Organohalogen concentrations and a gross and histologic ...

elations between histological changes and individual levels of contaminants
in subcutaneous adipose tissue were found but these were not consistent. In
conclusion, the findings were similar to several controlled toxicity studies of
PCBs, DDTs and dieldrin. The signs of chronic inflammation in relation to
triads in most of the bears could be a natural phenomenon in the East
Greenland polar bear, caused by e.g. infectious agents, and is not necessarily
a result from chronic exposure to toxic substances as organohalogens. However,
this could not be elucidated because we did not have access to samples
from non (or very low) exposed, free-ranging bears. It could not be concluded
whether the high lipid content was a function of lipid hyperphagia,
fasting, organohalogen toxicity or a combination of these.
The fifth paper reports the histology of kidneys and adrenals in 91 and 43
individuals, respectively. Of these, 38 (42%) exhibited glomerulonephritis
and/or -sclerosis. In addition, hyalinisation of tubular basement membrane -
accompanied by atrophy and fibrosis – was found in these individuals. One
case of tubular cellproliferation at the corticomedullary border was found in
a 7-year-old male. Tubular hyalin casts were positively correlated with the
degree of glomerular and tubular lesions (protein lost) while accumulations
of tubular protein droplets and PAS-positive pigments (e.g. bile pigment,
melanin, haemoglobin or byproducts from the metabolism of plant material
but not lipofuscin or haemosiderin) were found in all individuals. We could
not evaluate if these lesions had a clinical impact on the bears. Furthermore,
focal mononuclear cellinfiltrations were found in diverging degrees of the
cortex and medulla, independent of the glomerular and tubular changes.
The glomerular and tubular lesions were the same as those found in highly,
environmental polluted subpopulations of marine mammals and fish, laboratory
animals exposed to PCBs and estrogens, as well as industrial workers
chronically exposed to toxic organic chemicals. In addition, there was a clear
age dependency for severe glomerular and tubular lesions, as well as indications
of old females having a higher prevalence of moderate and severe
changes when compared to old males. However, this could not be evaluated
statistically due to a relatively low sample size in these two groups. This difference
could indicate that mature female polar bears are more sensitive to
extrinsic factor - like organohalogens and infectious agents - due to reproductive
related cycles of fasting and laction (discussed in Paper I). No significant
relations between histopathological changes and levels of organohalogens
were found. No histopathological changes were found in the adrenals.
We therefore propose that the renal lesions found in the polar bears
were a result of ageing, infectious agents, season and meaby chronic exposure
to organohalogens. However, a true cause and effect could not be concluded
due to the lack of reference material of not exposed individuals and
would require an experimental setup using a relevant phylogenetic Arctic
top predator.
The sixth paper deals with the female reproductive organs. Earlier field observations
from Svalbard from early to mid 1990-ies indicated – among others
– a relation between high organohalogen exposure in utero and neonatally,
and clitoral enlargement in two adult female polar bears, and clitoral
enlargement and lateral urethral opening in two yearlings, respectively. On
9th July 1999 samples from a 23-year-old female, which exhibited a significantly
enlarged clitoris resembling those previously reported in adult
female polar bears from Svalbard, was obtained at a Inuit hunt outside Scoresby
Sound. A first-time ever histological examination of clitoral enlargement
in polar bears revealed intense, chronic, ulcerative and perivascular
clitoriditis showing that the enlargement was an inflammatory reaction - and
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