Arch. Environ. Contam. Toxicol. 44, 125–131 (2003) DOI: 10.1007/s00244-002-1301-5

A R C H I V E S O F

Environmental Contamination a n d Toxicology © 2003 Springer-Verlag New York Inc.

Human Exposure to Polychlorinated Biphenyls in a Residential Community K. G. Orloff,1 S. Dearwent,1 S. Metcalf,1 S. Kathman,1 W. Turner2 1 2

Agency for Toxic Substances and Disease Registry, 1600 Clifton Road, MS-E32, Atlanta, Georgia 30333, USA Centers for Disease Control and Prevention, 1600 Clifton Road, MS-F17, Atlanta, Georgia 30333, USA

Received: 16 December 2001/Accepted: 15 April 2002

Abstract. Blood serum concentrations of polychlorinated biphenyls (PCBs) were measured in members of a residential community who lived near a chemical plant that formerly manufactured PCBs. Elevated blood serum PCB concentrations were detected in some of the older adults who were long-term residents of the community. Congener-specific analyses indicated that PCB congeners 153, 138/158, 180, 118, and 187 contributed 60 – 67% of the total PCBs detected in blood from adults and children. Blood PCB concentrations correlated strongly with age and length of residency in the neighborhood. However, blood PCB concentrations did not correlate with PCB concentrations in soil or house dust samples from the homes. Past exposures to PCBs may be a significant contributor to the elevated PCB concentrations detected in some adult members of the community.

A chemical company produced polychlorinated biphenyls (PCBs) at a plant in Anniston, Alabama, from 1935 to the 1970s. Hazardous wastes, including PCB still bottoms, were disposed in two unlined landfills located adjacent to the production facility. Environmental investigations documented the presence of PCB contamination in sediment samples from off-site drainage ditches and in soil samples from private residences near the facility. These findings led to property buyouts for some homeowners and remediation of off-site contaminated areas. PCB-contaminated soil in residential lots was excavated and back-filled with clean clay material and covered with topsoil and sod. However, some off-site PCBcontaminated soil and sediment still remain. Residents of the area expressed concern to state and federal health and environmental officials over their potential exposures to environmental PCB contamination. To assess these potential exposures, the Agency for Toxic Substances and Disease Registry (ATSDR) collected environmental (soil and house dust) and biological (blood) samples and analyzed them for PCB congeners.

Correspondence to: K. G. Orloff; email: [email protected]

Materials and Methods Target Population Families who lived within a radius of about one-half mile of the chemical manufacturing plant were invited to participate in this investigation. To be eligible for the study, at least one family member had to be a child between 1 and 7 years old. ATSDR staff and representatives of the community went door-to-door to invite eligible families to participate. A total of 18 families fully participated in this investigation. The participants were self-selected and lived in homes that were scattered throughout the residential neighborhoods surrounding the facility. Environmental samples of soil and house dust were collected from 18 homes, and blood samples were collected from 78 residents of these homes. Blood samples were taken from two other residents of the target area, although environmental samples were not collected from their homes. Prior to testing, each adult and a parent or legal guardian of each minor participant was required to sign an informed consent/ assent form. A separate informed consent form for environmental testing was also obtained for each house prior to testing. The test population ranged in age from 1 to 89 years old and consisted of 43 adults and 37 children (aged 16 or younger). The racial distribution of the participants was 81% black and 19% white; the gender distribution was 56% female and 44% male.

Biological Sampling and Analyses A licensed phlebotomist collected a 7-ml blood sample from each participant using a Vacutainer威 tube with no anticoagulant. After collection, the blood samples were allowed to clot for 2 h at room temperature. The tubes were then placed on ice until they were delivered to the laboratory for analysis. Blood collection supplies and laboratory analyses were provided by the National Center for Environmental Health laboratory at the Centers for Disease Control and Prevention in Atlanta, Georgia. Blood serum samples were analyzed for 37 PCB congeners using high-resolution gas chromatography isotope-dilution high-resolution mass spectrometry (HRGC/ID-HRMS) (Patterson et al. 1990). The 37 congeners selected were those that are most commonly detected in human blood samples based on published reports. Serum samples were spiked with 13C12-labeled internal standards, and the analytes of interest were isolated using a C18 solid phase extraction procedure followed by a multicolumn automated cleanup and enrichment procedure. The analytes were separated by HRGC using a DB-5 ms 30-m

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capillary column and quantified by ID-HRMS using selected ion monitoring at 10,000 resolving power. The concentration of each analyte was calculated from an individual standard linear calibration. Each analytical run was conducted blinded and consisted of three unknown serum samples, a method blank, and a quality control sample. Serum total lipids were calculated using an enzymatic summation method (Akins et al. 1989). Results were reported as concentrations of individual PCB congeners per unit volume of blood serum and also as lipid-based concentrations. Individual congeners were added together to yield total PCB concentrations.

