fed Lake Michigan bloater chub, Lake Michigan yellow perch, and Lake Erie coho also exhibited reduced numbers whelping, reduced kit weight, and/or reduced kit survival. Total Hg content was measured at 0.30 µg/g for Lake Michigan coho, 0.10 µg/g for Lake Michigan chub, 0.18 µg/g for lake Michigan perch, and 0.36 µg/g for Lake Erie coho, though no correlation was found between Hg concentrations and reproductive decline or mortality.

2.

Mink were fed diets containing either 5 ppm MeHg or 10 ppm mercuric chloride through the breeding season (Aulerich et al., 1974). Mink in the MeHg group began to exhibit signs of Hg poisoning on the 25^th day after treatment and all died between the 30^th and 37^th day. The average weight of this group was significantly less than controls after one month, and heart and kidney weights were significantly higher. Mink in the mercuric chloride group showed no signs of Hg poisoning, weight loss, or reduced whelping. Kit weight was significantly lower than controls at birth, but normalized by age 4 weeks. Mean Hg tissue content was significantly higher for the MeHg group only.

3.

Adult female mink were fed diets consisting of 40% pike homogenate that contained mean concentrations of 5.7 ppm MeHg and 5.8 ppm total Hg for periods of 25, 50, 75, or 100 days (Jernelöv et al., 1976). Total Hg and MeHg content increased in liver, spleen, muscle, kidney, and brain tissue samples and remained the same in fur samples. Concentrations of Se constant in all tests except kidney and liver, where a increase was observed. Of the total amount of Hg found, about 73% was MeHg, with the liver and kidney containing 46 and 55%, respectively.

4.

Adult and juvenile female mink were fed diets supplemented with 50 and 75% fish containing 0.44 ppm total Hg over a 145 day period (Wobeser et al., 1976a). Concentrations of Hg in the liver and kidney increased more rapidly than those in the brain. Adult tissue concentrations initially increased more rapidly than juveniles, but approached adult levels by the end of the study. No clinical or pathological signs of Hg poisoning were observed.

5.

Adult female mink were fed diets containing 1.1, 1.8, 4.6, 8.3, and 15.0 ppm Hg as MeHg chloride for 93 days (Wobeser et al, 1976b). Clinical intoxication was observed in mink in the 1.8 to 15.0 ppm groups, with an onset time that directly related to Hg dose. Mean concentrations of Hg in the tissues of mink that died were 11.9 µg/g brain, 16.0 µg/g muscle, 23.1 µg/g kidney, and 24.3 µg/g liver. Brain lesions and spleen abnormalities occurred in all treatment groups. Kidney abnormalities occurred in the 15.0 and 8.3 ppm groups and liver abnormalities were present in the 15.0, 8.3, 4.6, and 1.8 ppm groups.

6.

Mink fed a diet of 11 ppm PCB for 66 days were analyzed for Cd and Hg concentrations (Olsson et al., 1979). Concentrations of Cd in treated animals were higher than those in controls. Concentrations of Hg showed no significant difference between groups.

7.

Eighty-four ranch-bred mink were separated into four treatment groups and a control group, and fed commercial mink food supplemented with one of the following treatments: 1.0 ppm PCB (Aroclor 1254), 1.0 ppm MeHg, 1.0 ppm PCB plus 1.0 ppm MeHg, 0.5 ppm PCB plus 0.5 ppm MeHg (½MeHg/PCB group), or no supplement (Wren et al.,1987a). Mink were fed these diets for approximately two and a half months, when mink exposed to 1.0 ppm MeHg either alone or in combination with PCB, were switched to alternate day feeding as a result of unexpected mortality of 12 individuals. Mortality tapered off with the revised feeding schedule. The highest mean liver Hg levels occurred in the MeHg group, but had lowered to a similar level as the MeHg/PCB group by the end of the six-month trial. Both groups maintained higher Hg concentrations than the ½MeHg/PCB group. Kits born to MeHg treated mothers contained greater liver Hg concentrations than control kits. When tested at 35 days, Hg levels had lowered, with the ½MeHg/PCB group maintaining approximately twice the concentration of either of the two 1.0 µg/g MeHg groups. No significant differences were found of the test groups in examination of the thyroid gland, pituitary gland, adrenal gland, or serum T4 or T3 levels. Brain lesions were found in those mink that died of MeHg poisoning.

