PROCEEDINGS OF
THE EPA WORKSHOP
ON INTERACTIONS
BETWEEN SOCIAL
STRESS AND
ENVIRONMENTAL
HAZARDS
MAY 14-15, 2012
U.S. EPA Headquarters, East Building
Room 1153 (Map Room)
1201 Constitution Ave, N.W.
Washington DC 20004
Prepared By
Industrial Economics, Incorporated
Support for this Workshop
Was Provided Through
Contract #EP-W-10-002

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WORKSHOP CHAIRS
Onyemaechi C. Nweke, DrPH, MPH
Environmental Health Scientist
Office of Environmental Justice
Office of Enforcement and Compliance
Assurance
Devon Payne-Sturges, DrPH
Asst. Center Director for Human Health
National Center for Environmental
Research
PRESENTERS
Staci Bilbo, Ph.D.
Assistant Professor
Duke Institute for Brain Sciences
Duke University
Jane Clougherty, Sc.D.
Assistant Professor and Director of
Exposure Science
Graduate School of Public Health
University of Pittsburgh
Deborah Cory-Slechta, Ph.D.
Professor of Environmental Medicine and
Pediatrics
University of Rochester Medical School
Neal Fann
Office of Air Quality Planning and
Standards (OAQPS)
Office of Air and Radiation
U.S. Environmental Protection Agency
Robert-Paul Juster, M.Sc
Center for Studies on Human Stress
McGill University
CONTRACTOR SUPPORT
Lynne Messer, Ph.D., M.P.H.
Asst. Research Professor
Center for Health Policy
Duke Global Health Institute
Duke University
Madeleine Scammel, D.Sc.
Boston University School of Public Health
Joel Schwartz, Ph.D.
Professor of Environmental Epidemiology
Harvard School of Public Health
Peggy Shepard
Executive Director
West Harem Environmental Action, Inc
Rosalind Wright, M.D.
Associate Professor of Medicine
Channing Laboratory, Harvard Medical
School
Associate Professor of Environmental
Health
Harvard School of Public Health
Industrial Economics, Inc.
Amelia Geggel
Henry Roman
Eric Ruder
Scientific Consulting Group, Inc.
Suzie Warner
Michelle Watson
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TABLLE OF CONTENTS
Introduction	1
Purpose and Background 	1
Theme I: Science of the Impacts of Chronic Psychosocial Stress on Health 	3
Theme II: Interactions between Chronic Psychosocial Stress, Social Context, Health
and Environmental Hazards	5
Toxicological Evidence of the Interaction between Chronic Psychosocial Stress and
Environmental Hazards 	5
Epidemiological Studies on the Interaction between Chronic Psychosocial Stress and
Environmental Hazards 	6
Theme III: Measuring Chronic Psychosocial Stress and Social Context in Research... 8
Allostatic Load Model	8
Measuring Built Environment Metrics to Quantify Impacts of Chronic Social Stress ... 9
Cross Cutting Issues/Emerging Theories	11
Impacts of the Timing of Social Stress Exposure 	11
Resilience to Psychosocial Stress	12
Differences in Susceptibility 	12
Panel Discussion Summary 	13
Appendices
Workshop Agenda 	A-l
Workshop Abstracts 	B-l
Speaker Biosketches 	C-l
List of Workshop Attendees	D-l
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INTRODUCTION
The U.S. Environmental Protection Agency's Office of Environmental Justice and National
Center for Environmental Research convened the Workshop on Interactions between Social
Stressors and Environmental Hazards in May 2012 to examine the association between
negative health outcomes and exposure to psychosocial and chemical stressors. This
workshop sought to promote discussion among multiple stakeholders, including
environmental health researchers, EPA regulatory scientists and community advocates.
The workshop represents a sustained effort by the EPA to advance the science of
disproportionate environmental and health impacts experienced by minority and low income
populations. It is a follow-up to discussions initiated on the issue of social stressors at the
March 17-19, 2010 science symposium "Strengthening Environmental Justice Research and
Decision Making: A Symposium on the Science of Disproportionate Environmental Health
Impacts."
This report highlights the major issues presented and discussed during the May 2012
workshop.
PURPOSE AND BACKGROUND
Individuals with higher risk of exposure to environmental contaminants and an increased
susceptibility to adverse health outcomes following exposure may also experience higher
exposures to social stressors. Emerging evidence from epidemiological and toxicological
studies suggests that social stressors may modify the effects of environmental exposures on
health, potentially resulting in higher risks of adverse health effects in individuals exposed to
both kinds of stressors. This workshop aimed to share emerging research from multiple
disciplines related to the interactions between social stressors and environmental hazards.
Objectives for the workshop were as follows:
1.	Review research on the physiological effects of stress and biological pathways
through which psychosocial stress and social context may adversely influence health;
2.	Share toxicological and epidemiological evidence of the interactions between stress,
social context, and environmental hazards; and
3.	Discuss how to focus future research efforts on these interactions to best inform
policy decisions.
The workshop agenda divided presentations into three themes:
• Theme I: Science of the Impacts of Chronic Psychosocial Stress on Health
o Robert-Paul Juster presented "The Life Cycle Model of Stress: Detecting how
Chronic Stress and/or Trauma Harms Brains and Bodies" which gave an
overview of the biological pathways involved in chronic, psychosocial stress and
how stress may lead to adverse health outcomes.
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•	Theme II: Interactions between Chronic Psychosocial Stress, Social Context, Health
and Environmental Hazards
o Dr. Stacy Bilbo's talk, "Interactions between Social Context and Immune
and Neuroendocrine Systems in Laboratory Animals," detailed the
synergistic and gender-specific effects of early exposures to air pollution and
social stressors on neural development and cognitive impairments in mice.
o Dr. Rosalind Wright discussed how interactions between psychosocial
stressors and environmental exposures in utero may lead to increased risk of
wheezing and asthma in children during her presentation "Perinatal Stress
and Physical Environmental Influences on Urban Childhood Asthma:
Independent and Interactive Effects."
o Dr. Joel Schwartz presented "Evidence Review from Epidemiological Data -
Interactions between Air Pollution and Social Context and Implications for
Risk Assessment," which reviewed the epidemiological evidence of the
influence of social context on the effects of exposure to air pollution, lead,
and temperature increases as well as the importance of incorporating
population heterogeneity into risk assessments.
o Dr. Deborah Cory-Slechta, in "Combined Effects of Lead and Stress on
Impulsivity Measured and How These Effects are Mediated by Brain and
HPA Axis," presented her research on the synergistic and gender-specific
effects of exposure to lead and stress in animal models.
•	Theme III: Measuring Chronic Psychosocial Stress and Social Context in Research
o Robert-Paul Juster's second presentation, "The Allostatic Load Model:
Indicators, Indices and Methods to Measure the Antecedents and
Consequences of Chronic Stress throughout the Life Cycle," discussed the
concept of the allostatic load model and the development of methods to
measure chronic stress in a clinical setting.
o Dr. Lynne Messer's presentation, "Measuring Neighborhood Context for
Research Addressing Maternal and Child Health Disparities," shared her
research on methods to measure the relationship between the built
environment and maternal and child outcomes.
o Dr. Jane Clougherty presented "Disentangling Spatial Patterns in Social and
Environmental Exposures for Epidemiology" and detailed methods for using
spatial data and geographic information systems to better characterize the
relationship between stress, environmental hazards, and childhood asthma
exacerbation.
These presentations were followed by a panel discussion entitled "communication/ translation
of research on chronic psychosocial stress and environmental hazards to the public, policy
makers, public health practitioners and clinicians." This discussion included environmental
health researchers Dr. Cory-Slechta and Dr. Madeleine Scammel, community advocate Peggy
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Shepard, executive director of WE ACT for Environmental Justice, and regulatory scientist
Neal Fann of EPA's OAQPS.
This report presents a summary of each of the workshop themes and then describes several
emerging areas of research that appeared across presentations, including the influence of
timing of exposures on health outcomes, evidence for resilience to stress, and differences in
susceptibility. It concludes with a summary of the panel discussion. Four appendices are
included with this report: the workshop agenda, presentation abstracts, speaker biosketches,
and a list of workshop attendees.
THEME I: SCIENCE OF THE IMPACTS OF CHRONIC PSYCHOSOCIAL STRESS ON HEALTH1
Over the course of evolution, humans have developed a "flight-or-fight" stress response to
survive potentially life-threatening situations. This response involves subconscious
physiological changes that allow individuals to quickly adapt to immediate threats to their
well-being. Although these biological pathways evolved in response to urgent situations,
these same physiological changes occur in response to chronic psychosocial stress.
Activating the stress response to escape immediate threats to bodily harm offers a survival
advantage. However, chronic activation of these pathways is thought to play a role in the
development of numerous chronic diseases.
Mr. Juster and Dr. Wright gave broad overviews of the physiological mechanisms involved in
the stress response. The body mediates stress through two physiological systems; the
sympathetic-adrenomedullary (SAM) system and the hypothalamic-pituitary-adrenocortical
(HPA) axis. Following exposure to external stressors, individuals automatically and
subconsciously determine whether the situation presents a possible threat, in a process known
as appraisal. If the individual perceives the situation to be stressful, signals from the
hypothalamus stimulate the adrenal glands to produce hormones (epinephrine and
norepinephrine) that stimulate the "fight or flight" response of the SAM system. This
response increases heart rate, respiration, blood pressure, and blood flow to muscles, and
decreases digestion, among other changes. The HPA axis regulates the body's stress
response through the release of hormones in the brain (hypothalamus) and pituitary gland.
These hormones tightly control the amount stress hormones, such as Cortisol, released by the
adrenal glands. Because elevated Cortisol levels can be damaging, the body relies on negative
feedback loops to lower Cortisol levels when the stress response is no longer needed.
Chronic activation of the stress response affects multiple systems in the body and may lead to
endocrine, metabolic, autoimmune, and mental health issues. Dr. Wright noted that stress
may disrupt immune system function, increase oxidative stress, and alter gene expression.
The immune system responds to feedback from the autonomic nervous system which in turn
is influenced by hormones and cytokines (cell signaling molecules) released by the immune
system. Dr. Cory-Slechta stated that abnormal HPA axis response is associated with
numerous diseases including osteoporosis, heart disease, diabetes, autoimmune diseases,
Alzheimer's disease, and psychiatric disorders.
1 Mr. Juster gave the only full presentation on this theme. However, this section includes relevant information provided by other
speakers during the workshop.
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Chronic stress elevation brought on by long-term exposure to community violence or racism,
as well as chronic effects from acute stressors such as job loss or emotional trauma may
affect the development and size of certain brain regions. Different regions of the brain,
including the amygdala, hippocampus, prefrontal cortex, and hypothalamus, are involved in
the activation of the body's stress response. The amygdala regulates emotional response to
events, especially fear, anger, and aggression. The prefrontal cortex controls cognitive
processes such as moral behavior, planning, attention, and reasoning. The hippocampus is
involved in learning and memory. Mr. Juster illustrated this concept using research
observations on the effect of chronic stress on the development of mental health disorders
such as Post Traumatic Stress Disorder (PTSD). Studies show that individuals with
schizophrenia, depression, or PTSD are more likely to have a smaller hippocampus. Some
researchers propose that stress has a neurotoxic effect that causes the hippocampus to shrink
while other researchers argue that individuals with a smaller hippocampus are more
vulnerable to developing certain mental health problems such as PTSD. One model that
bridges these two hypotheses is the life cycle model of the effect of stress on development.
