TABLE OF OONTENTS
ACKNClWLEDGEI1ENI'S
1.
ISSUE
2 • ThTRODUcrION Ai'ID BACKGROUND
3 • D"TA INrERPRErATION/SIGNIFICANCE
4.
OJNCLUSIONS
5 • Rt:COMMENDATIONS
APPENDICES
A. Report on the effects of mercury on Florida Panthers. William Buck, DVM
B. Working Group Participants

ACKNCWLEDGEMENTS
'rhe Technical Subcorrmittee wishes to recognize and acknowledge the contributions and input of the rrany individuals representing the agencies comprising the Florida Panther Interagenc1 cemnittee.
Their involvement ani assistance have been invaluable in the preparation, review, analysis and interpretation of inforrration and data associated with this report.
Dr. Melody Roelke deserves special recognition for her early recognition of a problem with the panther and her dedication which inspired the entire subcomnittee. This report would not have been possible without her perseverance.
A special thanks is also offered to: Dr. William B. Buck,
Dr. George V. Kol1ias, Dr. Robert Ringer, and Dr. Stephen Sundlof; to
Sonjia Wilson for her assistance to Dr. Roelke and for typing the drafts and final document; report; to Mark Cantrell for the graphics contained in the to Clint ~bore who conducted the statistical analyses vital to the report; and to Dena Anderson for her efforts in assembling and shipping samples.
Additionally, personnel of the U. S. Fish and Wildlife Service's
Patuxent Wildlife Research Center, Laurel, Maryland, and the Florida Game ani Fresh Water Fish Comnission's Eustis Laboratory, Eustis, Florida, are to be commended for their rapid m1alysis of rraterials crucial to the developrrent of observations and reconrnendations presented in this report.
Dr. Don Schultz is also to be comnended for editing and assembling this report.
A <::omplete listing of individuals attending the November 16-17 and/or December 7··3, 1989, meetings is presented in Appendix B.

srATUS REPORT
MERCURY OJNTAMINATION IN
FLORIDA PANTHERS
1.
ISSUE
Extremely high levels of mercury (100 parts per million-ppm) were found in the liver of a Florida panther that died in the Everglades on July 26,
1989.
No definitive cause of death was identified, but mercury toxicosis is suspected.
Analysis of various tissue samples from other dead panthers recovered since 1978 also contained mercury at levels of concern.
2.
INrRODUcrION AND BACKGROUND
L~ February, 1989 the Florida Game and Fresh Water Fish Commission (GFC), the Florida Department of Environrrental Regulation (DER), and the Florida
Department of Health and Rehabilitative Services (HRS) released data that had been jointly <Xlllected beginning in 1984 reporting unexpectedly high levels of mercury (Hg) in edible portions (fillets) of largerrouth bass collected at 69 sites throughout Florida.
Mercury concentrations exceeded
0.5 parts per million (ppm), wet weight, at 32 sites and 1.0
ppm at 15 sites.
Concentrations as high as 4.4 ppm were reported from Southeast
Florida.
The current U.S. Food and Drug Administration action level for mercury in fish is 1.0 ppm, whereas Florida's action level is 0.5 ppm.
In
1989, HRS issued area-specific health advisories (based on average Hg concentrations) with the following criteria: Fish containing 0.5-1.5 ppm
Hg - limit consumption to one meal/week and eat no fish containing levels of 1.5 ppm or higher.
A rreeting in March, 1989, established a working group comprised of State agencies and the u.S. Fish and Wildlife Service (FWS) to coordinate the collection of fish sa~les and collate data from various sites within the state.
The State also expanded its fish sampling program to 150 sites in
1989.
The FWS provided technical assistance to State laboratories and took responsibility for further sampling of fish and sample analysi~ on FWS lands and offered to assist the National Park Service (NPS) in sampling of fish in the Everglades National Park (ENP) with sample analysis to be conducted at FWS labs.
The FWS and the ENP collected 77 samples of fish from the ENP in March and April.
Samples from one part of the ENP ranged between 0.5-1.5 ppm whereas samples from another section of the ENP exceeded 1.5 ppm.
Mercury levels in largerrouth bass collected by the FWS in 1989 from Loxahatchee National Wildlife Refuge were found to be between
0.5-1.5
ppm.
Appropriate health advisories were issued for the refuge and park in conjunction with HRS.
Shortly after the release of the original findings of high Hg levels in fish tissue, the GFC Division of Wildlife began investigating
Hg contamination in selected wildlife species of the Everglades in those areas where high Hg levels were found in fish.
The species examined thus far are muscle tissue from softshell turtles, alligators, mottled

duc'<s and white-tailed deer.
The laboratory analyses to date have verified that Hg bioconcentration was manifested in longer-lived species at the higher trophic levels.
Average Hg levels observed in alligator flesh was
2.92 ppm while average Hg levels observed in the other three species were well under 1.0 ppln.
Levels in largemouth" bass exceeded levels from fishes lower on the food chain.
Prior to the recent efforts, known surveys for ffi9L"cury in Florida biota ffive been limited to a few studies.
The possible occurrence of man-made lX'llutants in the Everglades ecosystem was examined by the ENP in an extensive survey in the early 1970's.
Between 1971 and 1973, a total of 95 samples representing various trophic levels was collected in ENP and adjacent areas.
Those animals sampled were various species of birds, crocodilians, both freshwater and marine fishes, and crustaceans.
M31TJIl\3.ls
were not collected during this study.
Mercury, as well as other trace elements and chlorinated pesticides were included in the analyses.
The samples included whole eggs of birds and crocodilians, muscle and brain tissues of birds, and whole-body analysis of fish, frogs and invertebrates.
Hg levels in these varied samples ranged from 0.05 ppm to 2.62 in the
95 samples analyzed.
The highest levels were found in freshwater vertebrates.
Freshwater fishes contained Hg levels ranging from 0.05 ppm to 0.94 ppm.
Alligator eggs ranged from 0.41
to 0.71 ppm, and white ibis ffid the highest levels, ranging from 1.0 ppm to 2.62 ppm.
Relatively low levels of Hg were found in freshwater crayfish.
The NPS report concluded that Hg concentrations were probably too low to have acute effects on wildlife, but could lead to long-term chronic problems, especially in freshwater ecosystems.
Another study was conducted in 1986 by the FWS in Loxahatchee National
Wildlife Refuge.
Mercury analyses were run on anhinga and little blue heron livers and whole bodies of largemouth bass and lake chubsuckers.
Mercury levels were high in anhingas from some rookeries, but not others
(range: 0.42 - 2.72, <rean - 1.5 ppm, on a wet weight basis).
Mercury in largemouth bass ranged from 0.56 - 1.05
ppm on a wet weight basis.
Neither of these fonner studies were effective in identifying the Hg problem in Florida.
Both were surveys, not designed to look specifically at Hg.
Both studies analyzed organs of birds and whole-body fish.
Neither study should be used as a benchmark to argue that Hg levels have increased dr&Tatically since those studies or the present work were conducted.
Rather, the earlier surveys suggest a Hg contamination problem existing at the tjJne of the earliest ENP study.
Much concern has nCM/ surfaced in Florida to determine the source of the
Hg contamination problem.
The traditional sources of excessive Hg in the ecosystem; pulp and paper plants, chor-alkali plants, or coal fired power plants, etc., '3Ie not evident in Florida.
While no generally accepted explanation has surfaced, a hypothesis has been suggested by
2

several concerned researchers.