8.

Mink were fed 25, 50, or 75% Hg-contaminated fish collected from the Oak Ridge Reservation (ORR) to study the effects on metal accumulation and reproduction (Halbrook et al., 1997). Concentrations of Hg in tissues of parents and offspring increased with increasing amount of ORR fish in the diet. Females in the 75% group experienced lower body weights, reduced litter size, and lower body weights in offspring

9.

From 1994-995, farm-raised female mink were fed Hg-contaminated whitefish and pike from the Bourassa Reservoir, Quebec, at levels to provide concentrations of 0.1, 0.5, and 1.0 ppm Hg in the diet (Dansereau et al., 1999). After 60 days, females were mated with 10-month old males fed a diet containing 0.1 ppm Hg for an equal length of time.  Female mink and offspring continued Hg exposure through and beyond the reproductive cycle, and were again mated to 10-month old males, 10 months after whelping.  Females in the 1.0 ppm group experienced mortality (30/50 of parents and 6/7 of offspring) after 11 months of exposure.  Length of gestation and number of kits born per female was not different among dosing groups, though the proportion of females giving birth was low for all mink except those exposed to 0.1 ppm Hg.  Hepatic concentrations of Hg for the 0.1, 0.5, and 1.0 ppm groups, respectively, were 28.2, 80.4 and 96.6 µg/g for female parents exposed for 430 days and 15.2, 49.5, and 99.8 µg/g for female offspring exposed for 330 days.  Detection of Hg in livers of kits that died before solid food was consumed indicated that exposure occurred in utero and/or during lactation.

10.

Fatty acid composition was measured in adipose tissue surrounding the lymph nodes in male and female minks fed control diets of freshwater and marine fish and similar diets laced with 62 mg Cu/kg diet (Käkelä and Hyvärinen, 1999).   Two fatty acid components of phospholipids were lower in Cu-treated groups than in freshwater-diet control groups.

11.

Vitamin levels were measured in liver, adipose tissue, and plasma of male and female minks fed control diets of freshwater and marine fish and similar diets laced with 62 mg Cu/kg diet (Käkelä et al., 1999).  Exposure to Cu had no effect on hepatic vitamin levels, and caused a decrease in vitamin E levels in adipose tissue of the freshwater group.  Exposure to Cu caused a decrease in vitamins A₁ and A₂ in the plasma to 50% the control values.  Exposure to Cu caused a significant increase in plasma levels of thyroxine.

IV.

Petroleum

1.

Thirty 8-week-old male mink kits were put into 3 groups of 10 and fed diets containing 0, 100, or 1,000 μg/g weathered Prudhoe Bay crude oil blended into standard mink feed (Beckett et al., 2002). Diets were fed to mink during a four-month period (July-November, 2000), and feed and water were provided ad libitum. One animal in the 100 μg/g treatment group died of urolithiasis in the left kidney and urinary bladder prior to the end of study. Mink (n=29) were anesthetized at the end of trial. A significant decrease in feed consumption occurred based on mean daily consumption values; 251.1g (0), 217.88 (100 μg/g), 196.6 (1,000 μg/g). There were no clinical signs of toxicity, and crude oil consumption did not affect body weight gain; 1012g (0), 1035g (100 μg/g), 977g (1,000 μg/g). Data suggest exposed mink suffered from anemia, and there was an upward trend in liver (52.66g 0, 59.78g 100 μg/g, 71.61g 1,000 μg/g) and spleen  (3.29g 0, 5.25g 100 μg/g, 5.61 1,000 μg/g) weights with increasing crude oil concentrations. Examination of tissues and brain sections indicated no significant alterations.

V.

Other

1.

