![]() |
|
![]() |
Biological Characteristics
Species
|
Adult
male Enhydra lutris grow
up to 1.5 to 2 m in length with a maximum weight of 45 kg; females are
considerably smaller. The average length for pups is about 60 cm, with a
weight of 2 kg (Orr and Helm, 1989).
The otter’s head is relatively rounded with small ears and a
broad snout; the body is long with the tail broad at the base but
tapering and equal to about a fourth of the body length (Orr and Helm,
1989). The forepaws are stumpy yet highly mobile with retractile claws
while the hind feet are flipper-like and are used for propulsion through
the water (Mason and MacDonald, 1986).
The fur of newborn pups is a light brown, wooly coat blending to
beige at the neck, which is covered within a few weeks by a coat of
longer guard hair with a distinctive yellowish tinge (Kenyon, 1981). The
adult fur grows in after a few months and is variable in color from
light beige to almost black, with sparse dark or silvery white guard
hairs (Kenyon, 1981). Sea otters are divided into three subspecies based
on slight cranial variations: Enhydra
lutris nereis or the southern sea otter found in California, Enhydra
lutris lutris or the Alaskan sea otter ranging from Prince
William Sound across the
Aleutians to Commander Island, and Enhydra
lutris gracile or the Asian sea otter from Kurile Islands and
the east coast of the Kamchatka Peninsla (Kenyon, 1981; Reidman, 1990).
|
Status
in Estuarine and Coastal Areas |
Sea
otters are non-migratory, full time residents in Pacific coastal areas,
inshore and out to about 120 foot depth.
Breeding occurs at sea throughout the year. Sea otter females gestate for
about 8 months and give birth to either a single pup or very rarely two
(Mason and MacDonald, 1986). Pups are semiprecocial at birth and are
capable of eating solid food after 17 days and diving after a few months
(Mason and MacDonald, 1986). The otter pup is dependent on the mother for
at least a few months and weaned at one year, but may remain with mother
after she has a new pup (Kenyon, 1981). The average life span of a sea
otter is believed to be about 12 to 16 years in the wild (VanBlaricom,
1988). |
Abundance
and Range |
There
now exist an estimated 150,000 sea otters found along the north Pacific
rim from the Kuril Islands into the Kamchatka Peninsula, the Commander
Islands east across the Aleutian Islands to Prince William Sound, and
spotted populations along the west coast of North America at southeast
Alaska, Vancouver Island, Washington from Pt. Grenville to Pillar Pt.
and central California from Point Sur to Diablo Canyon (Paine, 1993).
The 2001 USGS Washington sea otter census counted 555 otters along the
Washington coast. The 2002 USGS California sea otter census counted 2139
sea otters in California. |
Site
Fidelity
|
Sea
otters rarely wander more than a few miles from their established
feeding grounds (Kenyon, 1981). Otters prefer a protected inshore area
with a rocky bottom and an abundance of kelp, especially giant kelp,
which are used for rest (they wrap themselves while napping to keep from
drifting) and provide the ideal foraging grounds (Riedman, 1990). |
Ease
of Census
|
Moderate |
Feeding
Habits
|
Sea
otters eat a variety of marine life including red sea urchins, abalone,
rock crab, and squid. When preferential prey are scarce otters will also
eat mussels, kelp crabs, clams, turban snails, octopuses, barnacles, sea
stars, scallops, rock oysters, fat innkeeper worms, and chitons (Reidman,
1990). Individual otters will normally specialize in one or two of prey
items (Reidman, 1990). The different sea otter subspecies have been
shown to include different average proportions of prey type in their
diets (Mason and MacDonald, 1986). Otters will typically dive up to 60
feet while foraging and will bring their prey to the surface within
folds of skin serving as a bag under their left arms (Mason and
MacDonald, 1986). Using rocks as tools they will crack open shellfish
using their chest as a table while floating on their backs. Feeding
occurs both at day and night (Orr and Helm, 1989). |
|
||
I.
