HEALTH CONSULTATION
Public Comment Release
EVALUATION OF SOIL, BLOOD & AIR DATA FROM ANNISTON, ALABAMA
CALHOUN COUNTY, ALABAMA
EXECUTIVE SUMMARY
The U.S. Environmental Protection Agency (EPA) Region 4 asked the Agency for ToxicSubstances and Disease Registry (ATSDR) to investigate public health concerns in the area of achemical manufacturing facility in West Anniston, Alabama. ATSDR was asked to determinewhether polychlorinated biphenyls (PCBs) and pesticides in soil, blood, and air are a threat topublic health. (See Figure l, map of Anniston, AL.)
Describing the public health hazards at this site is complicated. There is an inadequatedescription of sampling and analytical methods for some of the data. This lack of informationhas caused us to make estimates of PCB exposure that may overestimate or underestimate healthrisk. For this reason, our estimates of exposure magnitude and our public health conclusionsmight change. The following conclusions are reached in this health consultation.
(1) Exposures to PCBs in soil in parts of Anniston present a public health hazard. PCBs inresidential soil present a public health hazard of cancerous and non-cancerous healtheffects for persons with prolonged exposure. PCBs in residential soils in some areas maypresent a public health hazard for thyroid and neurodevelopmental effects after exposuredurations of less than 1 year.
(2) PCB exposures may have been more severe in the past. However, the fact that youngchildren have elevated levels of PCBs indicates that exposure may still be occurring at highlevels.
(3) Exposures to PCBs in the air present an indeterminate public health hazard. Theuncertainty regarding the levels of PCBs in the air in Anniston over long exposure durations,combined with uncertainty regarding air levels of PCBs to which people would be exposed attheir homes, precludes a determination of whether PCBs in air present a health hazard. Moreinvestigation needs to be conducted to a) identify persons living near the air monitors at whichelevated air PCB levels have been detected and b) define the limits of the area with elevated air levels for PCBs.
(4) ATSDR's evaluation of the health hazard potential, particularly with regard to the size of theexposed population and the levels or duration of exposure, is limited by data gaps. Furthersampling and evaluation are needed to fully assess the scope of contamination and exposure. Weare concerned about the potential for health effects at this site.
Further investigation should be done to identify both exposure pathways and appropriate public health actions. This additional data will help us make more specific recommendations for protecting public health.
BACKGROUND AND STATEMENT OF ISSUES
Data Sources
Environmental contamination data were provided to ATSDR by Solutia, two community groups,and EPA. The data were collected for different purposes, analyzed by different laboratories, andreported to ATSDR with varying levels of completeness in the descriptions of methods andquality assurance. Data from all four sources will be used in this consultation so that the mostcomplete and current picture of the extent of chemical exposures can be assessed. However,sampling and analytical methods are not adequately described for all of the data. This lack ofinformation has caused us to make estimates of PCB exposure that may overestimate orunderestimate health risk. For this reason, our estimates of exposure magnitude and our publichealth conclusions might change. The sources of data are listed below.
- Soil and air PCB data developed by Solutia. Much of the available soil sampling datafrom Solutia were generated before 1996 and limited to total PCB levels. The sampleswere collected from drainage ditches and flood plains passing through or extending toareas near the facility. The samples, for the most part, were collected in response to aconsent decree issued by Alabama Department of Environmental Management [1]. Thesoil sampling described the nature and extent of offsite PCB contamination caused bysurface water transport, and is addressed in the public health assessment prepared by theAlabama Department of Public Health (ADPH) [2].
From February 1998 through June 1999, air data were collected over 3 days to16 monthsfrom 9 locations in Anniston. Only PCBs air results were reported. These data werereported by chlorine number (e.g., mono-, di-, tri-chlorobiphenyl) and as total PCBs.Since 1996, additional data sources have resulted from ongoing studies administered byAlabama Department of Environmental Management for other offsite areas, locatedprimarily in the flood plain of the receiving waterways (i.e., Snow Creek, ChoccoloccoCreek, and Coosa River). These data sets cover a wide geographic area and are notaddressed in this document.
An adequate description of the soil sampling and analytical methods (to verifyconcentration quantification and to identify specific location of samples relative toexposure scenarios for individual homes) are available [3,4]. However, ATSDR needsbetter descriptions of the methods used for the Solutia air data.
- Soil and blood PCB data developed by community group 1 (CG1). PCB analytical resultsfor approximately 660 soil samples and 2,970 blood samples were provided to EPA andATSDR. Most of the soil and blood PCB results were reported as total PCBs. The soilsamples were obtained from residential yards within approximately 2 miles of the Solutiafacility. The sample locations were described by street address. Additional informationabout sample location and depth for a given address was not provided. Persons whoconsented to blood sampling were part of a lawsuit involving environmentalcontamination in West Anniston [5]. Most of these persons reside near the Solutiafacility; however, some were former residents who have moved out of the area. Birthdates of the persons sampled and the date of sampling were provided for most of the blood samples. The blood samples were obtained during 1996 through 1999.