This hypothesis suggests that Hg is coming from a natural source, Le., the peat soils ccmnon in the state.
These often flooded, and highly anaerobic soils, provide a suitable environment for the lrethylation of inorganic Hg.
Metblymer=y is a product of primarily anaerobic bacteria and is the biologically active and toxic form of mercury.
Inorganic Hg is considered to be biologically innocuous.
The methylation process, of itself, is probably not a direct avenue for bioconcentration of mer=y in the food web.
Methylmercury in anaerobic soils is probably not bioavailable.
However, by burning peat soil, slow oxidation of peat, draining or other disturbances of peat, the methylmercury enters the food chain where it bioaccumulates in top carnivores of aquatic food chains.
While no research has yet been conducted in Florida to verify this hypothesis, work performed in Finland, a country with one third of its land covered in peat soil, has traced mercury contamination to various types of disturbance of that soil.
'lTne developing Hg problem began to focus on the Florida panther on
July 26, 1989 when panther *27, a 4-year old female, radio-instrumented since April 1988, died in the East Everglades near Everglades National
Park (Figure 1).
A necropsy performed on July 27 found no obvious cause of death.
In September, a FWS contract laboratory performed an initial contaminants screening for selected pesticides and heavy metals on tissues from this panther.
Both mercury and seleniwn levels in the animal's liver were high; rnercury was measured at 98 ppm and seleniwn at 22 ppm.
This value was so high that a second test was run at an FWS facility for o::mfirrration.
The second value was also high - 110 ppm.
Liver has been the primary organ of interest because of the comparability of panther liver data with liver values of domestic cats from published literature.
As a result of the concern raised by the data from panther *27, liver and hair samples taken from other dead panthers that had been archived over the past years, and some hair samples from living panthers were sent to both the FWS and GFC laboratories for analysis.
six liver samples contained rnercury levels of 7.8 ppm or higher (range of all 10 samples was 0.005 to 20.0 ppm).
Mercury levels in hair samples fran 10 individual panthers ranged fran 0.02 to 130.0 ppm.
Of these, six contained levels over 7.8 ppm.
On November 7 and 8, 1989, the Technical Subcomnittee of the Florida
Panther Interagency Ccmnittee met to address the relevance of the mercury situation to Florida panthers.
The objectives of this meeting were to:
(1) evaluate and discuss the significance of existing data; (2) develo,) sampling plans to more fully characterize the situation; and (3) develop a written report containing data sumnaries and specific recarrnendations for action.
3

3.
DIiTA ANALYSIS AND INI'ERPRETATION
The initial and perhaps most urgent question addressed by the subcommittee was whether panther #27 died fran mercury toxicosis. This question cannot be answered conclusively from direct evidence.
Indirect evidence for mercury toxicosis in this panther was suggested by the extraordinarily high levels of Hg in tissues from this animal (110 ppm in liver, 130 ppm in hair, and 6.3 ppm in brain).
Microscopic or histologic examination of brain tissue could have verified Hg toxicosis, however, the brain was too decayed for histopathological work.
It is the consensus of the subconmittee, based on the reported mercury levels, that panther #27 probably died as a result of Hg toxicosis.
Dr. William Buck, a consultant to the subcommittee, stated that i f panther #27 did not die as a result of the reported high Hg levels, she would have eventually.
This statement is supported by data available for danestic cats which are presumed to be physiologically similar to the panther.
Fatal levels of total Hg in danestic cats livers have been reported to range from 37 to 145.5 ppm.
( A]:pend ix A).
Following the recognition of possible Hg toxicosis in panther #27, additional samples from #27 and archived tissues of other panthers were submitted for analysis.
These were from panthers that had either died from non-mercury related causes, or were alive when the samples were taken.
All available data are presented in Table 1.
When the mercury data are examined by geographical location and age of the panther (3-7 years old or 8+ years old) there were striking differen~~s noted (Figure 2).
Based on geometric rreans, the liver mercury levels for the younger group of panthers living in the eastern region of southern
Florida was 85 times higher than those living in the western region.
In the western group, liver Hg concentration in old cats were 48 times greater than young cats.
No older panthers have been sampled from the eastern portion of the range, either due to a sampling error or the absence of older adults fr~n that population.
In order to extrapolate organ mercury levels of dead panthers to living animals for which no organ tissue is available, we examined hair and liver obtained at the time of death from a small number of panthers .'(n
=
6).
This set of data was subjected to statistical analysis to determine i f there was a correlation with the liver data (Figure 3).
Correlation at the 95 % level was found between liver and hair.
Using this information, and additional testing to verify this relationship, it may be possible to predict liver levels through additional hair analysis.
w1lo1e blood levels may also serve as a means to evaluate the mercury burdens in living animals without using invasive techniques such as liver biopsies.
Three different archived sources of blood were analyzed; whole blood, washed red-cells and red-cell fibrin clots.
Si.nce 97% of whole blood mercury is bound to hemoglobin in the red cells, whole blood values could be calculated fran the washed red-cells and red-cell fibrin clots.
The initial laboratory analyses of blood samples shows the same pattern of
4

=ntamination as the liver values based on age and geographical location
(Figure 4).
The rrost probable source of mercury contamination in panthers is via the food web.
Florida panthers are known to feed on both large and srrall prey and there appears to be regional differences in the kinds of prey items taken throughout the Florida panthers' range.
This is probably due in part to the availability of prey.
In areas with sufficient populations of larger prey, panthers will feed prinarily on white-tailed deer and hogs.
If larger prey are unavailable, smaller prey such as raccoons, armadillos, and rabbits are taken (Figure 5).
Within the Everglades National Park (ENP), panthers U4, U5, and #22, living in Long Pine Key (LPK) (also known as the Hole-In-The-Donut area), feed primarily on white-tailed deer which are relatively abundant.
The frequency of deer kills in this area averages one every 7-14 days.
Other prey items such as raccoons, rabbits, and armadillos are taken less often and comprise approxinately 20% of the diet.
Whole blood mercury levels for all <three of these panthers were relatively low: 0.21 - 0.23
]:pm.
Florida panthers #16 and #27 live in the area north of LPK known as the
East Everglades.
During the 15 rronths of radio-nonitoring prior to her death, panther #27 fed only on snall prey.
Of the twelve kills recovered, all were raccoon.
At the time of death, her liver mercury was exceedingly high; 98-110 ppm and her hair was 130 ppm.
Panther #16, when last sampled as a sub-adult (2-2.5 yrs. of age), fed on raccoons, otters, and marsh rabbits.
At this time his hair Hg was 82 ppm and his calculated blood level was 1.83 ppm.
As he matured, he shifted from killing smaller to larger prey.
At present panther U6 prinarily feeds on deer, hog, and alligators.
This area of the East Everglades appears to have a low deer density and panthers in this area depend nore on smaller prey (raccoons, rabbits and otters) to maintain themselves.
This dependence on small prey is the probable source of mercury contamination for the Florida panthers and may account for the extrerrely high mercury levels in the individuals tested from thi:, area (Table 1 and Figures 2-4).
It is presumed that the panthers are getting the mercury fran small prey such as racco<pns which feed on contaminated aquatic species.
Panther #21, after leaving her rrother, rroved east through the abandoned farm fields south of Hanestead and Florida City.
This area supports relatively low numbers of deer and she fed mainly on small prey, primarily raccoon, and only occasionally on deer.
