Program - Society of Toxicology

Society of Toxicology 2011
Program Description (Continued)
Abstract #
Tuesday Afternoon, March 8
1:00 PM to 2:00 PM
Room 140A
Exhibitor Hosted Session: Uses for Stereology in Toxicologic
Pathology
Presented by: WIL Research Laboratories
Unbiased stereological analysis is required for documentation of shifts in
neuronal and other cell populations as well as changes in lung parameters
such as aleveolar counts and size estimations. This session will introduce
the specialized terminology and basic mathematical and technical concepts
involved in stereological sampling and analysis.
Tuesday Afternoon, March 8
1:30 PM to 4:15 PM
Room 144
Environment and Disease
Symposium Session: Developmental Origins of Adult Disease:
The Effects of Low-Dose Lead
Chairperson(s): Erin Hines, U.S. EPA, Research Triangle Park, NC, and
Andrew Rooney, NIEHS, Research Triangle Park, NC.
Sponsor:
Metals Specialty Section
Endorsed by:
Neurotoxicology Specialty Section
Reproductive and Developmental Toxicology Specialty Section
Risk Assessment Specialty Section
Numerous epidemiology and animal toxicology studies support an association
between an adverse prenatal environment and the development of
diseases in later life. Experimentally, prenatal exposure to lead (Pb) at low,
environmentally-relevant doses causes physiological changes that increase
the likelihood of diseases in adulthood such as obesity, hypertension, and
neurological disorders. Although human epidemiological data also support
an association between increased Pb exposure and hypertension or cognitive
impairment, the exact mechanisms by which lead exerts these effects
in epidemiologic studies is unknown. We will discuss experimental animal
toxicology data that suggest several possible mechanisms for developmental
origins of adult diseases (DOAD) associated with exposure to low levels
of lead. Data support a sex-dependent mechanism resulting in increased
fat deposition and late-onset obesity, retinal degeneration, and motor
activity aberrations following low dose gestational lead exposure in male
mice. Lead-induced hypothalamic pituitary adrenal axis dysfunction is a
potential mechanism for a range of adult diseases and disorders, including
hypertension, diabetes, metabolic syndrome, schizophrenia, and cognitive
dysfunction. Epigenetic mechanisms have also been implicated, and
epigenetic pathways may present a mechanistic link between developmental
lead exposure and the etiology of Alzheimer’s disease. These data highlight
the importance of exposure windows for the development of adverse health
effects associated with low-level lead and have possible risk assessment
implications for ongoing assessments such as the NTP Monograph on Low-
Level Lead and the U.S. EPA Integrated Science Assessment for Lead.
#1697 1:30 DEVELOPMENTAL ORIGINS OF ADULT
DISEASE: THE EFFECT OF LOW-DOSE
LEAD (PB). ​E. P. Hines 1 and A. Rooney 2 . 1 EMAG,
NCEA, U.S. EPA, Research Triangle Park, NC
and 2 National Toxicology Program, Center for the
Evaluation of Risks to Human Reproduction, NIEHS,
Research Triangle Park, NC.
1:30 INTRODUCTION. ​Erin Hines
Abstract #
#1698 1:35 LOW-LEVEL GESTATIONAL LEAD
EXPOSURE IS A RISK FACTOR FOR LATE-
ONSET METABOLIC SYNDROME AND
NEURODEGENERATION. ​D. A. Fox. University
of Houston, Houston, TX.
#1699 2:15 DEVELOPMENTAL LEAD (PB)
EXPOSURE AND PERMANENT HPA
AXIS DYSFUNCTION: A POTENTIAL
UNIFYING BIOLOGICAL MECHANISM
FOR PB-ASSOCIATED DISEASES AND
DISORDERS. ​D. A. Cory-Slechta. Department of
Environmental Medicine, University of Rochester
Medical Center, Rochester, NY.
#1700 2:55 EARLY LIFE EXPOSURE TO PB AND
PROGRAMMED SUSCEPTIBILITY TO
NEURODEGENERATIVE DISEASE. ​N. Zawia.
Biomedical Sciences, University of Rhode Island,
Kingston, RI.
#1701 3:35 CONTRASTING THE DEVELOPMENTAL
AND ADULT ORIGINS OF ADVERSE
EFFECTS FROM LEAD IN THE DRAFT NTP
MONOGRAPH ON LOW-LEVEL LEAD. ​A.
A. Rooney. Center for the Evaluation of Risks to
Human Reproduction, NIEHS, National Toxicology
Program, Research Triangle Park, NC.
Tuesday Afternoon, March 8
1:30 PM to 4:15 PM
Room 204
Symposium Session: Does the Clock Make the Poison?
Influence of the Circadian Clock on Toxicological
Mechanisms and Outcomes
Chairperson(s): Helmut Zarbl, University of Medicine and Dentistry New
Jersey, Piscataway, NJ, and Louisa Hooven, Oregon State University,
Corvallis, OR.
Sponsor:
Disease Prevention Task Force
Endorsed by:
Carcinogenesis Specialty Section
The daily biochemical, physiological, and behavioral activities of many
organisms are synchronized by light/dark cycles. These temporal oscillations
are maintained by the circadian clock, which has intrinsic periodicity
of approximately 24 hours. The circadian rhythm of cells is controlled by
the interaction of multiple positive and negative feedback loops comprising
a molecular oscillator, which modulates expression through transcriptional
and epigenetic means. Environmental and occupational exposures leading
to disruption of circadian rhythm, including jet lag, light-at-night, and
shift work are associated with an increased risk of endometriosis, breast
cancer, and prostate cancer, prompting the International Agency for Cancer
Research to classify shift work as a probable human carcinogen (type 2A).
Disruption of the circadian clock is also associated with increased risk of
cancer, cardiovascular disease, diabetes, obesity, reproductive problems,
sleep disorders, drug and alcohol addiction, and psychiatric disorders.
Accumulating evidence indicates that the dynamic influence of the circadian
clock profoundly affects many critical pathways in toxicology. Exposure to
stressors, carcinogens, chemotherapeutic agents, and other xenobiotics can
alter circadian function in cells, rodents, and humans, while some chemopreventive
agents my reset the rhythm. Targeted disruption of clock gene
expression is advancing our ability to understand and manipulate the circadian
clock. Our panel of experts will review the state of this emerging area
and explore opportunities for disease prevention.
Tuesday
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