|
Organochlorine Contaminants |
|
1. |
Selected
tissues from sea otters found dead along coastal California between 1968
and 1980 were analyzed for chlorinated hydrocarbon residues (Risebrough,
1989). The following age versus liver DDE
concentrations (mg/g,
ww) were compared for individual otters and are taken from graphs:
Males : fetus (0), pup (0.5, 3.5, 5.0, 6.0, 6.25, 6.5,
7.0, 31), immature (0, 0.5, 1.0, 5.0, 9.5), sub-adult (0, 1.0,1.5, 2.0,
2.5, 3.0, 3.5, 4.0), adult
(0, 1.0, 1.5, 2.0, 3.0, 3.5, 4.5, 5.5), aged adult (0, 0.5, 1.5, 9.5); Females
: fetus (0), pup (1.5, 2.0, 4.0, 5.5, 7.0, 25.5), immature (1.0, 1.25,
1.5, 2.5, 6.5, 12.5), sub-adult (0, 0.5, 1.0, 1.15, 2.5, 4.0, 10.0),
adult (0, 1.0, 1.5, 4.0, 5.0, 6.0, 9.0), aged adult (0, 2.0, 2.5, 3.0). DDE
did not increase with age for either male or female otters. Livers
of adult sea otters were analyzed for DDE
and the following concentrations (mg/g,
ww) were found: Males : 1970 (0.75, 3.25), 1971 (1.25, 2.25),
1977 (5.0), 1978 (5.5, 5.75), 1979 (0.5), 1980 (0.25). Females :
1969 (3.5), 1973 (3.75, 8.5), 1977 (1.25, 1.5), 1979 (0, 1.0, 1.25,
6.5), 1980 (0.5). No significant changes were seen in DDE concentrations in liver samples over the time period 1969
– 1980. PCBs
concentrations
(mg/g,
ww) in livers taken from graphs are as follows: Males : 1968 (0.25,
0.25), 1970 (0.75, 1.1), 1971 (0.25, 0.25, 0.5, 0.75, 1.5), 1972 (0.25,
0.25, 0.5, 0.5, 0.75, 1.25, 1.6, 3.5, 3.75, 4.0), 1973 (0.75, 1.6), 1977
(1.0, 2.25), 1978 (0.25, 0.5, 0.75, 1.25), 1979 (0.25, 1.25), 1980 (0.25, 0.25, 0.75); Females: 1969 (0.75, 1.75), 1970
(0.25, 0.75, 1.25, 3.0), 1971 (1.0), 1972 (0.75, 0.75, 0.75, 1.0, 1.0),
1973 (0.25, 0.75, 1.0, 1.75, 3.25), 1977 (1.0, 2.0, 3.0), 1978 (0.25,
0.75), 1979 (0.25, 0.75, 1.5), 1980 (0.1, 1.5). |
|
2. |
Tissues
from sea otters (n=10) found dead or shot along coastal central
California during 1969 to 1970 were analyzed for organochlorine
pesticide contamination (Shaw, 1971). The following tissues were
analyzed (not every tissue was analyzed for each otter): fat (F), liver
(L), testis (T), ovary (O), brain (B), kidney (K), heart (H), adrenal
(A). The following concentrations (mg/g,
ww) were found and are listed in order of (DDE
/ DDD / DDT) for individual otters *1 through *10:
*1, drowned female from Morro Bay, L = (0.49 / 0.03 / trace), B =
(0.17 / 0.008 / trace); *2, male hit by boat at Monterey Bay, L = (14 / 0.59 /
0.74), T = (13 / 0.55 / 0.46), B = (9.2 / 0.39 / 0.42); *3, male died of natural cause at Monterey Wharf, F = (7.7
/ 0.20 / 0.19), L = (0.87 / 0.044 / 0.029), T = (2.1 / 0.072 / 0.056), B
= (0.53 / 0.13 / 0.14); *4, female died of natural cause at Point Lobos,
F = (1.1 / 0.024 / 0.059),
L = (0.55 / 0.04 / 0.059); *5,
female died of natural cause at Lover’s Pt.,
L = (7.8 / 0.044 / 0.049), O = (0.84 / trace / trace), A = (7.1 /
0.10 / 1.3); *6, male shot
at Morro Bay, F = (0.39 / 0.0068 / 0.015), L = (3.4 / 0.032 / 0.051), T
= (0.093 / 0.036 / 0.019), B = (0.025 / trace / 0.079), K = (0.0069 /
trace / trace), H = (0.012 / trace / trace);
*7, male shot at Cambria, F = (34 / 1.5 / 0.64), L = (0.11 /
0.012 / 0.0052), K = (0.64 / 0.032 / 0.020), T = (0.69 / 0.056 / 0.022);
*8, male shot at Cambria, F = (7.0 / 0.33 / 0.18), L = 0.03 / 0.0003 /
0.0013), K = (1.5 / 0.067 / 0.023), T = (0.20 / 0.021 / 0.013);
*9, female drowned at Hopkins Marine Station, F = (18 / 1.3 /
0.87), L = 0.059 / 0.0054 / 0.0065), K = (12 / 0.19 / 0.14), O = (1.26 /
0.15 / 0.201); *10, male
hit by boat at Monterey Bay, F = (3.7 / 0.40 / 0.26), L = (0.32 / 0.022
/ 0.016), K = (0.47 / 0.031 / 0.021), T = (5.7 / 0.24 / 0.24). |
|
3. |
Liver
samples from beach-cast sea otter carcasses or recently killed
individuals were collected from California (n=9) between 1988 and 1991,
southeast Alaska (n=7) during May 1991, and the Aleutian Islands [Adak
(n=5) between 1991 and 1992 and Amchitka (n=2) in 1992] and analyzed for
organochlorine contamination (Bacon et al., 1999).