Adversity early in life may affect brain development and lead to a smaller hippocampus.
Animal studies show that maternal separation and poor maternal care accelerate the
development of the amygdala and cause hippocampal atrophy. Children of depressed
mothers have higher Cortisol levels and larger amygdala and lower levels of Cortisol produced
in response to stress. Individuals with a smaller hippocampus may be predisposed to
developing certain mental health issues following exposure to social stressors. In summary,
the life cycle model suggests that chronic exposure to stress in early life has been associated
with hippocampal atrophy, which in turn may impair the brain's response to social stressors
later in life. A smaller hippocampus may predispose individuals to certain mental health
disorders such as PTSD
Finally, presenters briefly highlighted the issues of stress perception and appraisal, as well as
the concepts of harmful and helpful stress. Noting that the term stress has multiple colloquial
meanings, Mr. Juster offered an explanation for psychosocial stress that is potentially harmful
based on the exposed individual's appraisal, and described such potentially harmful stress as
that which involves situations that are novel, unpredictable, threaten the ego or involve a
sense of loss of control. Perception of stress was considered the "exposure agent" or trigger
for physiological responses by some presenters who argued that external events must be
perceived as stressful to lead to negative emotional and physiological responses. For
example, loud noise is not bothersome if it is not heard. Dr. Messer argued that stressors may
affect individuals negatively even without their direct acknowledgement of the stressor or of
their response to the stressor.
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THEME II: INTERACTIONS BETWEEN CHRONIC PSYCHOSOCIAL STRESS, SOCIAL
CONTEXT, HEALTH AND ENVIRONMENTAL HAZARDS
Multiple human and animal studies illustrate how early exposure to pollutants in combination
with severe or chronic stress can change the pattern of the developing brain, leading to
lifelong social and psychological effects. The timing and duration of exposures to both
chemical and psychosocial stressors play a critical role in the long term effect of exposure.
Stress exposure may change the genetic programming of developing fetuses or children and
can permanently alter physiology. The synergistic effect of exposures to pollution and social
stress often leads to more severe health outcomes than either exposure alone.
TOXICOLOGICAL EVIDENCE OF THE INTERACTION BETWEEN CHRONIC PSYCHOSOCIAL STRESS
AND ENVIRONMENTAL HAZARDS
Animal studies performed by Dr. Cory-Slechta and Dr. Bilbo involving exposure to
pollutants at levels equivalent to higher inner city exposures demonstrate that prenatal and
early postnatal exposures to social and chemical stressors have physiological effects that last
into adulthood. Exposures during critical periods of development, such as in utero, may lead
to permanent physiological or neurological changes. These studies in mice and rats focus on
air pollution and lead exposures and suggest that maternal stress interacts with exposure to
these contaminants and may harm developing fetuses.
Dr. Bilbo presented evidence that that concurrent exposure to air pollution and maternal
stress increases the likelihood of cognitive impairment in adulthood. Mice exposed only to
air pollution early in development (prenatally to diesel exhaust and postnatally to ozone)
showed airway hyper reactivity as adults long after the exposure period ended. When these
exposures were combined with maternal stress, markers of stress increased in both mothers
and pups. Offspring weighed less and had higher stress hormone levels. Male offspring
showed increased memory impairment and higher anxiety. The reason for these impairments
may be that stress and diesel exhaust affect the immune response in the brain, leading to
cognitive problems. These impairments may be mediated through impacts to microglial cells,
which along with other immune factors, aid other neural cells in development and maturation.
Both mothers and offspring showed evidence of neuroinflammation, including increases in
the immune signaling molecules cytokines and chemokines. These early exposures to
maternal stress and air pollution appeared to have lifelong health impacts in mice.
Dr. Cory-Slechta's research shows that prenatal exposure to lead in rats produced lifelong
changes in the stress response which is amplified by concurrent prenatal exposure to social
stress. Rats normally increase the stress hormone corticosterone over the first year of life, but
animals exposed to both prenatal stress and lead did not show this developmental pattern.
Male rats exposed to a plausible human exposure level of lead in utero displayed an elevated
stress hormone response following a stress challenge. Interestingly, rats of either gender
exposed at higher levels did not show this response. Rats exposed to both lead and stress
prenatally had impaired cognitive functions, including learning impairments and greater
impulsivity. Both lead and social stress appear to affect similar biological pathways,
including the HPA axis and the mesocorticolimbic system, which is involved in learning and
memory. Fetal exposure to either or both lead and stress appeared to cause lifelong
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alterations to both of these pathways. Although the placenta protects the fetus against normal
elevated maternal Cortisol levels during pregnancy, it may not be able to protect against high
levels due to chronic stress. A developing fetus will respond to the presence of excess fetal
glucocorticoids or lack of nutrition by permanently altering its physiology. These
physiological changes may be the mechanism for the cognitive impairments observed. Dr.
Cory-Slechta noted that epidemiologic studies show an association between maternal stress
during pregnancy and language development in human toddlers as well as attention deficits in
children.
These researchers observed that the interaction effects of stress on the observed relationship
between exposure to environmental toxins and stress and the development of cognitive
deficits appears to be gender specific. Dr. Bilbo reported that in her research in addition to
the observation that only males exposed to diesel exhaust in utero showed more anxiety-like
behaviors and impaired memory, these effects were also aggravated by concurrent exposure
to maternal stress in utero. Dr. Cory-Slechta noted that female rats exposed to both lead and
stress in utero showed signs of learning impairments. Exposure prenatally to stress or lead
alone did not produce these cognitive deficits. However, exposure to lead and stress
prenatally increased impulsivity in both female and male rats. Further work by Dr. Bilbo
suggests that a possible mechanism for observed gender-specific interactions between stress
and cognitive effects is through neuroimmunomodulatory pathways in which the early
immune system influences brain development during critical sensitive periods. She discussed
experiments that showed that exposure to E. coli during the neonatal period alone did not lead
to long-term effects. However, a second exposure during adulthood led to social and
cognitive deficits in male mice only. The differences in the immune response observed in
male and female mice may explain these findings. These animal studies suggest that
exposures to social and chemical stressors during the prenatal and neonate periods lead to
increased risk of adverse health and cognitive impacts later in life in a gender-dependent
manner.
EPIDEMIOLOGICAL STUDIES ON THE INTERACTION BETWEEN CHRONIC PSYCHOSOCIAL STRESS
AND ENVIRONMENTAL HAZARDS
Dr. Wright presented her research on the association between stress exposure and the risk of
developing asthma. Her research measured the number of negative life events such as
financial strain, racism, discrimination, interpersonal or community violence as well as
exposure to allergens in children and mothers. Children whose mothers had traumatic life
experiences had higher levels of certain immune factors indicative of asthma. These children
took longer to recover following a stress challenge at six months of age, as measured
behaviorally and via heart rate. Both prenatal and postnatal maternal stress, especially
postnatal financial strain, was associated with repeated wheeze episodes before two years of
age. Infants whose mothers reported the highest levels of social stress presented with wheeze
patterns similar to children exposed to black carbon. This finding is important because
repeated wheeze at a young age increases the risk of asthma. Children of atopic (allergic)
mothers exposed to high levels of allergens at home showed a linear relationship between IgE
(marker of reactivity to allergens) and stress. Non-sensitized mothers showed a large effect
of prenatal stressors on repeated wheeze in their children. Both high community violence and
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traffic-related air pollution were associated with repeated wheeze and may have had an
interactive effect. Maternal Cortisol levels may explain these findings. Mothers with children
who wheezed had greater diurnal changes in Cortisol levels. Prenatal maternal stress levels
may lead to changes in fetal immune response and, therefore, increased risk for wheezing.
Dr. Schwartz presented multiple epidemiological studies that emphasized the importance of
understanding how social and biological factors influence susceptibility to air pollution,
temperature changes, and lead exposure. Dr. Schwartz pointed to evidence that lower
socioeconomic status is associated with a higher prevalence of certain diseases, such as
diabetes, that increase susceptibility to air pollution and high temperatures. All-cause
mortality risk from air pollution also is inversely associated with educational attainment, a
marker of socioeconomic status. Chronic exposure to variability in summer temperatures is
associated with minority status. The odds of mortality, especially cardiovascular mortality,
from exposure to extreme high temperatures are modified by race, diabetes status, and
education. These results indicate that social factors influence the risk of mortality from air
pollution and temperature changes.
Lead exposure has long been associated with cognitive impairment. Recent studies have
shown that cognitive effects are seen below levels previously believed to be safe (10 ug/dL).
Minority, lower socioeconomic status, and medically underserved children have a higher risk
of exposure to lead and are more likely to be exposed to social stressors. Dr. Cory-Slechta
noted that low socioeconomic status leads to increased risk of chronic elevation of stress
hormones (such as glucocorticoids), which may increase the risk of certain diseases. Similar
to the animal studies summarized previously, epidemiological studies presented by Dr.
Schwartz suggest that concurrent exposure to lead and social stress increases the likelihood
and magnitude of cognitive function deficits in both adults and children. Residence in
neighborhoods with more psychosocial hazards was associated with cognitive deficits in
older adults. Men who reported greater stress levels showed a stronger association between
level of bone lead and cognitive impairments. The effects of lead exposure in children is also
modified by socioeconomic status (as measured by parental education or paternal
occupation), with lower levels of lead associated with cognitive deficits. Acute stress in these
children has been associated with modified vascular response. Hypertension risk is greater
for the combination of lead and social stress exposure than either exposure alone. Because
the risk of negative cognitive effects from lead may be greater in children and adults
concurrently exposed to high levels of social stress, policies that incorporate these findings
may better protect against cognitive impairments due to lead exposure.
Moving toward advancing the integration of these findings with environmental policy, Dr.
Schwartz outlined several problems with current risk assessment approaches, a key analytical
and decision-making framework at EPA. Studies have established that age, health status, and
genetics play a role in susceptibility to environmental exposures. However, most
toxicological studies rely on healthy, same-age animals with a similar genetic make-up. This
lack of diversity in animal models may lead to erroneous conclusions regarding the effects of
certain exposures. Dr. Schwartz used examples from studies on particulate matter and heat to
demonstrate that assuming average risk of adverse outcomes across a geographic area will
fail to account for actual risk. Setting standards based on these averages may fail to protect
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vulnerable individuals. Likewise, the mean response across multiple toxicological or
epidemiological studies will appear normally distributed even if individual studies show a
skewed response. Heterogeneity in human populations, whether due to social factors such as
income, or innate factors such as genetics or disease status, is likely to lead to a range of
thresholds for a given toxin. This range of thresholds may be best modeled assuming a linear
concentration-response rather than a single threshold to find the standard that will protect
vulnerable members of the population. Dr. Schwartz argued that heterogeneity has important
implications for risk assessment and policy decisions. Incorporating factors that influence
heterogeneity in exposure and susceptibility allows risk assessments to better reflect actual
risks. Understanding factors that change susceptibility may allow risk assessments to better
inform policy decisions and protect public health.