In 1974 and 1975, farm mink, ages 10 to 12 weeks were put in groups of 2 males and 8 females.  They were fed 0, 1, 2.5, 6.25, or 15.625 ppm polybrominated biphenyls (PBBs) mixed into mink feed, or 1.54 or 11.98 ppm PBB obtained from mixing PBB contaminated poultry or beef into mink feed (Aulerich and Ringer 1979).  Percent mortality for the mink in the groups as listed above, was 0, 0, 10, 90, 100, 10, and 100.  The PBB poisoned mink rejected food, lost weight, had an unthrifty appearance, and had fatty infiltration of the liver.  Female body weight during the study for the control ranged from 700 g to 950 g, and for treated females 525 g to 1025 g (estimated from graph).  Brain, heart, liver, lung, spleen, and kidney weights as percent of body weight for the control group were 1.03, 0.81, 3.70, 1.20, 0.41, 0.67; for the 6.25 ppm 1.53, 0.82, 5.47, 1.44, 0.41, 1.03; for the 15.625 ppm 1.60, 0.80, 5.52, 1.46, 0.39, 0.92; for the 11.98 ppm 1.77, 0.86, 5.58, 1.37, 0.38, 0.92.  Average body weight and days on diet for the control, 6.25, 15.625, and 11.98 ppm groups, respectively, were 854.78 g and 313 days, 567.11 g and 210 days, 561.60 g and 74 days, and 519.00 g and 54 days.  Average number of kits whelped per female, percent kit mortality, average kit birth weight, and kit weight at 4 weeks for controls were 5.6 kits, 23%, 9.1 g, and 128 g; and the range for treated groups 1, 2.5, and 1.54 ppm were 3.5-4.2 kits, 47-60%, 7.5-8.6 g, and 87-132 g.  The 1 ppm and 1.54 ppm groups’ kits weight at birth and 4 weeks were significantly different from controls.  Mortality (dead/total) for 0, 1, 2.5, 6.25, or 15.625 ppm groups was 0/10, 0/10, 1/10, 9/10, and 10/10.  No mink in the 6.25 ppm group reproduced, and no mink in the 15.625 ppm group survived to reproduction. 

2.

Captive 6-month-old mink at Michigan State University Experimental Fur Farm were fed dietary concentrations of 0, 0.50, 0.90, 1.62, 2.90, and 5.25 ppm sodium monofluoroacetate (compound 1080) for 28 days (n = 5 males and 5 females per group, Hornshaw et al., 1986b).  Significant reductions in body weight were observed in female mink fed 0.90 ppm, and in both sexes fed more than 0.90 ppm.  Change in male body weight (g) for 0, 0.50, 0.90, 1.62, 2.90, and 5.25 ppm groups, respectively, were +283, +354, +36, -204, -614, and –544, and for females they were +204, +53, -115, -117, -366, and –445.  Cumulative feed consumption ranged from 1316 to 7217 g, cumulative compound 1080 consumption ranged from 0-7.6 mg.   Ranges of red blood cells/mm³ (x 10⁶), white blood cells/ mm³ (x 10³), hemoglobin (g/dL), and hematocrit (%) were 9.26-9.89, 6.6-23.3, 21.1-23.2, and 50.5-54.3.  Hemoglobin in the 1.62 and 2.90 ppm treatment groups were significantly different from the control.  The range of organ weights were (% of brain weight): male/liver 321-839 and female/liver 263-715; male/spleen 15.5-48.0 and female/spleen 12.5-50.1; male kidney 63.9-104.4, and female/kidney 53.3-86.0; male/lung 84.0-112.4 and female/lung 74.0-96.5; male/heart 59.9-106.7 and female/heart 50.4-74.4; and testes 3.6-9.0.  Liver weights in all treatment groups, spleen weights for males and females combined in the 1.62, 2.90, and 5,25 ppm treatment groups, kidney weight for males in the 0.90 ppm treatment and for males and females in all treatments above 0.90, heart weight in males in the 0.90 treatment and higher, and heart weight in females in the 5.25 ppm treatment group were significantly different from controls. 

For mink in a separate reproductive study fed 0, 0.05, 0.20, and 0.80 ppm compound 1080, number of females bred/total females was 12/12, 11/12, 10/12, 2/12; number of females whelped/females bred was 9/12, 9/11, 7/10, and ½; mean number of live kits/female whelped 5.9, 6.0, 4.0, and 5; total number of kits were 6.1, 6.4, 4.0, and 6; percent of kits surviving after 3 weeks was 94, 85.2, 95.2, and 0; and percent of kits surviving after 6 weeks was 86.8, 75.6, 85.7, and 0.  Mean kit body weight in the 0.20 treatment group was significantly different from the control at 3 and 6 weeks, the difference was due to a decreased litter size in the 0.20 ppm group.  Mean kit body weight at birth ranged from 8.8-9.8 g, at 3 weeks 89.6-108.9, and at 6 weeks 235-292 g.  LC50 values were calculated to be 3.2 ppm.  Concentrations above 0.80 ppm led to decreased weights of liver, spleen, kidneys, and loss of coordination of hindquarters.  There was a trend towards reduced body weight at lower doses, however, feed consumption was not reduced.  Compound 1080 was suspected of causing the impaired reproduction in the mink.

