Public Comment Release
EVALUATION OF SOIL, BLOOD & AIR DATA FROM ANNISTON, ALABAMA
CALHOUN COUNTY, ALABAMA
It appears likely that the available sampling has not fully described the nature and extent of
contamination present. Many of the blood PCB and dioxin analysis results appear to be higher
than could be explained by the air and soil exposure point concentrations. Other sources of PCB
contamination and other routes of exposure (in addition to air inhalation and soil ingestion
assessed in this consultation) may exist.
Based on very high blood PCB levels of above 100 g/L in some individuals, it is apparent that
either (a) exposures are occurring similar to occupational exposures where health effects (e.g.,
respiratory, hematologic, dermal, hepatic) have been reported , or that (b) much higher
exposures occurred at some time in the past. The high blood PCB levels (i.e., hundreds of people
above 20 Âµg/L, and a thousand above 10 Âµg/L) suggest that the exposure pathways are not fully
described by our knowledge of contamination in Anniston. PCBs have long half-lives in the
body, so some of the exposures may have occurred many years ago. However, the occurrence of
high blood PCB levels in persons under 14 years old suggests that PCB exposures occurred more
recently and may still be occurring in Anniston. It is not fully understood exactly what are (and
were) the most important uncontrolled environmental sourcesf of PCBs and exposure routes in the Anniston community.
Blood PCB levels in children indicate that recent exposures to PCBs have occurred in at least
some portion of the population (see discussion in the "Child Health Initiative" section).
However, there is insufficient information regarding the blood PCB and dioxin/furan results to
determine whether the blood results alone confirm that widespread unusual exposures to these
contaminants are now occurring. (These substances are ubiquitous in the environment, and so
ATSDR expects some exposure to occur even without a local source for the contamination.) The
unusually high blood PCB levels seen in some individuals could conceivably have been caused
by high exposures in the past. However, uncertainties in the soil and air sampling (i.e., regarding
areas covered and whether there are hot spots) do not allow us to rule out a current source as
sufficient cause for the high blood levels.
Computational tools such as pharmacokinetic models can provide information that improves our
understanding of exposure in Anniston. Pharmacokinetic modeling combined with recent
congener-specific PCB analysis in blood would help determine the environmental levels
necessary to cause the blood levels seen. For example, using pharmacokinetic modeling we
could estimate the air levels for short-lived individual PCB congeners that would be necessary to
cause a given blood level for that congener. If the air PCB levels necessary to cause a blood PCB
level are far above the air PCB levels we see today, then that would suggest that blood PCB
levels are likely to have come from other sources. Similarly, we could use pharmacokinetic
modeling to determine whether an exposure 25 years ago could have caused blood levels seen today.
Our uncertainty regarding PCB exposure pathways for Anniston is such that we cannot use blood
PCB levels to make decisions on how to reduce exposures. We do not have an adequate
conceptual model for where the PCBs are and how people came into contact with them. Without
further information, actions we take to reduce exposure based solely on blood PCB levels may
have no effect on PCB exposure, and they may even increase PCB exposure. For example, some
people living close to the Solutia facility did not have elevated blood PCB, but others who live
miles from the Solutia facility did.
ATSDR's estimate of upper bound excess for individual cancer risk indicates that a health hazard
may exist for long term exposures to PCBs in air for people living near the Solutia facility.
Uncertainty regarding sources of PCBs and PCB levels in air indicate a need for further data
collection. The further data collection is needed to rule out the likelihood of ongoing exposures
that would present a public health hazard. These conclusions are based on the following findings.
The air monitor at the Miller property location is only several hundred yards from residences and
we do not know the location of the source for the PCBs measured. Therefore, there is a
reasonable (but small) likelihood that some persons may be chronically exposed to elevated
levels of PCBs in air (as found during the 3 day period for which we have data). Estimated
cancer risk based on exposure to the average level of 51.2 ng/m3 PCBs in airg over a 30 year
period is in the range where the need to take actions to reduce exposure risk. However, the
uncertainty regarding long term exposure levels, sources, and air transport of the PCBs to
residential areas necessitates additional characterization before such actions are taken.
Several air monitor locations have reported individual daily air PCB levels similar to the average
reported at the Miller property location, but there is inadequate description of the sources for the
PCBs measured at these locations. The air measurements indicate that a potentially hazardous
source is near residential areas. Furthermore, because we do not know the source of these air
levels, it is possible that areas of even higher air PCB concentration may exist. There are no air
monitoring data for areas reported to have elevated soil PCBs that are located North and
Northwest of Solutia.