Environmental Sampling and Analyses ATSDR staff used a metal trowel to collect a surface soil sample (0 –3 inches in depth) from an area in the yard that the parent or child identified as a frequent play area. In addition, ATSDR staff used a Nilfisk威 HEPA vacuum cleaner to collect an indoor house dust sample from a room frequented by family members; this was typically the living room of the house. The environmental samples were shipped by overnight mail to the Midwest Research Institute in Kansas City, Missouri, for analyses of PCB congeners. The analytical procedures followed standard EPA methods (Nelson 2000). Prior to analysis, the house dust samples were strained through a wire mesh screen to remove food particles, fibers, and other debris. The soil and house dust samples were extracted by refluxing in a soxhlet for 18 h with hexane:acetone (1:1) (SW-846, Method 3540). The samples were cleaned up using acid partitioning (SW-846, method 8290) and a Florisil威 column (SW-846, Method 3620). The samples were analyzed for PCBs using gas chromatography/mass spectroscopy with internal standard analysis (Method 680). The results were reported as PCBs per dry mass of sample.

Data Analyses Descriptive statistics were used to characterize the blood serum and environmental media PCB data. To assess correlations between biological and environmental data, Spearman rank correlation coefficients were calculated. The correlation coefficients for the blood data were calculated using the lipid-based concentrations of PCBs. Statistical analyses were conducted using SAS v.8.

Results Biological Samples The concentration of PCBs was measured in blood serum samples from 37 children and 43 adults. In adults, the blood PCB concentrations ranged from nondetected to 210 ␮g/L or ppb. The mean PCB concentration in adults was 14.3 ppb, and the median concentration was 2.2 ppb. Detectable concentrations of PCBs were measured in 35 of 43 adults. The detection level for total PCBs varied between samples but was generally less than 1 ppb. If the PCB concentrations in the blood samples without detectable PCBs are assumed to be one-half the detection level, the mean and median concentrations in adults were calculated to be 14.6 ppb and 2.7 ppb, respectively. The mean and median blood PCB concentrations in adults were substantially different because several of the participants had very high PCB concentrations (maximum of 210 ppb) that skewed the arithmetic mean. If the five adults with the highest PCB con-

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centrations are excluded, the mean PCB concentration in the remainder of the population of 38 adults was 3.5 ppb. In children (age 16 or less), the blood PCB concentrations ranged from nondetected to 4.6 ppb. The mean PCB concentration in children was 0.37 ppb, and the median concentration was nondetected. Detectable concentrations of PCBs were measured in 10 of the 37 children tested. Assuming the PCB concentrations in the samples without detectable PCBs to be one-half the detection level, the mean and median concentrations in children were calculated to be 1.59 and 1.10 ppb, respectively. In Figure 1, blood PCB concentrations are plotted as a function of age. The ages of the participants ranged from 1 to 89 years. In general, there was a tendency for blood PCB concentrations to increase with age, as has been reported for other populations (Miller et al. 1991; Gerstenberger et al. 1997). In Tables 1 and 2, descriptive statistics for the blood concentrations of individual PCB congeners in adults and children are presented. Mean concentrations of PCB congeners are reported both as ␮g/L and as ng/g serum lipid. Blood concentrations of PCBs can increase after the ingestion of large quantities of dietary fat (Phillips et al. 1989). To correct for this transient hyperlipidemia, blood serum concentrations of PCBs can be normalized by calculating them as a blood lipid concentration. As indicated, the mean concentration of total PCB congeners was in adults was 14.3 ␮g/L or 2,543 ng/g lipid, and in children 0.37 ␮g/L or 61.5 ng/g lipid.