3.

Captive mink were fed warfarin or sodium monofluoroacetate (Aulerich et al., 1987b). The authors were unable to obtain high enough concentrations of sodium monofluoroacetate (aconitase inhibitor) in the rabbits to cause mortality in the mink, so tests for secondary toxicity in mink were abandoned.  In 1984 – 1985, mink were fed warfarin for 4 weeks, mixed into diet directly, or fed to New Zealand white rabbits, which were sacrificed and mixed with mink feed to obtain correct concentrations.  Mink fed 7 ppm or more warfarin exhibited anorexia, lethargy, incoordination, and bloody feces.  For mink fed warfarin directly in their food, at 0, 2.2, 3.9, 7.0, 12.5, 22.5 ppm, mortality was 0, 0, 0, 10, 50, and 100%, and mean days to death were NA, NA, NA, 17, 16.6, and 12.2.  Weight change ranged from –138 g to +56 g in males and –46 to –213 in females, and cumulative feed consumption ranged from 5789 to 8001g for males and 2289 to 4851 for females.  Cumulative warfarin consumption ranged from 0 to 73.7 mg in males and 0 to 28.7 mg in females.  Feed consumption for males was significantly different from the controls in the 2.2 ppm group in week 3, the 22.5 ppm group in week 2, and in females in the 2.2 ppm group in week 3, in the 12.5 ppm group in acclimation and weeks 3 and 4, and in the 22.5 ppm group in week 2.  In mink fed warfarin in feed containing rabbit meat from warfarin-contaminated rabbits, there was no mortality.  Weight change ranged from +18 to +117 g in males and –54 to –127 g in females, and cumulative feed consumption ranged from 5180 to 7343 g in males and 3717 to 7203 in females.  Cumulative warfarin consumption ranged from 0 to 134.1 in males and 0 to 83.7 in females.  Male feed consumption was significantly different from the control in the 2.2 ppm group in week 2.   

 References for Mink

Aulerich, R. J. and R. K. Ringer. 1977. Current status of PCB toxicity to mink, and effect on their reproduction. Arch. Environm. Contam. Toxicol. 6:279-292.

Aulerich, R. J., R. K. Ringer, H. L. Seagran, and W. G. Youatt. 1971. Effects of feeding coho salmon and other Great Lakes fish on mink reproduction. Can. J. Zool. 49:611-616.

Aulerich, R. J., R. K. Ringer, and S. Iwamoto. 1973. Reproductive failure and mortality in mink fed on Great Lakes fish. J. Reprod. Fert., Suppl. 19:365-376.

Aulerich, R. J., R. K. Ringer, and S. Iwamoto. 1974. Effects of dietary mercury on mink. Arch. Environ. Contam. 2:43-51.

Aulerich, R.J., and R.K. Ringer.  1979.  Toxic effects of dietary polybrominated biphenyls on mink.  Arch. Environ. Contam. Toxicol. 8:487-498. 

Aulerich, R. J., S. J. Bursian, W. J. Breslin, B. A. Olson, and R. K. Ringer. 1985. Toxicological manifestations of 2,4,5,2', 4', 5'-, 2,3,6,2',3',6'-, and 3,4,5,3',4',5',-hexachlorobiphenyl and Aroclor 1254 in mink. J. Toxicol. Environ. Health 15:63-79.

Aulerich, R. J., R. K. Ringer, and J. Safronoff. 1986. Assessment of primary vs secondary toxicity of Aroclor 1254 to mink. Arch. Environ. Contam. Toxicol. 15:393-399.