Complete descriptions of the sampling and analytical methods used for the blood datawere not provided. However, the information that has been received is sufficient fordetermining whether PCB levels in the community were elevated [6]. ATSDR did notreceive a complete description of the sampling and analytical methods used for the soildata from Community Group 1 (CG1) to verify concentration quantification and toidentify specific location of samples relative to exposure scenarios for individual homes.
- Soil and air PCB and pesticide levels reported by EPA. EPA provided ATSDR with PCB and pesticide analytical results for surface soil samples obtained from 38 locations and PCB analytical results for air samples from five monitoring stations over a 3- day period. The samples were collected in June 1999. The soil samples were obtained in residential areas near the Solutia site, and the sampling locations were determined by regulatory agencies and CG1. These samples were intended to address community concerns about current exposures and to help gain an initial understanding of the general levels and distribution of PCBs within the community. Only air analytical results for PCBs were reported. The air PCB data were reported as Aroclor equivalents. The descriptions of the sampling and analytical methods EPA used for collecting the air and soil data were sufficient to verify concentrations and locations of samples relative to the exposure scenarios.
- Soil and dust PCB data developed by Community Group 2 (CG2). On October 14, 1999,EPA provided ATSDR with geographic information system (GIS) representations anddata that Solutia had sent to Alabama Department of Environmental Management [7]. Asecond community group, CG2, had generated these additional data. The samples werecollected during late 1996. Information about location and depth of samples at specificaddresses was provided. PCB analytical results for soil, indoor dust, and air samples (theair samples described previously that had been done by Solutia) were contained in thedata package. The 75 surface and 12 "core" soil samples and eight indoor dust samples(from three homes) were collected from residential areas within a 1-mile perimeter of theSolutia facility.
ATSDR has not verified concentration quantification because of incomplete descriptionsof the soil or dust sampling and analytical methods used for the CG2 data sets.
Summary of Data Provided
Quality assurance and control information
ATSDR did not receive quality assurance and quality control (QA/QC) data for laboratoryanalysis of the samples in data sets provided by CG1 and CG2. Analysis results can differsubstantially between laboratories, and QA/QC data help identify when the results may differ.The lack of QA/QC information may have caused us to make estimates of PCB exposure thatmay overestimate or underestimate health risk. QA/QC data were available for analysis resultsprovided by EPA and Solutia.
Blood PCB measurements
In May 1999, EPA received data involving individual PCB measurements for 1,409 persons fromCG1. Approximately 1,000 of these persons had current addresses in zip codes surrounding theSolutia facility (i.e., 36201, 36202, and 36203) (Figures 2 and 3). The data included eachperson's name, total PCB level measured in blood serum, date of birth, and date the serum wasdrawn. Of the 1,409 persons, 1,400 were reported as having a "positive" total serum PCB level.Testing procedures used were with a detection limit of either 3 or 5 micrograms of PCBs per literof blood (µg/L).8,a,b In late September 1999, CG1 sent ATSDR a list of 1,566 persons who had"negative" PCB test results. Sampling or analytical methods were not provided for any of theblood data provided by CG1. ATSDR contacted the laboratory that performed the analysis anddetermined that the methods used were adequate for determining whether PCB levels in thecommunity were elevated [8].
If the four persons with a total PCB level of "<3.0" in the original data set are counted as "notdetected" and are added to the 1,566 persons from the second data set, then there were a total of1,570 persons in whom serum PCBs were "not detected" and 1,400 in whom PCBs were"detected." Thus, the total number of persons for whom serum PCB results were reported was2,970. Most (2,173 [73%]) of these persons had addresses in Anniston zip codes (36201, 36201,36203, 36204, 36205, 36206, and 36207).
The detected PCB values in the community group ranged from 3.0 to 2,111.5 µg/L. The averagefor the entire group (detects and non-detects) was 14.2 µg/L, and for the 95th percentile was49.6 µg/L. More than half of the persons tested had blood PCB levels above the detection limit of5 µg/L. Table 1 provides summary statistics for all 2,970, with reported blood PCB analysisresults.
Table 1.
Summary statistics for blood PCB levels for the
data submitted by Community Group l | Number of people | 2,970 |
|---|
| Average age | 45 years |
|---|
| Range of ages at testing | 3 days to 94 years |
|---|
| Range of PCB levels | Non-detect to 2,111.5 µg/L |
|---|
| Average PCB level | 14.2 µg/L |
|---|
| Median PCB level | 2.5 µg/L |
|---|
| 75th percentile PCB level | 14.8 µg/L |
|---|
| 95th percentile PCB level | 49.6 µg/L |
|---|
*Nondetect = ½ detection limit. See footnote a on page 4.