Environmental Samples The concentration of PCBs detected in composite surface soil samples from 19 homes ranged from nondetected to 11.7 ppm. The mean concentration of PCBs in soil was 1.4 ppm, and the median concentration was 0.60 ppm. The EPA has established a Recommended Soil Action Level—Analytical Starting Point of 1 ppm for PCBs in residential soil (U.S. EPA 1990). Soil samples from four homes contained PCB concentrations in excess of 1 ppm (11.7, 5.14, 1.31, and 1.20 ppm). The concentration of PCBs detected in house dust samples from 18 homes ranged from nondetected to 10.3 ppm. The mean concentration of PCBs in house dust samples was 0.81 ppm, and the median concentration was 0.11 ppm. House dust samples from two homes contained PCB concentrations in excess of 1 ppm (10.3 and 1.71 ppm). Indoor surface loading concentrations of PCBs in house dust ranged from nondetected to 31.9 ␮g/m2 of floor surface area.

Discussion Biological Samples In the United States, no study of PCB blood concentrations in a statistically based sample of the population has been conducted. Therefore, there is no national reference range that can be used as a comparison population for this investigation. However, several studies have measured PCB concentrations in populations that had no known exposures to PCBs other than typical background levels (Sahl et al. 1985; Miller et al. 1991; Hovinga et al. 1992; Wolf et al. 1993; Hunter et al. 1997;

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Fig. 1. Blood serum PCB concentrations (ppb) versus age (years)

Hanrahan et al. 1999; Kearny et al. 1999; Humphrey et al. 2000). In these published studies, mean background PCB concentrations in adults range from about 1.2– 6.8 ppb. Relatively few studies have measured PCB concentrations in children. However, in two published studies (Jacobson et al. 1990; Schecter et al. 1994), PCB concentrations in blood serum from children were about 2– 4 ppb, which is less than for adults. The upper end distribution of PCB concentrations in the general population has not been well characterized. In a review paper, Kreiss (1985) estimated that the 95th percentile PCB blood concentration in adults is 20 ppb. This estimate was based on studies conducted in the 1970s and early 1980s. The production of PCBs in the United States stopped in 1977, and the use of PCBs has since declined. Therefore, it is likely that the 95th percentile blood PCB concentration would be considerably lower today. As discussed, there is no recent, large-scale study of the concentrations of PCBs in blood samples from the United States population that can be used to define a statistically significant elevated blood PCB concentration. Therefore, in the discussion that follows, blood PCB concentrations in excess of 10 ppb will be designated as being elevated. Although arbitrary, this designation seems reasonable, because 10 ppb PCBs is severalfold higher than average PCB concentrations in the general population. Furthermore, in one study of adult women, a 90th percentile PCB concentration of 10.6 ppb was reported (Wolff 1993). In this investigation, nine adults had a blood PCB concentration (11, 15, 16, 17, 22, 54, 93, 97, and 210 ppb) that

exceeded 10 ppb. Because PCBs are resistant to metabolism in the body, they bioaccumulate as a person ages. Therefore, blood PCB concentrations tend to increase with age. In Figure 1, the blood PCB concentrations in the participants are plotted as a function of age. As indicated, all of the people with blood PCB concentrations in excess of 10 ppb were aged 43 years or older. Although blood PCB concentrations increase with age, PCB concentrations in excess of 10 ppb are unusual in unexposed populations, even among older adults. In a recent study, PCB concentrations were measured in a control group of older adults (aged 50 to ⬎ 70 years) (Humphrey et al. 2000; Schantz et al. 2001). The mean blood PCB concentration in this population of older adults was 4.55 ppb; the maximum concentration detected was 25.9 ppb. Only 10 of 37 children tested in this investigation had a detectable PCB concentration in their blood serum. The average PCB concentration in the children was 0.37 ppb, or 1.59 ppb if nondetects are assumed to be one-half the detection level. The highest blood concentration detected in a child was 4.6 ppb, which was detected in an older child (a 13-year-old girl). Reference ranges for PCB concentrations in teenagers are not available, but they would likely be between those for young children and adults. Nevertheless, the PCB concentrations detected in children and teenagers were within the ranges detected in the few available comparison studies for children. There are 209 possible congeners of PCBs, which differ in the number and position of the chlorine atoms on the biphenyl ring structure. In this investigation, 37 PCB congeners were measured in the blood samples. As shown by the data in Tables

