Exposure Investigation Report
(a/k/a SOLUTIA INC./MONSANTO)
ANNISTON, CALHOUN COUNTY, ALABAMA
The Monsanto 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 landfill areas located adjacent to the production facility. Investigations conducted by Monsanto (now Solutia, Inc.) under a Consent Order with the Alabama Department of Environmental Management (1985) documented the presence of PCB contamination in sediment samples from off-site drainage ditches and in soil samples from private residences east and north of the facility. These findings led to the remediation of off-site contaminated areas and property buyouts for some homeowners.
Recent investigations have detected elevated blood levels of PCBs in some residents of the community surrounding the Solutia facility and other neighborhoods in Anniston . The source and exposure pathways by which residents have been exposed to PCBs have not been defined. Furthermore, it is uncertain whether significant exposures are still occurring. To address these questions, the Agency for Toxic Substances and Disease Registry (ATSDR) conducted this Exposure Investigation (EI).
Prior to conducting the EI, staff from ATSDR and the Alabama Department of Public Health (ADPH) met with community representatives to explain the EI and solicit their input. In March 2000, ATSDR met with families who lived within a 1/2-mile radius of the site and invited them to participate in the EI. In order to be eligible for the investigation, at least one family member had to be a child between 1 and 7 years old. ATSDR staff and representatives of the community group, CAP, went door-to-door in the designated neighborhoods to invite eligible families to participate. A total of 18 families fully participated in the EI. Environmental samples were collected from these 18 homes, and biological samples were collected from 78 residents of these homes. In addition, environmental samples, only, were obtained from one home; and biological samples, only, were obtained from two people who lived in the designated area.
ATSDR staff gave the participants an appointment to come to the Calhoun County Health Department where blood samples were collected. A few of the participants were unable to come to the collection center. ATSDR staff traveled to the homes of these individuals to collect the blood samples.
A licensed phlebotomist collected a 7-ml blood sample from each participant using a Vacutainer tube with no anticoagulant. After collection, the blood samples were allowed to clot for 2 hours 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 in Atlanta, Georgia.
Blood serum samples were analyzed for PCB congeners using gas chromatography/mass spectroscopy (GC/MS). 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.
ATSDR staff used a metal trowel to collect a composite 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 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 and total PCBs. The house dust samples were strained through a wire mesh screen to remove food particles, fibers, and other debris prior to analyses. Soil and house dust samples were analyzed for PCB congeners using gas chromatography/mass spectroscopy (GC/MS).
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.
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 analyses were conducted using the lipid-based concentrations of blood serum PCBs.
To interpret the complex PCB congener profiles in the EI participants, ATSDR employed principal components analyses (PCA). The goal of PCA is to linearly transform possibly correlated variables (PCB congeners) into a smaller number of uncorrelated variables called principal components (PC). The PC scores are then plotted to graphically reveal patterns in a complex data set that are not readily seen by visual inspection.
Principal components analyses (PCA) and cluster analyses were carried out using SAS V.8 statistical software . Blood PCB data (lipid-based) were normalized by expressing the concentration of the individual PCB congeners in a sample as a percentage of the combined sum of all PCB congeners. The factor loadings and scores were rotated according to the Varimax rotation to assist in the interpretation of the factors . The cluster analysis was performed using squared Euclidean distances with an average linkage .
The concentration of PCBs was determined in blood serum samples from 37 children (16 years old or less) and 43 adults. In adults, the blood PCB concentrations ranged from non-detected to 210 parts per billion (ppb). The mean concentration in adults was 14.2 ppb, and the median concentration was 2.2 ppb. In children, the blood PCB levels ranged from non-detected to 4.6 ppb. The mean concentration in children was 0.37 ppb, and the median concentration was non-detected.
Among the adults, five people had a blood PCB concentration in excess of 20 ppb; the PCB levels in these five people were: 22, 54, 93, 97, and 210 ppb. These five high values skewed the arithmetic mean of the adult population. If the five individuals with elevated PCB levels are not included in the mean, the average PCB concentration in the rest of the population of 38 adults was 3.5 ppb.