Aulerich, R. J., S. J. Bursian, M. G. Evans, J. R. Hochstein, K. A. Koudele, B. A. Olsen, and A. C. Napolitano. 1987a. Toxicity of 3,4,5,3',4',5'-hexachlorobiphenyl to mink. Arch. Environ. Contam. Toxicol. 16:53-60.

Aulerich, R. J., R. K. Ringer, and J. Safronoff.  1987.  Primary and secondary toxicity of warfarin, sodium monofluoroacetate, and methyl parathion in mink.  Arch. Environ. Contam. Toxicol. 16:357-366. 

Aulerich, R. J., S. J. Bursian, and A. C. Napolitano. 1988. Biological effects of Epidermal Growth Factor and 2,3,7,8-Tetrachlorodibenzo-p-dioxin on developmental parameters of neonatal mink. Arch. Environ. Contam. Toxicol. 17:27-31.

Aulerich, R. J., S. J. Bursian, A. C. Napolitano, and T. Oleas.  2000.  Feeding growing mink (Mustela vison) PCB Aroclor 1254 does not affect baculum (os-penis) development.  Bull. Environ. Contam. Toxicol. 64:443-447. 

Bäcklin, B. and A. Bergman. 1992. Morphological aspects on the reproductive organs in female mink (Mustela vison) exposed to polychlorinated biphenyls and fractions thereof. Ambio 21:596-601.

Bäcklin, B.M., E. Persson, C.J.P. Jones, and V. Dantzer.  1998.  Polychlorinated biphenyl (PCB) exposure produces placental vascular and trophoblastic lesions in the mink (Mustela vison): a light and electron microscopic study.  APMIS 106:785-799.

Beckett, K.J., R.J. Aulerich, L.K. Duffy, J.S. Patterson and S.J. Bursian. 2002. Effects of dietary exposure to environmentally relevant concentrations of weathered Prudhoe Bay crude oil in ranch-raised mink (Mustela vison). Bull. Environ. Contam. Toxicol. 69:593-600.

Bergman, Å., M. Athanasiadou, S. Bergek, K. Haraguchi, S. Jensen, and E. K. Wehler. 1992a. PCB and PCB methyl sulfones in mink treated with PCB and various PCB fractions. Ambio 21:569-576.

Bergman, Å., B. Bäcklin, B. Järplid, L. Grimelius, and E. Wilander. 1992b. Influence of commercial polychlorinated biphenyls and fractions thereof on liver histology in female mink (Mustela vison). Ambio 21:591-595.

Bleavins, M. R., R. J. Aulerich, and R. K. Ringer. 1980. Polychlorinated biphenyls (Aroclors 1016 and 1242): Effects on survival and reproduction in mink and ferrets. Arch. Environ. Contam. Toxicol. 9:627-635.

Bleavins, M. R., R. J. Aulerich, and R. K. Ringer. 1983. Hexachlorobenzene-induced effects on the lymphocyte blastogenic response to Concanavalin A in the mink and European ferret. Environ. Toxicol. Chem. 2:411-418.

Bleavins, M. R., S. R. Bursian, J. S. Brewster, and R. J. Aulerich. 1984a. Effects of dietary hexachlorobenzene exposure on regional brain biogenic amine concentrations in mink and European ferrets. J. Toxicol. Environ. Health 14:363-377.

Bleavins, M.R., R.J. Aulerich, and R.K. Ringer.  1984b.  Effects of chronic dietary hexachlorobenzene exposure on the reproductive performance and survivability of mink and European ferrets.  Arch.  Environ. Contam. Toxicol. 13:357-365. 

Blus, L. J., C. J. Henny, and B. M. Mulhern.. 1987. Concentrations of metals in mink and other mammals from Washington and Idaho. Environ. Pollut. 44:307-318.

Brunström, B. 1992. Induction of cytochrome P-450-dependent enzyme activities in female mink (Mustela vison) and their kits by technical PCB preparations and fractions thereof. Ambio 21:85-587.

Brunström, B., B.-O. Lund, A. Bergman, L. Asplund, I. Athanassiadis, M. Athanasiadou, S. Jensen, J. Örberg. 2001. Reproductive toxicity in mink (Mustela vison) chronically exposed to environmentally relevant polychlorinated biphenyl concentrations. Environ. Toxicol. and Chem. 20:2318-2327.

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