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Table 1. Blood serum concentrations of PCB congeners in adults (n ⫽ 43) Congener

Mean (␮g/L)

Median (␮g/L)

Maximum (␮g/L)

Rank (mean ␮g/L)

Percenta

28 52 49 44 74 66 101 99 87 110 118 105 151 149 146 153 138/158 128 167 156 157 178 187 183 177 172 180 170 189 201 196/203 195 194 206 209 Total

0.0159 0.0141 0.0070 0.0109 0.3083 0.0732 0.0549 0.6501 0.0493 0.0227 1.1310 0.2646 0.0512 0.0211 0.4697 2.8719 2.1100 0.0738 0.1193 0.2634 0.0709 0.1906 0.8014 0.2274 0.2306 0.1319 1.5063 0.5996 0.0195 0.5154 0.3983 0.0706 0.4520 0.2600 0.1526 14.2815

0 0 0 0 0.052 0 0 0.081 0 0 0.096 0 0 0 0.057 0.399 0.282 0 0 0.045 0 0.027 0.106 0.033 0 0 0.296 0.113 0 0.101 0.085 0 0.089 0.057 0

0.365 0.211 0.121 0.161 5.449 1.675 1.185 13.207 1.054 0.449 19.798 5.494 1.035 0.708 6.042 41.529 30.912 2.586 1.636 2.833 0.944 2.597 12.644 4.770 3.082 1.599 19.262 7.356 0.280 6.622 5.505 1.012 5.818 3.746 1.969

32 33 35 34 12 23 26 6 28 29 4 13 27 30 9 1 2 22 21 14 24 18 5 17 16 21 3 7 31 8 11 25 10 15 19

7.0 9.3 7.0 9.3 65.1 37.2 14.0 79.1 30.2 14.0 76.7 48.8 23.3 4.7 76.7 79.1 72.1 18.6 41.9 67.4 27.9 51.2 79.1 53.5 48.8 48.8 74.4 67.4 14.0 72.1 69.8 18.6 67.4 53.5 32.6

a

Mean (ng/g lipid) 3.0 2.5 1.3 2.0 55.2 13.8 10.3 119.7 9.3 4.4 204.0 48.4 9.4 4.3 83.6 514.2 374.6 14.7 21.1 45.6 12.4 34.4 145.1 41.8 40.4 22.5 269.2 105.6 3.5 87.9 71.5 13.0 80.1 46.8 27.4 2,543.1

Percent of samples with detectable concentrations.

1 and 2, the congeners that contributed most to the total blood concentration of PCBs in the participants were 153, 138/158, 180, 118, and 187 (IUPAC designation). These congeners contain from five to seven chlorine atoms and are components of commercial PCB mixtures. Because these congeners contain chlorine atoms on the meta and/or para position of the biphenyl ring, they are resistant to metabolic degradation and bioaccumulate in humans (Hansen 1998; Brown 1994). As a collective group, commercial mixtures of PCBs have an estimated half-life of 2– 6 years (Shirai and Kissel 1996). However, the half-life of individual congeners may be considerably longer or shorter. For example, the halflife of PCB congener 153 was estimated to be 12.4 years, whereas the half-life of PCB congener 28 was estimated to be 1.4 years (Brown et al. 1994). In the adults with blood PCB concentrations in excess of 10 ppb, PCB congeners 153, 138/158, 180, 118, and 187 accounted for 62% of the total PCB concentrations. In the other adults, they accounted for 60% of the total PCBs. This indicates that the same PCB congeners composed the bulk of the

blood PCBs in adults with either normal or elevated PCB concentrations. Furthermore, the PCBs with long biological half-lives accounted for most of the total PCB concentrations, as has been observed in other studies (Hansen 1998; Humphrey et al. 2000). In children, the same six PCB congeners accounted for 67% of the total blood PCB concentrations. The total PCB concentrations in children were generally lower than for adults. As a result, the children typically lacked detectable quantities of the minor PCB congeners that were detected at low concentrations in adults. The absence of detectable quantities of these minor PCB congeners in children slightly increased the relative proportion of the major congeners.

