Neurobiological scientists (such as psychologists with expertise
on the psychophysiology of chronic stress and resulting health effects),
neurobehavioral toxicologists, neuropsychologists, and psychiatric or psychological epidemiologists.
To examine what is known about the potential effects of possible chronic stress on public health. Some studies provided information on
possible chronic stress occurring in communities near hazardous waste sites. Focus areas
for the panel included the pattern of stress acute, chronic, or both that may occur
among community members living near hazardous waste sites; the effects of
psychological stress on physiological responses to exposure; and whether
neurobehavioral disorders caused by chronic low-dose exposure to
neurotoxicants, which may manifest as psychological distress, are a public health
phenomenon near hazardous waste sites.
What is known about the long-term health effects of chronically increased stress among
individuals living near hazardous waste sites?
Background
Research into the psychological effects of disasters began with the study of
natural disasters in the 1950s. Scientists and clinicians recognized that a small number of
people exposed to the stress of various natural disasters, such as fires, hurricanes,
and floods, could develop psychological sequelae such as major depression, chronic
anxiety, and post-traumatic stress disorder (PTSD). Current thought among disaster
relief workers holds that most people will suffer no or only transient effects from the
stress of a natural disaster (i.e., acute stress disorder) or, in other words, "people
reacting normally to an abnormal situation" (B. Flynn, 1995, personal communication). For excellent
summaries on the psychological sequelae to natural disasters, see Rubonis and Bickman (13), Dew and
Bromet (14), and Green and Solomon (15).
There are important differences between technologic and natural disasters that are
believed to affect the psychological and social responses to technological disasters.
In addition to direct health effects, exposure to technologic disasters acute exposure,
as in chemical spills; or chronic exposure, as in residence near a leaking hazardous
waste site can cause people to experience psychological uncertainty, worry, and chronic stress.
Some postulate that the chronic stress documented to occur in some communities near hazardous waste
sites could possibly lead to an array of biopsychosocial effects, including physical health effects from chronic
stress (possible health outcomes affected by stress include cardiovascular, gastrointestinal
disorders, and skin), increases in the prevalence of certain psychological disorders,
and social disruption.
Sociologists studying communities near leaking hazardous waste sites have
defined this kind of situation as a "chronic technological disaster" (Kroll-Smith and Couch
[16]). Unlike a natural disaster which has a discernible low point and a recovery
phase during which life begins to return to "normal" many chronic technological
disasters have no discernible starting points, no distinct low points, may last for
many years, and may leave behind people at risk for latent health effects (2). These
events are not clear-cut, easily defined disasters, and the slow onset and recovery
may make the adjustment more difficult (17).
The first scientific studies of the health
effects of stress associated with environmen al contamination occurred after the Three Mile Island (TMI)
accident. Baum and colleagues (18) found indicators of psychophysiological effects from
stress, including elevated levels of psychological distress, perceived threat, subclinical anxiety
disorders, and depression in many of the community members they surveyed at TMI
as compared with controls. The comparison revealed biological signs of chronic stress consisting of
increased blood pressure (elevations were subclinical) and higher than normal levels of urinary cortisol and
norepinephrine metabolites. They also found that the psychophysiological pattern of anxiety, poor concentration,
and biological indicators of stress in community members affected remained subclinically
elevated for 6 years and only returned to normal levels 10 years after the accident.
Baum and colleagues then looked for this same chronic stress response in a community located near a leaking
hazardous waste site and found similar results. Baum and Fleming (7) concluded that "distress and mental
health outcomes also represent major outcomes of environmental disasters."
The findings of Baum and colleagues
are supported by observations made by a group of researchers in California who studied the towns affected by the
Cantara loop railway spill (10). They studied the physical, psychological, and psychophysiological reactions of
those who had been exposed to a spill of metal sodium. Psychological assessments of the residents showed
increased worry, perceived decreases in social support, and biological changes indicative of chronic
stress. Testing also showed greater levels of depression, anxiety, and somatic
symptoms which the researchers felt were possibly connected to chronic arousal
states in the exposed versus a control population. They postulated that "physiological
and psychosocial effects of the chemical spill trauma precede long-term physiological manifestations."