She is the sibling of panther U6
(a male) and =nsumed basically the same diet as he did, but had a
=nsiderably lQl,;er whole blood mercury level than he did (0.54 ppm vs. 1.83
j:pffi)
(Table 1).
This may reflect the males proximity to the Shark River
Slough drainage basin and his consequent contamination fran small orey.
In
=ntrast, a similarly aged, dispersed panther (#22) living in the i.PK
area and feeding primarily on deer, had a low blood mercury level consistent
'NLth those of ~1e adults in the same area.
5

Fcxxl consumption by panthers in the western portion of their range (Big
Cypress Swamp Fakahatchee Strand ecosystem) ShCMS a similar pattern of regional differences as related to the availability of prey species.
Those panthers living in the Fakahatchee Strand State Preserve (FSSP) take prirrarily raccoons, whereas those living north of State Road 84 in the northern Fakahatchee Strand (NFS) Bear Island area of the Big Cypress
National Preserve, and private ranches to the north, take primarily de<>.I
and hogs.
The rrercury levels in the north versus south Fakahatchee Strand follow a similar pattern as that shown in the Everglades system: those animals consuming primarily sooll prey have considerably higher Hg levels
(FSSP: liver 19-20 ppm, blood 1. 7 ppm) than those consuming large prey
(NFS: liver 0.05-7.8
ppm, blood 0.35 ppm).
Florida panther reproductive success appears to be closely associated with the type of rrajor prey item available (Figure 6).
ill those areas where deer and/or hog are the primary food item the panthers are reproductively successful.
ill the Lone Pine Key of the ENP and the northern Big Cypress swamp, litter size ranges fran 2-4 offspring.
Adult females have been documented to rear young at a rate of 1.04-1.09 kitt.ens
per female radio-collar-year (number of females x total radio-collarye.ar/documented > 6 Il'Onth-old kittens).
ill cont.rast, in the Fakahatchee
Strand State Preserve where sooll prey are the primary prey, the female panthers are not as productive, with a litter size of one offspring and
0.38 kittens produced per female radio-collar-year.
This probably is the result of poor nutritional status.
However this may be exacerbated by chronic mercury toxicity which can cause abortions, stillbirths, and congenital anorralies. In addition, there may be behavioral and developmental problems that would result in early neonatal death.
6

4.
Q)NCLUSIONS
The Technical Subcommittee made the following conclusions based on available data.
.
1.
Mercury contamination of the Florida Panther has been docurrented.
2.
Panther #27 contained levels of mercury in its liver consistent with mercury toxicosis reported fran laboratory experiments and field observations of danestic cats.
3.
It is likely that mercury toxicosis was involved in the death of panther #27.
4.
Elevated mercury levels have been docurrented in other dead and live panthers. None were as high as panther #27, but sorre are at levels of concern.
5.
Panthers with higher elevated mercury levels were found in the
Fakahatchee Strand and East Everglades area.
These areas appear to be mercury "hot spots".
6.
The presurred source of contamination is contaminated prey, probably raccoons, which bioaccurnulate mercury throuCJh the aquatic food web known to be contaminated with mercury in certain areas.
7.
The "hot spots" were correlated with a low availability of deer and hogs and a high conswnption rate of small IUaII1lll3.1s such as raccoons.
8.
The reproductive success in female Florida Panthers is lower in those areas where slTall prey (principally raccoons) is the predaninant food source.
This may be the result of poor primary nutritional status but also may be D:lllljXJunded by mercury contamination.
9.
Three living panthers are of irrrnediate concern.
Panther #16 had highly elevated levels of mercury in hair and blood when tested in
February, 1988 that exceed the subcamtittees action levels.
Panthers
#23 and #9 have the same prey base as panther #27 (primari:iy raccoons) and may be exposed source.
to high levels of mercury through this similar food
10.
land management practices and public use regulations that increase deer populations or, where appropriate, hogs and other noncontarntnated prey, could shift panthers away fran contaminated prey species.
11.
Mercury contamination is a serious threat of tl1e Florida Panther.
to the continued existence
7

5.
~DATIONS
'nIl' by k>chnical subcormi \:tAA recOlllllends tJJa\: the following actions be taken the involved agencies.
Agency assignlW'Jlts follow each action.
!,.
Ml\NAGf~~AC!'IONS.
1.
Recapture all collared panthers on a routine basis am. test for
O:ll1tamination.
Number 9 and offspring, 23 and 16 should be checked on a priority l.>asis as determined by the subcolllnittee due to historically high bl(~ levels, preferred prey, and/or location in sus~cted roorcury "hot spot".
In addition, any othe. panthers that a meet these criteria based on laboratory results or location will be imnediate1y tested.
Blcxxl am.
hair samp:tes will be analyzed on a rapid tumarolmd basis.
Where Whole blood level exceeds 1.4 ppm wet weight met'cury the ~rk'ing group will inmadiately convene to recanoend a oourse of action for that animal, to the FPIC.
The value of 1.4
ppm ffiO,'1tioned in Managerrent Action #:I.) is derived from the table in
Appendix A entitled "TisSl1e Concentrations of Mel;CUry I\Ssociated with
Signs and Lesions of Alkylmercury Toxi=sis".
The table depicts a level of 14-17 ppm mercury in blood as ind.icating toxicosis.
The subcal~ittee used 10% of these values (1.4-1.7
ppm) as an appropriate number upon the recam'<c-mdation of Dr. William Buck who states "A
O(Xl1ll:)O rule of thumb is that the a minimal toxic dose of chemical is ahout 10% of lethal dose.
Although recognizing that this may be extending the rule too far, one could assUI\\e tl1at the concentrations of mercury in the various tissues aSf>ociated with minimal toxicosis in the cat ~uld be about 10 percent of those listed • • . for lethal toxi=sis."
(Appendix A, page 4).
The Envimnrrental Protection Agency, when setting criteria of to:dcants for aquatic endangered species, uses a value of 1% of the toxic dose that ~uld kill 50% of the species.
Thus, the subcomnitt.ee
felt that t.he 10% value was a rational one.
(GFC, NPS am. FWS).
2.
3.
Increase efforts tc capture W1collared panthers and analyze blood and mir for ~cury.
(GFC.
!ncl\.lded in the SSP recorrmendations).
Identify other potential iOOl;CUry "hot spots" for the Florida Panther through the use of historical a.nd current mercury data and lnf(ll-"l1'l'ttion.
The two areas that llre considered cUrrently as "hot spots" are
Fall.ahatchee strand, sout.h of Alligator Alley, and. the East Everglades area.
(FWS, NPS, GFC aoo
DM) -
4.
T-Cike action through public use regulations to increase the numbers of nonco!~~nated prey such as deer (and.
hogs where appropriate) in areas identlfled as mercury "hot spots".
The GFC and DNR have already closed the Fakahatchee Stram State Preserve to hunting for deer and.
hogs
The East EyE>rglaoos area has been designated for addition to the •
~~Ilades
National Park.
Consideration should be given to tightening
~chie~e~~a~=;~t-~oarn~ itafta lengthy delay is expected until the area .
B us • (GFC and.
NPS)
8

5.
Condnct habitat ffi'\nag",l00nt actiona that will increase the numbers of non-contaminated prey species such as deer (and hogs where appropriate>. Specific areas tllat.
should be ernphasizoo inclooel a.
Fakah~tctl.E;"U~t:rarrl.§.t:at~~s~.