The following mean organochlorine concentrations (mg/g,
ww) were found: Aleutian ( |
|
4. |
Liver
samples from 23 sea otters that were obtained in 1991 to 1992 from
beached carcasses or freshly killed specimens in central California
(n=9), southeast Alaska (n=7), and the Aleutian Islands (n=7) were
analyzed for organochlorine contaminants (Estes et al., 1997). The
following average concentrations (ng/g, ww) were found: Aleutian
Islands |
|
5. |
Liver,
kidney and brain samples from adult sea otter carcasses collected
between 1992 and 1996 along the central California coast from Half Moon
Bay to Diablo Canyon were analyzed for organochlorine contamination
(Nakata et al., 1998). The otters had died prior to collection by
trauma, disease, emaciation, neoplasia, esophageal impaction, intestinal
perforation, or unknown causes. The following are the concentrations (ng/g
ww) found for individual otters (A – T) and listed in order of ( |
|
6. | Carcasses of adult sea otters were collected for brain, liver, and kidney tissues along the coast of California (Kannan et al. 2004). Contaminants in 11 livers were detected at the following levels (ng/g wet weight): 140-8,700 total PCBs, 290-5,900 DDTs, 5.8-500 HCHs, 10-500 chlordanes, 40-9,200 monobutylin + butylin. Contaminants in 4 kidneys were detected at the following levels (ng/g wet weight): 480-4,600 total PCBs, 1,400-8,600 DDTs, 6.4-19 HCHs, 30-190chlordanes, 4-265 monobutylin + butylin. Contaminants in 3 brain samples were detected at the following levels (ng/g wet weight): 69-330 total PCBs, 300-1400 DDTs, 3.3-8.1 HCHs, 2.6-39 chlordanes, 3.9-140 monobutylin + butylin. |
|
II.
|
Cholinesterase-inhibiting
pesticides |
|
|
No
direct exposure data available. |
|
III.
|
Trace
Elements, Metals and Metalloids |
|
1. |
Kidney
and liver samples taken from sea otters found dead along coastal
California between 1968 and 1980 were analyzed for metals contamination
(Risebrough, 1989). The following mean concentrations (mg/g,
dw) were found and listed as (number of samples, liver, kidney): Silver
(n=117, 2.45, trace), Mercury (n=124,
4.42, 2.35), Cadmium
(n=124, 15.8, 37.0), Iron (n=124, 1078, 497), Manganese
(n=123, 12.3, 3.54), Magnesium
(n=89, 909, 840), Copper (n=124,
132, 31), Zinc (n=124, 213,
159). The following
observations were made concerning the individual metal results: Silver
– The liver concentrations were higher in females than males. Mercury
– In both liver and kidneys Hg
concentrations increased with body length. Liver concentrations were
about twice that of kidneys. Cadmium
– Sea otters concentrate high quantities of Cd,
particularly in the kidneys. Concentrations increase with age and higher
concentrations are found in adult females than in adult males. No
increase in kidney Cd was
observed over the years of the study period. Magnesium
– In kidneys, Mg
concentrations increased with body length for males, but this
relationship was not seen in females. Copper
– Cu
concentrations were about four times higher in liver than in kidneys. Manganese
– Mg
concentrations were three to four times higher in the liver than in the
kidney and the concentrations increased with body length and weight in
kidneys of males, but not of females.
Zinc –
Concentrations of Zn in
kidneys were strongly correlated with Cd
concentrations, and with body lengths and weights. |
|
2. |
Lead
concentrations
and stable isotopic compositions of Pb
were measured in third post-canine or first molar teeth of
pre-industrial (excavated and from about 1900 years before present) and
contemporary sea otters (1986 and 1987) from Amchitka Island, Alaska to
determine if changes had occurred in the magnitude and source of
assimilated Pb (Smith et
al., 1990). The following
concentrations (ng/g, dw) were found: Pre-industrial (n=5, including 2
replicate sets, r1 and r2) (19, 14, 72r1, 67r1, 48, 49r2, 61r2).
Contemporary (n=5, includes 1 replicate set) (130, 42, 140, 23r, 25r,
26). No significant difference was found in the amount of Pb
accumulation in the older and contemporary otter, however
isotopic compositions revealed there were different sources of Pb.
In the pre-industrial otter Pb
was derived from natural deposits in the Aleutian Arc. In the
contemporary otter, Pb was
primarily from industrial processes originating from Asia and western
Canada. |
|
3. |
Lead
concentrations and stable isotopic compositions of lead were measured in third post-canine or first molar teeth
of six pre-industrial (excavated, dating from 500 to 3000 years before
present) and seven contemporary sea otters (collected between 1987 and
1989) from the coast around Monterey Bay, California to determine if
changes had occurred in the magnitude and source of assimilated Pb
(Smith et al., 1992). The
following concentrations (ng/g, dw) were found: Pre-industrial: (61,
170, 170, 45, 130, 72); Contemporary:
(93, 200, 1900, 1800, 960, 140, 300). No relationship was observed
between animal age and tooth Pb
concentration in the pre-industrial and contemporary otters. Lead
isotopic compositions indicate multiple and distinct sources of
accumulated Pb.