Other recent findings also suggest that the experience of exposure to hazardous
substances and the resulting psychosocial changes can result in adverse physical and
psychological health effects. In 1994, epidemiologists at the University of Texas
investigated the physical and psychological effects found in a community that had
been exposed to a toxic cloud of hydrogen fluoride (11). These researchers first
performed a study that documented both short- and long-term physical health effects
in those exposed to the vapors. Then, they evaluated the psychological effects of this
exposure situation and found that a linear relationship exists between the degree
of gas exposure and increased psychological distress. Specific findings included
increased anxiety and somatic concerns among the affected persons.
Panel Discussion
The panel members generally agreed that the background literature on long-term
health effects from chronic stress associated with living near a hazardous waste site
is sparse; however, the panel also referred to knowledge on effects of chronic stress
gained from related studies on chemical or natural disasters and in the occupational
setting.
Stress is a whole-body process with effects that can be measured using self-reports
from groups or individuals as well as from other more objective measurement techniques. There are
inherent difficulties in self-reporting measures because the reports may reflect concerns or actual changes
related to the incident. Other methods used to evaluate the consequences of dealing with a stressor for a
prolonged period include direct behavioral observations by a trained observer; psychophysiological measures of
stress, such as increased blood pressure, heart rate, and changes in skin conductance; and biochemical
parameters, such as measurable changes in stress hormones (cortisol) and in the catecholamine levels,
such as norepinephrine and epinephrine. Though these indicators may provide some
clues to the altered whole-body response to stress, interpretation of the results may
be problematic (e.g., the timing of cortisol measures is crucial because the secretion
of cortisol shows a daily, biphasic variation). It is important to control for
other factors such as smoking, exercise, and diet, which may elevate measurements.
The panel discussed studies conducted using the methods mentioned above. A
study by Davidson and colleagues (19)found that, compared with a control group,
residents near TMI showed significant stress effects over the first 5 years of follow-up. The effects noted
included increased symptom reporting; difficulties with attention and concentration; and alteration in heart
rate, blood pressure, levels of urinary catecholamines (epinephrine and norepinephrine), and blood cortisol
levels. In other research on effects of chronic stress in communities exposed to toxic
substances, residents living near a hazardous waste site showed alterations in psychological and
psychophysiological stress indicators similar to those seen at TMI (20).
An important general discussion point was that the critical factors and
underlying causes for sensitivity to the effects from stress are not clearly
understood. Studies done at TMI and the toxic waste site, as well as other studies, conclude that effects
may be largely related to event characteristics and the responses of each person to
the event. These responses can range from little concern to extreme agitation.
The differing reactions most likely reflect many factors, such as the characteristics of the
event (e.g., did actual chemical exposures occur?); imagery associated with the
episode; media coverage; and the individual's coping mechanisms, perceptions of the
situation, appraisal of threat, and perceived sense of control over the circumstances.
Data Gaps and Recommendations
How well do commonly measured
indices of stress used in the past to study
natural disasters or combat-related trauma in Vietnam veterans apply to residents
living near hazardous waste sites?
What are the age-specific effects of living near a hazardous waste site?
How do children respond? How do the elderly respond? More information is needed on how
these special populations respond to this type of experience.
What is the time course of the physical and psychological responses to chronic
stress? During periods of recorded stress at TMI, physical measures showed increased stress
compared to controls; however, self-reports of stress showed no differences. Are psychophysiological
baselines being shifted to future stress?
There is a need to quantify the effects of chronic stress on the health
of these communities, especially when conditions express themselves in nonspecific outcomes
(e.g., increased frequency of headaches). It is recommended that ATSDR evaluate
existing instruments for their adequacy in assessing the prevalence of these
nonspecific health outcomes.
