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Confounding factors such as age, gender, and hormonal and nutritional status not only
modulate the intake and bioaccumulation of PTSs as detailed above, they also strongly affect
the immune response of marine mammals (Ross et al. 1993, 1994; Hall et al. 2003a; Lalancette
et al. 2003). The endocrine system exerts a strong control on the immune response in mam-
mals and any physiological or chemically induced modulation of the hormonal status could
have profound impacts on the immune response, therefore affecting sensitivity to immu-
notoxic compounds (Pillet et al. 2006). Numerous environmental contaminants including
PCBs and PBDEs have a direct impact on the endocrine system of marine mammals (Hall
et al. 2003b; Sormo et al. 2005; Tabuchi et al. 2006). Most of these “endocrine disruptor” com-
pounds also have demonstrated immunotoxic effects that could therefore result from either
a direct effect on immune cells or from the chemically induced alterations of the hormonal
balance. An analogous situation is observed with vitamin status. PCBs or hexachlorocyclo-
hexanes appeared to modulate vitamin A and E homeostasis in pinnipeds and polar bear
(Jenssen et al. 2003; Debier et al. 2004; Mos et al. 2007) with potential consequences on the
immune response (Mora et al. 2008). Moreover, effects of retinol on morbillivirus infections
have recently been partially elucidated (Trottier et al. 2009). These indirect impacts of vitamin
A on pinniped resistance to phocine distemper virus (PDV) certainly deserve more attention.
6.3.4 Environmental Contaminants and Health Risks in Marine Mammals
Several studies from different geographical areas have addressed the impact of environmen-
tal pollutants on marine mammal species, investigating morphological changes of certain
organs or an increased susceptibility to infectious diseases of animals inhabiting contami-
nated regions or with higher contaminant body burdens. Higher levels of PCBs and mer-
cury in tissues were associated with prevalence of infections in harbor porpoises (
Phocoena
phocoena
) and bottlenose dolphins (
Tursiops truncatus
) stranded in the United Kingdom and
Germany (Siebert et al. 1999; Bennett et al. 2001; Jepson et al. 2005; Davison et al. 2011). The
pathologies reported in these studies included severe parasitic pneumonia often associ-
ated with secondary bacterial infections, as well as bacterial septicemia, which is usually
associated with an immunosuppressive status. Thymic atrophy and splenic depletion were
associated with increasing levels of PCBs and PBDEs in the subcutaneous blubber of harbor
porpoises from northern European waters (Beineke et al. 2005). This study also pointed out
a positive correlation between high PBDE levels, poor health status, and lymphoid deple-
tion of the thymus in
Phocoena phocoena
. In general, lymphoid depletion was associated
with bacterial infections, such as severe dermatitis, pneumonia, peritonitis, or myocarditis.
The most common causes of pathological lesions were not primary pathogenic agents, such
as highly pathogenic viruses, but rather nematodes and opportunistic bacterial infections,
again suggesting a deficient immune system (Beineke
et al. 2005). Recently, Nakayama et al.
(2009) have demonstrated a significant association between butyltin levels and the parasitic
infection status of lung nematodes in finless porpoises (
Neophocaena phocaenoides
).
In the Saint-Lawrence Estuary beluga whale (
Delphinapterus leucas
) population, cancer was
the second leading cause of death overall, and tumors have been identified in 27% of adult ani-
mals, representing the highest rate of cancer in a cetacean population (Martineau et al. 2002).
This high incidence of neoplastic diseases has been potentially attributed to carcinogenic effects
and/or reduced antitumoral immune responses due to environmental factors, including high
environmental levels of PAH (De Guise et al. 1995b; Martineau et al. 2002). The high occur-
rence of opportunistic infections and parasitic infestations reported in these beluga whales
strongly supports the hypothesis of a chemically induced immunodeficiency as a possible
cause of the above-mentioned reduced antitumoral immune response (Martineau et al. 2002).
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