THEME III: MEASURING CHRONIC PSYCHOSOCIAL STRESS AND SOCIAL CONTEXT IN
RESEARCH
Researchers have developed a number of techniques to quantify the level of exposure to
chronic psychosocial stress. These measures include determining clinical biomarkers of
chronic social stress, as discussed in Mr. Juster's presentation of the allostatic load model, as
well as developing methods to measure the influence of the built environment on health
outcomes, as detailed by Drs. Messer and Clougherty. These approaches to measuring
chronic social stress allow researchers to better elucidate the relationship between stress,
environmental exposures, and health impacts.
ALLOSTATIC LOAD MODEL
Mr. Juster presented the concept of allostatic load to understand how chronic stress can lead
to health problems. This theory proposes that the body reaches stability by continuously
changing physiological parameters to match environmental conditions in a process called
allostasis. The body evaluates environmental stressors and reaches set points that both meet
environmental demands and conserve resources. This framework of how social stress may
lead to adverse health outcomes proposes that through the process of constant readjustment to
match stressful conditions, the body may wear out physiological systems that allow
adaptation to changing conditions. This "wear and tear," known as allostatic load, may be the
mechanism for the development of adverse health outcomes from chronic stress exposure.
The theory of allostatis allows a more complete understanding of how psychosocial stress
may lead to certain health outcomes.
Traditional understanding of how the body maintains stability, known as homeostasis, posits
that physiological systems rely on internal negative feedback loops to ensure that
physiological parameters do not deviate from fixed set points. The model of allostasis was
first proposed by Sterling and Eyer2 in 1988 and offers a more dynamic understanding of the
interaction of biological functions and describes how the body changes set points in response
to external influences. For example, the allostatic model explains why chronically stressed
rats will continue to have high blood pressure after the removal of experimental stressors.
2 Sterling, P. and Eyer, J., 1988, Allostasis: A new paradigm to explain arousal pathology. In: S. Fisher and J. Reason (Eds.),
Handbook of Life Stress, Cognition and Health. John Wiley & Sons, New York.
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Rather than returning to a baseline blood pressure, as expected with the homeostatic model,
rats increased the set point of their blood pressure in response to external stressors. The
allostatic model proposes that the body has mechanisms to anticipate physiological changes
and that behavior can influence physiological response. Consider the experience of feeling
dizzy after standing up too quickly. Once the individual realizes the cause (standing up too
fast), he or she may choose to change behavior (stand up more slowly) to avoid feeling
lightheaded. Rather than understand the dizziness response only as a physiological reaction
to gravity, allostasis incorporates the change in behavior. Allostatic changes begin with
primary mediators (e.g. stress hormones) that act as messengers to cause primary effects such
as cellular changes. The combined effects of these subclinical changes may lead to secondary
outcomes, such as changes in blood pressure, cholesterol, glucose levels, etc. These clinical
markers can be a sign of the presence or risk of developing stress-related diseases (tertiary
outcomes).
Because allostatic load may indicate the presence or risk for certain diseases, researchers such
as Mr. Juster are investigating methods to allow clinicians to test levels of allostatic load. To
measure allostatic load, researchers are developing an "allostatic index" consisting of four to
ten biomarkers spanning the neuroendocrine, immune, cardiovascular, and respiratory
systems and metabolic and anthropometric measures. Several major studies in the United
States, Taiwan, and Europe have shown a correlation between higher allostatic load, as
measured by an allostatic index, and lower socioeconomic status, lower self-rated health, less
social mobility, higher job strain, career instability, minority status, and older age. Allostatic
states that may be indicative of risk of poor health include both an inadequate stress response
as well as a continued heightened response with failure to recover. Some of the ongoing
research on allostatic load aims to find the parameters that best predict adverse health
outcomes in order to give clinicians a tool to measure allostatic load prior to the development
of disease. Generally speaking, the allostatic model suggests that a holistic approach to
patient treatment in the clinical setting should aim to reduce arousal of the stress response in
order to prevent or mitigate disease.
MEASURING BUILT ENVIRONMENT METRICS TO QUANTIFY IMPACTS OF CHRONIC SOCIAL STRESS
Drs. Messer and Clougherty presented their work developing methods to measure and
analyze the impact of neighborhoods and the built environment on health outcomes. Their
research focuses on designing and validating novel techniques to accurately assess how
neighborhoods influence exposures to social stress and to environmental toxins as well as the
risk of negative health effects from these exposures. Dr. Messer's work aims to quantify the
effect of the built environment on pregnancy outcomes and Dr. Clougherty's research looks
at factors that influence asthma exacerbation in urban children.
Dr. Messer noted that studies show neighborhoods have modest but lasting associations with
health disparities, and that where people live can influence their level of exposure to both
social stress and environmental toxins and their risk of adverse health outcomes. In order to
better understand factors in the built environment that influence health outcomes, she
assessed tax parcels in Durham, NC for descriptive variables, including the condition (peeling
paint, broken windows, etc.), nuisances (such as litter, discarded furniture and graffiti), and
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property descriptors (property type and vacancy status). She combined visual assessments of
properties with data on crime, tenure, and amenities and analyzed data on a parcel-level,
census block-level, and primary adjacency community level (parcels adjacent to index block).
Her research found that certain housing and property metrics were associated with higher
odds ratios for pre-term birth, small for gestational age, decreased birth weight, and decreased
birth weight percentile for gestational age. In a follow-up study, the Healthy Pregnancy-
Healthy Baby Cohort assessed the influence of genetic, environmental and social factors on
birth outcomes. Unadjusted models showed relationships between certain built environment
metrics and the mother's psychological state, while adjusted models demonstrated a
significant relationship between living in a rental property and negative paternal support as
well as "John Henryism" (working harder when faced with adversity). This research
demonstrated a methodology to measure the built environment that assesses, rather than
samples, an entire community and showed that neighborhood conditions may influence birth
outcomes.
Dr. Clougherty presented her recent work designing a study in New York City that uses
resident-defined neighborhood boundaries to elucidate the relationship between residential
location, exposure to both traffic-related air pollution (TRAP) and social stressors, and
childhood asthma exacerbation. This research will involve 25 focus groups where residents
identify stressors of concern. Further surveys will determine if individuals' stress level is
related to these stressors. The spatial patterns of social stressors and air pollution will be
assessed using data from multiple sources, including census tracts, school districts, police
precincts, etc. Because TRAP is a complex mixture of pollutants that varies across space and
because social stressors and pollutants cluster spatially, this study will use statistical
techniques that correct for spatial confounding and autocorrelation to understand the effects
of air pollution, psychosocial stress, and socioeconomic status on asthma hospitalizations in
children. Dr. Clougherty stated that stratifying geographic areas by effect modifiers of risk,
such as markers of socioeconomic status (e.g., education) or other sources of variability, such
as disease prevalence, will more accurately portray the distribution of risk. This study will
examine the effects of social stressors and TRAP on hospitalization rates for asthma in
children and explore whether social stress modifies the effects of air pollution on asthma
exacerbation.
Drs. Clougherty and Messer discussed a number of issues related to data source availability
for understanding spatial relationships of synergistic effects between social stressors and
environmental contaminants. In order to accurately classify exposures and population
characteristics by neighborhood, researchers need to integrate data from multiple sources.
However, neighborhoods often do not map to administrative boundaries, such as census tracts
or school zones and these administrative borders may not line up with each other. Dr.
Clougherty's study will use statistical techniques to combine exposure and population
variables from multiple, incongruous administrative areas. However, Dr. Messer compared
several geographic units of analysis and found that census blocks and census tracts acted as
good proxies for most neighborhood exposures, except for walkability. Dr. Clougherty
discussed the potential for exposure misclassification when using metrics with differing
scales of spatial variation. For example, the percentage unemployed varies block by block,
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while differences in racial composition range across a larger geographic area. Additionally,
social stressors identified by residents may be difficult to measure directly and researchers
must consider related indicator variables as surrogates. Dr. Clougherty noted that the metrics
chosen as markers for susceptibility may influence observed spatial differences in
susceptibility. Dr. Messer noted that additional metrics not assessed in her work may
influence birth outcomes and that further research will continue to refine metrics used to
assess neighborhoods. Understanding these factors can lead to more accurate assessments of
the interaction between social stressors, environmental hazards, and the risk of adverse health
effects.
Understanding associations between neighborhood effects may lead to interventions that
improve birth outcomes and reduce the rate of hospitalizations for asthma. Research that
develops innovative methods for measuring the influence of neighborhoods on exposure to
chronic social stress and environmental toxins, may give policy makers better tools to set
standards that protect vulnerable populations.
CROSS CUTTING ISSUES/EMERGING THEORIES
IMPACTS OF THE TIMING OF SOCIAL STRESS EXPOSURE
Multiple presenters discussed the theory that timing of exposures to both social stress and
chemical contaminants influences the nature of the interactions and the ultimate impacts of
these exposures. Toxicological studies in animals and epidemiological evidence in humans
support the idea that these exposures have the greatest impact during certain vulnerable
periods during growth and development. Early exposures may cause genetic modifications
that lead to lifelong cognitive and physical health problems. Susceptibility to social stressors
and environmental contaminants may depend on the age and timing of exposure.
Evidence in both animal and human studies indicates that quality care during young
childhood appears to prevent many health effects associated with exposure to social stress.
Dr. Wright noted that the degree of vulnerability to maternal stress in children is highly
regulated by social context. Exposure and response to maternal stress begins in utero and
continues to develop after birth. Increased levels of stress hormones in children due to
exposure to social stressors may impact immune function and lead to health effects in
adulthood. Some individuals are more highly sensitive to stress exposure due to genetic
make-up. However, one of the key factors in avoiding later health effects from exposure to
social and chemical stressors is attentive and supportive care of young children. Responsive
care seems to prevent increased levels of stress hormones in children and poor quality care
seems to increase vulnerability to stress. Interventions during this period of development
may improve lifelong health.
Exposures to social and chemical stressors early in life may influence health in adulthood due
to genetic modifications known as epigenetics. This process involves molecular changes that
regulate the level of expression of certain genes without altering the underlying DNA
sequence. Epigenetic changes during fetal and early childhood development can have
lifelong impacts. Dr. Cory-Slechta stated that exposure to elevated Cortisol during fetal
development may permanently alter the HPA axis in a similar manner to lead exposure. Mr.