There remains uncertainty in the interpretation of measures of stress. ATSDR
should attempt to define criteria for when a change in these stress measures is
considered a problem. In toxicologic terms, when are changes in stress indicators
considered "adverse" or capable of causing unwanted health effects in a person and
in a community?
Although there is some background information on what the disease
outcomes are and how they are related to chronic stress, these outcomes are not fully
characterized. What do the physiological and biochemical changes in these populations mean (i.e., what is
their relationship with diagnosable illnesses?).
Are there certain neurobehavioral effects found in individuals exposed to chronic low-doses of toxins who live near hazardous waste sites that, if detected, could constitute sentinel health events at these sites? If they exist, can their early detection be
used as an intervention screening tool?
Background
Before the beginning of industrial hygiene, employees in some industries were
chronically exposed to very high levels of chemicals that led to toxic effects on their
nervous systems, specifically in the neurobehavioral diseases of sensory, motor, and
cognitive functions, as well as memory and attention. Examples of chemicals that are
known neurotoxins at occupational levels of exposures are carbon disulfide,
hexacarbons, mercury, lead, organophosphates, and organic solvents.
Historically, there have been far fewer episodes of neurotoxic effects found in
the general community as compared with the occupational population, and most of
those episodes resulted from contaminated food. During Prohibition in the United
States, there was an outbreak of "Ginger Jake" paralysis, which was associated with
drinking extracts of Jamaican ginger that were contaminated with tri-ortho cresyl
phosphate (21). In 1968, an outbreak of Yusho (the name of the disease caused by
polychlorinated biphenyls [PCBs]) occurred in Japan after adults and children
drank rice oil contaminated with high levels of PCBs. Chloracne and numbness and
weakness of the extremities occurred in the adults. Children born to mothers exposed to the oil during pregnancy
had abnormal pigmentation, decreased reflexes, and intelligence quotients of 70 (22).
The most well-known case of environmental contamination leading to
neurotoxic effects in a community occurred in Minamata, Japan. Metallic mercury used as a
catalyst by a local factory was discharged into the bay. The bacteria and microscopic aquatic
life in the bay bottom converted the metallic mercury to organic mercury compounds, especially methyl
mercury. The fish and shellfish in the bay picked up the high levels of methyl mercury. After a period of time, an
epidemic of neurologic effects (e.g., paresthesias, ataxia, and deafness) was noticed in the fisher
people who lived by the bay. These effects were traced back to the mercury in the
bay. Median doses of 11 milligrams per kilogram of methyl mercury in fish resulted
in these effects (22).
Neurobehavioral disorders, such as lead poisoning, have occurred in communities
exposed to high doses of lead.
There is still a great deal of controversy about the potential occurrence of
neurobehavioral effects with chronic, low-dose exposure to hazardous substances.
The panel discussed this specific concern.
Panel Discussion
Much is known and substantial evidence has been found about the neurobehavioral
effects in humans resulting from exposures to neurotoxic substances; however, much
of this information comes from observations from high exposures in occupational
settings. Occupational exposures to neurotoxins differ significantly from chronic
low-dose exposures experienced by most community members near a hazardous waste site.
Occupational exposures tend to be high-level, sometimes short-term
exposures that happen to a more homogeneous population (i.e., healthy adult
employees).
How does our knowledge about occupational neurobehavioral effects compare with
the possible effects of chronic low-dose exposures? Existing literature (Baum and
Bowler [5, 7, 10, 18, 20, 23]) points to measurable changes in memory and attention as
neurobehavioral effects observed in groups living near hazardous waste sites. What is the cause of these
neurobehavioral effects chronic low level toxic exposure or effects of concern over a possible exposure?
Neuropsychological methods are used to test for neurobehavioral effects.
Field batteries, such as ATSDR's Adult Environmental Neurobehavioral Test Battery
(AENTB), are sufficiently sensitive to detect psychophysiological effects associated
with chronic stress, such as decrements in memory and concentration. The data gathered
could then be interpreted epidemiologically in light of several potential
confounders, such as clear indicators of exposure to a neurotoxin, test administration bias, subject bias,
ethnic or cultural factors, education, sex, and age. The need to document exposure to neurotoxins points to the
lack of selectivity in the neurobehavioral testing methods (i.e., the inability to differentiate whether
changes in memory and attention are toxicant-induced effects versus stress-related effects).