Pre-industrial animals contained Pb derived
from natural continental sources in northern California. Essentially all
of the Pb in contemporary
otters was derived from industrial sources represented by particulate
aerosols, likely originated from past and current uses of lead-containing
gasoline. |
|
4. |
Carcasses
from sea otters found dead along the California coast during 1992 to
1996 were divided into brain, liver, and kidney samples and analyzed for
contamination from tributyltin (TBT)
and its degradation products monobutyltin
(MBT) and dibutyltin (DBT) (Kannan
et al., 1998). The
following concentrations (ng/g, ww) were found for individual otters (A
– AI) and are listed in order of (MBT
/ DBT / TBT
): A-liver (360 / 5820 /
3020), A-kidney (11 / 54 / 200), A-Brain (12 / 24 / 105); B-liver (236 / 3090 / 1970),
B-kidney (17 / 200 / 210), B-brain (<7 / 9.3 / 72);
C-liver (<7 / 51 / 56), C-kidney (<7 / 3.7 / 10), C-brain
(<7 / <2.4 / 3.9);
D-liver (<7 / 54 / 135), D-kidney (<7 / 7.5 / 7.7), D-brain
(<7 / <2.4 / 2.7); E-liver
(<7 / 49 / 75), E-kidney (14 / 6.8 / 9.3), E-brain (<7 / 2.8 /
1.8); F-liver (<7 / 21 /
19), F-kidney (<7 / <2.4 / 4);
G-liver (81 / 860 / 2130), G-kidney (7 / 24 / 120);
H-liver (26 / 220 / 140), H-kidney (<7 / 15 / 16);
I-liver ( 360 / 2360 / 1600);
J-liver (190 / 2080 / 2900), J-kidney (11 / 110 / 170);
K-liver (25 / 53 / 48); L-liver
(10 / 104 / 100); M-liver
(18 / 85 / 130); N-liver
(14 / 83 / 180); O-liver
(19 / 83 / 200); P-liver
(220 / 410 / 760); Q-liver
(14 / 120 / 120); R-liver
(<7 / 29 / 32); S-liver
(12 / 52 / 28); T-liver (14
/ 94 / 150); U-liver (17 /
144 / 170); V-liver (18 /
110 / 53); W-liver (31 /
110 / 53); X-liver (140 /
1520 / 950); Y-liver (17 / 220 / 190);
Z-liver (140 / 1840 / 2050);
AA-liver (310 / 1560 / 670);
AB-liver (12 / 310 / 330); AC-liver
(140 / 1290 / 920); AD-liver
(14 / 90 / 55); AE-liver
(18 / 240 / 43); AF-liver
(9.4 / 34 / 66); AG-liver
(8 / 120 / 60); AH-liver
(24 / 95 / 59); AI-liver
(16 / 200 / 260). Total
butyltin concentrations in kidney and brain were about 7 and
18 fold less than those in liver. Based on the mean body weight of 21.1
kg for the otters analyzed, the average burden of BT
in the liver was estimated to be 1.3 mg. The hepatic concentrations of BTs
were correlated with the length and weight in adult males, however the
same correlation did not exist with females. In female livers DBT
was the predominant butyltin
whereas in the male livers TBT
was the predominant butyltin.
Concentrations of butyltins varied greatly according to sampling
location. Otters collected from enclosed marinas such as Monterey Harbor
or Morro Bay contained at least an order of magnitude greater
concentration than otters collected from open locations, like San
Simeon. The following are the mean concentrations (ng/g, ww) found in
otters from the various locations and listed as (MBT
/ DBT / TBT
): Morro Bay (n=4) (84 /
1020 / 1060), Moss Landing (n=2) (193 / 2940 / 1530), Half Moon Bay
(n=1) (<7 / 51 / 56), San Simeon (n=1) (<7 / 54 / 135), Estero Bay
(n=4 male) (10 / 56 / 71), Estero Bay (n=4 female) (23 / 150 / 104),
Pismo Beach (n=2) (17 / 83 / 190), Monterey Harbor (n=8) (160 / 1400 /
1200), Montara Beach (n=1) (18 / 85 / 130), Hazard Canyon (n=1) (14 / 90
/ 55), Jalama Beach (n=1) (220 / 410 / 760), Diablo Canyon (n=2) (14 /
137 / 55), Port San Luis (n=1) (8 / 120 / 60), Carmel (n=1 female) (24 /
95 / 59), Carmel (n=1 male) (16 / 200 / 260). |
|
IV.
|
Petroleum |
|
1. |
On
March 24, 1989, Exxon Valdez ran aground in Prince William Sound, Alaska
spilling an estimated 42 million liters (11,000,000 gallons) of Prudhoe
Bay crude oil (Garshelis, 1997). Sea otter carcasses
collected by location following the spill include: Prince William
Sound: 421 (391 oiled
and 30 un-oiled). Kenai
Peninsula: 165 (53 oiled and
112 un-oiled). Kodiak-Alaska
Peninsula: 190 (151 from Kodiak Island Group and 39 from Alaska
Peninsula of which 91 were oiled
and 99 were un-oiled. |
|
2. |
The
best estimate for sea otter mortality as a result of the Exxon
Valdez oil spill at Prince William Sound, Alaska ranges from 2,650
to 3,905 individual sea otters (Bonnell et al., 1996). |
|
|
||
I. |
Organochlorine |
|
|
No
response data available |
|
II. |
Cholinesterase inhibiting pesticides |
|
|
No
response data available |
|
III. |
Metals |
|
|
No
response data available |
|
IV.