'l'he DNR's existing larrl lTanagement program should be exparrle:.l., where appropriate.
b.
Florida Panther National Wildlife Refu:!e: The FWS plans to
IiiiPleinent an a"qressi~8"habitat improvement program for deer.
It should be given a hi gll priority.
c.
Everglades National Park.
The National park Service plans to restore the natural ecosystem in the Hole-In~The-Donut area t.hat is currently overrun with exotics.
This restoration plan should increase deer numbers. It should be given a high priority.
(j •
B.
d. Big eypresf;..Nat.ional Preserve.
In consultation with the GFC the National Park SE'.rvi(,.'e neoos to develop aOO aggressively linplement. a natural wildlife habitat management plan to increase tile natural abundance and diversity of deer habitat.
The existing fire llunagerrent program should be expaOOed for wildlife purpo~es.
Place further emphasis on tile acquisition of the Golden Gates Estates for habitat management to increase the population of noncontaminated prey in the area adjacent to t.he Fakahatchee StraOO "hot spot".
Develop a management agreenlerlt. betw<.>Eln the State and the FWS for nanagement of these larDS for the ~'lorida panther by the Florida
Panther National Wildlife Refuge upon State acquisition.
(DNR and FWS)
AOOl'rIQNI\L TESTIN::l AcrIONS
1.
Determine the ratio of inorganic to organic rrercury (rrethy1Jrercury) in selectoo tissues from the following panthers: 11verbrain #7, 27.
kidney #7, 8, 27 (FWS).
#7, 8, 27,
PO)
59.
2.
Analy~e.
selected tissue from panther #27 and two other panthers for approprlate priority pollutants to includel arrl PCB's lFWS).
metals, organochlorines
.
3.
Conduct lOO:CUry analyses on liver, brain (where available) aOO muscle
(where avallable) tissue from six archivoo bobcats from the Racooon
Point area of Big Cypress National Preserve, six from Fakahatchee
Strand State Preserve, and up to six from Everglades National Park
<G!'C and FWS).
•
4.
C"bfld~lct mercury analys",s on l~ver, muscle, and brain tissue from a:ch~Ved otters includlng
I SlX from Fakahatchee Strand State Preserve
~~~n ~:rqRalacd(X)()esnNPto~nt
.
1'l rea kOf Big Cypress a lOna l Par <GFC 800 FWS).
National preserve, arrl four'
9

'j.
>5.
Conduct a sampling IxexJniln t.o be rompleted by February 1, 1990, to determi ne mercuty levell; in six raccoons taken frolO each of nine locations inclucl ing; four site') in the Everglades National park
(Ic,-,=, fron the Shark Rivm: Slough, one fram Hole-Tn-The Donut, one frem tile FASt Everglades), one site in Conservation area l1lunber 3 north of
Alligator Alley, and four sites in Big C:ypress/Fakahar.ch<;.'e drainage
(Florida Panther National Wildlife Refuge or Bear Island, Hacooon
Point, Fakahatchee Stmnc1 south of Alligator Alley and Big Cypress
'.outJ, ot the loop road).
A muscle sample and a liver sample frem each raccoon will be submitted for analysis.
Other tissues to include kidney, brain, blood, hair and addition muscles and liver will be retained for possible fllture analysis (GFC, FWS, NPS).
The suOComni ttee re(..'Ql1lI\(mds that blood and hair samples of all panthers captured be routinely analyze:} for mercury (GF\; and NPS).
i 'I'ne BLlbccmnittee should ITOve forward to develop a protocol to use the captive Texas cougar (hdd by GFC - Gainesville) for experimental procedures (experil11€'ntal prot<x:ol - GFC, Dr. Roelke).
C. f',OlJOCE lDEN'J'IFICI\TION l\Nl.l
ELIMINATION
1.
Strongly support the State of Florida's current efforts to identify and rectify the souroe of the mercury contanunation.
Write the
Federal Congressional Delegations to alert them
Panther.
Attach a ropy of this report to the problem with the to the letters.
At the appropri<Jt.e time, write a letter to State Legislators endorsing the recalmendations of the State Task Foroe. (FPIC Chairman)
10

TABLE 1.
MERCURY DATA FRCM FLORIDA PANrHERS
Patuxent Lab Analyses Eustis Lab Analyses
Sampling
Sex Date l\ge
1
M 4/18/ 85 OA
F 1/26/ 85
OA
10/28/ 85
OA
Lcx::ale
2
N.FS
S.FS
S.FS
F 4/13/ 87
8/ / 88
F 10/31/ 88
OA
OA
S.FS
cap.
A S.FS
M 2/ / 86 SA S.FS
M
M
1/15/ 89
2/27/ 86
12/ / 87
OA
A
FS/B1
A B1
A B1
ENP F 4/11/ 88
F 12/13/86
6/10/88
A
A
ENP
M 2/2/ 88 SA E.ENP
M
F
F
3/10/87 YA
8/ /88 A
P.R.
B1
7/23/88 YA
8/19/88 YA
3/24/88 SA
H.A.
cap.
ENP
Liver Hair Brain EDTA PM ROC Clot Liver Kidney Muscle
7.8
11.2
0.82
0.17
1.7
Bl00d
3
20.0
0.73
20.0
19.0
14.0
0.10
1.12* 3.3
16.3
21.0
8.5
2 .J./1. 4
0.76
0.J.9
0.31* 0.82
4
0.05
0.28
8.5
13.0
0.05
6.4
0.16
82.0
14.0
7.1
0.24
0.02*
0.23
0.21
1.83*
0.044
0.54
0.22
4.9
0.046
1.3 0.21/0.11
0.06
11.9
0.91 0.19
0.09
4

Estimated age of panther.
81'.= subadl1lt (1-2 yrs.l, YA= young adlllt (2-3 yr~.), A= adlllt (4-7 yrs.l,
01'.= old adlllt (8+ yrs.).
Locale where panther was found or captured.
FS= Fakahatchee Strand; N.FS= Northern
Fakahatchee Strand; S.FS= Southern Fakahatchee Strand; BI= Bear Island; BCNP= Big Cypress
National Preserve; ENP= Everglades National Park; E.ENP= Eastern ENP; P.R.= private ranch north of BCNP; Gap.= panther in captivity; H.A.= Homestead area; C.S.= near Corkscrew
Swamp; Ccrb.= Corbett Managem2.nt Area, Palm Beach Ccunty; SIR= Seminole Indian Reservation;
RP= Raccoon Point.
Blood.
EDTA signifies whole blood mixed with EDTA; PM; post-rrortem serwn; RBC= washed red blood cells; clot= blood clot.
Sample sent for analysis.
No results to date.
Analyses =ndueted in 1985 at a midwestern hunan toxicology laboratory.
Calculated whole blood Hg levels, based on absolute value found in either washed red blood
(RBC) or in fibrin clot.
(97%l (RBC or fibrin clot Hq value) = calculated whole packed cell volume blood level

FIGURE 1
c .
\
, ~
\
"-
\.
\
\
\.
"--
'---..
-
..........
---."
\...
_...
~.~
\
\
I ' iNorthern Fakahatchee:
\
.
\
\
,
\
\
'
\ .
\.
\
Panther Refuge;
Bear Island & i
L.
Private Lands
.....J
I
,-'------~
, Fakahatchee Strand
State Preserve '
Eastl
Evergla~es
Big Cypress
National Preserve
Long Pine Key/
Hole-in-the-Donu
J

FIGURE 2
1.4
. .