Blood serum concentrations of PCBs were also calculated as a blood lipid concentrations. For adults, the mean blood PCB concentration was 2,537 ng/g lipid , and the median concentration was 392 ng/g lipid. Previous studies have shown that blood concentrations of PCBs can be influenced by the intake of dietary fat . Therefore, blood PCB concentrations are best expressed as a blood lipid concentration so comparisons can be made between individuals and with other studies. However, to date, few published studies have reported PCBs as blood lipid concentrations. In this EI, blood PCB concentrations are reported as µg/L (ppb) and as ng/g lipid.
The concentration of PCBs detected in composite surface soil samples from 19 homes ranged from non-detected to 11.7 ppm. The mean concentration of PCBs in soil was 1.4 ppm, and the median concentration was 0.60 ppm.
The concentration of PCBs detected in house dust samples from 18 homes ranged from non-detected to 10.3 ppm. The mean concentration of PCBs in house dust was 0.81 ppm, and the median concentration was 0.11 ppm.
Indoor surface loading concentrations of PCBs in house dust ranged from non-detected to 2,960 ng/ft2. The mean surface loading concentration was 192 ng/ft2, and the median concentration was 6.6 ng/ft2.
In the United States, no study of PCB blood levels 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 EI. However, several studies have measured PCB levels in populations that had no known exposures to PCBs other than typical background levels. The results from these studies are listed in Tables 1 and 2.
As indicated in Table 1, mean background PCB levels in adults range from 3.7 to 6.8 ppb. The geometric mean and median PCB values calculated from these studies are somewhat lower, since these statistical measures of central tendency reduce the influence of individuals with unusually high PCB levels in the test population.
In comparing the results of these studies, several caveats must be considered. First, different analytical methodologies were used, which could account for some of the variability between studies. Earlier studies used packed column gas chromatography with electron capture detectors; more recent studies have used glass capillary columns with mass spectroscopy to detect individual PCB congeners. In addition, different populations were studied, and background PCB exposures of these populations could vary. In the United States, dietary intake of PCBs is thought to be the major source of exposure . Therefore, regional variations in food consumption patterns could explain some of the variability in the studies. The age of the participants in these studies also varied. Since blood PCB levels increase with age [6,7], some of the variability between studies might be accounted for by the different age distributions of the study populations. Finally, these studies were conducted over the time period, 1982-1995. Since production of PCBs in the United States was halted in 1977, PCB releases to the environment have decreased. This could cause PCB blood concentrations to decrease over time, although this speculation has not been adequately documented.
In spite of these limitations and differences between studies, the results are fairly consistent. These studies suggest that mean PCB levels in blood serum from adults without unusual PCB exposures are 3 to 7 ppb, with lower levels being reported in more recent studies.
The upper end distribution of PCB levels in the general population has not been well characterized. In a review paper, Kreiss estimated that the 95th percentile PCB blood concentration in adults is 20 ppb . Since this estimate was based on studies conducted in the late 1970s and early 1980s, it is likely that the 95th percentile level would be lower today. However, in the absence of a more recent estimate, ATSDR will assume that a blood PCB level in excess of 20 ppb is significantly elevated.
In this EI, five adults had a blood PCB level (22, 54, 93, 97, and 210 ppb) that exceeded 20 ppb. It was noted that the blood serum sample from the individual with 22 ppb PCBs was hyperlipidemic (total lipid = 1,417 mg/dl). Following a heavy fat meal, blood PCB levels can be temporarily elevated by the transient lipidemia . Therefore, the elevated blood PCB level in this individual may have been spuriously elevated by the presence of hyperlipidemia.
If the five individuals with elevated PCB levels are excluded, the mean PCB level in the rest of the adult population is 3.5 ppb, which is within the normal background range. Therefore, these results indicate that PCB exposures for most of the adult EI population were within the normal background range.
Blood concentrations of PCBs were also calculated as a blood lipid concentration. For adults, the mean blood concentration was 2,537 ng/g lipid, and the median concentration was 392 ng/g lipid. The large difference in these values indicates that the mean value is skewed by the inclusion of the elevated individuals. If the five highest concentrations are not included, the mean PCB concentration in the rest of the adult population is 544 ng/g lipid.