Data Gaps and Recommendations
The components of existing field neurobehavioral testing batteries would
likely capture anxiety-related responses on a group basis. Therefore, they would be useful
as tools for screening groups of people, but would not be useful as clinical instruments or
individual screening instruments. They also would not be useful for separating physiological from psychological
effects. To gain maximum usefulness for community evaluations, there is a need for community-based norms for many
tests. These screening measures would be helpful in determining the magnitude of a
problem in a community, but not for determining specific intervention strategies.
Existing field neurobehavioral testing
batteries are not capable of detecting adverse health effects resulting from chronic, low-dose exposures, which
would constitute sentinel health effects. It is unlikely that differences between
groups can be detected by existing field neurobehavioral testing batteries, such
as AENTB. Results on specific subtests would be helpful in identifying issues for further
evaluation. However, results from existing batteries would not allow attribution of
observed group differences to physiological versus psychological mechanisms.
What is known about how to clinically differentiate between organic behavioral disorders caused by exposure to certain
neurotoxicants and purely psychologic responses to possible exposures? This discussion will consider methodological
questions such as testing for stress and neurobehavioral effects as well as other issues.
Background
The previous discussions were based on instruments designed to screen large
groups of people for neurological and behavioral problems possibly related to chronic low-dose exposure to
neurotoxins. This discussion relates to the individual, clinical workup of a person concerned about possible
health problems from a previous neurotoxic exposure, with consideration of methodological
questions such as testing for stress and neurobehavioral effects.
Panel Discussion
Dr. Rosemarie Bowler and Dr. Eugene Emory were co-leads on this topic. Dr.
Rosemarie Bowler discussed work she has done studying communities that have been exposed to acute chemical
spills. A study of approximately 1,500 people who were evacuated following a spill of Catacarb was presented (23).
Catacarb contains boron, potassium, metavanadate, and diethanolamine. Environmental data
suggested that exposures to the spill were low; however, despite the low exposures,
there were a substantial number of self-reported health effects at statistically
significant levels compared with the effects reported by the control group. These
effects included problems with memory, anxiety, depression, sleep disorders, headaches, chemical sensitivity,
dermatological problems and rashes, visual problems, respiratory and gastrointestinal problems, and eye
discharge. Dr. Bowler's clinical evaluations of the residents affected by the Catacarb showed that
60% had post-traumatic stress syndrome and 30% showed cognitive deficits involving verbal learning and memory.
In another study performed with a community that had experienced a spill of metam sodium following a railroad
accident, Dr. Bowler found a significant increase in salivary cortisol, a physiological indicator of
elevated stress, compared with the level found in controls (10). In both of these
studies, it was noted that all of the effects (self-reported versus objective) were
observed within a relatively short period following exposures. It was not possible to
differentiate whether these changes resulted from chronic psychological stress or the
effects of exposures to neurotoxins.
There are many considerations in diagnosing organicity (i.e., effects of neurotoxic
exposures on the brain versus the psychological stress from the exposure). The issues and
questions to be considered when attempting to differentiate organic effects from psychological effects are
as follows:
Is the agent a known neurotoxicant (i.e., dangerous to the human nervous
system)?
What are the exposure variables (e.g., the duration of exposure, level of exposure, and patients' prior
knowledge of the effects of neurotoxicants)?
Are the symptoms consistent with neurotoxic effects (such as
micromercularism, which results from chemical mercury poisoning, or cognitive and attentional deficits
associated with moderate lead exposure)?
Are mediating factors taken into consideration (e.g., age, prior exposures,
prior illnesses, premorbid mental health, premorbid personality, social support, other central nervous
system [CNS] trauma, and prior sensitization to other toxins)?