005
0.05
7.8
1----1.1-+----.;.
1
2.5
1
\
\
Naples
19.0
20.0
20.0*
[;;J 3 7 yrs
~
8+ yrs
* following 16 months in captivity
>-=-<-'
~f-'----j
1 10 .0]
~_~---J
13.
Flamingo

FIGURE 3
10000 -
L...
Q)
->
1000
100
-+---' c
Q) x
:=;
-+---' cD
CL
10
0.1
1
-
0.Q1
O. 1
!
!
!
!1.l
1
~,
10 100
Figure
3.
Estimated regression of log(l iver Hg) on log(hair Hg), with prediction limits.

FIGURE 4
I
I
\
.
.
!,
\
"---..
\ , - - -
'\
\
\ \
\
.
\
.
\ .
\
\.
\
.\
IO.2i}.
~ \.
\
0.044
0.24
\
10.02#
I 0.069
0 . 3 5 ' . .
I
. " - . _ .
.:::::---'---'.---..-y-,,-,,<-
0.31
1.7
1.12#
0.76+
I ppm
I
~
3 -
8+
7 yrs yrs
" 1 month in captivity
# calculated from clot or washed red cells
+ post mortem hemolysed blood
4.1+
1.
1.7
83
J
#
1
0.221
L - _ - - - - j
0. 23
1
0.2JJ

FIGURE 5
~
Raccoons and/or armadillos
~ Deer and/or hogs
Flamingo

FIGURE 6
~
(
\
"
.
\
.
\
.
.........,
'\
.
r--.---:J \ \ .
IT9
.
\.
\.
.
4 k itt ens/ yr
\
. (n = 6/12.5 yr/13 kittens)
\.
\\.
. ' , , - . _ .
\
\
\
\.
\
I.:::.----.-.-.~,,_,L,
..
/..J
0.38 kittens/yr
(n = 3/8 yr/2 kittens)
(n
1.09 kittens/yr[
= 3/5.5 yr/6 kittens)

APPENDIX A
EFFECTS OF MERCURY ON FLORIDA PANTHERS
Report to the Ad Hoc Interagency Working Group of the
FLORIDA PANTHER INTERAGENCY COMMITTEE
November 16-17, 19~9 by
William B. Buck, DVM
National Animal Poison Information Network
2004 S. Wright Street--SRIB
Urbana, IL 61801
Background
The detection of approximately 100 ppm (wet weight basis) total mercury in the liver and 130 ppm in hair of panther No.
27 found dead in south Florida prompted concern as to the roll of this element in the death of this animal.
Analyses of liver and hair in arChived specimens from other panthers taken since 1985 revealed mercury concentrations greater than 20 ppm in 6 panthers and greater than 10 ppm in 5.
Mercury concentrations in hair roughly correlated with those in livers.
These and other related findings induced the calling together of the ad hoc working g:::oup to evaluate the problem and to recommend remedial procedures.
MercurY
There are four (4) general forms of mercury: 1) metallic, 2) inorganic salts, 3) aryl (ring) organic and 4) alkyl organic mercurial compounds.
The relative hazard to mammals of these forms are least for elemental mercury and greatest for alkyl mercurial compounds such as methyl mercury.
In bodies of water, the soil and the gastrointestinal (GI) tracts of mammals, the various for;ms of mercury are capable of being transformed via microbial action, at least partially, to alkyl mercurials.
Alkyl mercurials (methyl and ethyl mercurials) tend to attach to the red blood cells and concentrate in the brain and skeletal muscle tissues, as well as the liver and kidney.
Other forms of mercury (inorganic and aryl mercurials) tend to concentrate in liver and kidney tissues, but not in brain and muscle.
When taken orally, elemental mercury is very poorly absorbed, while alkyl mercurials (e.g., methylmercury) are almost 100 percent absorbed.
Aryl and inorganic forms of mercury are only partially absorbed from the GI tract.

Biomagnification of Mercury
Mercury contamination of water systems, regardless of its original form (elemental, inorganic or organic) is likely to be biomagnified in the ecosystem as alkyl mercury (methyl or ethyl mercury).
Thus, predators at the top of the food chain are most likely to be exposed to the higher biomagnified levels of alkyl mercurials such as methylmercury.
Panthers'are in this category.
The scientific literature contains numerous reports on the effects of mercury in animals and birds.
However, there are fewer than a dozen good reports on cats--all dealing with the domestic cat.
The comments and suggestions in this report are based upon the unsubstantiated assumption that panthers are comparable to domestic cats in their response to ingestion of mercury in their diet.
Effects of Methylmercury in Domestic Cats (See attached handouts)
1) Dietary levels and toxic effects: a) Daily doses of 0.02 mg/kg for two years caused no adverse effects.
b) Daily doses of 0.046 mg/kg body weight for 60 wks,
0.074 mg/kg' for 40 wks or 0.176 mg/kg for 14 wks caused clinical signs of toxicosis but not death.
c) Daily doses of 0.25 mg/kg 8-14 wks caused clinical signs of toxicosis and death.
d) In a study on the effects of methymercury on pregnant cats, 0.083 mg/kg daily for 58 days caused no signs of poisoning, except 1 of 6 cats aborted and cannibalized all the fetuses.
If one wants to extrapolate mg/kg body weight to ppm in the diet, divide the percentage of body weight that the cat eats daily by 100, then mUltiply that by the mg/kg body weight dose.
Thus, assuming that a cat eats 10 percent of their body weight daily, a dosage of 0.046
mg/kg would be 0.046 x 10 equals 0.46 ppm methylmercury in the diet.
Under these assumptions, cats eating a diet containing from 0.46
to 1.
76 ppm methylmercury would likely develop signs of mercury poisoning after several months or years on such a diet.
2) Clinical signs of methylmercury toxicosis in cats
The signs of poisoning are predominantly associated with the brain.
Electroencephalographic changes can be detected 2-3 weeks before observable signs are present.
Signs usually seen in order of occurrence include a)
2

3) changes in temperament, mood and personality, b) posterior weakness and incoordination, c) gradual onset of ataxia with zigzag and sudden movements, d) hind-limb rigidity, e) compensatory widening of stance, f) highstep gait, g) intention tremors, h) loss of righting reflex and inability to land on feet when jumping, i) tonic-clonic seizures, j) glassy stare, k) vocalization,
1) hypersalivation, m) urinary incontinence, impaired vision and other senses after seizures longer than 24 hours, but no hearing loss, m) coma and n) death.
Abortion and teratogenic changes have also occurred, even when the dam shows minimal signs of poisoning.
Postmortem changes is cats associated with alkylmercury toxicosis
The lesions of alkylmercury toxicosis in cats are located in the brain.
No lesions have been observed in the spinal cord, peripheral nerves, kidneys or other organs.
The leptomeninges may be gray discolored.
Microscopically, there may be a) disintegration of the visual, aUditory and other sensory neurons of the cerebral cortex, b) neuronophagy, c) axonal swelling and demyelination, d) loss of nerve cell processes, e) vacuolation of neuropils, f) proliferation of microglia, g) loss of granular and Perkinje cells of the dorsal cerebellum, h) endothelial hypertrophy and hyperplasia, i) meningitis, and j) vascular necrosis.