There are few studies in the published scientific literature that have reported blood concentrations of PCBs on a lipid-adjusted basis, so only limited comparisons can be made between the EI participants and other populations with background exposures. In a study of non-fasting adults, a mean blood serum PCB concentration of 666 ng/g lipid was reported . In another study of Canadian adults, the median blood plasma PCB concentration (50th percentile) was reported to be 263 ng/g lipid . However this value is likely to be less than the actual PCB total, since only 15 PCB congeners were included in the total, and the blood samples had been diluted 10-15 percent by a citrate anticoagulant. Therefore, based on these limited studies, the lipid-based PCB concentrations in most of the EI participants were comparable to those reported in other normal populations.
Relatively few studies have measured PCB levels in children. However, based on two published studies (Table 2), PCB levels in blood serum from children are about 2 to 4 ppb, which is less than for adults. In the EI population , the average blood PCB level in children was 0.37 ppb, and the median value was 0. These levels are less than the values cited in the reference studies.
Only 10 of 37 children tested in the EI had a detectable PCB level in their blood serum. The highest blood level 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, all of the PCB concentrations detected in children from the EI were within the ranges detected in the reference studies for children (Table 2). ATSDR concludes that none of the children tested in the EI had a significantly elevated blood PCB level.
Because PCBs are resistant to metabolism in the body, they bioaccumulate as a person ages. Therefore, blood PCB levels tend to increase with age. In Figure 1, the blood PCB levels in the EI participants are plotted as a function of age. As indicated, all of the people with elevated blood PCB levels (> 20 ppb) are aged 45 or older. In people below the age of 40, none of the PCB concentrations exceeded 8.2 ppb. The absence of elevated PCB levels in people below 45 years old suggests that PCB exposures in the past may have exceeded more recent exposures.
To assess the relationships between blood PCB levels, age, and length of residency in the vicinity of the manufacturing plant, Spearman rank correlation coefficients were calculated. Age was strongly correlated with the blood PCB level (rs = 0.729, p < 0.001). Length of residency was also correlated with the blood PCB level (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 level and length of residency in the vicinity of the Solutia facility (rs = 0.310, p = 0.0054). This suggests that people were exposed to PCBs while living at their current residences, although it is not known when the exposures occurred or what the source of PCBs was.
PCB Congener Analyses
There are 209 possible congeners of PCBs, which differ in the number and position of the chlorine atoms on the biphenyl ring structure. The congeners that contributed most to the total blood concentration of PCBs in most of the EI participants were PCB congeners 153, 138/158, 180, 187, and 118 (IUPAC designation). In general, these congeners accounted for more than 50 percent of the total PCBs in individuals with elevated or normal PCB levels.
Several studies have reported that these same congeners are the major ones detected in blood, breast milk, and adipose tissue samples from other human populations [10, 11]. The presence of relatively high concentrations of these congeners in humans is likely related to several factors: (1) they are major constituents of commercial PCB mixtures (e.g., Aroclor 1260), (2) they bioconcentrate in animal food chains, and (3) they resist metabolic degradation.
To interpret the PCB congener profiles in the EI participants, ATSDR employed principal components analyses (PCA) [see description in Methods section]. As shown in Figure 2, most of the children were in Cluster A, and most of the adults were in Cluster B. In general, the blood samples from children in Cluster A contained the major PCB congeners discussed above, but they lacked other, minor PCB congeners that were detected in individuals in Cluster B. In addition, the children generally had lower total PCB levels.
All of the adults with elevated blood PCB levels grouped in Cluster B, along with other adults with normal PCB levels. This indicates that the PCB profiles in adults with normal or elevated PCB levels were similar; they differed only in the total concentration of PCBs.
Two of the EI participants (A* and C*) had distinctly different PCB profiles. These two individuals were teenagers who lived in different homes. Blood samples from both of these individuals contained several lower chlorinated PCB congeners. Lower chlorinated congeners tend to be more susceptible to metabolic degradation; hence, they have shorter biological half-lives. In particular, PCB congeners 52 and 44, which lack chlorine atoms on the meta and para position of the biphenyl ring, are especially susceptible to metabolic degradation . Therefore, the presence of these congeners in human blood serum suggest relatively recent exposure. Nevertheless, the total concentrations of PCBs in blood samples from these individuals (0.66 and 4.6 ppb) were within the normal range.