What are the general effects observed
on neuropsychological function (e.g., are there perceptual disturbances, changes in states of consciousness or
awareness, or memory impairment)?
What are the specific effects on neuropsychological functions such as verbal
learning and short-term memory?
Are the deficits observed consistent across neuropyschological domains?
Have developmental (i.e., age-specific) issues been considered? In children,
the maturation of the nervous system influences their susceptibility. Children
are frequently the most sensitive population to neurotoxins, and assessing the
effects of an exposure on the youngest (preverbal) children may be difficult.
Other diagnostic considerations in differentiating neurotoxicity versus
psychological effects include looking for inconsistent test performance, varied
medical history, secondary gain (e.g., dependency, avoidance of activity, and
financial gain), consistent history of exposure, and whether test results indicate an organic versus a
psychological disorder.
When performing individual clinical tests, the following pattern of results
indicate a probable organic cause rather than a psychological cause. Neuropsychological
findings consistent with organic impairment are 1) impairments in cognitive flexibility,
memory (especially sustained concentration and visual memory), verbal fluency, motor speed, grip
strength, reaction time, and visual-spatial and visual-motor deficits; and 2) intact functions or normal
scores in the area of word knowledge, simple attention, malingering scores (i.e., frequency of pretending illness or
disability), and comprehension.
Data Gaps and Recommendations
There is a need for long-term, longitudinal studies of neurotoxic substances.
These studies would examine exposure, specific effects of exposure on neuropsychological
functions, developmental issues such as maturation of the nervous system, and how factors such
as premorbid personality and other CNS trauma affect responses. Also examined would be aging and
susceptibility to neurotoxins.
There is a need for further study on
the issues related to psychological effects of exposures to hazardous substances. Among the factors to be
considered in these studies are actual or perceived control over the exposure
situation or ability to develop a personal solution, community factors affecting responses, cultural
impacts, and what actual measures of stress should be taken.
Multiple indicators of psychological
stress should be included when evaluating communities that have experienced exposure to hazardous
substances. This stress battery would involve multiple psychological indicators and physiological measures
of stress, as well as biochemical indicators such as cortisol responses/catecholamine
levels and immune system functions. In terms of the physiological measures that
could be used to differentiate psychological from neurotoxic reactions, cortisol
levels may be good indicators of cognitive coping strategies and catecholamine
levels may be indicative of physical coping.
When interpreting results of stress batteries, it is very important to
consider how factors such as perceived control over the situation and having or not having
community and social support networks may affect stress responses in the communities at hazardous waste sites.
Given what is known regarding the psychobiology of stress, are there interactions
between chronic stress and exposure to neurotoxicants that could shift the dose-response curve for
neurotoxins?
Background
This section discusses how to investigate the hypothesis that biological changes
caused by chronic stress could shift the dose-response curve of the body to various
types of neurotoxins, thereby changing the possibility of human health effects from
possible exposures. According to Casarett and Doull's Toxicology (22), a dose-response relationship describes
the correlation between the characteristics of exposure to a toxin and the spectrum of effects that it
causes. Other factors can also influence the body's response to toxins (e.g., age, gender, general health).
Three assumptions must be met if a dose-response curve is to accurately show the
relationship between exposure and effect: 1) the observed response is caused by
the chemical administered; 2) the response is related to the dose; and 3) there is a
way to measure, quantify, and express the toxicity.
Panel Discussion
Neurotoxicants can have a multitude of effects, including systemic effects.
Neurotoxicity can include an early noticeable effect on a specific part of the nervous
system and/or a delayed health effect that may manifest with aging or illness.
Three assumptions must be met if a dose-response curve is to accurately show the
relationship between exposure and effect: 1) the observed response is caused by
the chemical administered; 2) the response is related to the dose; and 3) there is a
way to measure, quantify, and express the toxicity.
One of the panelists, Dr. Jean Harry presented on how to investigate this
possible interaction experimentally. Currently, there are no human studies available to
support this hypothesis.