The blood PCB levels measured for a large number of persons (hundreds and perhaps as many asa thousand) in this group are high when compared with blood levels for the rest of the U.S.population [9,10]. The blood levels for the community group are also high compared with morerecent data collected by the Centers for Disease Control and Prevention's National Center forEnvironmental Health (NCEH). Estimates from the 1970s of the 95th percentile of the "typicalcU.S. range" for PCBs in the blood indicate that 20 µg/L was unusual at that time. In addition, thevery highest blood PCB level reported in 13 studies of nonoccupationally exposed populationsfrom the 1970s was 79 µg/L. Most of the high values reported in studies from the 1970s werebelow 60 µg/L [11]. On the basis of more recent blood analysis results for "typical U.S."populations and on declining environmental PCB levels, we expect that blood PCB levels in theU.S. population are now even lower than they were in the 1970s [12]. ATSDR estimates that the95th percentile of the typical U.S. population range may now be as low as 10 µg/L.
In addition, the blood PCB levels reported for many of the community members are higher thanlevels reported for many persons who worked daily with PCBs and who were studied for healtheffects decades ago [13]. There were 41 persons with blood PCB levels above 100 µg/L and 1037persons with blood PCB levels above 10 µg/L. There were 521 persons (17% of the entire group)with PCB levels above 20 µg/L (Table 2).
Table 2.
Number of persons sampled with blood PCB levels above 10, 20, and 100 µg/L | Of all persons (N=2,966) | Number | Percentageof total |
|---|
| Number of persons above 10 µg/L | 1,037 | 34.9 |
|---|
| Number of persons above 20 µg/L | 521 | 17.5 |
|---|
| Number of persons above 100 µg/L | 41 | 1.4 |
|---|
Most of the high PCB levels (e.g., those over 100 µg/L) were in persons over 50 years of age at the time their blood was sampled (Table 3). However, 346 persons under the age of 50 had greater than 10 µg/L PCB, including one 38-year-old person with a blood PCB level of 124 µg/L. Two children less than 6 years of age had blood PCB levels between 10 and 20 µg/L, and one 12-year-old had a blood PCB level of 26 µg/L. Five persons aged 20 to 30 years had levels ranging from 23.8 to 46.9 µg/L. Furthermore, 121 persons less than 50 years of age had blood PCB levels above 20 µg/L, representing 6.7 % of all persons in this age group who had blood PCB tests (Table 4 and Figures 4 and 5).
Table 3.
Age distribution of persons sampled for blood PCB levels Blood PCB
level (µg/L) | Age (years) |
| 0-5.9 | 6-19.9 | 20-29.9 | 30-39.9 | 40-49.9 | 50-59.9 | 60-69.9 | 70-79.9 | 80 | Not
reported | Total | <50 | <30 | >50 |
| Non-detect | 27 | 138 | 318 | 384 | 356 | 174 | 61 | 21 | 4 | 87 | 1,570 | 1,223 | 483 | 260 |
| <10 | 0 | 3 | 13 | 81 | 108 | 79 | 37 | 22 | 2 | 19 | 364 | 205 | 16 | 140 |
| 10-100 | 2 | 2 | 16 | 79 | 245 | 245 | 219 | 115 | 26 | 46 | 995 | 344 | 20 | 605 |
| >100 | 0 | 0 | 0 | 1 | 1 | 9 | 13 | 7 | 6 | 4 | 41 | 2 | 0 | 35 |
| Total | 29 | 143 | 347 | 545 | 710 | 507 | 330 | 165 | 38 | 156 | 2,970 | 1,774 | 519 | 1040 |
Table 4.
Number of persons less than 50 years old who had PCB levels above 10, 20, and 100 µg/L Of persons less than 50 years of age
(N=1774) | Total number | Percentageof total |
| Number of persons above 10 µg/L | 346 | 19.6 |
|---|
| Number of persons above 20 µg/L | 121 | 6.7 |
|---|
| Number of persons above 100 µg/L | 2 | 0.1 |
|---|
Based on comparison of the distribution of blood values to reference or "typical" distributions ofPCB values, more than 500 (i.e., all those with blood levels above 20 µg/L, including 120persons younger than 50 years of age)--and perhaps more than 1,000--persons (i.e., all thosewith levels above 10 µg/L) in the 2,970 tested have high blood PCB levels. There may be morepeople with high blood PCB levels in the Anniston area.
We are concerned about the possibility of more people with high blood PCB levels. The potentialsources of PCB exposure for the persons tested thus far have not been adequately identified andcharacterized. For example, we do not know where those persons worked or what street theylived on over the past few years. Furthermore, hot spots for PCB contamination have beenidentified by sampling done by CG1 and CG2, but a thorough sampling of the areas around thosehot spots has not been done. Because of the incomplete characterization of sources of exposure,it is unknown if the available sampling has defined the limits of the contaminated area or thepathway (or pathways) causing PCB exposures. Therefore, it is prudent to assume that otherpersons from the Anniston area also have high blood PCB levels.
