HEALTH CONSULTATION
Public Comment Release
EVALUATION OF SOIL, BLOOD & AIR DATA FROM ANNISTON, ALABAMA
CALHOUN COUNTY, ALABAMA
The U.S. Environmental Protection Agency (EPA) Region 4 asked the Agency for Toxic Substances and Disease Registry (ATSDR) to investigate public health concerns in the area of a chemical manufacturing facility in West Anniston, Alabama. ATSDR was asked to determine whether polychlorinated biphenyls (PCBs) and pesticides in soil, blood, and air are a threat to public health. (See Figure l, map of Anniston, AL.)
Describing the public health hazards at this site is complicated. There is an inadequate description of sampling and analytical methods for some of the data. This lack of information has caused us to make estimates of PCB exposure that may overestimate or underestimate health risk. For this reason, our estimates of exposure magnitude and our public health conclusions might 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 in residential soil present a public health hazard of cancerous and non-cancerous health effects for persons with prolonged exposure. PCBs in residential soils in some areas may present a public health hazard for thyroid and neurodevelopmental effects after exposure durations of less than 1 year.
(2) PCB exposures may have been more severe in the past. However, the fact that young children have elevated levels of PCBs indicates that exposure may still be occurring at high levels.
(3) Exposures to PCBs in the air present an indeterminate public health hazard. The uncertainty 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 at their homes, precludes a determination of whether PCBs in air present a health hazard. More investigation needs to be conducted to a) identify persons living near the air monitors at which elevated 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 the exposed population and the levels or duration of exposure, is limited by data gaps. Further sampling and evaluation are needed to fully assess the scope of contamination and exposure. We are 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
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, and reported to ATSDR with varying levels of completeness in the descriptions of methods and quality assurance. Data from all four sources will be used in this consultation so that the most complete 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 of information has caused us to make estimates of PCB exposure that may overestimate or underestimate health risk. For this reason, our estimates of exposure magnitude and our public health conclusions might change. The sources of data are listed below.
From February 1998 through June 1999, air data were collected over 3 days to16 months from 9 locations in Anniston. Only PCBs air results were reported. These data were reported by chlorine number (e.g., mono-, di-, tri-chlorobiphenyl) and as total PCBs. Since 1996, additional data sources have resulted from ongoing studies administered by Alabama Department of Environmental Management for other offsite areas, located primarily in the flood plain of the receiving waterways (i.e., Snow Creek, Choccolocco Creek, and Coosa River). These data sets cover a wide geographic area and are not addressed in this document.
An adequate description of the soil sampling and analytical methods (to verify concentration quantification and to identify specific location of samples relative to exposure scenarios for individual homes) are available [3,4]. However, ATSDR needs better descriptions of the methods used for the Solutia air data.
Complete descriptions of the sampling and analytical methods used for the blood data were not provided. However, the information that has been received is sufficient for determining whether PCB levels in the community were elevated [6]. ATSDR did not receive a complete description of the sampling and analytical methods used for the soil data from Community Group 1 (CG1) to verify concentration quantification and to identify specific location of samples relative to exposure scenarios for individual homes.
ATSDR has not verified concentration quantification because of incomplete descriptions of the soil or dust sampling and analytical methods used for the CG2 data sets.
Quality assurance and control information
ATSDR did not receive quality assurance and quality control (QA/QC) data for laboratory analysis of the samples in data sets provided by CG1 and CG2. Analysis results can differ substantially 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 that may overestimate or underestimate health risk. QA/QC data were available for analysis results provided by EPA and Solutia.
In May 1999, EPA received data involving individual PCB measurements for 1,409 persons from CG1. Approximately 1,000 of these persons had current addresses in zip codes surrounding the Solutia facility (i.e., 36201, 36202, and 36203) (Figures 2 and 3). The data included each person's name, total PCB level measured in blood serum, date of birth, and date the serum was drawn. 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 liter of 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 the blood data provided by CG1. ATSDR contacted the laboratory that performed the analysis and determined that the methods used were adequate for determining whether PCB levels in the community were elevated [8].
If the four persons with a total PCB level of "<3.0" in the original data set are counted as "not detected" and are added to the 1,566 persons from the second data set, then there were a total of 1,570 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 was 2,970. 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 average for the entire group (detects and non-detects) was 14.2 µg/L, and for the 95th percentile was 49.6 µg/L. More than half of the persons tested had blood PCB levels above the detection limit of 5 µg/L. Table 1 provides summary statistics for all 2,970, with reported blood PCB analysis results.
