327
Chapter fourteen: Toxicology and poisons
is still challenging, and extrapolation to local or global population level effects is extremely
difficult (Fedorenkova et al. 2010; Van Straalen et al. 2010). It is important to reiterate that
not all responses to the presence of a toxicant are adverse, and in many cases are essential or beneficial (such as protective hermetic effects). There are a number of populations
of marine mammals that have been shown to have concentrations of contaminants over
established traditional thresholds of concern (i.e., Basu et al. 2009; Doucette et al. 2012; Rea
et al. 2013). However, from a population perspective, the ramifications of high concentrations of contaminants observed are unclear. Additionally, as has been emphasized in this
chapter and elsewhere, toxic thresholds which have been established in model organisms
(i.e., humans, rats, mink) might not be relevant to marine mammals, which have evolved
in a drastically different environment than their terrestrial counterparts.
In some instances where the etiology of mass die-offs is deduced (i.e., UMEs due to
HABs) the pathology of toxins may be known from laboratory animal models or observational studies (Silvagni et al. 2005), however, observations of intoxication are often limited
to dead/moribund or severely intoxicated animals. Pathology associated with chronic
low level or sub-lethal exposure to poisons is poorly understood, and observing changes
in complex traits such as foraging ecology and behavior are often difficult and dependent on low numbers of observations (Kvitek et al. 1991; Cook et al. 2011). The study of
cognitive deficits as a result of exposure to particular poisons in humans is often subtle
and dependent on baseline markers of typical development. In some cases, associations
between an adverse outcome (neurologic disease) and a toxicant (mercury) are noted but
cannot be causally determined due to the observational nature or lack of controlled study
design (Van Hoomissen et al. 2015). It is unclear whether these poisons have the same
effects on marine mammals as for non-marine mammals, or furthermore if cognitive deficits have significant effects on the behavior or fitness of marine mammals. For instance,
concentrations of THg in the brainstems of polar bears were associated with decreased
N-methyl-d-aspartate (NMDA) receptor levels, however, it is unclear if these subclinical
effects are associated with any gross pathologies or observable behavioral changes (Basu
et al. 2009). Linking an observed biochemical or physiologic change to an adverse effect
can be rather elusive and frustrating for marine mammal toxicologists. However, progress is being made.
The study of marine mammal toxicology and their unique adaptations to dealing with
both new and old poisons is inexorably linked to other fields of study. Nutrition, physiology, ecology, and genetics are all components of toxicology, and developments in these
fields shape the future advancement of toxicologic research. The interaction between environmental, wildlife, and human health is beginning to be appreciated with the promotion
and implementation of the One Health Initiative, and the field of marine mammal toxicology can undoubtedly benefit from a holistic approach to examining the effects of poisons
on marine mammal health.
Glossary
Acclimation: The ability of an individual organism to respond to changes in environmental or physiologic conditions.
Adaptation: An evolved phenotypic trait which has arisen through natural selection.
Bioaccumulation: Net accumulation of a chemical compound in an organism from all
sources (air, diet, water) resulting from a higher rate of absorption than excretion.
Biomagnification: An increase in contaminant concentration from one trophic level to the
next attributable to accumulation from diet.
Chapter fourteen: Toxicology and poisons
is still challenging, and extrapolation to local or global population level effects is extremely
difficult (Fedorenkova et al. 2010; Van Straalen et al. 2010). It is important to reiterate that
not all responses to the presence of a toxicant are adverse, and in many cases are essential or beneficial (such as protective hermetic effects). There are a number of populations
of marine mammals that have been shown to have concentrations of contaminants over
established traditional thresholds of concern (i.e., Basu et al. 2009; Doucette et al. 2012; Rea
et al. 2013). However, from a population perspective, the ramifications of high concentrations of contaminants observed are unclear. Additionally, as has been emphasized in this
chapter and elsewhere, toxic thresholds which have been established in model organisms
(i.e., humans, rats, mink) might not be relevant to marine mammals, which have evolved
in a drastically different environment than their terrestrial counterparts.
In some instances where the etiology of mass die-offs is deduced (i.e., UMEs due to
HABs) the pathology of toxins may be known from laboratory animal models or observational studies (Silvagni et al. 2005), however, observations of intoxication are often limited
to dead/moribund or severely intoxicated animals. Pathology associated with chronic
low level or sub-lethal exposure to poisons is poorly understood, and observing changes
in complex traits such as foraging ecology and behavior are often difficult and dependent on low numbers of observations (Kvitek et al. 1991; Cook et al. 2011). The study of
cognitive deficits as a result of exposure to particular poisons in humans is often subtle
and dependent on baseline markers of typical development. In some cases, associations
between an adverse outcome (neurologic disease) and a toxicant (mercury) are noted but
cannot be causally determined due to the observational nature or lack of controlled study
design (Van Hoomissen et al. 2015). It is unclear whether these poisons have the same
effects on marine mammals as for non-marine mammals, or furthermore if cognitive deficits have significant effects on the behavior or fitness of marine mammals. For instance,
concentrations of THg in the brainstems of polar bears were associated with decreased
N-methyl-d-aspartate (NMDA) receptor levels, however, it is unclear if these subclinical
effects are associated with any gross pathologies or observable behavioral changes (Basu
et al. 2009). Linking an observed biochemical or physiologic change to an adverse effect
can be rather elusive and frustrating for marine mammal toxicologists. However, progress is being made.
The study of marine mammal toxicology and their unique adaptations to dealing with
both new and old poisons is inexorably linked to other fields of study. Nutrition, physiology, ecology, and genetics are all components of toxicology, and developments in these
fields shape the future advancement of toxicologic research. The interaction between environmental, wildlife, and human health is beginning to be appreciated with the promotion
and implementation of the One Health Initiative, and the field of marine mammal toxicology can undoubtedly benefit from a holistic approach to examining the effects of poisons
on marine mammal health.
Glossary
Acclimation: The ability of an individual organism to respond to changes in environmental or physiologic conditions.
Adaptation: An evolved phenotypic trait which has arisen through natural selection.
Bioaccumulation: Net accumulation of a chemical compound in an organism from all
sources (air, diet, water) resulting from a higher rate of absorption than excretion.
Biomagnification: An increase in contaminant concentration from one trophic level to the
next attributable to accumulation from diet.