Even though PCBs are persistent in the body, they are still slowly removed from the body overtime. The length of time that it takes for this removal varies by the congener. For somecongeners, this process takes many years; for other congeners, this takes less than a year. Theestimated length of time is usually based on the length of time that it takes to remove half of theamount (termed a "biological half-life"). Research scientists have determined the biological half-life for the various PCB congeners. Using this information, we can estimate how long ago aperson might have been exposed to a particular PCB congener. If a person has a PCB congenerwith a short half-life in their blood, then it is likely that that person was exposed to the congenerwithin the preceding few years.
The long persistence of some PCB congeners in the body suggests the possibility that many ofthe high blood PCB levels in current and former Anniston residents could have been caused byexposures that occurred years or even decades ago. This possibility increases concern about thepotential for adverse health effects. If the exposures did happen years ago, they must have been high exposures to have caused the blood PCB levels detected today. Estimated biological half-lives for total PCBs range from 3 to 24 years [14]. Thus, if the elevated blood PCB levelsdetected in Anniston residents today were caused by exposures that happened 20 years ago, thenthe blood levels 20 years ago would have been about twice what they are today (if half-lives forthe PCBs in Anniston are 24 years). The blood PCB levels would have been 16 times higher 20years ago if the PCB half-lives are 5 years.
Some of the blood data indicate that elevated PCB exposures occurred in the past few years. Forexample, elevated blood PCB values recorded for children (Table 5) indicate that exposuresoccurred as recently as 1994.d Furthermore, five of the congeners that were elevated in adultsmeasured during the 1996 exposure investigation (EI) have biological half-lives of less than1 year (congeners 105, 118, 138, 153, and 180) [15]. In 12 persons from the EI, the total of justthose five congeners was greater than 20 µg/L, and in three the total was greater than 100 µg/L.Therefore, it seems clear that for the persons evaluated in the EI, the PCB exposures were notdecades old. Because we do not know the sources of exposure for the 1,000 or more personswith elevated PCBs demonstrated in the CG1 data set, we cannot exclude the possibility thatexposures are still occurring as they did for the persons measured in the EI. Congener-specificPCB analysis for persons living in Anniston could be used (with pharmacokinetic modeling) todetermine whether exposures are still occurring by similar analysis of the proportion of shorthalf-life congeners in total serum PCB.
Table 5.
Detected blood PCB levels and ages for persons younger than 14 at the time of blood sampling. Age when
sampled (years) | Year of blood sample | Blood PCB level (µg/L) |
| 2 | 1996 | 11.1 |
|---|
| 2 | 1996 | 17.2 |
|---|
| 9 | 1998 | 11.8 |
|---|
| 12 | 1998 | 26.3 |
|---|
The large number of persons in whom PCBs were not detected indicates that many persons in thearea, including persons who live near the Solutia facility, have "typical" blood PCB levels. Thereis also a wide range of blood values across the group sampled (700-fold difference between thehighest and the lowest detection). The difference between highest and lowest detection is nearly50-fold, even among persons aged 50 years or less. This finding may indicate that many personsdo not (or did not) come into contact with the PCB sources that the persons with the higher bloodPCB levels contacted. This suggests a heterogeneous source of exposure (i.e., hot spots, variationin exposure pathways), a time differential (e.g., much higher exposures happened in the past),varying ethnic or cultural practices (i.e., geophagiae has been reported among persons living inthis area), or persons with occupations that would cause exposure to PCBs.
PCB levels in children younger than 6 years of age at the time of testing
Geographic information system (GIS) analysis indicates that 648 children younger than 6 years ofage lived within a 1-mile radius of the Solutia facility (1990 national census). Blood analysisresults are available for 16 children under six (at date of testing) within that same 1-mile radius.Of those 16 children, two had a blood PCB level above the detection limit (Figure 6). Both ofthese children were approximately 2 years old when tested. One child had a blood PCB level of17.2 µg/L, and the other had 11.1 µg/L. There are no reference values for "typical" blood PCBlevels in children to use for comparison with these children. However, on the basis of theexpected accumulation rate for PCBs in blood and the values seen in adults, we expect that areference 95th percentile value for "typical" children would be below 10 µg/L.
The child with a reported blood PCB value of 17.2 µg/L lived in a home where two adults (maleand female) and three other children (ages 4 to 12) were also tested. The male adult and the2-year-old child were above the detection limit for PCBs in blood. The male adult's blood PCBwas 32.9 µg/L. The female adult is the mother of the 2-year-old. The 2-year-old child with ablood PCB value of 11.1 µg/L lived in a home where two adults (male and female) were alsotested. The woman's blood PCB level was 19.2 µg/L, and the man's was below the detection limit.