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 as a 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 more recent data collected by the Centers for Disease Control and Prevention's National Center for Environmental Health (NCEH). Estimates from the 1970s of the 95th percentile of the "typicalc U.S. range" for PCBs in the blood indicate that 20 µg/L was unusual at that time. In addition, the very highest blood PCB level reported in 13 studies of nonoccupationally exposed populations from the 1970s was 79 µg/L. Most of the high values reported in studies from the 1970s were below 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 the U.S. population are now even lower than they were in the 1970s [12]. ATSDR estimates that the 95th 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 than levels reported for many persons who worked daily with PCBs and who were studied for health effects decades ago [13]. There were 41 persons with blood PCB levels above 100 µg/L and 1037 persons 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 | Percentage of 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 | Percentage of 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 of PCB values, more than 500 (i.e., all those with blood levels above 20 µg/L, including 120 persons younger than 50 years of age)--and perhaps more than 1,000--persons (i.e., all those with levels above 10 µg/L) in the 2,970 tested have high blood PCB levels. There may be more people with high blood PCB levels in the Anniston area.
We are concerned about the possibility of more people with high blood PCB levels. The potential sources of PCB exposure for the persons tested thus far have not been adequately identified and characterized. For example, we do not know where those persons worked or what street they lived on over the past few years. Furthermore, hot spots for PCB contamination have been identified by sampling done by CG1 and CG2, but a thorough sampling of the areas around those hot 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 the pathway (or pathways) causing PCB exposures. Therefore, it is prudent to assume that other persons 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 over time. The length of time that it takes for this removal varies by the congener. For some congeners, this process takes many years; for other congeners, this takes less than a year. The estimated length of time is usually based on the length of time that it takes to remove half of the amount (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 a person might have been exposed to a particular PCB congener. If a person has a PCB congener with a short half-life in their blood, then it is likely that that person was exposed to the congener within the preceding few years.
The long persistence of some PCB congeners in the body suggests the possibility that many of the high blood PCB levels in current and former Anniston residents could have been caused by exposures that occurred years or even decades ago. This possibility increases concern about the potential 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 levels detected in Anniston residents today were caused by exposures that happened 20 years ago, then the blood levels 20 years ago would have been about twice what they are today (if half-lives for the PCBs in Anniston are 24 years). The blood PCB levels would have been 16 times higher 20 years 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. For example, elevated blood PCB values recorded for children (Table 5) indicate that exposures occurred as recently as 1994.d Furthermore, five of the congeners that were elevated in adults measured during the 1996 exposure investigation (EI) have biological half-lives of less than 1 year (congeners 105, 118, 138, 153, and 180) [15]. In 12 persons from the EI, the total of just those 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 not decades old. Because we do not know the sources of exposure for the 1,000 or more persons with elevated PCBs demonstrated in the CG1 data set, we cannot exclude the possibility that exposures are still occurring as they did for the persons measured in the EI. Congener-specific PCB analysis for persons living in Anniston could be used (with pharmacokinetic modeling) to determine whether exposures are still occurring by similar analysis of the proportion of short half-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 the area, including persons who live near the Solutia facility, have "typical" blood PCB levels. There is also a wide range of blood values across the group sampled (700-fold difference between the highest and the lowest detection). The difference between highest and lowest detection is nearly 50-fold, even among persons aged 50 years or less. This finding may indicate that many persons do not (or did not) come into contact with the PCB sources that the persons with the higher blood PCB levels contacted. This suggests a heterogeneous source of exposure (i.e., hot spots, variation in 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 in this 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 of age lived within a 1-mile radius of the Solutia facility (1990 national census). Blood analysis results 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 of these children were approximately 2 years old when tested. One child had a blood PCB level of 17.2 µg/L, and the other had 11.1 µg/L. There are no reference values for "typical" blood PCB levels in children to use for comparison with these children. However, on the basis of the expected accumulation rate for PCBs in blood and the values seen in adults, we expect that a reference 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 (male and female) and three other children (ages 4 to 12) were also tested. The male adult and the 2-year-old child were above the detection limit for PCBs in blood. The male adult's blood PCB was 32.9 µg/L. The female adult is the mother of the 2-year-old. The 2-year-old child with a blood PCB value of 11.1 µg/L lived in a home where two adults (male and female) were also tested. The woman's blood PCB level was 19.2 µg/L, and the man's was below the detection limit.
ATSDR received, through EPA, blood analysis results for 20 dioxin, furan, and coplanar PCB congeners 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 summary data 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 2,970 persons. 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 of birth 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 a comparison group of 360 persons from studies in five states (see Appendix B). This comparison group 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" 95th percentile 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's estimate of a reference 95th percentile in Table 6. TEQs are derived using 1998 World Health Organization 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) is more 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 comparison group (39.6 ng/L).