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Juster discussed how stress during prenatal development affects the programming of the HPA
axis. From birth through two years, the hippocampus rapidly develops and may be most
affected by stress early in life. As discussed previously, the hippocampus plays a key role in
the stress response, signaling the adrenal gland to release stress hormones. Controlled
experiments in animals support the idea that attentive care may mitigate the effect of social
stress exposure on the hippocampus. Dr. Bilbo presented studies that indicate augmented
maternal care in mice (attentive grooming and nursing behaviors) increases the expression of
anti-inflammatory cytokines by altering the expression of the glucocorticoid receptor in the
hippocampus through epigenetic changes. These levels of gene expression were not due to
genetic inheritance alone, as mice fostered by more attentive mothers showed the same
pattern of epigenetic changes and pups later fostered by less attentive mothers reversed these
epigenetic changes. These molecular responses occurred during the first week of life and
lasted into adulthood. As mentioned earlier, male mice exposed to E. coli as pups and again
as adults showed signs of cognitive and social deficits. However, these results were seen
only in pups lacking attentive care. Pups with augmented maternal care did not show deficits
following the second immune challenge. Attentive maternal care appeared to give lifelong
protection. These animal studies support the idea that intervention may mitigate the harm
from social stress exposure, with long-term health benefits.
Concurrent early exposure to environmental contaminants and social stressors may affect
physical and mental health in adults. Dr. Schwartz discussed how childhood socioeconomic
status predicts adult socioeconomic status as well as lifetime lead exposure. Mr. Juster noted
that the timing of stress exposure may influence which areas of the brain are affected.
Epigenetic changes due to psychosocial stress may explain this association. For example, Dr.
Schwartz noted that low optimism and higher anxiety scores were linked to increased gene
expression (decreased methylation) in individuals exposed to air pollution. Evidence from
both human and animal studies demonstrates that the timing of exposure to social stress and
environmental contaminants may have lifelong effects.
RESILIENCE TO PSYCHOSOCIAL STRESS
Several presenters noted that despite clear associations between chronic social stress and
negative health outcomes, certain types of stress may be beneficial by encouraging resilience.
Appropriate stress response is important for normal social functioning. Mr. Juster discussed
that among individuals who grew up in lower socioeconomic status households those who
had the "shift and persist" personality trait had the lowest allostatic load. This personality
trait tends to frame adversity more positively and continues to focus on the future despite
hardships. This correlation was not seen in children from higher socioeconomic status
households. Stress that motivates individuals may teach resilience rather than lead to
negative health outcomes. However, most studies detailed in this workshop found chronic
social stress detrimental to later health status.
DIFFERENCES IN SUSCEPTIBILITY
Multiple speakers presented findings showing that socioeconomic status, race, gender,
genetics, disease status, and other factors influence the effect-modifying potential of social
stress on the relationship between environmental exposures and adverse health outcomes.
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Speakers emphasized that this heterogeneity should be taken into account when setting
standards and that current policy decisions may not adequately protect vulnerable
populations. Multiple toxicological and epidemiological studies demonstrate that social
stress acts as an effect modifier for multiple environmental exposures, including air
pollutants, lead, and temperature changes and that risk of exposure to social stress and to
environmental toxins is correlated with socioeconomic and minority status. Studies in
rodents show how gender influences the response to stress and pollutant exposures. Detailed
analyses of geographic differences in susceptibility suggest that both exposure levels to social
and chemical stressors as well as risk of adverse health outcomes from these exposures vary
by neighborhood. By understanding characteristics that lead to heterogeneous responses to
contaminants, policy makers can choose policy options that take into account distributional
effects and design policies that reduce disparities in health.
PANEL DISCUSSION SUMMARY
The workshop ended with a panel discussion about ways to translate research on social
stressors and environmental toxins to improve public policy and how best to communicate
results to the public, policy makers, and clinicians. The panel was comprised of Peggy
Shepard, a community advocate, EPA regulatory scientist Neal Fann, and environmental
health scientist Dr. Madeleine Scammel. Dr. Cory-Slechta moderated the panel. The
discussion was framed by a series of questions on how researchers, regulators, and
communities can coordinate to improve public policy and public knowledge to reduce
exposures to environmental and social stressors.
• What are the traditional ways that EPA would incorporate information on sensitive
populations in regulatory development decisions?
Mr. Fann answered that EPA sets the standards for criteria pollutants, such as particulate
matter (PM) and ozone, to be protective of sensitive subpopulations. The Transport Rule
demonstrates an example of how environmental justice analyses are used to justify decisions,
rather than used as an integral part of the rulemaking process. Through an environmental
justice analysis EPA determined the baseline distribution of risk of mortality from PM by
county and by race, income, and educational attainment. The analysis showed that PM-
related mortality decreased across the population and the most substantial decrease was seen
in these sensitive subgroups. Mr. Fann added that this analysis was completed later than the
economic and other regulatory analyses and did not directly inform policy decisions made in
developing the Transport Rule. These types of analyses are data- and time-intensive, and are
often difficult to complete early in the regulatory process. However, incorporating this
information earlier in the process may facilitate the inclusion of equity considerations
throughout the policy development process.
Panelists debated whether EPA has a mandate to assess impacts on vulnerable
subpopulations. Ms. Shepard stated that the 1994 Executive Order 12898 on environmental
justice includes an unfulfilled mandate for such assessments and that guidance on cumulative
impact from the 1990's has still not been incorporated into agency decision-making. Other
panelists commented that EPA assesses impacts of rules on vulnerable subpopulations, even
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when not mandated to perform these analyses. All panelists agreed that EPA needed to
expand its ability to perform these assessments.
•	What types of data would be helpful to a regulatory analyst and decision maker in
conducting environmental justice analyses?
Better characterization of the distribution of exposures and health effects across subgroups
would help inform analyses of environmental justice concerns. Reports detailing the
monetized benefits for a given rule do not give information on risks for sensitive subgroups
or on equity issues. The data needed to fully assess environmental justice concerns often
comes from multiple sources, including state and county databases. For this reason, data on
social factors and psychosocial stress may not be consistently formatted or straightforward to
compile. EPA has had many discussions on ways to improve data interoperability, with the
goal of providing spatial tools that combine data on exposure, health, ecosystem services,
susceptibility factors, etc. These databases would allow researchers, community groups and
community planners easier access these types of data.
Mr. Fann raised the importance of presenting data in a way that managers will feel confident
in the conclusions of an assessment. Some methods used in environmental justice analyses
are relatively new and EPA has not adopted standard approaches for these evaluations. For
example, EPA has not yet established standard indicators for socioeconomic status. Current
regulatory processes reflect careful review of existing analytical methods. For instance, the
EPA has a well-vetted approach for analyzing the benefits and costs of rules. Therefore, a
degree of "analytical inertia" exists that must be overcome in order to update these methods
to include environmental justice concerns. Since each program office is autonomous,
changes in approaches for incorporating environmental justice into regulatory analysis can
take time. Nevertheless, EPA has made important strides in incorporating environmental
justice issues into the regulatory process. As EPA continues to develop and refine
approaches for characterizing vulnerable subpopulations and understanding the distribution of
impacts, incorporating environmental justice concerns in the regulatory process will become
easier. Including analyses that detail the impact on environmental justice in an executive
summary of a regulatory impact analysis, rather than attached as an appendix, will help show
that these considerations play an important role in the decision-making process.
•	Is there an opportunity to accommodate emerging data related to interactions between
social stress and environmental hazards in your assessments?
Two panelists spoke of pilot studies by EPA that improved knowledge of the exposure levels
of vulnerable communities. Ms. Shepard mentioned a study where WE ACT and Columbia
University worked with EPA to perform community-based monitoring of PM2.5 in Harlem.
This study found PM2.5 levels twice as high as the standard. Ms. Shepard stated that these
results were used to defend the new standards in court. Because of this study, EPA provided
additional resources for community-based air monitoring in New York.
Mr. Fann reported that an EPA pilot in Detroit illustrated that states can develop innovative
ways to implement NAAQS that incorporate environmental justice concerns. The study
looked at two implementation approaches, the typically-used least cost approach and the
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multiple risk based approach. The former method allows the state to just meet the standard.
The latter aimed to find the maximum human health benefit by incorporating data on the
distribution of exposure among the population and information on how controls on key
industrial sectors would reduce exposure for highly exposed subgroups within the population.
This approach both meets the air quality standard and improves health and equity across the
population.
•	How can the research community best approach studies on social stress and
environmental contaminants to inform EPA 's regulatory process?
Several researchers and EPA analysts spoke about the need for better communication
between EPA and academic researchers. Dr. Scammel noted that often researchers and EPA
are not aware of each other's data needs. She suggested regular conference calls between
researchers and EPA to help encourage more policy-relevant research. Dialogue between
academics and EPA would provide a forum for researchers to present results in a format that
allows analysts to easily incorporate this information into regulatory analyses. For example,
better understanding of dose-response information for vulnerable subgroups helps analysts
better determine the distributional impacts of proposed rules. Dr. Cory-Slechta mentioned
that the funding opportunities at other agencies, such as the National Institutes of Health do
not always match EPA's research needs. Direct grants from EPA, such as the Cumulative
Risk Grants, encourage researchers to improve understanding of distributional impacts on
vulnerable and sensitive subpopulations.
Participants agreed on the need for cross-disciplinary and multidisciplinary research
approaches. For example, the National Academy of Sciences' Science and Decisions:
Advancing Risk Assessment offers a new paradigm for non-cancer risk assessment. The study
of social stressors readily fits this updated risk assessment paradigm. Dr. Cory-Slechta noted
that recently EPA recognized the importance of multidisciplinary approaches and added
social and behavioral scientists to its Scientific Advisory Board. Audience members noted
that environmental health risk assessors should work with researchers in the social and
natural sciences to improve understanding of environmental justice concerns.
•	What are ways to help communities identify environmental hazards and learn how they
can effect change in institutions to improve their lives?
Panelists spoke of the importance of using community knowledge in understanding
environmental justice issues. Ms. Shepard discussed how after WE ACT surveyed the
community, the organization found that it was not working on any of the top concerns of
residents (e.g. garbage, rats, litter, drugs, crime). Now the organization incorporates the
community's interests into its agenda. She stated that workers are often aware of potentially
harmful occupational exposures. Encouraging individuals to share this knowledge with their
peers and neighbors can help initiate community action on these issues.
Community-based research that partners with EPA and academic researchers can inform
studies on vulnerable subpopulations. These partnerships help shape research questions and
allow data to be used to inform public policy. For example, Ms. Shepard discussed a
partnership between the University of Pennsylvania and a small town in Pennsylvania that led
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to improved water quality. Researchers heard from residents that the town had poor quality
tap water. Upon further analysis, the researchers found that the town's water was
contaminated and used that data to work with residents to ensure that they had access to clean
water. Several community advocates who partner with Dr. Scammel on research efforts
noted the importance of explaining to the community how results will be used to increase
community participation and ensure that the concerns of the community are met.
Encouraging community knowledge to guide scientific studies will improve understanding of
environmental justice issues and lead to results that can be incorporated into regulatory
decision making.
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Agenda
Day 1 - Monday May 14, 2012
Session Title	Speakers	Time
Welcome	Workshop Chairs:	1:00 p.m. -1:15 p.m.