Blood dioxin measurements
ATSDR received, through EPA, blood analysis results for 20 dioxin, furan, and coplanar PCBcongeners for 10 persons from CG1. The blood PCB levels, sum dioxin toxicity equivalence(TEQ), and the year of birth of the 10 persons are shown in Table 6. Congener-specific summarydata are presented in Table 7. The criteria for choosing these 10 persons were not provided.Persons tested for dioxins did not correspond to the highest 10 total PCB values for the 2,970persons. For example, nine persons with PCB levels between 200 and 800 µg/L were not tested for dioxins.
Table 6.
Total blood PCB, sum dioxin toxicity equivalence (TEQ)* levels, and year ofbirth for the blood dioxin/furan/coplanar PCB analysis Reference
number for
the person | Total PCBs in
blood (µg/L) | Sum TEQ for dioxins, furans and PCBs in blood
(ppt, lipid basis) | Year of birth |
| without PCBs | with PCBs |
| 1 | 2111.5 | 179.8 | 371.3 | 1913 |
| 2 | 187.5 | 37.5 | 98.6 | 1936 |
| 3 | 166.0 | 39.6 | 112.9 | No data |
| 4 | 151.5 | 74.0 | 310.3 | 1919 |
| 5 | 149.7 | 32.8 | 44.5 | 1946 |
| 6 | 145.0 | 38.3 | 72.3 | No data |
| 7 | 124.1 | 37.5 | 445.9 | 1931 |
| 8 | 120.8 | 36.6 | 122.7 | 1924 |
| 9 | 103.0 | 60.0 | 292.8 | 1921 |
| 10 | 76.3 | 36.1 | 56.0 | 1944 |
* Derived using 1998 World Health Organization toxicity equivalence factors [16].
ATSDR has developed an estimate of the 95th percentile values for the 20 congeners for acomparison group of 360 persons from studies in five states (see Appendix B). This comparisongroup is not a matched "control group" for the 10 persons measured in Anniston; however,statistics derived from this group represent ATSDR's best estimate of a "reference" 95thpercentile for the U.S. population. The average, median, minimum, and maximum of the dioxin,furan, and PCB congeners measured for the 10 persons in Anniston are compared with ATSDR'sestimate of a reference 95th percentile in Table 6. TEQs are derived using 1998 World HealthOrganization toxicity equivalence factors [17].
Of note for the dioxin comparisons,
The highest sum dioxin toxicity equivalent (TEQ) (445.8 nanograms per liter or ng/L) ismore than 10 times the 95th percentile of the comparison group (39.6 ng/L).
The minimum Sum TEQ (44.5 ng/L) is just above the 95th percentile for the comparisongroup (39.6 ng/L).
The median sum TEQ without PCB contribution (37.9 ng/L) is just below the 95thpercentile for the comparison group (39.6 ng/L).
The penta and hexa biphenyls, the penta and hexa furans, and octa dioxin seem to bemore markedly elevated than other congeners.
The maximum value for a dioxin, furan, or PCB congener does not seem to be strongly related to the total PCB value. For example, the highest sum TEQ (445.8 ng/L) and penta PCB (4,050 ng/L) were for Individual 7 from Table 5. The highest octa dioxin (5,909.8 ng/L) and tetra PCB (713 ng/L) were for Individual 9 from Table 5. The highest hexa PCB (2,807 ng/L) was for Individual 4. The highest penta and hexa furans were for Individual 1.
Table 7.
Summary statistics for dioxins/furans/coplanar PCBs in 10 persons from Anniston area, and 95th percentiles for a comparison group developed by ATSDR | Congener | Number of
persons
measured | Statistics for the measurements
(in parts per trillion, lipid based)* | 95th percentile for
a comparison
group ** |
| Average | Median | Minimum | Maximum |
| 2378 tetra dibenzodioxin | 10 | 4.68 | 3.9 | 2.2 | 8.4 | 4.9 |
| 12378 penta dibenzodioxin | 10 | 12.7 | 11.7 | 8.1 | 23.8 | 9.6 |
| 123478 hexa dibenzodioxin | 10 | 15.2 | 14.1 | 10.4 | 23.7 | 10.1 |
| 123678 hexa dibenzodioxin | 10 | 92.5 | 89.5 | 63.1 | 158 | 114.4 |
| 123789 hexa dibenzodioxin | 10 | 11.4 | 11.3 | 7.8 | 16.2 | 12.8 |
| 1234678 hepta dibenzodioxin | 10 | 128.5 | 71.3 | 31.1 | 286.6 | 157.3 |
| Octa dibenzodioxin | 10 | 1,593.7 | 1046.9 | 598.1 | 5,909.8 | 1,372.9 |
| 2378 tetra dibenzofuran | 7 | 1.6 | 1.6 | 1.4 | 1.9 | 1.8 |
| 12378 penta dibenzofuran | 0 | | | | | 1.9 |
| 23478F penta dibenzofuran | 10 | 42.2 | 18.4 | 7.1 | 223.9 | 12.1 |
| 123478 hexa dibenzofuran | 10 | 28.3 | 17.2 | 13.3 | 95.9 | 11.7 |
| 123678 hexa dibenzofuran | 10 | 18.1 | 10 | 6.2 | 83.5 | 9.2 |
| 123789 hexa dibenzofuran | 0 | | | | | 2.2 |
| 234678 hexa dibenzofuran | 10 | 3.7 | 3.5 | 1.5 | 6 | 4.3 |
| 1234678 hepta dibenzofuran | 10 | 20.7 | 21.4 | 14.8 | 26.7 | 25.6 |