The blood levels of PCBs that cause adverse health effects have not been well characterized. In occupational studies, exposures to PCBs have been associated with chloracne and subtle evidence of liver damage, although it is possible that polychlorinated dibenzofuran impurities in the PCBs might have contributed to the toxicity [13, 14]. Slight elevations in serum enzymes of hepatic origin, such as gamma-glutamyl transferase, have been reported in workers with blood serum PCB levels of several hundreds of parts per billion . However, in occupational studies, it is difficult to unequivocally attribute the observed health effects to PCBs because of the possible confounding effect of concurrent exposure to other chemicals. Nevertheless, based on one such study, a blood PCB level of 200 ppb was suggested as a no effect level .
Based on this criterion, only one of the EI participants had a blood PCB level that exceeded this level of concern. However, it should be recognized that occupational studies have examined only a limited number of health endpoints and have limited statistical power to detect an effect. Therefore, no firm conclusions can be drawn regarding a safe blood level for PCBs in adults.
Several studies have reported that low level PCB exposure during fetal or neonatal development can effect the infant's neurobehavioral development [15, 16]. However, several limitations of these studies have been noted: (1) possible exposure to other neurotoxic chemicals besides PCBs (e.g., dioxins, mercury, lead, or organochlorine pesticides) that may have contributed to the effects, (2) inadequate control for confounding socioeconomic variables such as maternal smoking, alcohol, and other drug use, and (3) inadequate control for maternal birth weight and nonspontaneous deliveries [17, 18]. In addition to these methodological limitations, different studies have measured different neurobehavioral endpoints, which impedes comparisons between studies.
Therefore, these studies suggest, but do not conclusively prove, an association between prenatal or neonatal exposures to PCBs and neurobehavioral and developmental effects in young children. Furthermore, these purported effects were reported to occur in populations with background exposures to PCBs, so a threshold effect level has not been defined. Because of these limitations, it cannot be determined whether the low level PCB exposures detected in the EI participants could affect neonatal development. Nevertheless, to minimize any potential health risks, it is prudent public health policy to reduce exposure to environmental PCB contamination.
The concentration of PCBs detected in composite surface soil samples from 19 homes ranged from non-detected to 11.7 ppm. Soil samples from four homes contained PCB concentrations in excess of 1 ppm (11.7, 5.14, 1.31, and 1.20 ppm).
At Superfund sites, the U. S. Environmental Protection Agency (EPA) has set a Recommended Soil Action Level - Analytical Starting Point of 1 ppm PCBs for residential properties . Higher action levels may be set if warranted by site-specific conditions.
The concentration of PCBs detected in house dust samples from 18 homes ranged from non-detected to 10.3 ppm. House dust samples from two homes contained PCB concentrations in excess of 1 ppm (10.3 and 1.71 ppm). The EPA has not established an action level for PCBs in house dust.
By calculating the Spearman rank correlation coefficient, ATSDR was able to show that 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 finding was expected since soil constitutes about 50 percent of the mass of house dust .
Statistical analyses failed to demonstrate a significant correlation between blood PCB levels 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 (ng/ft2) concentration (rs = 0.046, p = 0.70). Further analyses in which the EI population was divided into adults and children also failed to demonstrate any significant correlations between blood and environmental PCB levels. The absence of a correlation between blood PCB levels and soil or house dust PCB levels suggests that residents have been exposed to other sources of PCBs besides those in soil and house dust.
Characterization of PCB Exposures
In the general population, the major background source of PCB exposure is from food . 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 comercially-available foods have contributed to the body burden of PCBs in the EI participants. However, for those EI participants with elevated PCB levels, additional sources of PCB exposure are likely.
The EI participants with elevated blood PCB levels share several characteristics: (1) They are older adults, aged 45 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. In addition, three of the five individuals with elevated blood PCB levels reported eating clay that they collected in the neighborhood.
In recent years, the potentially responsible party 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, water, and air, and by indirect contact from eating locally-raised animal or plant foodstuffs.
Once PCBs get inside the body, they are resistant to metabolic degradation and are stored in adipose tissue for long periods of time. The biological half-life of PCB congeners vary, but for PCB mixtures, a collective half-life of 2 to 6 years has been estimated . Therefore, the high body burdens of PCBs seen in some long-term residents may be the result of exposures that occurred years ago. This conclusion is supported by the absence of elevated blood PCB levels in younger residents of the community (Figure 1), as well as by the strong correlation between blood PCB level and length of residency.