Onyemaechi Nweke, DrPH, U.S. EPA
Devon Payne-Sturges, DrPH, U.S. EPA
Theme I: Science of the Impacts of Chronic Psychosocial Stress on Health
The Life Cycle Model of Stress:	Robert-Paul Juster, Center for Studies on 1:15 p.m. - 2:15 p.m.
Detecting how Chronic Stress and/or Human Stress, McGill University
Trauma Harms Brains and Bodies
Theme II: Interactions between Chronic Psychosocial Stress, Social Context,
Health and Environmental Hazards - Evidence from Epidemiology and Toxicology
Interactions Between Social Context
and Immune and Neuroendocrine
Systems in Laboratory Animals
Staci Bilbo, Ph.D., Assistant Professor,
Duke Institute for Brain Sciences, Duke
University
2:15 p.m. - 3:15 p.m.
BREAK

3:15 p.m. - 3:30 p.m.
Perinatal Stress and Physical
Environmental Influences on Urban
Childhood Asthma: Independent and
Interactive Effects
Rosalind Wright, M.D., Associate Professor
of Medicine, Channing Laboratory,
Harvard Medical School and Associate
Professor of Environmental Health,
Harvard School of Public Health
3:30 p.m. - 4:30 p.m.
END OF DAY 1
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DAY 2: Tuesday May 15, 2012
Welcome Remarks/Re-cap	Workshop Chairs:	8:15 a.m. - 8:30 a.m.
Onyemaechi Nweke, DrPH, U.S. EPA
Devon Payne-Sturges, DrPH, U.S. EPA
Theme II: Interactions between Chronic Psychosocial Stress, Social Context,
Health and Environmental Hazards - Evidence from Epidemiology and Toxicology
(continued)
Evidence Review from Epidemiological	Joel Schwartz, Ph.D., Professor of	8:30 a.m. - 9:30 a.m.
Data - Interactions between Air	Environmental Epidemiology, Harvard
Pollution and Social Context and	School of Public Health
Implications for Risk Assessment
Combined Effects of Lead and Stress
on Impulsivity Measured and How
These Effects are Mediated by Brain
and HPA Axis
9:30 a.m. -10:30 a.m.
Deborah Cory-Slechta, Ph.D., Professor of
Environmental Medicine and Pediatrics,
University of Rochester Medical School
BREAK
10:30 a.m. -10:45 a.m.
Theme III: Measuring Chronic Psychosocial Stress and Social Context in Research
The Allostatic Load Model: Indicators, Robert-Paul Juster, Center for Studies on 10:45 a.m. -11:45 a.m.
Indices and Methods to Measure the Human Stress, McGill University
Antecedents and Consequences of
Chronic Stress Throughout the Life
Cycle
LUNCH
11:45 a.m. -1:15 p.m.
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DAY 2: Tuesday May 15, 2012 (continued)
Theme III: Measuring Chronic Psychosocial Stress and Social Context in Research
(continued)
Measuring Neighborhood Context for
Lynne Messer, Ph.D., M.P.H., Assistant
1:15 p.m. -2:15 p.m.
Research Addressing Maternal and
Research Professor, Center for Health

Child Health Disparities
Policy, Duke Global Health Institute

Disentangling Spatial Patterns in Social
Jane Clougherty, Sc.D., Assistant
2:15 p.m. - 3:15 p.m.
and Environmental Exposures for
Professor and Director of Exposure

Epidemiology
Science, Graduate School of Public
Health, University of Pittsburgh

BREAK

3:15 p.m.- 3:30 p.m.
Panel Discussion:
Facilitator:
3:30 p.m. - 4:30 p.m.
Communication/Translation of
Research on Chronic Psychosocial
Stress and Environmental Hazards to
the Public, Policy makers, Public Health
Deborah Cory-Slechta, Ph.D., Professor of
Environmental Medicine and Pediatrics,
University of Rochester Medical School

Practitioners and Clinicians
Panelists:
Peggy Shepard, WE ACT for
Environmental Justice
Madeleine Scammel, D.Sc., Boston
University School of Public Health
Neal Fann, U.S. EPA

Adjourn	4:30 p.m.
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Abstracts
Theme I: Science of the Impacts of Chronic Psychosocial Stress on Health
Title: The Life Cycle Model of Stress: Detecting How Chronic Stress and/or Trauma Harms Brains
and Bodies (Robert Juster, Center for Studies on Human Stress, McGill University)
Chronic exposure to stress hormones, whether it occurs during the prenatal period, infancy, childhood,
adolescence, adulthood or aging, has an impact on brain structures involved in cognition and mental
health. Likewise, lifelong brain changes in turn shape our ability to adapt or mal-adapt to environmental
stressors in measurable ways. Of critical importance is the timing and duration at which major stressors
and/or traumas are experienced, as this will profoundly affect individuals" neurological development and
their vulnerabilities or resistance. The consequences of chronic stress and/or trauma at different life stages
depend on which brain regions are developing or declining at the time of the exposure. With regard to
brain regions involved in the regulation of stress hormones, the (1) prefrontal cortex, (2) amygdala, and
(3) hippocampus are each critically important and differentially sensitive to psychosocial stress.
According to the life cycle model of stress, smaller regional volumes in these three substrates will lead to
distinct biological signatures that can be used to predict differential risk-profiles for specific
psychopathologies in adulthood, as well as inform when certain traumas might have occurred in early life.
While direct measurements of central nervous system substrates are costly and invasive, indirect
assessments using peripheral biomarkers routinely collected in blood draws and other vehicles (saliva,
hair) can be used to determine physiological dysregulations among, for instance, stress hormone levels as
well as in allostatic load biomarkers discussed under Theme III of this workshop.
Background reading:
Lupien, SJ. McEwen, BS. Gunnar, MR. Heim, C. 2009. Effects of Stress Throughout the Lifespan on the
Brain, Behaviour and Cognition. Nature Rev. Neurosci. 10: 434-445. Doi: 10.1038/nrn2639
Available at: htto://www.nature.com/nrn/iournal/v 10/n6/abs/nrn2639.html
Theme II: Interactions between Chronic Psychosocial Stress, Social Context, Health and
Environmental Hazards - Evidence from Epidemiology and Toxicology
Title: Evidence from Toxicology - Interactions between Social Context and Immune and
Neuroendocrine Systems in Laboratory Animals (Staci Bilbo, Ph.D., Assistant Professor, Duke
Institute for Brain Sciences, Duke University)
Maternal and child health are influenced by multiple host, social, and environmental factors, but very
little is known about the interactions of these forces at the neural level. Poverty is associated with
combined environmental and psychological stressors, including toxin exposure, poor air quality, and sub-
standard housing, which we believe can interact and possibly synergize to worsen physiological
outcomes. Specifically, the presence of psychosocial stressors may increase vulnerabilities to chemical
stressors such as air pollution during pregnancy, and result in adverse outcomes (such as asthma) in the
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offspring that would not otherwise occur. Our work is designed to test the hypothesis that combined
stressors early in life synergize to produce long-term changes in cognitive, affective, and physiological
(e.g., asthma) outcomes. We are using a murine model that includes a significant social stressor (restricted
bedding material) and an environmental exposure of known importance to health outcomes (air pollution).
Recent data suggest that asthma and mental health problems, such as cognitive disability and depression,
are strongly linked, independent of precipitating factors such as poverty. Thus we are interested in making
the connection between neural and respiratory developmental outcomes associated with exposure to social
and environmental stress. While we are using an animal model approach, we are working concurrently to
understand the outcomes from this research within the context of human exposures and outcomes.
Background reading:
Bilbo, SD. Schwarz, JM. 2009. Early-life Programming of Later-life Brain and Behavior: A critical role
for the immune system. Front. Behav. Neurosci. 3(14): 1-14. Doi: 10.3389/neuro.08.014.2009
Available at: htto://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737431/
Title: Perinatal Stress and Physical Environmental Influences on Urban Childhood Asthma:
Independent and Interactive Effects (Rosalind Wright, Associate Professor of Medicine, Channing
laboratory, Harvard Medical School and Associate Professor of Environmental Health, Harvard
School of Public Health)
Children in lower socioeconomic status (SES) urban communities and ethnic minorities are at increased
risk for wheezing respiratory illnesses and asthma compared to their higher SES counterparts. Such
disparities may be explained by differential environmental exposures, including both psychosocial
stressors and physical toxins, which cluster in more socially disadvantaged communities. Thus,
transdisciplinary studies that consider both individual- and community-level psychosocial determinants
and physical toxins together may help us better understand heterogeneities in urban asthma expression.
Candidate factors identified in our ongoing urban cohort studies include community violence exposure,
ambient pollution, and indoor aeroallergens. Both community- and individual-level stress have been
linked to asthma expression, and urban low-SES families exposed to higher community violence are also
more likely to experience chronic stress over other life domains (e.g., financial strain, discrimination,
housing problems). Lower-SES populations, experiencing greater cumulative stress, may also be more
likely to be exposed to other environmental toxins linked to asthma expression, such as household
allergens related to poorer housing stock or traffic-related air pollution. Epidemiological data will be
reviewed, demonstrating the independent effects of stress on childhood asthma when controlling for these
co-varying physical determinants. These data also exemplify how co-occurring psychosocial and physical
exposures may combine to influence or modify respiratory health risk in these urban children.
Background reading:
Peters, JL. Cohen, S. Staudenmayer, J. Hosen, J. Platts-Mills, TA. Wright, RJ. 2012. Prenatal Negative
Life Events Increases Cord Blood IgE: Interactions with dust mite allergen and maternal atopy. Allergy.
67(4): 545-551. Doi: 10.1111/j. 1398-9995.2012.02791 x
Available at: htto://onlinelibrarv.wilev.com/doi/10.1111 /i. 1398-
9995.2012.02791.x/abstract;isessionid=B4CAAD364E7ADB0F7F04523EBE174BEA.d02t01
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Wright, RJ. 2009. Moving Towards Making Social Toxins Mainstream in Children's Environmental
Health. Curr. Opin. Pediatr. 21(2): 222-229. Doi: 10.1097/MOP.0b013e3283292629
Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2752500
Title: The Interaction of Social Factors and Environmental Exposures in Risk: Issues and Results
from Epidemiologic Studies (Joel Schwartz, Ph.D., Professor of Environmental Epidemiology,
Harvard School of Public Health)
While the principle that social factors may modify response to environmental agents has long been
understood, few quantitative risk assessments for major environmental rulemakings have taken this
interaction into account. Conceptual issues, methodologic issues, and data limitations have contributed to
this lack, but all of these are changing. Recent epidemiologic studies have provided the basis for
differential responses to heat, air pollution, and lead. In addition, methodologic and data improvements
are allowing examination of cumulative risk, critical windows for exposure, and transgenerational effects.
As a result, it is becoming possible to examine not just the overall burden of environmental exposures, but
the distribution of risk. This is illustrated with some examples from air pollution and climate change, as
well as a simulation study.