Correlation Analysis To assess the relationships between blood PCB concentrations and age and length of residency at current address, Spearman

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Table 2. Blood serum concentrations of PCB congeners in children (n ⫽ 37) Congener

Mean (␮g/L)

Maximum (␮g/L)

Rank (mean ␮g/L)

Percenta

28 52 49 44 74 66 101 99 87 110 118 105 151 149 146 153 138/158 128 167 156 157 178 187 183 177 172 180 170 189 201 196/203 195 194 206 209 Total

0.0049 0.0046 0.0041 0.0046 0.0090 0.0034 0.0043 0.0178 0.0035 0.0033 0.0275 0.0044 0.0026 0.0028 0.0181 0.0774 0.0405 0.0025 0.0026 0.0049 0.0025 0.0038 0.0211 0.0062 0.0072 0.0057 0.0391 0.0105 0.0028 0.0074 0.0097 0.0015 0.0048 0.0029 0.0017 0.3697

0.181 0.170 0.150 0.170 0.163 0.126 0.159 0.175 0.101 0.122 0.284 0.109 0.098 0.105 0.236 0.813 0.581 0.092 0.099 0.113 0.093 0.088 0.265 0.097 0.013 0.147 0.536 0.193 0.105 0.129 0.216 0.054 0.116 0.108 0.065

15 18 22 18 10 25 21 7 24 26 4 20 31 28 6 1 2 33 30 15 24 23 5 13 12 14 3 8 28 11 9 35 17 27 34

2.7 2.7 2.7 2.7 13.5 2.7 2.7 24.3 5.4 2.7 27.0 5.4 2.7 2.7 27.0 27.0 13.5 2.7 2.7 5.4 2.7 5.4 24.3 10.8 8.1 5.4 21.6 8.1 2.7 8.1 8.1 2.7 8.1 2.7 2.7

a

Mean (ng/g lipid) 0.619 0.581 0.514 0.581 1.337 0.430 0.792 3.016 0.346 0.416 4.935 0.584 0.335 0.768 3.186 14.492 6.922 0.314 0.338 0.651 0.319 0.500 3.730 0.965 1.159 0.751 7.032 1.673 0.359 1.038 1.346 0.184 0.721 0.370 0.222 61.517

Percent of samples with detectable concentrations.

rank coefficients were calculated. Age was strongly correlated with the blood PCB concentration (rs ⫽ 0.729, p ⬍ 0.001). Length of residency was also correlated with the blood PCB concentration (rs ⫽ 0.645, p ⬍ 0.001). By calculating the Spearman partial correlation coefficient, it was determined that if age were controlled for, there was still a significant correlation between the blood PCB concentration and length of residency (rs ⫽ 0.310, p ⫽ 0.0054). In these calculations, a participant’s length of residency was equated to how long he or she had lived at the current address. However, many of the participants indicated that they had lived at more than one house in the area over the course of their lives. Therefore, the length of residency value may have underestimated how long some people actually lived in the vicinity of the facility. If this information had been incorporated into the calculations, the correlation coefficient between blood PCB concentrations and length of residency may have been even higher. Nevertheless, these statistical analyses suggest that people were exposed to PCBs while living near the facility, although it is not known when the exposures occurred or what the source of PCB exposure was.

Environmental Samples Environmental sampling at the homes indicated the presence of PCB contamination in soil and house dust samples from many of the houses. This contamination poses a potential source of exposure, because children may intentionally (pica behavior) or inadvertently ingest soil and house dust (Calabrese et al., 1989; Stanek and Calabrese 1995). Soil and house dust ingestion by adults has not been well studied, but it is likely to be less than for children (Calabrese et al. 1990). However, in some adult populations, intentional ingestion of clay and soil may occur (geophagia) (Vemeer and Frate 1979; Feldman 1986). To examine the correlations between the concentrations of PCBs in blood and environmental samples, the Spearman rank correlation coefficients were calculated. As indicated by the results in Table 3, there was a significant correlation between the concentrations of PCBs in soil and house dust samples from individual homes (rs ⫽ 0.628, p ⬍ 0.0052). This correlation is expected because soil typically constitutes about half of the mass of house dust (Paustenbach et al. 1997).