| 1234789 hepta dibenzofuran | 1 | | | | 1.9 | 3.3 |
| Octa dibenzofuran | 0 | | | | | 6.7 |
| 3344 tetra chlorinated biphenyl | 5 | 275.2 | 175 | 41 | 713 | 105.9 |
| 33445 penta chlorinated biphenyl | 10 | 1,268.3 | 756 | 104 | 4,050 | 51.3 |
| 334455 hexa chlorinated biphenyl | 10 | 867.9 | 481 | 136 | 2,807 | 38.5 |
| Sum Toxicity Equivalent (TEQ) | 10 | 192.7 | 117.8 | 44.5 | 445.8 | 39.6 |
| Sum TEQ without PCBs | 10 | 57.1 | 37.9 | 32.7 | 179.7 | |
* Values above the comparison population 95
th percentile are shaded. Values more than four times the 95
th percentile are shaded and in bold.
** See
Appendix B.
Air monitoring
ATSDR reviewed air monitoring data from two sources, EPA and Solutia. On June 28 throughJuly 1, 1999, EPA's Region 4 and its Science and Ecosystem Support Division conducted an airmonitoring study using 24-hour, high-volume sampling methods at five locations around theSolutia facility [18] (Figure 7, Table 7) [19,20]. The five locations were
A detention pond near Montrose Avenue,
Miller Property Site between railroad and Tenth St. near Crawford Avenue,
The South Landfill near State Road 202 and Clydesdale Avenue,
The West Landfill near First Avenue and Jefferson Street, and
Wellborn High School (Background Site).
Sample locations were on Solutia property, except Wellborn High School.
Air concentrations throughout the 3-day EPA study were highest at the Miller Property andlowest near Wellborn High School. Concentrations were generally highest when it rained duringthe first 2 days of the study. PCBs in air at all the sites more closely resembled an Aroclor 1242pattern more than the other eight Aroclor patterns assessed in EPA's analysis. Total PCB levelswere not reported. A sum of Aroclor 1242 and Aroclor 1254 will be used to estimate total PCBlevels for health effects assessment. Total PCB levels in the air summed in this way averaged 63nanograms per cubic meter (ng/M3) for the Miller Property site. Averages for the four stationswere from 2 to nearly 10 times above the only detection reported for air near the background siteat Wellborn High School.
Solutia provided PCB analysis data for air samples taken between February 18, 1998, and July 1, 1999 [21] (Figure 7 and Table 8). The Solutia data are consistent with the air data provided by EPA. The Solutia data are from the same areas of Anniston as the EPA monitoring stations, which provided a longer period of observation. The Solutia data provided comparison to four background locations, including the Wellborn High School location sampled by EPA. Sample analysis results are available from both EPA and Solutia for June 28 through July 1, 1999, for several air monitor locations.
Table 8.
Summary data for air PCB sampling locations | Sampling location | Map key for Figure 7 | Sampled by | Number of samples | Time period covered | PCB levels in air (ng/M3) |
| high | low | average |
| East of the Solutia facility |
| Solutia location 1 "ANN SW" | 1 | Solutia | 23 | 2/18/98 to 7/1/99 | 80.7 | 0.1 | 37.6 |
| Solutia location 2 "ANN NE" | 2 | Solutia | 26 | 2/18/98 to 7/1/99 | 39.1 | 0.1 | 14.4 |
| Detention Pond near Montrose Ave | 3 | EPA | 3 | 6/28/99 to 7/1/99 | 53.3 | 19.9 | 31.4 |
| Solutia | 23 | 4/9/98 to 7/1/99 | 39.2 | ND | 14.4 |
| Miller Property site | 8 | EPA | 3 | 6/28/99 to 7/1/99 | 85.1 | 27.5 | 62.8 |
| Solutia | 3 | 6/28/99 to 7/1/99 | 58 | 14.7 | 39.6 |
| Average of the two monitors at the Miller Property | 51.2 |
| West of the Solutia facility |
| West End Landfill near 1st Ave and Jefferson St | 6 | EPA | 3 | 6/28/99 to 7/1/99 | 33.4 | 14 | 22.1 |
| Solutia | 3 | 6/28/99 to 7/1/99 | 12.2 | 7.8 | 10 |
Wellborn High School
(background location)* | 9 | EPA | 3 | 6/28/99 to 7/1/99 | 6.5 | ND | < 6.5 |
| Solutia | 3 | 6/28/99 to 7/1/99 | 1.1 | 0.2 | 0.7 |
| South of the Solutia facility |
| Solutia location 4 "WEL" | 4 | Solutia | 24 | 4/9/98 to 7/1/99 | 48.9 | ND | 9.8 |
| Solutia location 5 "SO L" | 5 | Solutia | 24 | 2/24/98 to 7/1/99 | 11.2 | ND | 1.9 |
| South Landfill near Hwy 202 and Clydesdale Ave | 7 | EPA | 3 | 6/28/99 to 7/1/99 | 23.1 | 9.7 | 16.2 |
| Solutia | 4 | 6/28/99 to 7/1/99 | 12.6 | 4.5 | 6.7 |
* Air PCB levels for the other background locations (described as "urban areas in Alabama") averaged 0.5, 1.5, and0.3 ng/m
3 [
22].