4) Tissue concentrations of mercury associated with signs and lesions of alkylmercury toxicosis in cats signs of poisoning and death have occurred in cats having the following tissue concentrations of total mercury:
Tissue
Blood
Concentration (oom wwbl
13-17 (1 cat aborted wi th 5.4 ppm)
Brain
Liver
Kidney
Skeletal Muscle
10-18
40-74
21-37
15-24
3

A common rule of thumb is that a minimal to~ic dose of chemical is about 10% of the lethal dose.
Although recognizing that this may be extending the rule too far, one could assume that the concentrations of mercury in the various tissues associated with minimal toxicosis in the cat would be about 10 percent of those listed above for lethal toxicosis.
Mechanism of Alkylmercury Action
Alkylmercurials are readily absorbed across the GI mucosa.
They readily cross the placental barrier, and thus, may cause learning disorders in both the dam and her offspring.
Although the exact mechanism(s) of action is not known, learning, behavioral and early electrical functional deficits may be due to calcium and neurotransmitter disturbances.
Alkylmercurials a) destroy neurons in the cerebrum and cerebellum, and b) damage the blood-brain barrier.
Thus, there may be direct toxic effects of solutes normally excluded from the brain 2.£ there may be failure of transport mechanisms to supply neurons with essential amino acids and other metabolites.
They may inhibit protein synthesis through inhibition of aminoacyl-tRNA transferases.
Antioxidants such as vitamin E and selenium tend to protect against alkylmercury toxicosis.
Interpretation of the Presently Available Data Regarding the
Florida Panther
1) Liver and hair mercury concentrations (100 and 130 ppm, respectively) in panther No. 27 are compatible with a diagnosis of mercury toxicosis.
2) Evidence of clinical signs of mercury toxicosis before death of panther No.
27 is not available.
3) Selenium concentrations in liver and kidney tissues of domestic animals greater than 5 ppm are associated with toxicosis.
4) The selenium concentration of 22 ppm in the liver of panther
No. 27 should be given consideration as to its relationship to the death of this panther.
The protective relationship between selenium and mercury is an important factor, however, and may partially nullify the toxic properties of both elements.
:
Additional InfOrmation Needed
1) Mercury concentrations in blood, brain, tissues of the panther (alkylmercury tends to as well as liver).
muscle and kidney be in these tissues
2) Form of mercury (organic vs.
inorganic) tissues.
in liver and kidney
4

3) conce;ttrations of alkylmercury in prey consumed by panthers.
Because ~t has been observed that those panthers with the highest me 7 cury (arc~ived
~h~~e ~hose w~th
~t ~s ~mportant specimens) content were those eating raccoon, the lowe~t content were eating deer and wild hog, to determ~ne the mercury content of raccoon being consumed by the panther.
.
4) Selenium concentrations in blood (and. liver and kidney tissues when available) should be monitored in both panthers and their prey.
RECOMMENDATIONS
The following are some of the recommendations of this member of the ad hoc task force:
1) Continue to analyze for mercury and selenium concentrations in archived panther tissues.
Because molybdenum is reputed to be concentrated in peat soils, this element and copper should also be analyzed in the archived specimens.
2) Monitor blood and hair from live panthers for mercury, (and at least 10 % of the specimens for selenium, copper and molybdenum).
Any panthers that die in the future should be necropsied and the various tissues analyzed for the above elements.
3) Monitor the prey of panthers for mercury and other elements
(listed above).
The raccoon and otter and other prey that feed on aquatic life should be targeted for monitoring.
4) Change the land management practices in the mercury contaminated areas to encourage the natural inhabitation of deer and wild hog, to provide mercury-free prey for the panther.
5) When a panther is found to contain 2 ppm or greater concentration of mercury in its blood, i t should be removed from its environment and placed in the captive breeding program that is being established.
6) At the present time there is no recognized and ac~epted therapeutic protocol that would be likely successful for use in the Florida Panther.
However, experimental use of such chelating agents as dimercaptosuccinic acid (DMSA) could be evaluated in those panthers brought in because of mercury contamination.
BIBLIOGRAPHY
A list of scientific articles on mercury derived by computer search is attached.
Some of the more relevant articles are cited below:
5

Hatch, R.C.
1988.
organomercurials in dogs, cats and calves.
In
VET PHARM THERAP. Booth and McDonald, eds. pp 1056-1058.
osweiler, G. D.
et al.
1985.
Organic and inorganic mercury.
In
CLINICAL AND DIAGNOSTIC VET TOX. Keldall-Hunt pub. pp 121-131.
Khera, K.S.
1973.
Teratogenic effects of methylmercury in the Cat:
Note on the use of this species as a l110del for teratogenicity studies.
Teratology 8:293-304.
Charbonneau, S.M.
et al.
mercury in the adult cat.
1974.
Subacute toxicities of methyl
Toxic Appl Pharm.
27:569-581.
Charbonneau, S.M. et al.
1976.
Chronic toxicity of methyl mercury in the adult cat.
Interim report.
Toxicity 5:331-349.
Takeuchi, T. et al.
1977.
The outbreak of Minamata disease (methyl mercury poisoning) in cats on Northwestern ontario reserves.
Environ. Res.
13:215-228.
Harada, M. and A.M.
Smith.
1974??
Minamata disease: A medical report.
In MERCURY pp 180-192.
Eaton, R.D.P., D.C. Secord and P.
Hewitt.
1980.
An experimental assessment of the toxic potential of mercury in ringed seal liver for adult laboratory cats.
Toxic Appl Pharm.
55:514-521.
Houpt, K.A. et al.
1988.
A tuna fish diet influences cat behavior.
J.
Toxic Environ Health 24:161-172.
Books on Mercury
MERCURY IN THE ENVIRONMENT An Epidemiological and Toxicological
Appraisal.
1972.
L.
Friberg- and :J.
Vostal eds.
CRC press.
Cleveland, OH 44128.
pp 215.
MERCURY, Environmental Health Criteria
Organization. Geneva. pp 129.
1.
1976.
World Health
MERCURY HAZARDS TO FISH, WILDLIFE, AND INVERTEBRATES: A Synoptic
Review.
1987.
U.S. Dept. of Interior, Fish and Wildlife s~rvice contaminant Hazard Reviews Report No.
10.
(BioI. Rept.
85 1.10).
pp 90.
6
..

Use
Electrolytic chlorins""(chlorinealkali plants)
~
Electrical apparatus (batteries, switches, fluorescent lights)
Paint (anti-fouling formulations)
Instruments
Catalysts
Dental preparations
Agriculture (fungicides)
...
-
....
Generall~boratory
Pharmaceuticals
Pulp and paper (slimicides)
Amalgamation
Other
Total
Pounds
1,572,000
1,382,000
739,000
391.000
221,000
209,000
204,000
126,000
52,000
.
42.000
..
15,000
1,082,000
6,035,000

.,
.,
..

0.4-1.0
2.0-3.0
0.25 (fish)
0.176
0.074
0.046
0.02
10:90 d
2-3wk
55-96 d
14wk
40wk
60wk
2 years
10-20 mglkg
10-20 mglkg
14-24 mglkg
Buck et al., 1987; Charbonneau et al., 1976 clinical signs clinical signs marked toxicosis toxicosis toxicosis toxicosis no signs

(in sequence)
-
• EEG changes-2-3 weeks before onset of signs
• Changes in temperament, mood, personality and behavior
• Posterior weakness and incoordination
• Gradual onset of ataxia (zigzag with sudden movements)
• Hind-leg rigidity
• Compensatory widening of stance
• High-step gait
• Intention tremors
• Loss of righting reflex and inability to land on feet when jumping
• Tonic-clonic seizures
• Glassy stare
• Vocalization
• Hypersalivation
• Urinary incontinence
• Impaired vision and other senses after seizures far more than 24 hours; but no hearing loss
..
