To study stock structure of bottlenose dolphins, we use a
multi-disciplinary approach including photo identification, genetic, and
radiotelemetry techniques. Photo-identifications of dorsal fins in the
Charleston, South Carolina area are collected to compare with other areas
along the Atlantic coast. Biopsy sampling and subsequent genetic analysis of
mitochondrial and satellite DNA of bottlenose dolphin skin samples collected
in the Charleston area are compared to other areas along the Atlantic coast.
Radio and satellite tracking data are plotted to determine the distribution of
animals and migration patterns.
To monitor the health status of individuals and the role of
contaminants on health, a multi-disciplinary investigative approach is taken
using data obtained from stranded animals, animals captured in the wild, and
in vitro studies. Deaths of all stranded cetaceans are investigated by
performing detailed necropsies. Tissues are banked for archive and contaminant
analysis. Live capture-release of bottlenose dolphins allows for collection of
important health assessment data including morphometric measurements, blood
cell and chemistry analysis (CBC + differential, a full blood panel, thyroid
panel, morbillivirus, steroid panel, vitamin A), urinalysis, and fecal
analysis. Also, blubber, blood, and milk are collected for contaminant
analysis to determine the role contaminants play in the health of the
individual. In vitro studies on dolphin cell lines are used to determine
responses of biomarkers to chemical contaminants.

My experience as a graduate student was at the Institute of
Wildlife and Environmental Toxicology (TIWET) at Clemson University working
under Drs. Mike Hooper and Ed Pivorun in an inter-disciplinary and unique
approach that prepared me for my present position at NOAA. When I first came to
the program, I was a research assistant for Mike Hooper's student, Dale Hoff,
who was performing a risk assessment on badgers, Taxidea taxus, inhabiting the
Rocky Mountain Arsenal, a Superfund site heavily contaminated with dieldrin. In
order to define potential exposure of badgers to dieldrin, we defined home
ranges for individual animals. Here, I gained radiotelemetry experience that is
now helping me track bottlenose dolphins. From this research with Dale Hoff, my
thesis evolved – "Dieldrin Effects on the Biochemistry and Control of
Cold Adaptation in the Deer Mouse, Peromyscus maniculatus". With the help
of Ed Pivorun and Mike Hooper, I learned innovative laboratory techniques
(biomarker approaches and physiologic techniques) to study the effects of
dieldrin on brain chemistry and adaptation physiology (i.e. torpor). My
experience gained in non-lethal biomarker approaches learned at TIWET is now
helping to define my in vitro studies on dolphin cell lines as a method to
determine the effect of chemical contaminants on the health of marine mammals.
My personal research interests center around the recent
findings of scientists conducting a thirty-year study in Sarasota Bay, Florida -
that first-born bottlenose dolphin calves rarely survive. The mechanism for this
high mortality is unknown and could involve organochlorine contaminant transfer
from the mother to the calf. Marine mammals, particularly odontocetes, have the
highest organochlorine burden of any wildlife species worldwide. A large
percentage of this contaminant burden is transferred directly to the first born
neonate during lactation with up to 80% of the maternal organochlorine burden
transferred to the first born calf. Normally in an adult, the blood-brain
barrier acts to effectively block contaminants from entering the brain. However,
in the immature brain of newly born mammals, the blood-brain barrier is not well
developed. Organochlorine contaminants have the potential to pass through the
blood-brain barrier and exert a toxic effect. Dieldrin, chlordanes, toxaphene,
endosulfan, and polychlorinated biphenyls, all of which have been found in
bottlenose dolphin blubber, are neurotoxic to the central nervous system. I
hypothesize that contaminants pass through the undeveloped blood-brain barrier
in cetacean neonates and cause toxicity, thereby explaining the high mortality
observed in first-born bottlenose dolphin calves in Sarasota Bay. The hypothesis
consists of three objectives. The first objective is to define, quantify, and
model contaminant exposure of first-born neonates in bottlenose dolphins as well
as other odontocete neonates. The second objective is to determine neurotoxic
effects in odontocete neonate brains. The last objective is to construct a risk
assessment model to evaluate contaminant-induced neurotoxic risk on neonates.