Background reading:
Schwartz, J. Bellinger, D. Glass, T. 2011. Exploring Potential Sources of Differential Vulnerability and
Susceptibility in Risk From Environmental Hazards to Expand the Scope of Risk Assessment. Am J
Public Health. 101 Suppl 1: S94-101. Doi: 10.2105/AJPH.2011.300272
Available at: http://aiph.aphapublications.org/doi/abs/10.2105/AJPH.2011.3002727url ver=Z39.88-
2003&rfr id=ori:rid:crossref.org&rfr dat=cr pub%3dpubmed
Title: Gender-Dependent Effects of Maternal lead (Pb) Exposure, Prenatal Stress and the
Combination on Impulsivity Assessed Using a Delay of Reward Paradigm (Deborah Cory-Slechta,
Ph.D., Professor of Environmental Medicine and Pediatrics, University of Rochester Medical School)
Elevated Pb exposure and prenatal stress are co-occurring risk factors and have common adverse effects
that include attention deficits. This may reflect the fact that both target the mesocorticolimbic system of
the brain, critical to executive function, and the hypothalamic-pituitary adrenal (HPA) axis, the
physiological system that mediates the body's stress response. Correspondingly, it might be predicted
that when combined, Pb and prenatal stress would have enhanced effects relative to either alone. We
examined the effects of Pb, prenatal stress and the combination of these factors on impulsivity, a
component of attention deficit, in a rat model using a delay of reward (i.e., self-control) paradigm that
provides a choice in each trial of the behavioral test session between a short delay followed by a small
reward or a long delay followed by a large reward. The long delay value was increased over behavioral
test sessions. Effects of Pb, prenatal stress and the combination were more pronounced in males, who
exhibited a slower behavioral shift from the long delay to the short delay choice as long delay values
increased, and, particularly Pb and prenatal stress-treated males, omitted more trials and responded
prematurely more frequently. Females, particularly Pb and prenatal stress-treated, showed an almost
exclusive long delay lever preference in initial training, but no differences in preference from controls as
the long delay value increased. Pb and prenatal stress treated females, however, showed significant
increases in inter-trial interval responses that were without functional value, as long delay value
increased. These findings suggest difficulties, particularly in response to combined Pb and prenatal stress,
in behavioral transition as reward value changes.
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Background reading:
Cory-Slechta, DA. Virgolini, MB. Rossi-George, A. Thiruchelvam, M. Lisek, R. Weston, D. 2008.
Lifetime Consequences of Combined Material Lead and Stress. Basic Clin. Pharmacol. Toxicol. 102(2):
218-227. Doi: 10.1111/j.l742-7843.2007.00189.x
Available at: http://www.ncbi.nlm.nih.gov/pubmed/18226077
Cory-Slechta, DA. Stern, S. Weston, D. Allen, JL. Liu, S. 2010. Enhanced Learning Deficits in Female
Rats Following Lifetime Pb Exposure Combined with Prenatal Stress. Toxicol. Sci. 117(2): 427-438.
Doi: 10.1093/toxsci/kfq221
Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2940413/
Theme III: Measuring Chronic Psychosocial Stress and Social Context in Research
Title: The Allostatic Load Model: Indicators, Indices and Methods to Measure the Antecedents and
Consequences of Chronic Stress Throughout the Life Cycle (Robert-Paul Juster, Center for Studies on
Human Stress, McGill University)
The allostatic load model represents an interdisciplinary approach to comprehensively conceptualize and
quantify chronic stress in relation to pathologies throughout the life cycle. Allostatic load represents the
biological damage individuals experience when chronically stressed that is easily quantified using an
index representing neuroendocrine, immune/inflammatory, cardiovascular, and metabolic system
functioning. Our recent review of nearly 60 empirical studies suggests that allostatic load indices
incorporating sub-clinical ranges for numerous biomarkers predict clinical outcomes better than
traditional biomedical methods that address only clinical thresholds for single biomarkers. Importantly,
allostatic load algorithmic inclusion of neuroendocrine and/or immune/inflammatory biomarkers is
stronger than metabolic syndrome parameters or systemic clusters. In reviewing the literature, it was
consistently found that increased allostatic load corresponds either cross-sectionally or longitudinally to a
plethora of antecedents (e.g., socioeconomic disadvantage, poor social networks, workplace stress,
maladaptive personality traits, genetic polymorphisms, etc.) with dire consequences (e.g., mortality,
cardiovascular disease, psychiatric symptoms, cognitive decline, physical/mobility limitations,
neurological atrophy, etc.). In addition to the cumulative physiological toll consistently found with
increasing age in populations worldwide, the risk and protective factors of allostatic load differ according
to sex at a given developmental period as well as a function of gender-specific factors that include social
support, work/home balance, hostility, caregiving, and spirituality. Targeting these factors during key
periods of development is therefore essential to improving public health. The allostatic load model offers
a useful framework to foster refined prevention, detection, and treatment strategies vis-a-vis physical
health and psychological well-being throughout the life cycle.
Background reading:
Juster, RP. McEwen, BS. Lupien, SJ. 2010. Allostatic Load Biomarkers of Chronic Stress and Impact on
Health and Cognition. Neurosci. Biobehav. Rev. 35(1): 2-16. Doi: 10.1016/j.neubiorev.2009.10.002
Available at: http://www.sciencedirect.com/science/article/pii/S01497634090Q1481
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May 14-15,2012
Title: Measuring the Neighborhood Context for Research Addressing Maternal and Child Health
Disparities (Lynne Messer, Ph.D., M.P.H., Assistant Research Professor, Center for Health Policy,
Duke Global Health Institute)
Background: The built environment, a key component of environmental health, may be an important
contributor to health disparities, particularly for reproductive health outcomes.
Here I will report on research that investigates the relationship between seven indices of the quality of the
residential built environment and adverse reproductive outcomes for Durham, NC.
Methods: We surveyed approximately 17,000 residential tax parcels in central Durham assessing over 50
individual variables on each. These directly-observed data were combined with tax assessor, public
safety, and US Census data to construct seven indices (housing damage, property disorder, security
measures, tenure, vacancy, crime count and nuisance count) representing important domains of the
residential built environment. Fixed slope random intercept multilevel models estimated the association
between the residential built environment and five adverse birth outcomes. Models were adjusted for
maternal characteristics and clustered at the primary adjacency community unit.
Results: Five built environment indices (housing damage, property disorder, tenure status, vacancy status,
and nuisances) were associated with each of our five outcomes (pulmonary tuberculosis, small- for-
gestational-age [SGA], low birthweight, continuous birthweight and birthweight-percent for gestational
age) in the unadjusted context, but some estimates were attenuated following adjustment. In models
adjusted for individual-level covariates, housing damage remained statistically significantly associated
with SGA, birthweight and birthweight-percent for gestational age.
Conclusion: This work suggests a real and meaningful relationship between the quality of the residential
built environment and birth outcomes, which we argue are a good measure of general community health.
It also suggests that measuring the built environmental context is feasible and yields important and unique
information for use in health disparities work.
Background reading:
Miranda, ML. Messer, LC. Kroeger, GL. 2012. Associations between the Quality of the Residential Built
Environment and Pregnancy Outcomes among Women in North Carolina. Environ. Health Perspect.
120(3): 471-477. Doi: 10.1289/ehp. 1103578
Available at: htto://www.ncbi.nlm.nih.gov/pmc/articles/PMC3295337
Messer, LC. Vinikoor-Imler, LC. Laraia, BA. 2012. Conceptualizing Neighborhood Space: Consistency
and variation of associations for neighborhood factors and pregnancy health across multiple neighborhood
units. Health Place. In press. Doi: 10.1016/j.healthplace.2012.03.012
Available at: http://www.sciencedirect.eom/science/article/pii/S 1353829212000603?v=s5
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EPA Workshop on Interactions between Social Stressors
and Environmental Hazards
May 14-15,2012
Title: Disentangling Spatial Patterns in Social and Environmental Exposures for Epidemiology (Jane
Clougherty, Sc.D., Assistant Professor and Director of Exposure Science, Graduate School of Public
Health, University of Pittsburgh)
Growing epidemiological and toxicological evidence suggests that chronic stress may modify individual
susceptibility to environmental pollutants - possibly mediated through allostatic load pathways including
immune, endocrine, and metabolic alterations. A persistent problem in the epidemiology of combined
effects, however, is persistent spatial confounding between social and physical environmental exposures.
A further complication is that publicly-available data on chronic community stressors is aggregated to
different administrative data (e.g., crime rates by police precinct, poverty rates by census tract).
This presentation will explore GIS-based methods for validating the selection of community stressors and
neighborhood scales, methods for re-appropriating stressor measures across administrative units, and for
quantifying spatial autocorrelation among multiple social and pollution exposures (which indicates the
potential for spatial confounding and effect modification). We will employ case examples and preliminary
data from our New York City-focused EPA STAR grant.
Background reading:
Clougherty, JE. Kubzansky, LD. 2009. A Framework for Examining Social Stress and Susceptibility to
Air Pollution in Respiratory Health. Environ Health Perspect 117(9): 1351-1358.
Doi: 10.1289/ehp.0900612
Available at: http://ehp03.niehs.nih.gOv/article/info:doi/10.1289/ehp.0900612
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EPA Workshop on Interactions between Social Stressors
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Speaker Biosketches
Staci Bilbo, Ph.D.
Assistant Professor, Duke Institute for Brain Sciences, Duke University
Dr. Staci Bilbo received a bachelor's degree from the University of Texas at Austin in 1998, her Ph.D. in
Psychology and Brain Sciences from Johns Hopkins University in 2003, and continued her training with a
postdoctoral fellowship in the Center for Neuroscience at the University of Colorado at Boulder. She is
now an Assistant Professor of Psychology and Neuroscience at Duke University. Current research in her
laboratory focuses on understanding the consequences of early life events, including infection, stress,
environmental toxins, and maternal obesity on neural and immune system development, using rodent
models.
Jane Clougherty, Sc.D.
Assistant Professor and Director of Exposure Science, Graduate School of Public Health,
University of Pittsburgh
Jane Clougherty is an Assistant Professor and Director of Exposure Science at the University of
Pittsburgh Graduate School of Public Health, Department of Environmental and Occupational Health. Her
work focuses on differential susceptibility to air pollution by chronic stress, and she has developed several
of the early epidemiological and toxicological models for exploring these synergistic effects. Dr.
Clougherty completed her doctorate in Environmental Health at the Harvard School of Public Health in
2006. From 2008-2010, she managed the New York City Community Air Survey (NYCCAS), one of the
largest GIS-based studies to date on intra-urban variability in multiple pollutants. She is currently
leading an effort under an EPA STAR grant to extend the NYCCAS work to explore spatial patterning in
chronic stress across NYC, and synergistic effects on childhood asthma hospitalizations.
Deborah Cory-Slechta, Ph.D.