Charbonneau et al., 1976

•
•
•
•
•
•
•
•
•
Gray discoloration of leptomeninges
Microscopic disintegration of visual, auditory and other sensory neurons of cerebral cortex
Neuronophagia
Axonal swelling and demyelination
Loss of nerve cell processes
Vacuolation of neurophils
Proliferation of microglia
Loss of granular and Perkinje cells of dorsal cerebellum
Proliferation of Bergman glial cells
Endothelial hypertrophy and hyperplasia
Meningitis·
Vascular necrosis
No lesions in spinal cord, peripheral nerves, kidneys or other organs

• Exact mechanism not known
• Destroys neurons in cerebrum and cerebellum
• Damage blood-brain barrier
• May be direct toxic effects of solutes normally excluded from brain or
• Failure of transport mechanisms to supply neurons with essential amino acids and other metabolites
• Could be defect in protein synthesis in neurons
(structural changes occur in ribosomes)
• Antioxidant effects of Vitamin E and selenium protect against alkylmercury toxicosis
• May also inhibit aminoacyl-tRNA transferases (thus preventing amino-aceylation and protein synthesis)

• Readily cross the placental barrier.
• Thus, behavioraLand learning disorders in both parents and offspring -.
• Teratogenic and embryotoxic effects occur
• Learning, behavioral and early electrical functional deficits (visual evoked responses) may be due to calcium and neurotransmitter disturbances
.'

of
Tissue
Concentration
wet wt.}
Blood
Cerebral cortex
Cerebellum
Spinal cord
Sciatic nerve
Liver
Kidney _
Gastrocnemius muscle
14-17
17-18
27-29
8-10
8-10
72-74
37
22-24
Charbonneau et al., 1974; Davies and Nielsen, 1977

26
• 90 days on a
~ef of seal liver (100 g/day) produced no toxic effects
• 90 days of beef liver plus 0.25 mg/kg methylmercury produced clinical signs and histologic signs of mercury toxicosis
• The clinical and pathologic features of mercury poisoning in cats are similar to those observed in humans
Eaton et al., 1980; Takeuchi, 1968

518
Tissue
Liver
Kidney
Cerebral cortelt
Cerebellum
Muscle
Heart
" ~:,:'r.·' -.
<':" .:' .
~~;.:..
....
......" •.
i~:'i',.( Lunnlll~
,
'~:_:,
4'
\:':~~:~:.:.:
: :
..
I
, ' .
Sciatic
EATON. SECORD. AND HEWITT
".
TABLE 3
Hg
(ppm)
TEItMI:-:AL MEItCUItY CO:-lCENTItATIO:-:S I='" CATS TISSUES
..
(ppm)
Seal liver fed (g)
Control
(C) L.
25 M.50
H. 100
, Total
Inorganic
Total
Inorganic
Total
Inorganic
TotaY
Inorganic
TOlal
Inorganic
0.51
=
0.85"
0.47 :: 0.09
0.35 :: 0.11
0.29
=
0.16
0.01:: 0.03
0.04 :: 0.02
Total
Inorganic
Total
Inorganic
Total
Inorganic
0.66 :: 0.23
0.26 ::
0.12 :: 0.08
0.03 :: 0.01
." 0:,'3 "~
0.05 :: 0.03 ..
0.11:: 0.17
0,04
0.06
1.08
0.71
=
0.54
=
0.30
1.05
0.77
=
0.:!5
=
0.21
0.23
0.04
=
0.16
=
0.03
0.22
=
0.08
0.07:: 0.03
0.53
0.05
O.:!O
0.04
=
0.08
=
0.Q2
=
0.06
=
0.02
0.24
=
0.06
·0.06 :: 0.02
0.07
O.O:!
0.05 :: O.O::!
2.:!7
1.60
=
1.30
=
1.28
1.82 :: 0.70
I.J I
=
0.52
0.34 :: 0.14
0.06 :: 0.01
0.48 :: 0.11
0.07 :: 0.03
0.66 :: 0.23
0.06 :: 0.02
0.41 :: 0.22
0.08:: 0.03
0.43 :: 0.18
0.07:: 0.03
0.09 :: 0.02
0.05 :: 0.02
o!
:!.n :::
1.28
2.86 :: 0.51
2.02 :: 0.48
0.61 :: 0.21
0.04 :: O.O:!
0.89 :: 0.31
C.'!7 :: 0.41
1.24 :: 0.21
0.06 :: 0.01
0.77 :: 0.34
0.58:: O.oJ
o.n :::
0.23
0.14
:!: 0.06
0.19 :: 0.06
0.07 ::: 0.03
Methylmercury chloride (MM)
40.25 :: 11.51
18.19
=
9.7:!
21.60:: 7.58
8.68:: 5.81
10.43:: 2.36
1.12:: e.:! I
1'!.27:: 2.99
1.95
== 0.89
15.08:: 4.24
0.78:: O.~O
8.92:: 2.08
0.35:: 0.19
10.80:: 3.67
0.47:: 0.21
2.01:: 0.59
0.15:: 0.03

I
\
. I
\
1
,I ~ :,'
,
; i
1
C. Control
L. 25 g seal Ii ver x 517 days
M. 50 g seal liver x 517 days
H.
100 g sea.l liver
da.ys
MM. 0.25 mgllcg
MMc daily
TABLE 4
Se:LENIU~1
A:-.'O TOTAL MERCURY COl'TENT IS FIVE GROVPS OF FIVE ens (ppm)
Liver Kidn.-:y
Hg
0.10::: 0.05"
(N ""
Se
5 x 5)
0.64 ::: 0.06
Hg
::x 0.07
1.20:= 0.41
2.35:!: 0.99
3.21::: 1.78
40.12 ::: 10.20
0.99
"t: O.lot
1.02 ::: 0.29
1.57 :!: 0.48
2.72 '::: 0.69
0.95 ::: 0.26
1.51 :: 0.60
2.20
:= 0.4)
20.58
:!:
7.63
(N '"
Se
.5 )( 5)
1.46 := 0.26
. 2.18
=
0.59
'2.)1 := 0.69
2.75
:= 0.30
1.98 ::: 0.35
.. Mean:!: SD.
.
'
:,-; ~ od·· ..
~·
(.t.": "".
....
~ '.' , i . .
,
I
,
\
!
\

, j EFFECT OF SEAL LIVER MERCl:RY O~ C\TS "17
TABLE 2
PREEXI'[RI~IE~T"l "~D TER~II~"1.
MEkCI;RY LEVEl..S
I~
HAIR .... :-:D BI.OOD 01'
1:- FI\·E'OIET ... RY GROl'r$ OF 8
-lll C."I~
/
Preexperimenl:ll <ppml Termin:,llrr€,(
If-
Group
Bldl,tl
Tot:.1
Hair
Inor·
~aOlc
I"or·
Tl'tal I;:lmc Tl'I:,1
Blood
I "lW' j;:lnic
" j
T"lal
Hair
Im'r· gallic
C.
Control 7.9<1
::: 1.20"
_ I .