|
Petroleum |
|
1. |
The
demographic consequences of the Exxon
Valdez oil spill
in Prince William Sound in March 1989 on the sea otter population was
investigated by surveys of otter
abundance, pup production, activity, and foraging (Garshelis and
Johnson, 2001). Pre-spill data was compared to data collected during a
seven year period after the oil spill in
the western Prince William Sound. This western survey area was the area
most affected by the oil spill and
included Green Island, Appelgate Rock, Knight Island, Montague Island,
and Naked Island. Counts
(converted to densities) of independent sea otters conducted over the 7
year post-spill time period were consistently equal to or higher than
counts made before the spill (1977-1985) for three of four oiled
sites and one un-oiled site. The
following are numbers of otters counted listed in order of years as
(1984, 1989, 1990, 1991, 1993): Green
Island (8, 25, 23, 27, 36), Naked
Island (21, 35, 16, 17, 12), Knight
Island (70, 69, 55, 110, 101), Port Bainbridge (126, 150, 89, 62, 126),
Port Nellie Juan (32, 42, 27, 24, 39), Passage Canal (2, 2, 1, 2, 5). Pup
production, measured as the ratio of
pups to all otters other than pups, did not differ significantly
between pre- and post-spill (1990) at un-oiled Montague Island or at the
heavily oiled Green Island,
however, the pre-spill pup ratio was significantly higher for Appelgate
Rock, the most heavily oiled
of sites, for the 1990 survey. Pup ratios at Appelgate Rock for the 1994
and 1996 surveys were near pre-spill levels.
Pup ratios at Knight Island were higher in the post-spill
surveys, and at the lightly oiled
Naked Island the post-spill ratios were also higher.
Foraging
success about Gibbon’s Anchorage at Green Island was similar in
1980-81, 1990, and 1991 with clams being the primary prey and either
crabs or mussels being the next most common prey. At Knight Island,
foraging success was higher at oiled than
at un-oiled sites for adult females , but was not different for adult
male otters. |
|
2. |
Medical
condition and degree of oiling
was evaluated for 339 sea otters collected between March 30 and August
21, 1989 and rehabilitated at Valdez Otter Rehabilitation Center (VORC),
the Seward Otter Rehabilitation Center (SORC), and at a temporary care
facilty at Homer following the T/V Exxon Valdez oil
spill (Williams et al., 1990).
Degree of oiling was
based on % body coverage oiled as follows: heavily
oiled = >60%, moderately
oiled =30 to 60 %, lightly
oiled = < 30% of body coverage or light sheen on fur, and
unoiled = no visible evidence of oiling.
Based on these criteria, otters received at rehab centers are as
follows: VORC: 78 (50%) heavily
or moderately oiled, 51
(33%) lightly oiled, and 11
(7%) unoiled, 16 (10%) not documented; SORC: 19 (10%)heavily
or moderately oiled, 72
(39%) lightly oiled, 44
(23%) unoiled, 52 (28%) not documented; Homer: 6 otters unoiled,
12 not documented. Blood
samples were drawn from otters upon arrival at the rehab centers.
Samples were analyzed for petroleum
hydrocarbon concentrations and initial results indicated a
positive correlation between total
petroleum hydrocarbon concentration and mortality. Blood
variables analyzed include: Hematocrit (HCT, %), Glucose (GLU, mg/dL),
Blood urea nitrogen (BUN, mg.dL), Serum glutamic pyruvic transaminase (SGPT,
mg/L), Serum glutamic oxalacetic transaminase (SGOT, IU/L),
Lactate dehydrogenase (LDH, IU/L), creatinine phosphokinase (CPK, mg/L),
and creatinine (CREA, mg/dL). Normal values for unoiled otters from a
spill free area are as follows (Low value/High value): HCT (50.3/62.1), GLU (87.6/150.2), BUN (34.3/63.6), SGPT
(96.4/240.0), SGOT (87.0/511.0), LDH (94.7/419.3), CPK (169.8/490.3),
CREA (0.5/1.4). The following mean values were observed in rehabilitated
otters that survived and were eventually released: Heavy oiled – (HCT 52.5 n=7, GLU 105.7 n=6, BUN 72.2 n=5,
SGPT 329.5 n=2, SGOT 574.6 n=5, LDH 746.6 n=5, CPK n/a, CREA 0.6 n=5); Moderately
oiled - (HCT 48.2 n=7, GLU 110.7 n=7, BUN 70.6 n=7, SGPT
251.5 n=6, SGOT 484.3 n=7, LDH 629.0 n=7, CPK 1283 n=5, CREA 0.5 n=7); Lightly
oiled - (HCT 48 n=8, GLU 155.9 n=8, BUN 48.8 n=8, SGPT 420.4
n=8, SGOT 738 n=8, LDH 538.7 n=7, CPK 746 n=8, CREA 0.8 n=8).