The air monitoring locations were not chosen for the purpose of establishing a PCB source.There are no air monitors to the north and northwest of the Solutia facility where a number ofpersons were reported with high blood PCB levels. Furthermore, soil sampling provided by CG1(e.g., 14th or Hamm Streets) and provided by CG2 (e.g., Crane or Carter Streets) shows that localareas of soil contamination that are more than a ½ mile from any air monitor (Table 9). There areresidences within 300 yards of the monitor location on the Miller property. The monitor at thedetention pond near Montrose Avenue is within 20 yards of the 700 block of Montrose. Themonitor at the detention pond near Montrose Avenue is also within 200 yards of the 800 block of Montrose and within 300 yards of the 500 through 700 block of Zinn Parkway Drive.
Soil, sediment, and dust sampling
The largest number of soil and sediment samples was provided by Solutia. However, because ofthe site conceptual model operating at the time the Resource Conservation and Recovery Act of1976 required Solutia to sample soil and sediment. These samples were limited, with fewexceptions, to drainage ditches and areas frequently flooded near the Solutia facility. The Solutiasamples demonstrated that PCB contamination had been previously carried off the Solutia facilityby water flowing through drainage ditches. The human health hazard posed by PCBs thatmigrated into residential areas through this pathway is addressed in the two health consultationsprepared by ADPH in 1995 and 1996 [23,24] and by the 1999 public health assessment for thissite [25]. Most of the soil-, dust-, and sediment-mediated exposure described by the ADPHconsultations has been addressed through relocations and remediation undertaken by Solutia. Thesampling conducted by Solutia in response to recommendations in the ADPH consultations doesnot address dioxin, furan, or pesticide contamination.
Soil samples outside of the flood plain have been taken by CG1, EPA, and CG2. Each of thesedata sets demonstrates PCB contamination outside the flood plains associated with ditchesdraining from Solutia. The data sets do not overlap enough in terms of area covered or samplingmethods for ATSDR to draw conclusions about whether the PCB levels observed by EPA areconsistent with the levels observed by either CG1 or CG2.
The data developed by the four sources (including Solutia) are summarized in Table 9. The CG1 soil data set is shown in Figures 8 and 9. The EPA data is shown in Figure 10. The CG2 data is shown in Figure 11.
Table 9.
Summary descriptions of total PCB levels reported for soil samples | Sample set | Number of samples | In flood plain
connected to Solutia? | minimum
(ppm) | maximum
(ppm) | Range of top 10
sample locations
(ppm) |
| CG1 | 655 | mostly no | ND ** | 840.4 | 17.4 to 840.4 |
| EPA | 38 | mostly no | ND | 15.2 | 1.4 to 15.2 |
| CG2 | 75 surface and 12
"core" soil samples | about half and half | ND | 644.7 | 112.6 to 644.7 |
| Solutia | 593* | mostly yes | ND | 2810 | 502 to 2810 |
* This is the number of samples assessed in the ADPH public health assessment. More samples were taken by Solutia.
** ND = nondetected.
Table 10 shows residential areas identified as having one or more soil samples with PCB levels between 10 and 20 ppm, between 20 and 100 ppm, or greater than 100 ppm. (Addresses are rounded to nearest hundred so that individual houses are not identified.)
Table 10.