Professor of Environmental Medicine and Pediatrics, University of Rochester Medical School
Deborah Cory-Slechta is a Professor of Environmental Medicine and Pediatrics at the University of
Rochester Medical School. She previously served as Chair of its Department of Environmental Medicine
and Director of the NIEHS Environmental Health Sciences Center, and as Dean for Research. She also
was the Director of the Environmental and Occupational Health Sciences Institute (EOHSI) and Chair of
the Department of Environmental and Community Medicine at the UMDNJ-Robert Wood Johnson
Medical School. Dr. Cory-Slechta has served on multiple national review and advisory panels, including
the National Institutes of Health, the National Institute of Environmental Health Sciences, the Food and
Drug Administration, the National Center for Toxicological Research, the Environmental Protection
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Agency, the National Academy of Sciences, the Institute of Medicine, and the Agency for Toxic
Substances and Disease Registry. She currently serves on the Advisory Committee for Childhood Lead
Poisoning Prevention of the CDC. Her research has focused largely on the relationships between brain
neurotransmitter systems and behavior, and how such relationships are altered by exposures to
environmental toxicants, particularly the role played by environmental neurotoxicant exposures in
developmental disabilities and neurodegenerative diseases.
Neal Fann
Office of Air and Radiation, U.S. Environmental Protection Agency
Neal Fann serves in the Office of Air and Radiation of the U.S. Environmental Protection Agency, where
he has developed extensive experience in quantifying and characterizing the human health impacts, and
monetized benefits, of changes in criteria and toxic air pollution. In this role, he has performed technically
complicated and policy-relevant benefits assessments in support of major EPA regulatory actions
including the Cross-State Air Pollution Rule and the Mercury and Air Toxics Rule, among many others.
Mr. Fann manages the PC-based environmental Benefits Mapping and Analysis Program (BenMAP)
software, a model relied upon by EPA, stakeholder groups, researchers and international analysts to
quantify the impacts and monetized benefits of air quality improvements. To ensure that this model
remains the state-of-the-science and is properly specified with the best available data, he continually and
critically evaluates the newest air pollution epidemiology and economics literature.
Mr. Fann also regularly contributes to the academic literature, publishing air pollution, risk assessment,
and environmental justice assessments in journals including Risk Analysis and Environmental Science &
Technology. Most recently he wrote a commentary in Environmental Health Perspectives, articulating
the benefits of tighter integration between air pollution epidemiology and risk assessment. His other
recent publications include: a national assessment of the public health burden of recent levels of PM2.5
and ozone in the U.S. and a proof of concept approach for maximizing the public health benefits of air
quality improvements while achieving a more equitable distribution of risk. Prior to joining EPA, Mr.
Fann received a Master of Public Policy at the Sanford School of Public Policy at Duke. He holds a
bachelor degree in Economics and Political Science from Trinity University.
Robert-Paul Juster
Center for Studies on Human Stress, McGill University
Robert-Paul Juster is currently a researcher and doctoral candidate in the Integrated Program in
Neuroscience at McGill University and is affiliated with the Centre for Studies on Human Stress. His
work applies the allostatic load model of chronic stress to detect health risks in vulnerable populations.
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Lynne C. Messer, Ph.D.
M.P.H., Assistant Research Professor, Center for Health Policy, Duke Global Health Institute
Lynne C. Messer is a socio-environmental and reproductive / perinatal epidemiologist whose work
focuses on the social and structural determinants of maternal and child health disparities. Her
methodological work includes better-defining neighborhood environments, developing environmental
exposure measures for infant mortality outcomes and addressing the limits of causal inference in
observational studies. She is also interested in the psychosocial mechanisms through which socio-
environmental exposures result in health disparities for women and children.
Madeleine Kangsen Scammell, D.Sc.
Boston University School of Public Health, Boston, MA
Madeleine Kangsen Scammell is an Assistant Professor of Environmental Health and a Core Director of
the Partners in Health and Housing Prevention Research Center (CDC) and the BU Superfund Research
Program (NIEHS). Her research is mostly community-driven and community-based and includes mixed-
methods analysis that incorporate qualitative and quantitative data obtained using social science and
epidemiological research methods. She applies these methods in mapping and monitoring community-
identified environmental health hazards and analyzing cumulative exposures to chemical and non-
chemical stressors. She is the PI of an EPA STAR grant to develop new analytic techniques for
examining the cumulative risks of exposure to social and chemical stressors.
Joel Schwartz, Ph.D.
Professor of Environmental Epidemiology, Harvard School of Public Health
Dr. Joel Schwartz is a Professor of Environmental Epidemiology at the Departments of Environmental
Health and Epidemiology, Harvard School of Public Health. He has extensive experience in air pollution.
He examined both acute and chronic effects of air pollution exposure. His recent research has established
that exposure to fine combustion particles in the air at concentrations well below current standards are
associated with a range of adverse health effects from increased respiratory symptoms, to increased
hospital admissions, to increased deaths. This work has led to a tightening of the U.S. air quality
standards. In addition, he has also done considerable work on health effects of ozone exposure. He has
several international collaborations underway in this area. Recent work has been focused on the
cardiovascular effects of air pollution, and on factors that modify the response to air pollution. Recent
work has suggested diabetics are more susceptible to such effects.
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EPA Workshop on Interactions between Social Stressors
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May 14-15,2012
Peggy M. Shepard
Executive Director, Co-Founder, WE ACT For Environmental Justice
Peggy Shepard is co-founder and executive director of WE ACT For Environmental Justice (WE ACT),
based in West Harlem, which has a 22-year history of engaging Northern Manhattan residents in
community-based planning and campaigns to affect environmental protection and environmental health
policy locally and nationally. WE ACT has successfully combined grassroots organizing, environmental
advocacy and environmental health research to become a national leader in advancing the perspective of
environmental justice in urban communities. A former journalist, Ms. Shepard has served as chair of the
EPA's National Environmental Justice Advisory Council (NEJAC). She received the Jane Jacobs Medal
from the Rockefeller Foundation in 2008 for Lifetime Achievement, the 10th Annual Heinz Award For
the Environment, and an Honorary Doctorate from Smith College in 2010.
Ms. Shepard served as chair of the National Environmental Justice Advisory Council (NEJAC) to the
U.S. Environmental Protection Agency, and currently serves as co-chair of its Research and Science
workgroup. She is a member of the Regional Health Equity Council, Region 2, Office of Minority Health,
HHS; the Environmental Justice Advisory Committee to the NYS Department of Environmental
Conservation and the NYC Mayor's Sustainability Advisory Board. Ms. Shepard is a former member of
the National Advisory Environmental Health Sciences Council of the National Institutes of Health and the
National Children's Study Federal Advisory Committee, NIH. She has served as guest editor of an
Environmental Health Perspectives monograph, Advancing Environmental Justice Through Community-
Based Participatory Research, April 2002, and is co-author of Promoting Environmental Health Policy
Through Community Based Participatory Research: A Case Study from Harlem, New York, Jan. 2006,
Journal of Urban Health. A lecturer on issues of environmental justice and community-based health
research, she graduated Howard University and Solebury and Newtown Friends Schools.
Rosalind Wright, M.D.
Associate Professor of Medicine, Channing Laboratory, Harvard Medical School and Associate
Professor of Environmental Health, Harvard School of Public Health
Dr. Rosalind Wright is internationally recognized for work examining independent effects of stress as
well as interactions between stress and other environmental toxins (e.g., air pollution, aeroallergens, diet)
on asthma in urban, minority populations. Specifically, her research program focuses on the epidemiology
of chronic respiratory disease in both adults (adult-onset asthma, COPD) and children (childhood
asthma). Utilizing multiple longitudinal cohort designs, Dr. Wright is investigating the role of varied
psychosocial stressors (e.g., adverse life events, violence, social deprivation) on asthma morbidity.
Whereas earlier psychosomatic models have supported a role for psychological stress in contributing to
variable asthma morbidity among those with existing disease, a growing appreciation of the interactions
between behavioral, neural, endocrine, and immune processes suggest a role for these psychosocial
factors in the genesis of asthma as well.
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EPA Workshop on Interactions between Social Stressors
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May 14-15,2012
List of Participants
Janet Angbazo
MBBS MPH
Rockville, MD
Peter Ashley
Environmental Health Scientist
Office of Healthy Homes and Lead Hazard
Control
U.S. Dept. of Housing and Urban Development
Washington, DC
Rupa Basu
Oakland, CA
Thomas Bateson
Epidemiologist
National Center for Environmental Assessment
U.S. EPA
Washington, DC
Adam Baumgart-Getz
Environmental Scientist
Community & Tribal Programs Group
U.S. EPA "
Durham, NC
Staci Bilbo
Assistant Professor, Psychology & Neuroscience
Duke University
Durham, NC
Uni Blake
Director Environmental Affairs
Hometown Energy Group
Schenevus, NY
George Bollweg
U.S. EPA Region 5
Chicago, IL
Michael Broder
Science Coordinator
Office of the Science Advisor
U.S. EPA
Washington, DC
Ashley Bubna
Student Contractor
Office of Research and Development
U.S. EPA
Arlington, VA
Rich Callan
U.S. EPA
Washington, DC
Jessie Can-
Research Analyst
Environmental & Occupational Health
University of Pittsburgh
Pittsburgh, PA
Ann Carroll
OSWER, Office of Brownfields and Land
Revitalization
U.S. EPA
Washington, DC
Dolon Chakravartty
Analyst, Data Coordination and Access Program
Toronto, ON, Canada
Jane Clougherty
Assistant Professor and
Director of Exposure Science
Environmental & Occupational Health
University of Pittsburgh
Pittsburgh, PA
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EPA Workshop on Interactions between Social Stressors
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May 14-15,2012
Cappy Collins
Preventive Medicine
Mount Sinai School of Medicine
New York, NY
Margaret Conomos
Health Statistician, Environmental Information
U.S. EPA
Washington, DC
Gelena Constantine
EJ Coordinator
Office of Research & Development
Office of Science Policy
U.S. EPA
Washington, DC
Deborah Cory-Slechta
Professor, Environmental Medicine
University of Rochester School of Medicine
Rochester, NY
Maria Costantini
Principal Scientist
Health Effects Institute
Boston, MA
Alva Daniels
ORD /NCER/ U.S. EPA
Washington, DC
Heather Dantzker
Project Manager
Environmental Risk & Toxicology
ICF International
Fairfax, VA
Sally Darney
Sustainable & Health Communities Program
Office of Research & Development
U.S. EPA
Research Triangle Park, NC
Matthew Davis
Office of Children's Health Protection
U.S. EPA
Washington, DC
INDUSTRIAL ECONOMICS, INCORPORATED
Michael Dellarco
Bethesda, MD
Michelle DePass
Assistant Administrator
Office of International & Tribal Affairs
U.S. EPA
Washington, DC
David Diaz-Sanchez
Chief, Clinical Research Branch
U.S. EPA
Chapel Hill, NC
Melissa Dreyfus
Environmental Health Scientist
Office of Superfund Remediation and
Technology Innovation
U.S. EPA
Washington, DC
Mari Eggers
Research Associate, Center for Biofilm
Engineering
Little Big Horn College
Bozeman, MT
William Eggers III
Professor, Extended Studies
Montana State University
Bozeman, MT
Kristie Ellickson
Saint Paul, MN
Paul English
Branch Science Advisor
California Department of Public Health
Richmond, CA
Amanda Evans
U.S. EPA/ASPH
Cincinnati, OH
Neal Fann
U.S. EPA
Research Triangle Park, NC
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EPA Workshop on Interactions between Social Stressors
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May 14-15,2012
Zaida Figueroa
U.S. EPA
Manassas, VA
Michael Firestone
Senior Science Advisor
Office of Children's Health Protection
U.S. EPA
Washington, DC
Julie Fitzpatrick
Office of Science Advisor
Risk Assessment Forum Staff
U.S. EPA
Washington, DC
Robert French
NorthStar Learning Centers
New Bedford, MA
Amelia Geggel
Associate
Industrial Economics, Inc.