The following are values for otters that died during
rehabilitation: Heavily oiled
– (HCT 60.3 n=6, GLU 53.2 n=6, BUN 189.6 n=7, SGPT 287.3 n=4, SGOT
960.8 n=6, LDH 1332 n=5, CPK 6654 n=5, CREA 1.2 n=6);
Moderately oiled - (HCT
59.2 n=11, GLU 101.8 n=7, BUN 144.5 n=10, SGPT 1384 n=7, SGOT 3917 n=8,
LDH 2194 n=7, CPK 2469 n=6, CREA 1.1 n=9);
Lightly oiled - (HCT
49.3 n=8, GLU 119.4 n=11, BUN 108.2 n=11, SGPT 610.1 n=10, SGOT 1009
n=10, LDH 1798 n=10, CPK 4902 n=9, CREA 0.8 n=9).
The hematocrits taken upon arrival showed no correlation with the
degree of oiling or
survival, although heavily and
moderately oiled otters often developed anemia after several
weeks in captivity. Plasma glucose was below normal values in the heavily
oiled otters that subsequently died. Blood urea nitrogen was
about 2-fold higher than normal for otters that died, and was elevated
in heavily oiled
otters that survived. The indicators of kidney and liver damage (BUN,
SGPT and SGOT) were highly variable. Liver enzymes were elevated in
otters that did not survive. Although the serum creatinine
concentrations were two-fold higher in otters that died, these
concentrations were still within normal value range. Three
disorders were commonly diagnosed in oiled
sea otters: hypothermia or hyperthermia, hypoglycemia, and emphysema.
More than 36% of otters received at VORC were hypothermic on arrival,
27% were hyperthermic usually with moderate
to light oiling.
Hypoglycemia, tested in more than 45% of otters received, was a major
contributor to thermoregulatory and metabolic problems of heavily
oiled otters that subsequently died. Mild to severe pulmonary
emphysema was seen in 45 post mortem otter examinations, and 70% of all
otters that died showed some form of pulmonary emphysema. |
|
3. |
Clinical
records and laboratory data for 21 oiled
sea otters collected during the Exxon Valdez oil
spill and that died within 10 days of arrival at the
rehabilitation center were examined (Lipscomb et al., 1994).
Degree of oiling was based on % body coverage oiled as follows: 7
otters heavily oiled =
>60%, 5 otters moderately oiled
=30 to 60 %, and 9 otters lightly
oiled = < 30% of body coverage or light sheen on fur.
Shock was the most common terminal syndrome, characterized by
hypothermia, lethargy, and hemorrhagic diarrhea. A high proportion of
otters had seizures at or near the time of death. Anorexia was also
relatively common. The
following hematological findings: Leukopenia (decrease in white
blood cell count) was the most common blood condition for otters of all
degree of oiling and was
characterized by decreased mature neutrophils with increased numbers of
immature neutrophils and decreased lymphocytes. Azotemia (accumulation
of nitrogenous waste products in the blood) was also common in otters
all three conditions of oiling.
Hyperkalemia (abnormally high blood potassium) and hypoproteinemia/hypoalbuminemia
(abnormally low blood protein and albumin) were found less common than
azotemia, but were probably also related to diarrhea and shock.
Increased hepatocellular leakage-associated serum transaminases were
only slightly less common than azotemia. Histopathological
exams were performed on 51 oil
contaminated otters collected during the Exxon Valdez oil
spill and that subsequently died in rehabilitation centers.
The degree of oiling was as
follows: 16 otters heavy oiling,
13 otters moderate oiling,
22 otters light oiling. The
examinations revealed the following: Interstitial pulmonary emphysema
was the most common lesion occurring in 11 of 15 heavily
oiled otters, in 5 of 11 moderately
oiled otters, and in 3 of 20 lightly
oiled otters. Incidence of emphysema was threefold higher in
oil-contaminated versus uncontaminated otters. Gastric erosions were
found in 2 heavily oiled, 7
moderately oiled and 4 lightly
oiled otters. Hepatic lipidosis occurred in 8 heavily
oiled, 5 moderately oiled
and 1 lightly oiled otter.
Renal lipidosis was found only in otters that also had hepatic lipidosis.
Centrilobular hepatic necrosis was seen in 4 heavily
oiled, 3 moderately oiled
and 4 lightly oiled otters.
No evidence of aspiration pneumonia, a condition associated with mammal
ingestion of petroleum hydrocarbons,
was found in oil-contaminated
sea otters. |
|
4. |
Hydrocarbon analysis was performed on
tissues taken from heavily oiled (60%
or more body coverage) and moderately
oiled (30 to 60% body coverage) sea otter carcasses (n=10)
recovered dead from Western Prince William Sound, Alaska several days
after the Exxon Valdez oil spill
of March 1989 (Mulcahey and Ballachey, 1994). Tissues analyzed included
kidney, liver, muscle, intestine, fat, and brain. Aliphatic
and aromatic hydrocarbons
were found in all tissues of each of the ten oiled
otters and the mean concentrations (ng/g) were compared to 12
unoiled otters and listed in order of (kidney, liver, muscle): Total
aliphatic hydrocarbons: Unoiled otters (3800, 2800, 3200), Oiled
otters (7700, 6200, 6100); Total
aromatic hydrocarbons: Unoiled otters (170, 160, 170), Oiled
otters (1500, 1100, 600). The ten oiled
otters were separated into three groups based patterns of hydrocarbons
in tissues. The first group (n=4) had relatively low mean concentrations
of both total aliphatic
(6000 ng/g) and total aromatic
hydrocarbons (700 ng/g) in tissues, expected of animals that
died soon after exposure to crude oil.