Streets and blocks identified by EPA, CG1, and CG2 data sets as containing soils with PCB levels above 10, 20, or 100 ppm | Block (rounded to nearest 100) and street | Between
10 and 20
ppm | Between
20 and
100 ppm | Greater
than 100
ppm | Data set* |
| Across Rd (between Eulation Rd and Carter St) | | yes | | CG2 |
| 800 Boynton Ave (multiple addresses)# | | yes | yes | CG2 |
| 1000 Carter St | yes | | | CG1 |
| 800 Crawford St (multiple addresses)# | | yes | yes | CG1, CG2 |
| 1900 Duncan Ave | yes | | | CG1 |
| 2500 Eulation Rd | | | yes | CG1 |
| 100 Front St | yes | | | CG1 |
| 1300 Front St | | yes | | CG1 |
| 2400 Gurnee Ave | yes | | | CG1 |
| 1000 Hamm St | yes | | | CG1 |
| 2300 W Jefferson St | | yes | | CG1 |
| 300 McArthur Dr | | yes | | CG1 |
| 900 McDaniel Ave | yes | | | EPA, CG1 |
| 1500 McDaniel Ave | yes | | | CG1 |
| 3000 McKleroy Ave | yes | | | CG1 |
| 2000 Moore Ave | yes | | | CG1 |
| 2600 Moore Ave | yes | | | CG1 |
| 200 Mountain View Rd | | | yes | CG1 |
| 600 N Marshall St | yes | | | CG1 |
| 800 Montrose Ave | yes | | | CG2 |
| 2200 Old Birmingham Hwy | yes | | | CG1 |
| 1700 Patch Place | yes | | | CG1 |
| 1500 W 8th St | | | yes | CG2 |
| 1400 W 10th St | yes | | | EPA |
| Snow creek drainage ditch at Crane Ave and W 11th Street | | | yes | CG2 |
| 11th St. drainage ditch at Carter St | | | yes | CG2 |
| 1700 W 13th St | yes | | | CG1 |
| 2000 W 14th St | yes | | | CG1 |
| 3100 W 14th St | yes | | | CG1 |
| 1100 W 16th St | yes | | | CG1 |
| 700 Zinn Dr | yes | | | CG1 |
* EPA = Environmental Protection Agency; CG1 = Community Group 1; CG2 = Community Group 2.
# These locations have been purchased by Solutia.
The locations of the samples for the data sets were not reported in a manner that allows evaluation of specific residential exposure scenarios. For example, we do not know how close to a residence any particular sample was taken, nor do we know whether samples were near a garden, in a children's play area, or from a generally inaccessible area.
A simple analysis (regression) of the relationship between soil and blood levels does not show anassociation (i.e., soil PCB does not predict blood PCB) and it is unclear as to why. There areseveral reasons for this, including:
The 1996 EI by ADPH of 103 people just east of the Solutia facility did show arelationship between soil and blood PCB. It therefore seems reasonable to expect thatsome of the 2,970 people in the larger CG1 group may have similar exposure patterns tothe 103 persons in the EI, and would show a relationship between blood and soil levels. However, exposure patterns among many of the 2,970 from a much larger area of Anniston may be quite different from the 103 persons studied in the EI. The length of time an individual lived at an address with soil analysis information islikely to vary, and that length of time will affect the relationship between soil PCB levelsand blood PCB levels. Information regarding how long people lived at an address was notprovided to ATSDR. PCBs have long half-lives in blood, which means that blood levelsare likely to be most closely related to an average concentration of the places they havelived over many years rather than the soil concentration at their current residence.
A better understanding of the factors that would lead to a lack of relationship between blood andsoil PCB levels may help ATSDR and ADPH intervene or make recommendations to reducePCB exposures. A survey is being conducted by the community that will provide informationregarding other exposure pathways (for example, cultural or "medicinal" ingestion of clay,consumption of local produce, occupational history). In addition, representatives of CG1 haveagreed to provide residential history information to ATSDR. The survey and residential historyinformation may help clarify the relationship between soil and blood PCB levels by allowingATSDR to assess persons for whom a soil pathway is likely to predominate.
The Community Group 2 report also presents analysis results for dust samples taken in houses inthe 800 block of Boynton Avenue. Of eight samples taken in three residences, none were abovedetection limits of 0.7 parts per meter. The locations of the samples for the data sets were notreported in a manner that allows evaluation of specific residential exposure scenarios. Forexample, we do not know the quantity of dust collected, the size of the areas sampled, or thelocation of samples within the homes.
The pesticides DDT and chlordane were found in a few of the 40 soil samples taken by EPA in1999. The DDT and chlordane analyses were performed as part of the laboratory cleanupprocedures associated with the PCB analysis. The scope of the EPA sampling and analysis planwas to investigate PCB contamination at a select few locations around the Solutia facility. DDTand chlordane were not part of the original EPA sampling and analysis plan. The two highestDDT levels were 171.9 and 5.1 ppm, with five of 38 samples above 1 ppm. The two highestchlordane levels were 113.7 ppm and 24.4 ppm, with nine of 38 samples above one. The levelswere not high enough nor were the occurrences frequent enough to suggest widespread hazardouscontamination in West Anniston. Based on available information, it appears likely that the DDTand chlordane were the result of individual uses of these pesticides (e.g., to control termites orfire ants) at some time in the past. Nonetheless, any sampling plans for this area should consider the possibility that off-label and illegal pesticide applications may be occurring.
Next Section Table of Contents