A methodology does not exist that would allow for discrimination between stress or
neurotoxicant-mediated effects in community-based studies. Any efforts would also
require knowledge of the toxic chemical present and its expected biological effects.
Experimental animal data exist to suggest that stress levels can modulate a toxic
response; however, the question of specificity remains. Given that stress can induce
or unmask a latent effect of a toxicant, there is the possibility that chronic
stress could alter basal levels of neurofunctioning and shift the threshold for
neurotoxicity. Indeed, one may find a shift in the dose response to a
neurotoxicant; however, a specific effect of the neurotoxicant needs to be examined in greater detail than the
generalized non-specific end points. Detecting such a shift would require the knowledge of toxicant-specific
biological mechanisms of actions, which most often are not known.
A possible question to be investigated is what end points should be measured
to determine if a shift in dose-response has occurred?
Data Gaps and Recommendations
The following data gaps will affect the ability to investigate the proposed
question:
Neurotoxic end points may be specific to the chemical, but most often
they are not.
We often do not know the optimal range of dose to measure the effects.
We may know the mechanism of action but not the health consequences
of the measured biochemical response (e.g., catecholamines).
The panel had the following recommendations for investigating the
effects of stress on susceptibility to neurotoxicants:
There needs to be an examination of shifts in general toxicity or other target
organs with end points not confounded by stress. Experimental descriptive animal
models need to be used to test the hypothesis about the synergistic interaction
between stress and specific neurotoxic effects of chemicals. Animal models of
stress, such as auto-analgesia, reactivity (startle response), learned helplessness,
and yoked-control could be used.
Target organs other than the nervous system, such as the
cardiovascular and gastrointestinal systems, must be included in the examination.
Common cellular pathways (i.e., mechanisms of action) need to be
investigated.
The expected toxicant-induced
responses need to be identified and a shift in that
specific endpoint rather than an unrelated endpoint should be found.
What is known about the proportion of individuals who are most sensitive to the uncertainty of possible exposures? This
question includes consideration of populations who are medically, psychologically, and physiologically sensitive.
Background
In public health practice, consideration of medically, psychologically, and
physiologically sensitive populations who are unusually sensitive or susceptible is
especially important. Identification of those unusually susceptible to a pathogenic
influence-be it bacterial, viral, or toxic-enables specifically targeted interventions to be
designed to prevent exposure or to mitigate exposure that has already occurred. People may be unusually
susceptible to a chemical because of a medical condition that interferes with the body's detoxification process or
excretion of a toxin. They may be culturally at risk because of traditional practices that expose them to a
greater than average dose of a toxin (e.g., native tribes who live extensively on
"country" food, such as fish and wild game, that may have bioaccumulated [i.e.,
toxins have built up in the organism]). Other people can be physiologically at risk
because of a genetic variant in an enzyme needed for the detoxification of a chemical.
Panel Discussion
Dr. Lawrence Schell was the discussant for this topic. Dr. Schell stated that there is
substantial scientific evidence to demonstrate that there are categories within
populations that are defined in biological terms, such as the very young and the very
old, that are unquestionably more susceptible to toxic effects than others. In addition,
other subpopulations might show more psychological effects and other indirect effects because of their cultures.
Biological/Developmental Factors
Sensitivity to a given toxicant exposure varies with stage of human development.
The fetus is the clearest example of heightened sensitivity, but aspects of sensitivity
may be present in later stages of development such as the neonatal period, childhood, and
adolescence. Specific "windows of injury" may exist when exposure occurs during
critical periods of growth and development. According to the theory of critical periods, there exist specific
developmental periods when environmental factors can be especially disruptive, with immediate or
late-developing effects. These critical periods may be related to times of rapid cell proliferation, cell
migration, or other processes that are specific to the development of each organ
system, as well as the interaction of these processes. Another developmental
theory-set point theory-states that physiological parameters are "tuned" (i.e.,
operating limits and modal functioning parameters set) within the individual at
specific times of development and that these "set point" times may be influenced by
the environment.