Because sampling methods are not known for the Community Group1 and for the Community
Group 2 data sets, there is a fairly high degree of uncertainty regarding exposure point
concentrations for soil ingestion pathways. However, soils sampled at approximately 30 separate
street blocks (see Table 9 with addresses above) appear to be high enough to indicate that a
public health hazard exists. On the basis of ATSDR's analysis of this uncertain data, PCB
detections residential soil ingestion exposure pathways warrant concern for the potential for non-cancer (e.g., neurodevelopmental, immune, and thyroid effects) and cancer effects for exposure
durations of approximately 30 years. In some areas PCB levels may range high enough to warrant
concern for effects (e.g., neurodevelopmental and thyroid effects) for exposure durations of
approximately 1 year. Given the uncertainty in location of and methods for sampling in the CG1
and CG2 data sets, additional sampling (and further health hazard assessment) is needed to
confirm exposure point concentrations for residential yards.
If maximah from the available data sets are used to estimate average exposure point
concentrations over intermediate or chronic exposure durations, then soil concentrations of
PCBs in some areas are high enough to present a public health hazard based on the potential
for chronic cancerous and non-cancerous health effects. Furthermore, residential soils in
some locations above may present risks for thyroid and neurodevelopmental effects for
intermediate exposure durations (less than 1 year of exposure). Studies of animals who
ingested similar doses of PCBs showed that some animals experienced changes in thyroid
hormone levels [27,28] and other animals experienced changes in behavior, deficits in memory
and learning function, and hyperactivity [29,30]. The relevance of these results to human health
is uncertain and should be further evaluated. While neurobehavioral effects have been observed
in infants of women exposed to PCBs before and during pregnancy, it is not known if children
who ingest PCBs would experience similar effects . Moreover, because sampling methods
and locations are not known there is substantial uncertainty in using these soil data to estimate
exposure point concentrations. Furthermore, the use of maxima to estimate averaged exposure
point concentrations is likely to result in a protective bias. Comprehensive sampling, focused on
areas where PCBs were detected by CG2 and by CG1, would reduce uncertainty regarding health
risks for these residences.
Soil levels of DDT and chlordane reported by EPA indicate that a public health hazard may exist
in two locations in Anniston with observed levels of 171.9 ppm DDT (700 block of West 14th
Street) and 113.7 ppm chlordane (1900 block of Cooper Avenue). Further soil sampling is
needed to determine exposure point concentrations for these contaminants at these locations, and to determine whether soil contaminated with these pesticides is more widespread.
The environmental data available for Anniston addressed soil and air contamination near the
Solutia facility. Other pathways that may be a source of PCBs should include ingestion of local
fish, chickens, and possibly pork.
PCBs have been reported in fish sampled from water bodies within 25 miles of Anniston (i.e.,
Choccolocco Creek, Coosa River). Fishing advisories have been posted for the affected areas.
Effectiveness of the fishing advisories is not known.
Several community members have reported that hogs were raised near the Solutia facility in the
past, and that at one point Solutia (known as Monsanto at the time) purchased hogs from local
community members. It is not known whether hogs are being raised near the facility now.
During site visits, ATSDR's staff observed flocks of chickens in a number of yards in West Anniston.
ATSDR's analysis of the potential size and geographic (or temporal) limits of the exposed
population was limited by the way in which persons were chosen for blood sampling. The blood
analysis data was not developed in a way designed to define all exposed persons, nor was it
designed to describe a group exposed by a particular pathway. Furthermore, we cannot rule out
the possibility of more contaminant exposure sources and pathways (e.g., more areas of soil
contamination). Therefore, we do not know whether more persons have unusually high blood
PCB or dioxin/furan levels.
ATSDR's analysis was limited by a lack of information regarding occupational history,
residential history, and behavior for the persons who had their blood analyzed. Further spatial
analysis (using geographic information systems) of blood, soil, and air data is needed when
additional data have been collected (data regarding residence history, behavior, and occupational
history). This analysis would be done to ascertain whether a relationship between environmental
contamination (in soil and air) and blood contamination exists. Residential history information
for persons, in conjunction with blood PCB information, may help identify areas with soil
ATSDR's analysis was also limited by the fact that the soil sampling in residential areas was not
designed to describe exposure point concentrationsi. Information regarding where a sample was
taken (for example, was it taken near the front door, in a garden, or in a child's play area) is
necessary to more accurately estimate exposure point concentrations. Therefore, the exposure
point concentrations and the risk for adverse health effects could be higher or lower than we have
estimated. Furthermore, the soil sampling in residential areas was not designed to describe the
nature and extent of contamination. Therefore, the contamination could be more widespread.
The lack of sample analysis methods as well as quality assurance and control data for the blood
data reduces our certainty that individual results are accurate. Therefore, ATSDR chose to limit
conclusions to those that are based on an overall assessment of the blood analysis results
(although individual blood analysis results may be used to help guide further investigation).
Similarly, the lack of sample analysis methods and quality assurance and control data for the soil
data provided by CG1 and CG2 reduces our certainty that PCB levels at a particular location are
accurate. Therefore, considering this lack of information on analysis methods and the lack of
information on sampling methods, ATSDR chose to limit conclusions to those that are based on
an overall assessment of the soil analysis results from CG1 and CG2. The soil analysis results
may be used to help guide further investigation.