The median sum TEQ without PCB contribution (37.9 ng/L) is just below the 95th percentile for the comparison group (39.6 ng/L).
The penta and hexa biphenyls, the penta and hexa furans, and octa dioxin seem to be more 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 | |
ATSDR reviewed air monitoring data from two sources, EPA and Solutia. On June 28 through July 1, 1999, EPA's Region 4 and its Science and Ecosystem Support Division conducted an air monitoring study using 24-hour, high-volume sampling methods at five locations around the Solutia facility [18] (Figure 7, Table 7) [19,20]. The five locations were
Sample locations were on Solutia property, except Wellborn High School.
Air concentrations throughout the 3-day EPA study were highest at the Miller Property and lowest near Wellborn High School. Concentrations were generally highest when it rained during the first 2 days of the study. PCBs in air at all the sites more closely resembled an Aroclor 1242 pattern more than the other eight Aroclor patterns assessed in EPA's analysis. Total PCB levels were not reported. A sum of Aroclor 1242 and Aroclor 1254 will be used to estimate total PCB levels for health effects assessment. Total PCB levels in the air summed in this way averaged 63 nanograms per cubic meter (ng/M3) for the Miller Property site. Averages for the four stations were from 2 to nearly 10 times above the only detection reported for air near the background site at 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 | ||
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 of persons 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 local areas of soil contamination that are more than a ½ mile from any air monitor (Table 9). There are residences within 300 yards of the monitor location on the Miller property. The monitor at the detention pond near Montrose Avenue is within 20 yards of the 700 block of Montrose. The monitor 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 of the site conceptual model operating at the time the Resource Conservation and Recovery Act of 1976 required Solutia to sample soil and sediment. These samples were limited, with few exceptions, to drainage ditches and areas frequently flooded near the Solutia facility. The Solutia samples demonstrated that PCB contamination had been previously carried off the Solutia facility by water flowing through drainage ditches. The human health hazard posed by PCBs that migrated into residential areas through this pathway is addressed in the two health consultations prepared by ADPH in 1995 and 1996 [23,24] and by the 1999 public health assessment for this site [25]. Most of the soil-, dust-, and sediment-mediated exposure described by the ADPH consultations has been addressed through relocations and remediation undertaken by Solutia. The sampling conducted by Solutia in response to recommendations in the ADPH consultations does not address dioxin, furan, or pesticide contamination.
Soil samples outside of the flood plain have been taken by CG1, EPA, and CG2. Each of these data sets demonstrates PCB contamination outside the flood plains associated with ditches draining from Solutia. The data sets do not overlap enough in terms of area covered or sampling methods for ATSDR to draw conclusions about whether the PCB levels observed by EPA are consistent 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 |
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 |
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 an association (i.e., soil PCB does not predict blood PCB) and it is unclear as to why. There are several reasons for this, including:
The length of time an individual lived at an address with soil analysis information is likely to vary, and that length of time will affect the relationship between soil PCB levels and blood PCB levels. Information regarding how long people lived at an address was not provided to ATSDR. PCBs have long half-lives in blood, which means that blood levels are likely to be most closely related to an average concentration of the places they have lived 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 and soil PCB levels may help ATSDR and ADPH intervene or make recommendations to reduce PCB exposures. A survey is being conducted by the community that will provide information regarding other exposure pathways (for example, cultural or "medicinal" ingestion of clay, consumption of local produce, occupational history). In addition, representatives of CG1 have agreed to provide residential history information to ATSDR. The survey and residential history information may help clarify the relationship between soil and blood PCB levels by allowing ATSDR 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 in the 800 block of Boynton Avenue. Of eight samples taken in three residences, none were above detection limits of 0.7 parts per meter. 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 the quantity of dust collected, the size of the areas sampled, or the location of samples within the homes.
The pesticides DDT and chlordane were found in a few of the 40 soil samples taken by EPA in 1999. The DDT and chlordane analyses were performed as part of the laboratory cleanup procedures associated with the PCB analysis. The scope of the EPA sampling and analysis plan was to investigate PCB contamination at a select few locations around the Solutia facility. DDT and chlordane were not part of the original EPA sampling and analysis plan. The two highest DDT levels were 171.9 and 5.1 ppm, with five of 38 samples above 1 ppm. The two highest chlordane levels were 113.7 ppm and 24.4 ppm, with nine of 38 samples above one. The levels were not high enough nor were the occurrences frequent enough to suggest widespread hazardous contamination in West Anniston. Based on available information, it appears likely that the DDT and chlordane were the result of individual uses of these pesticides (e.g., to control termites or fire 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.
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