Exposure itself varies with
developmental stage, whether the intake is passive or active. Absorption can vary with developmental stage
whether the absorption is passive dermal, respiratory, or gastrointestinal (GI). The heightened GI absorption
of lead during infancy is a prime example. Another would be the heightened affinity
of fetal neurons for methyl mercury in comparison with that of their mothers. Intake
of toxicants also varies developmentally. Infants and children breathe more rapidly
per unit body weight than adults and their higher dietary intakes related to their
growth mean a greater intake of foodborne and waterborne toxicants per unit of body weight compared with
adults' intakes. Furthermore, there are developmental stage-specific behaviors, such as mouthing, that
increase intake of dust and contaminants. Metabolism, detoxification, and excretion vary with
developmental stage as well.
Interaction of Culture and Environment
In addition to extra sensitivity because
of biological factors, heightened susceptibility to exposure can occur because of cultural factors. An
example of this is Native American groups that are at heightened risk because of their religious beliefs and
subsistence diets that generally involve greater contact with indigenous wildlife as well
as water and soil. A specific example comes from the experience of the Mohawk Indians of Akwesasne (St.
Regis Mohawk Reservation, New York) with contaminants from a Superfund hazardous waste site on the
St. Lawrence River. Traditional Mohawk subsistence lifestyle includes consuming locally grown plants
and local game, including fish from the St. Lawrence River, waterfowl, and wild
mammals. Because of the PCB levels in locally caught fish, the St. Regis Mohawk
Environmental Health Services and the New York State Department of Health suggested in the
mid-to-late 1980s that people limit consumption of locally caught fish or, if of childbearing age, to avoid
consumption entirely. Locally grown foods and waterfowl are suspect as well.
Avoiding locally caught fish and other types of subsistence food constitutes a
significant departure from the traditional diet and a loss of one aspect of traditional
culture (24). The social importance of diet should not be underestimated. Today,
diet is a common marker of ethnicity, and it is also integrated into a culture in several
ways. For example, in Native American cultures, the traditional subsistence methods were carefully
taught to each generation. This teaching itself was an important component of culture building in each
generation; however, if eating locally obtained foods is no longer healthy, children are not taught how to obtain,
prepare, serve, or consume them and a core component of the culture is affected. In
addition, Native Americans are caught between two diet-related health risks. They
are already at high risk because of obesity, with its attendant health risks of
diabetes and cardiovascular disease. To reduce the risk of these conditions, they are advised
to eat fish and vegetables-the very foods that are lost from the local diet because of
contamination. One may ask, "Which poses the greater risk, consumption of contaminated food or consumption of
processed foods?" Thus, the loss of the traditional diet constitutes not only a loss of the culture but can be
perceived as a direct blow to one's health.
Culturally imbedded values can strongly impact reactions to the discovery of a
hazardous waste site in one's community (25). For example, among many Native
American groups, land has a different meaning than it does in mainstream American
culture. In some groups, land has religious meaning and/or is a symbol of sovereignty and
cannot be sold. In contrast, in mainstream American culture, land rarely has this significance. Thus, most
U.S. residents would move away from a hazardous waste site without feeling that their religion has been affected.
Some lands are regarded as sacred by mainstream culture. Arlington National Cemetery is a
good example, because many Americans would be dismayed if a hazardous site were discovered
there. There probably are sacred lands in every culture, but, in some cultures,
all of one's homeland is sacred in some sense. Restricting access to, or use of,
such lands because of contamination could be disturbing and stressful.
Culture has other, wider effects on susceptibility to toxic exposures;
culture can affect symptom expression. Certain "diseases," called culture bound syndromes, are
found only among specific cultures. These syndromes include susto (a folk illness
that is attributed to a frightening event). This illness is found among some Latinos in
the United States and among people in Mexico, Central America, and South America.