0.1\6 7.50
:: 0.86
I.~~
:: 0.26
L.
"15'~ seal liver )( :5', d:ly!' I\.l-l
::: 2.~ I o.~
•
202.(1{1
:: IDO
IU2
~ 4.~O
:!.90
:: 0.29
l-C 50 I,; ~eal liver x 5, days
H. 100 I;!
seal liver
'>t
5., days
2H9
II.'~
7.:'6
::: O.1.t5
1.<.:::
0.62
~'i.(lO
:: M.M)
1\(,2.(10
::: 11(1.(1(1
15.(.() ..
.).
•
=~.~O .:. 11.94
2UO 7.57
1.07
=
6.~0 :: 1.26
:: O.4:!
~1
.~...
"y,:'
~
0 .,,,
......
mg!k~lday
....
l_.:~.:(,~\"
,
._::.:.:'
'~~~;.~_
•• '.;' 1<"."1,
,.;,:~,,: e b' ,., i
Mean' ::: SO;
9.10' 0.50
I :!331.t.OO
340.00
170.00
:!UO
lo2:!.OO
::: 128.70
:: 17.40
:: 6.9(1
~ Too small to mea~ure.
, Due to an error in giving first dose of methylmercury chloride in sc\cn of the ~IM group. this figure is

Laboratory for Animal Services, Cornell University, New
York State College of Veterinary Medicine, Ithaca, NY
J.
Toxic Chemicals Laboratory, Cornell University, New York
State College of Agriculture and Life Sciences, Ithaca, NY
When observed in their home cages, cats fed commercial tuna fish cat food were less active, vocalized less, and spent more time on the floor and more time eating than cats fed commercial beef cat food. There were no differences in response to human handling between the two groups. _
There w.ere no differences in learning ability on a twochoice point maze or in reversal learning in the same maze between beef- and tuna-fed cats. The behavior of the groups differed in a 15-min open field test only in the number of toys contacted. Cats fed the tuna had elevated tissue levels of mercury and selenium.

""
TABLE 5. Mercury and Selenium Content of the Diet
.r
ppm, Dry weight
Mercury Selenium Diet
Red-meat tuna cat food"
Beef (control)"
0.55
0.10
2.90
1:15
"Commercially canned.
'.
"

.
,~
\
TABLE 6. Mercury and Selenium In Cat Tissues after 188 Days of Feeding a Commercially Canned Red Meat Tuna or Beef (Conlrol) Diel
_ . _ . _ r
Brain· Kldnet liver' Musde'
Olet Hg
Se \
Hg Se
Se Hg Se
Red-meat tuna
•
Beef (control)
Red-meat tuna
Beef (control)
, Male cats
0.68
0.06
± 0.04
1.43
±
0.13
0.97
± 0.19
10.47
± 2.21
3.80
±
0.76
11.83
± 0.44
1.17
± 0.17
±
0.01
0.74
±
0.10
0.09
± 0-01 2.07
± 0.13
0.06
±
0.01
1.73
± 0.09
O.OS
± 0.01
Femafecats
1.02
0.06
± 0.23
152 ± 0.09
157
±
0.19
13.43
:I: 0.70
4.2G
±
0.36
8.93
±
± 0.01
0_84
±
0.04
0.10
± 0.01
2.17
:I: 0.17
0.09
o.n
1.19
± 0.12
±
0.01
1.118
± 0.03
0.05
± 0.01
2.02
0.82
± 0.27
± 0.06
1.89
0.90
± 0.11
:I: 0.03
_"""-
'Mean :I: standard error, in ppm dry weight; all differences between respective treatment means were significant (p
<
0.01).

~
.'

.
-.
..
~.
TABLE 7.
Su~ of Toxicologic findings of Oiher Investigators Who Have fed Cats with or without Added Mercury Compounds
..
..
"
..
Duration of
J
. : &perfmental design feeding Toxicologic symptoms
I .
Reference
• .Adult cats were fed {Ish containIng
_ " ll1dded methylmercury at levels
.
(pglkg body welght'd) of: 74
.
176
.
,.,
276-S26d.
92-119 d
P~1c changes In brain at both fftdfng levels
NeB let al.
(1'J76)
Adult cats were fed fish con(;inlng added methylmercury at levefs
(pglkg body welght'dl of: 46
·74
176·
. Young kittens were fed fish that contained up to 0.5 ppm mercury
420d
280d
98 d .
7-11 mo
Minicmll nonprogressive neurological deficit
Oinical signs of methylmercury toxicity at the two highest feeding levels
Proliferation of smooth endoplasmic reticulum; dilation of rough endoplasmic reticulum; floccular degeneration of· hepatic mitochondria
Charbonneau et al.
(19761
Chang and
Yamaguchi
(19741

(119/g
healthy~
,
Tissue location/Comments N liver Kidney Muscle Brain Reference
Mercury-poisoned
Clay lake, Onlario, found dead
Experimenlally killed by methylmercury In food
1
9
96.0
33.4
58.0
39.2
36.0
15.7
30.0
"
18.9
••
Ihis report
O'Connor and
Nielsen t 980
Normal
Northeastern USA
• males
• females
. Soulh-eenlral Onlario louisiana
14
15
4
100
4.3"
2.2"
3.0
1.3
.
1.4
0.9
• •
• •
Wren at a/1980'
Beck 1977
Georgia
• Ware Counly
• Echols Counly
Wisconsin
6
4
49
9.1
5.1
3.3
8.5
4.6
4.2
1.4
0.7
Halbrook 1978
Halbrook 1978
Sherty and SI.
Amanl19U2
·Converted from methylmercury concenlrations reported in original paper, assuming Ihal melhylmercury represenls
50% of tolal mecury In Oller ~ver.

APPENDIX B
Attendance lists for November 16-17, and December 7-8, 1989, m=etings in
Gainesville, Florida.
Sonny Bass, NPS, Homestead, FL, 305/245-5266
Chris Belden, FGFWFC, Gainesville, FL, 904/336-2230
Dr. William B. Buck, U. of Illinois, Urbana, IL, 217/244-7732
John Christian, USFWS, Atlanta, GA, 404/331-3580
Dennis B. Jordan, USFWS, Gainesville, FL, 904/392-1861
Dr. George V. Ko11ias, U. of Florida, Gainesville, FL, 904/392-4751
Ted Lange, FGFWFC, Eustis, FL, 904/357-6631
Todd Logan, USFWS, Naples, FL, 813/643-2636
Tan Logan, FGFWFC, Tallahassee, FL 904/488-3831
Dr.
Del Ni..rrm:>, NPS, Ft.
Collins,
0),
303/491-0695
Robert J. Pennington, USFWS, 'lero Beach, FL, 407/562-3909
Bob Prather, USFWS, 1'al1ahassee, FL, 904/681-7456
Dr. Robert Ringer, Michigan State U., East Lansing, MI, 517/336-1391
Bruce Rodgers, NPS, Atlanta, GA, 404/331-4916
Dr. Melody Roelke, FGFWFC, Gainesville, FL, 904/336-2230
Haner Royals, FGFWI''C" Eustis, FL, 904/357-6631
Dr. Don Schultz, USFWS, Atlanta, GA, 404/331-6343
Jim Stevenson, FDNR, Tallahassee, FL, 904/488-0338
Dr. Steve Sundlof, U. of Florida, Gainesville, FL, 904/392-1841
..