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Table 3. Spearman rank correlation coefficients (p values) for PCB concentrations in environmental and biological samples Soil Soil House dust (ppm) House dust (␮g/m2) Blood (ppb), all Blood (ppb), adults Blood (ppb), children

1.0 0.628 (p ⫽ 0.0052) 0.555 (p ⫽ 0.017) ⫺0.128 (p ⫽ 0.264) ⫺0.173 (p ⫽ 0.287) ⫺0.109 (p ⫽ 0.514)

House dust (ppm)

House Dust (␮g/m2)

0.628 (p ⫽ 0.0052) 1.0

0.555 (p ⫽ 0.017) 0.966 (p ⬍ 0.001) 1.0

0.966 (p ⬍ 0.001) 0.078 (p ⫽ 0.511) 0.045 (p ⫽ 0.786) ⫺0.039 (p ⫽ 0.824)

0.046 (p ⫽ 0.696) 0.008 (p ⫽ 0.959) ⫺0.109 (p ⫽ 0.534)

Further statistical analyses failed to demonstrate a significant correlation between blood PCB concentrations and the concentration of PCBs in either soil (rs ⫽ ⫺0.128, p ⫽ 0.26), house dust (rs ⫽ 0.078, p ⫽ 0.51), or the house dust loading (␮g/m2) concentration (rs ⫽ 0.046, p ⫽ 0.70). Further analyses in which the test population was divided into adults and children also failed to demonstrate any significant correlations between blood and current environmental PCB concentrations. The absence of a correlation between blood PCB concentrations and soil or house dust PCB concentrations (Table 3) suggests that other sources of PCBs, besides those in soil and house dust, have contributed to the body burdens of PCBs.

Conclusions In the general population, the major background source of PCB exposure is from food (ATSDR 2000). Among foodstuffs, the major contributors to the body burden of PCBs are fish, meat, and poultry. It is likely that trace levels of PCBs in commercially available foods have contributed to the body burden of PCBs in the participants. However, for those participants with elevated PCB concentrations, additional sources of PCB exposure are likely. Elevated concentrations of PCBs have been detected in fish from a creek near the plant, which prompted the state to issue a fishing advisory for the waterway. In addition, there are reports that in the past, hogs raised in areas adjacent to the plant were contaminated with high concentrations of PCBs (Grumwald 2002). Therefore, past consumption of locally raised animals and fish from nearby waterways may have been a significant source of PCB exposure. The participants with blood PCB concentrations in excess of 10 ppb share many of the following characteristics: 1. They are older adults, aged 43 years and above. 2. They reported no known occupational exposure to PCBs. 3. They grew up in neighborhoods near the facility and have lived there most of their lives. 4. They ate locally grown fruits and vegetables and locally raised chickens and eggs. 5. They ate fish caught in local rivers and lakes.

In addition, six of the nine individuals reported that in the past they ate clay from the neighborhood. Geophagia, including clay eating, has been reported to be a cultural or social tradition in some Southern societies (Vermeer and Frate 1979; Feldman 1986). Once PCBs get inside the body, they are stored in adipose tissue and are resistant to metabolic degradation. The major PCB congeners detected in the participants of this investigation have long biological half-lives. Therefore, exposures to PCBs that occurred years ago could have contributed to the high body burdens of PCBs seen in some long-term residents of the area. This hypothesis is supported by the absence of elevated blood PCB concentrations in younger residents of the community (Figure 1), as well as by the strong correlations between blood PCB concentrations and age and length of residency in the area. Furthermore, analyses of environmental data (soil and house dust) failed to show a correlation between current environmental concentrations of PCB contamination and blood PCB concentrations. In recent years, the chemical manufacturing company has purchased, remediated, and restricted access to some off-site, PCB-contaminated properties. However, it is likely that prior to remediation, long-term residents of the area had exposure to environmental contamination by direct contact with contaminated soil, sediment, surface water, and air and by indirect contact from eating locally raised animals, plant foodstuffs, and fish. Therefore, past exposure to environmental PCBs may have exceeded current ones and could be responsible for the elevated blood PCB concentrations seen in some older, longterm residents of the community.

Acknowledgments. The authors thank Cheryl Browder of the Alabama Department of Public Health for her assistance in conducting this investigation. The authors also thank the residents of the community for their generous assistance and participation in this investigation.

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