Nervios (a general state of vulnerability to stressful life experiences and to
a syndrome brought on by difficult life circumstances) is common among Latinos in
the U.S. and Latin America. There is a similar concept of "nerves" among Greeks in
North America (nerva), and pibloctoq (an episode of extreme excitement, which
lasts up to 30 minutes and is often followed by convulsive seizures and coma lasting
up to 12 hours) is found among Alaskan Eskimos (26). Culture can also affect how
symptoms are reported. People in some societies may be more comfortable reporting a
certain type of symptom (bodily versus emotional); alternatively, certain symptoms may be emphasized. Thus,
the biological effects of a hazardous waste site may be experienced and reported differently depending on the
culture of the people affected by it.
Culture affects the individual's role in day-to-day activities, thereby directly
influencing behavior that could lead to exposure. People with cultures that involve
more subsistence activities will have a greater chance of contact with hazardous waste in the land or native plants and animals affected by
contamination.
The psychological stress found among some people reacting to exposures to
hazardous waste may be mediated by social support. Culture-as a shared system of
values, rights, obligations, and expectations-defines the conditions under which
support is given, the members of the social network, and the types of support available (27).
Measuring social support in a multicultural situation will probably not accurately define social support in
each cultural group.
A disaster is the result of an unexpected loss of apparent or perceived control of
natural or manmade forces. Baum and Fleming have shown that in the United States
a key psychological dimension in predicting health-related reactions to disasters is
individual control (7). Furthermore, they have shown that disasters caused by human failure,
including the creation of a hazardous waste site, produce greater stress and health effects than natural disasters.
In the United States, hazardous waste sites are more likely found near communities
populated by minority groups, especially African-American and Hispanic groups. Minority
communities may have a tradition of distrust of government authorities. A culture of distrust may prepare
residents for the discovery that the government's control of hazardous waste has broken down and human
exposure to toxicants is likely. Models of reaction to hazardous waste sites that are based on the assumption
that the loss of control is a significant feature may require modifications when
applied to communities that have a history of disempowerment and genuinely expect
ill treatment by governments.
Members of subordinated cultures and minority groups that have been dominated
by a mainstream culture may perceive less control of events and circumstances because of their
history of powerlessness against mainstream culture. The premise that accidents caused by breakdowns in
technology are different from nature-caused misfortunes is culturally limited (25). While members of
mainstream American culture may perceive human failure as more surprising, less forgivable,
and less understandable than nature-based "failure," non-mainstream members may
see human systems as more prone to disaster, less trustworthy, and their failure not
as surprising as compared with circumstances created by nature.
Two types of control may be considered in a multicultural context
(28). Primary control refers to control exerted by changing existing circumstances. It is proactive
and the form of control emphasized on most scales that measure control. Secondary
control refers to control exerted by changing one's self to suit the existing circumstances. Primary
control is the type most Western observers prefer, and secondary control may be viewed as noncontrol,
an absence of responsibility for circumstances. Secondary control may be more typical of non-Western
cultures. Among these heterogeneous groups, accommodation to the natural environment
may be more common, and fewer technological means are used to make large-scale changes to
the environment.
Data Gaps and Recommendations
Little work has been done on how various subcultures within the United
States respond to exposure to hazardous substances.
Measurement of control mechanisms in toxicant-impacted
populations will need to take into account different cultures' varying styles of coping.
Cultural factors affect the actual risk
of exposure, the perception of risk from exposure, the perception of consequences of exposure, and the
perception and expression of personal symptoms. Reactions to the breakdown of control over
hazardous waste exposure depend on culturally defined expectations of control over
human-made and natural forces.
Non-Western cultures and minority groups that have been dominated by
mainstream culture and society may experience hazardous waste sites differently
and more severely than people integrated into mainstream American culture. Health
consequences of hazardous waste sites
may exacerbate already existing social and health problems.
Recommendations for working with sensitive populations:
Create a true and equal partnership with the affected community.
Base the project in the community. This will mean learning the community values
and empowering the community to solve its problems.
Use a holistic approach. The indirect effects of hazardous waste exposure (e.g.,
cultural damage, socioeconomic impacts, and psychological distress) may have more severe health effects
than the chemicals.