Cambridge, MA
Lauren Gordon
Project Coordinator
Child Health Advocacy Institute
Children's National Medical Center
Washington, DC
Richard Gragg
Associate Professor, Environmental Science and
Policy, School of the Environment
Florida A&M University
Tallahassee, FL
Molly Greenberg
Environmental Programs Assistant
Environmental Justice
Ironbound Community Corporation
Newark, NJ
Peter Grevatt
U.S. EPA
Washington, DC
Jacquelyn Hayes
Children's Environmental Health Program
U.S. EPA Region 9
San Francisco, CA
Diane Henshel
Biologist
Office of Science Advisor
Risk Assessment Forum
U.S. EPA
Washington, DC
Richard Hertzberg
Adjunct Professor
Environmental Health
Emory University
Atlanta, GA
Margaret Hicken
Research Fellow, Epidemiology
University of Michigan
Ann Arbor, MI
Maeve Howett
Assistant Clinical Professor, Nursing
Emory University
Atlanta, GA
Olivier Humblet
Postdoctoral Fellow
Center for Health and Community
University of California- San Francisco
San Francisco, CA
Tamara Lewis Johnson
NIH-NIAID
Bethesda, MD
Rhona Julien
Environmental Health Scientist
Indoor air
U.S. EPA
Boston, MA
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EPA Workshop on Interactions between Social Stressors
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May 14-15,2012
Robert-Paul Juster
Center for Studies on Human Stress
McGill University
Montreal, QC Canada
Kristopher Kraus
Climate Research Coordinator
Earth Gauge
National Environmental Education Foundation
Washington, DC
Sandra Kuntz
Associate Professor
College of Nursing
Montana State University
Missoula, MT
Jennifer Kwan
Mathematical Statistician
NICHD/NCS
National Institutes of Health
Rockville, MD
Robert Laumbach
Assistant Professor
Environmental and Occupational Medicine
UMDNJ-Robert Wood Johnson Medical School
Piscataway, NJ
Charles Lee
Deputy Associate Assistant Administrator for
Environmental Justice
OECA
U.S. EPA
Washington, DC
Jonathan Levy
Professor, Environmental Health
Boston University School of Public Health
Boston, MA
Stephen Linder
Professor
School of Public Health
The University of Texas Health Science Center
at Houston
Houston, TX
INDUSTRIAL ECONOMICS, INCORPORATED
Danelle Lobdell
U.S. EPA
Research Triangle Park, NC
Nica Louie
Environmental Health Scientist
U.S. EPA
Arlington, VA
Brigid Lowery
Director, Center for Program Analysis
OSWER
U.S. EPA
Washington DC
Richard Lukasik
Contractor
U.S. EPA
Arlington, VA
Robert MacPhail
Neurotoxicology
U.S. EPA
Research Triangle Park, NC
Mana Mann
Pediatrics
Mount Sinai School of Medicine
New York, NY
Valerie Marshall
Management Analyst
Office of Administration and Resources
Management
U.S. EPA
Boston, MA
Karen Martin
Biologist, Office of the Administrator
U.S. EPA
Washington, DC
Lawrence Martin
Office of Science Advisor
U.S. EPA
Washington, DC
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EPA Workshop on Interactions between Social Stressors
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May 14-15,2012
Pamela Maxson
Children's Environmental Health Initiative
Duke University
Durham, NC
Sabrina McCormick
Professor
Environmental and Occupational Health
George Washington University
Washington, DC
Leyla McCurdy
National Environmental Education Foundation
Washington, DC
Cynthia McOliver
Environmental Health Scientist
ORD/National Center for Environmental
Research
U.S. EPA
Arlington, VA
Lynne Messer
Center for Health Policy and Inequalities
Research
Duke Global Health Institute
Durham, NC
Greg Miller
Office of Children's Health Protection
U.S. EPA
Washington, DC
Rachel Morello-Frosch
Associate Professor
ESPM and SPH
Berkeley, CA
Brittany Morey
PhD Student
Community Health Sciences
UCLA School of Public Health
Los Angeles, CA
Ginger Moser
U.S. EPA
Research Triangle Park, NC
Anand Mudambi
Office of the Science Advisor
U.S. EPA
Washington, DC
Patricia Murphy
National Center for Environmental Assessment
U.S. EPA
Edison, NJ
Nicholas Newman
Director, Pediatric Environmental Health and
Lead Clinic
General Pediatrics
Cincinnati Children's Hospital Medical Center
Cincinnati, OH
April Nowak
Environmental Justice Coordinator
Enforcement, Compliance and Environmental
Justice, Region 8
U.S. EPA
Denver, CO
Leanne Nurse
Program Analyst
Office of Public Engagement
U.S. EPA
Washington, DC
Barry Nussbaum
Chief Statistician
Office of Environmental Information
U.S. EPA
Washington, DC
Onyemaechi Nweke
Physical Scientist
Office of Environmental Justice
US Environmental Protection Agency
Tamra Old Coyote
Water Quality Project Coordinator
Little Big Horn College
Crow Agency, MT
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EPA Workshop on Interactions between Social Stressors
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May 14-15,2012
Christina Park
Health Science Administrator
National Children's Study
NICHD
Bethesda, MD
Devon Payne-Sturges
Assistant Center Director
Nation Center for Environmental Research
U.S. EPA
Washington, DC
Joanne Perodin
Washington, DC
James Quackenboss
Research Scientist
Exposure Measurements and Analysis Branch
Human Exposure & Atmospheric Sciences
Division, Exposure Measurements and Analysis
Branch, ORD/NERL,
U.S. EPA
Las Vegas, NV
Kathleen Raffaele
U.S. EPA
Washington, DC
Rebecca Rehr
MPH Student
Maryland Institute for Applied Environmental
Health
University of Maryland School of Public Health
College Park, MD
Deldi Reyes
Environmental Justice Coordinator
U.S. EPA Region 9
San Francisco, CA
Henry Roman
Principal
Industrial Economics, Inc.
Cambridge, MA
Arlene Rosenbaum
Technical Director
ICF International
Rohert Park, CA
Elizabeth Rudd
Social Science Analyst
Housing and Urban Development
Policy Development and Research
Washington, DC
Eric Ruder
Principal
Industrial Economics, Inc.
Cambridge, MA
Zubair Saleem
Economics and Risk Analysis Staff / OSWER
U.S. EPA
Washington, DC
Tamara Saltman
Policy Analyst, Office of Air and Radiation
U.S. EPA
Washington, DC
Yolanda Anita Sanchez
Environmental Health Scientist
OSWER, OSRTI, U.S. EPA
Washington, DC
Madeleine Kangsen Scammell
Assistant Professor
Boston University School of Public Health
Department of Environmental Health
Boston, MA
Ted Schettler
Bolinas, CA
Rita Schoeny
Senior Science Advisor
Office of Science Policy/ORD
U.S. EPA
Washington, DC
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EPA Workshop on Interactions between Social Stressors
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May 14-15,2012
Brad Schultz
Research Environmental Scientist
Office of Research & Development (NERL)
U.S. EPA
Research Triangle Park, NC
Amy Schulz
Professor
Health Behavior and Health Education
University of Michigan School of Public Health
Ann Arbor, MI
Joel Schwartz
Professor of Environmental Epidemiology
Harvard School of Public Health
Boston, MA
Deborah Segal
Arlington, VA
Emily Selia
U.S. EPA
Washington, DC
Perry Sheffield
Department of Preventive Medicine
Mount Sinai School of Medicine
New York, NY
Edmond Shenassa
Associate Professor & Director
Maternal & Child Health Section
University of Maryland
College Park, MD
Peggy Shepard
Executive Director
WE ACT for Environmental Justice
New York, NY
Pamela Shubat
Toxicologist
Health Risk Assessment
Minnesota Department of Health
St. Paul, MN
Jan Shubert
LCSW
Office of Emergency Management
U.S. EPA
Washington, DC
Jane Ellen Simmons
National Health and Environmental Effects
Research Laboratory
U.S. EPA
Research Triangle Park, NC
Kam Sripada
Presidential Management Fellow
Office of Children's Health Protection
U.S. EPA
Washington, DC
Barry Steffen
Social Science Analyst
Policy Development and Research
U.S. Department of Housing and Urban
Development
Washington, DC
Elaine Symanski
Associate Professor
Epidemiology, Human Genetics &
Environmental Sciences
University of Texas School of Public Health
Houston, TX
Zaria Tatalovich
Acting Chief
Surveillance Systems Branch/ Division of
Cancer Control and Population Sciences
National Cancer Institute
Bethesda, MD
Linda Teuschler
Mathematical Statistician
ORD/National Center for Environmental
Assessment
U.S. EPA
Cincinnati, OH
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EPA Workshop on Interactions between Social Stressors
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May 14-15,2012
Veronica Tinney
Graduate Student
The George Washington University School of
Public Health
Washington, DC
Pamela Tucker
ATSDR
Atlanta, GA
Nicolle Tulve
U.S. EPA
Research Triangle Park, NC
Michael Wenstrom
Environmental Protection Specialist
Environmental Justice
U.S. EPA Region 8
Denver, CO
Kelly Widener
ACD of Research Communications
National Center for Environmental Research
U.S. EPA
Arlington, VA
Larke Williams
Environmental Engineer
ORD/Office of Science Policy
U.S. EPA
Washington, DC
Sacoby Wilson
Assistant Professor
Maryland Institute for Applied Environmental
Health
University of Maryland-School of Public Health
College Park, MD
Holly Wilson
Community Air Toxics, Lead
Office of Air and Radiation
U.S. EPA
Research Triangle Park, NC
Michael Wright
National Center for Environmental Assessment
U.S. EPA
Cincinnati, OH
Rosalind Wright
Associate Professor of Medicine
Channing Laboratory, Harvard Medical School
Associate Professor of Environmental Health
Harvard School of Public Health
Boston, MA
Tina Yuen
ASPH Fellow
National Center for Environmental Research
U.S. EPA
Arlington, VA
Jose Zambrana
Physical Scientist
National Center for Environmental Research
U.S. EPA
Washington, DC
INDUSTRIAL ECONOMICS, INCORPORATED
September 19, 2012
D-8

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