The second group of otters (n=3) had higher mean concentrations of total
aliphatic (10,000 ng/g) and total
aromatic hydrocarbons (2000 ng/g), expected of otters that
survived long enough after crude oil
exposure to concentrate hydrocarbons in tissues and start metabolizing
them. The final group of otters (n=3) had even higher concentrations of total
aliphatic (11,000 ng/g) and total
aromatic hydrocarbons (300 ng/g) in tissues, with especially
high concentrations of aliphatic hydrocarbons in intestinal tissues and aromatic
hydrocarbons in fat tissues. This pattern is expected of heavily
oiled otters that survived long enough after exposure to crude oil for hydrocarbons to move into tissues, but died
before the hydrocarbons were sufficiently metabolized to reduce
concentrations. |
|
5. |
Blood
and fur samples were taken from sixteen oiled
sea otters following the Exxon Valdez oil
spill that were captured from the southern Kenai Peninsula,
Alaska between 17 and 23 June 1989 (Hill and Tuomi, 1990). These otters
were randomly divided into two groups of eight and one group was
“de-oiled” by prescribed washing while the other group remained oiled. After fourteen days a second set of blood and fur
samples were taken and comparisons were noted to reveal any affects of oiling.
The following data was recorded from 1) a subjective grading system (1 =
poor, 2 = improving, 3 = ideal) to measure fur condition, 2) from a
visual field dichloromethane (FDCM) test, and 3) from complete blood
counts and chemistry: 1) Comparison of subjective scores of coat
condition for the washed and unwashed otters demonstrated that on some
days washed otters had better average scores, but on other days
unwashed, oiled otters had
better average scores 2) FDCM testing revealed only one fur sample as
containing Prudhoe Bay crude oil,
when at least eight otters were known to have contamination. 3) blood
chemistry revealed the following, listed as *Individual otter number (PCV
= packed cell volume, PT = serum glutamic pyruvic transaminase, LDH =
lactic dehydrogenase, CPK = creatine phosphokinase, WBC = white blood
cell count, Seg = segmented white blood cells, OT = glutamic oxaloacetic
transaminase, note listed in order of day 1 value–day 14 value): Unwashed, oiled otters:
*1 (PCV 49-48, PT 196-88, LDH 424-261, CPK 524-80), *2 (PCV
48-47, PT 190-117, LDH 542-353, CPK634-221, WBC 10,700-9,300, Seg
92-83), *3 (PCV 44-40, PT 217-251, WBC 11,900-6,800, Seg 88-72), *4 (PCV
53-29, PT 258-179, WBC 10,000-5,700, Seg 90-80), *5 (PCV 50-49, PT
236-107, LDH 427-161, CPK 1133-55), *6 (PCV 44-49, PT 289-98), *7 (PCV
50-43, PT 1130-158, LDH 574-296, CPK 485-147, WBC 8,000-9,600, Seg
84-90), *8 (PCV 49-37, PT 292-122, LDH 359-383, CPK 520-218, WBC
12,100-16,700, Seg 86-97) Washed
otters: *9 (PCV 52-48, PT 155-151, LDH 393-246, CPK 356-109), *10 (PCV
52-40, PT 144-168, WBC 8,700-13,400, Seg 83-78), *11 (PCV 53-48, PT
265-123, LDH 541-175, CPK 399-87), *12 (PCV 43-35, PT 178-309, OT
289-421), *13 (PCV 48-43, PT 287-182, LDH 487-349, CPK 166-343), *14 (PCV
51-47, PT 181-97, WBC 9,600-7,000, Seg 83-73), *15 (PCV 51-50, PT
146-111), *16 (PCV 49-42, PT 336-126, LDH 544-306, OT 615-215, CPK
1486-76, WBC 9,000-12,000, Seg 85-87). |
|
6. |
Blood
samples (n=25) were obtained from adult male sea otters collected
between September 1 and October 4, 1990 which inhabited both Exxon
Valdez oil spill affected
areas in western Prince William Sound (n=15) and a reference area in
eastern Prince William Sound not affected by the oil
spill (Bickham et al., 1998).
Flow cytometry was used to evaluate the sublethal, genetic damage
caused by the clastogenic effect of crude
oil exposure. This damage is measured as the coefficient of
variation (CV) of the G1 peak of the white blood cells. The mean CV for
the exposed otters was 4.8% and the mean genome size was 62.2, while the
mean CV for the unexposed otters was 5.1% with a mean genome size of
62.2. The values were not
significantly different between the exposed and unexposed otters meaning
that the mean genome sizes and dispersion of the DNA about the mean
value were not significantly increased in the population potentially
exposed to oil. Although
the mean CV’s did not differ, the variance of the CV’s was
significantly increased in the exposed otters, which is indicative of
genotoxic damage based on a separate statistical approach. |
|
|
||
Bacon,
C.E., W.M. Jarman, J.A. Estes, M. Simon and R.J. Norstrom. 1999.