Air sampling is not available for some areas where high blood PCB levels were reported (e.g.,
Northwest of the Solutia facility). Furthermore, no source was determined for the elevated air
levels and no boundary to the area with elevated air levels has been described by the air monitor
locations or results. Data concerning ambient temperature and rainfall during air sampling are
needed. These data are important because the average air PCB level is likely to be affected by
soil temperature and rainfall at the time of sampling, if air levels are the result of vaporization of PCBs in soil.
Susceptible populations for PCBs include young children and women of childbearing age, those
with incompletely developed glucuronide conjugation mechanisms (e.g., Gilbert's syndrome or
Crigler and Najjar syndrome), or with hepatic infections that have caused decreased capacity to
detoxify and excrete PCBs [32,33].
Persons with elevated blood PCB levels may also form a susceptible population with regard to
risk of continuing PCB exposures. There are several reasons why this may be true.
First, higher blood levels should tend to correlate with recency of exposure to elevated
levels of PCBs. For example, we expect that a group with elevated blood PCB levels
would have more people living near soil with high PCBs than a group with typical blood
PCB levels would. Therefore, additional time without exposure mitigation is more likely
to lead to more PCB exposure for persons who have elevated blood PCB levels than it is
for persons who have typical blood PCB levels.
Second, high blood PCB levels should also tend to correlate with long-term internal doses
of PCBs. In other words, we expect that a group with elevated blood PCB levels would
have more people who have experienced long-term internal doses of PCBs than a group
with typical blood PCB levels. We expect this correlation for two reasons. The first is that
any recent behavior that has lead to elevated PCB levels is likely to have also occurred in
the past. If someone ate PCB-contaminated fish from the Coosa River last week, then
there is a reasonable likelihood that they have eaten fish from the Coosa River in past
years too. The second reason is that in some people the elevated PCB level in their blood
today is due to a past exposure that has not yet been cleared from their body. Therefore, a
person with an elevated blood PCB level today may be "still exposed" to the PCBs in
their body from environmental exposures that happened many years ago.j If individuals
have been exposed to elevated levels of PCBs over a long period of time, then there is the
possibility that the PCBs have caused accumulated damage (e.g., based on long-term, low
level stress to the liver, or thyroid gland, or immune system). Persons with accumulated
damage in organs affected by PCBs could then be more susceptible to the effects of
additional PCB exposure if the accumulated damage has caused diminished capacity in
Finally, if threshold mechanisms are responsible for some or all of the health effects
caused by PCBs, then those with higher blood PCB levels are more likely to exceed
thresholds than those with lower blood PCB levels.
ATSDR CHILD HEALTH INITIATIVE
ATSDR's Child Health Initiative recognizes that the unique vulnerabilities of infants and
children demand special emphasis in communities faced with contamination of environmental
media. There are several reasons why particular attention should be paid to children's health as it
is related to environmental contamination in West Anniston.
There is reason to believe that children are now being exposed to PCBs above the "typical" U.S.
exposures. Two lines of evidence support this belief. First, a reputable clinical laboratory reports
that blood PCB levels are above 10 Âµg/L in several children, including children as young as 2
years of age. Second, soil levels in residential areas are reported to contain PCBs. In fact, some
residential areas are reported to have PCB levels that are high enough to warrant concern for
health effects for exposure durations of as little as one year. Higher soil ingestion rates, including
pica ingestion rates, are considered by some experts to be likely during a several year period in
early childhood .
Sampling done for the data sets provided to ATSDR was not designed to "catch everything" or to
statistically estimate the full problem. Therefore, we are likely to have missed some
contamination, and some exposed children. As many as 658 children live within 1 mile of a
presumed source of the PCBs (Solutia), and 2 of the 16 children sampled within that 1 mile
radius have elevated blood PCB levels. It seems likely that we would find more children with
elevated blood PCB levels if we sampled more methodically.
Sampling for all media and for the blood analysis does not describe the nature and extent of
contamination. Furthermore, the sampling does not describe exposure pathway concentrations,
and it does not adequately describe proximate sources of contamination. Given the wide range in
blood levels seen in persons of similar age living in the same area, it seems likely that there is
heterogeneity in the "local" PCB source in residential neighborhoods (i.e., hot spots of
contamination). There is a potential that children are living near an undiscovered hot spot.
PCBs are a suspected human carcinogen. Cancer is a disease that takes a long time to develop.
Early life exposures to carcinogens are anticipated to be more likely to cause cancer than
exposures later in life. This is one of the reasons why EPA chose to consider early life exposures
to PCBs "more potent" than later life exposures in their evaluation of the cancer potency of PCBs
PCBs may adversely affect neurological or behavioral developmental in young children. Studies
over the last decade have suggested that early behavioral development in humans is affected by
early life exposures to PCBs . Recent studies that have methodically examined PCB dose in
human populations have confirmed and extended those suggestions .
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