Comparison of organochlorine contaminants among sea otter (Enhydra
lutris) populations in California and Alaska. Environ.
Toxicol. Chem. 18(3):452-458. |
||
Bickham,
J.W., J.A. Mazet, J. Blake, M.J. Smolen, Y. Lou and B.E. Ballachey.
1998. Flow cytometric determination of genotoxic effects of exposure to
petroleum in mink and sea otters. Ecotoxicology 7:191-199. |
||
Bonnell,
M.L., R.G. Ford, A.J. Brody. 1996. Assessing the threat of oil spills to
southern sea otters. Endangered Species Update 13(12):38-42. |
||
Estes,
J.A., C.E. Bacon, W.M. Jarman, R.J. Norstrom, R.G. Anthony and A.K.
Miles. 1997. Organochlorines in sea otters and bald eagles from the
Aleutian Archipeligo. Marine Pollut. Bull. 34(6):486-490. |
||
Garshelis,
D.L. 1997. Sea otter mortality estimated from carcasses collected after
the Exxon Valdez oil
spill. Conserv. Bio. 11(4):905-916. |
||
Garshelis,
D.L. and C.B. Johnson. 2001. Sea otter population dynamics and the Exxon
Valdez oil spill: disentangling the confounding effects. J.
Applied Ecol. 38: 19-35. |
||
Hill,
K. and P.A. Tuomi. 1990. Field test for detecting crude oil on the fur
of sea otters. In: Sea Otter Symposium 17-19 April 1990. USFWS
Biological Report 90 (12), Anchorage, AK. 485 pp.
|
||
Kannan, K., N. Kajiwara, M. Watanabe, H. Nakata, N.J. Thomas, M. Stephenson, D.A. Jessup, and S. Tanabe. 2004. Profiles of polychlorinated biphenyl congeners, organochlorine pesticides, and butylins in southern sea otters and their prey. Environ. Toxicol. Chem. 23:49-56. |
||
Kenyon,
K.W. 1981. Sea Otter, Enydra lutris.
In: Handbook
of Marine Mammals, Vol.1 The Walrus, Sea Lions, Fur Seals, and Sea Otter.
Academic Press, San Diego, CA. 235 pp. |
||
Lipscomb,
T.P., R.K. Harris, A.H. Rebar, B.E. Ballachey and R.J. Haebler. 1994.
Pathology of sea otters. In: Marine
Mammals and the Exxon Valdez. Academic Press, San Diego, CA.
395 pp. |
||
Mason,
C.F. and S.M. MacDonald. 1986. Otters:
Ecology and Conservation. Cambridge University Press, London,
UK. 236 pp. |
||
Mulcahey,
D.M. and B.E. Ballachey. 1994. Hydrocarbon residues in sea otter tissue.
In: Marine Mammals and the Exxon
Valdez. Academic Press, San Diego, CA. 395 pp. |
||
Nakata,
H., K.Kannan, L.Jing, N. Thomas, S. Tanabe and J.P. Giesy.
1998. Accumulation pattern of organochlorine pesticides and
polychlorinated biphenyls in southern sea otters (Enhydra lutris nereis) found stranded along coastal
California, USA. Environ. Pollut. 103:45-53. |
||
Orr,
R.T., R.C. Helm. 1989. Marine Mammals
of California. University of California Press, Berkeley, CA.
93 pp. |
||
Paine,
S. 1993. The World of the Sea Otter.
Sierra Club Books, San Francisco, CA. 132 pp. |
||
Reidman,
M. 1990. Sea Otters.
Monterey Bay Aquarium Foundation. Monterey Bay, CA. 80 pp.
|
||
Risebrough,
R.W. 1989. Accumulation pattern of heavy metals and chlorinated
hydrocarbons by sea otters, Enhydra
lutris in California. U.S. Department of Commerce, National
Technical Information Service. 51 pp. |
||
Shaw,
S.B. 1971. Chlorinated hydrocarbon pesticides in California sea otters
and harbor seals. California Fish and Game 57(4):290-294. |
||
Smith,
D.R., S. Niemeyer, J.A. Estes and A.R. Flegal. 1990. Stable lead
isotopes evidence anthropogenic contamination in Alaskan Sea Otters.
Environ. Sci. Tech. 24:1517-1521. |
||
Smith,
D.R., S. Niemeyer and A.R. Flegal. 1992. Lead sources to California sea
otters: industrial inputs circumvent natural lead bio-depletion
mechanisms. Environ. Res. 57:163-174. |
||
VanBlaricom,
G.R., J.A. Estes. 1988. The Community
Ecology of Sea Otters. Springer-Verlag, Berlin.
247 pp. |
||
Williams,
T.M., J. McBain, R.K. Wilson and R.W. Davis. 1990. Clinical evaluation
and cleaning of sea otters affected by the T/V Exxon Valdez oil spill.
In: Sea Otter Symposium 17-19 April 1990. USFWS Biological Report 90
(12), Anchorage, AK. 485 pp.
|