Therefore, the available evidence suggests that past exposures to environmental PCB contamination exceeded current exposures. Nevertheless, this study and others conducted by the EPA have documented that elevated levels of PCBs remain in off-site soils and sediments. Since the future use of these areas cannot be predicted, they should be remediated to prevent further human exposure to environmental contamination.
- Five of 43 adults had an elevated blood PCB level (> 20 ppb).
- Blood PCB levels in 37 children were not elevated.
- Blood PCB levels were correlated with age and length of residency near the Solutia facility. Available evidence suggests that PCB exposures in the past may have exceeded more recent exposures.
- PCB concentrations in excess of 1 ppm were detected in surface soil samples from four homes and in house dust samples from two homes.
- Blood PCB levels were not correlated with soil or house dust PCB levels.
- Homes with PCB contamination in soil in excess of EPA action levels should be evaluated for possible remediation.
- Residents should minimize further exposure to areas of known PCB contamination.
Kenneth G. Orloff, Ph.D., DABT
Exposure Investigations and Consultations Branch
Division of Health Assessment and Consultation
Susan Metcalf, MD
Exposure Investigations and Consultations Branch
Division of Health Assessment and Consultation
John E. Abraham, PhD
Exposure Investigations and Consultations Branch
Division of Health Assessment and Consultation
- R. Canady, Agency for Toxic Substances and Disease Registry, Draft Health Consultation; Evaluation of Soil, Blood, and Air Data from Anniston, Alabama; February 14, 2000.
- A. C. Rencher; Methods of Multivariate Analysis; John Wiley and Sons, Inc.; New York 1995.
- R. R. Sokal and C. D. Michner; A Statistical Method for Evaluating Systematic Relationships; University of Kansas Science Bulletin 38 1409-1438 (1958).
- DL Phillips et al; Chlorinated hydrocarbon levels in human serum: effects of fasting and feeding; Arch. Environ. Contam. Toxicol. 18 495-500 (1989).
- Agency for Toxic Substances and Disease Registry; Toxicological Profile for Polychlorinated Bihenyls (update); Draft for Public Comment; December 1998.
- DT Miller et al; Human exposure to polychlorinated biphenyls in greater New Bedford, Massachusetts: A prevalence study; Arch. Environ. Contam. Toxicol. 20 410-416 (1991).
- SL Gerstenberger et al; concentrations of blood and hair mercury and serum PCBs in an Ojibwa population that consumes Great Lakes region fish; Clinical Toxicol. 35 377-386 (1997).
- Kathleen Kreiss; Studies on populations exposed to polychlorinated biphenyls; Env. Health Perspec. 60 193-199 (1985).
- MP Longnecker et al; Correlations among human plasma levels of dioxin-like compounds and polychlorinated biphenyls (PCBs) and implications for epidemiologic studies; Arch. Env. Health 55 195-200 (2000).
- Larry G. Hansen; Stepping backward to improve assessment of PCB congener toxicities; Env. Health Perspec. 106 171-189 (1998).
- H Humphrey et al; PCB congener profile in the serum of humans consuming Great Lakes fish; Env. Health Perspec. 108 167-172 (2000).
- JF Brown; Determination of PCB metabolic, excretion, and accumulation rates for use as indicators of biological response and relative risk; Environ. Sci. Technol. 28 2295-2305 (1994).
- H Ouw et al; Use and health effects of Aroclor 1242, a polychlorinated biphenyl, in an electrical industry; Archives Environ. Health 31 189-194 (1976).
- A. Fischbein et al; Dermatological findings in capacitor manufacturing workers exposed to dielectric fluids containing polychlorinated biphenyls (PCBs); 37 69-74 (1982).
- JL Jacobson et al; Effects of in utero exposure to polychlorinated biphenyls and related contaminants on cognitive function in young children; J. Pediatrics 116 38-45 (1990).
- WJ Rogan and BC Gladen; Study of human lactation for effects of environmental contaminants: the North Carolina breast milk and formula project and some other ideas; Environ Health Perspect. 60 215-221 (1985).
- SL Schantz; Developmental neurotoxicity of PCBs in humans: What do we know and where do we go from here? Neurotox. Teratology 18 217-227 (1996).
- RF Segal; Epidemiological and laboratory evidence of PCB-induced neurotoxicity; 26 709-737 (1996).
- U.S. Environmental Protection Agency, Solid Waste and Emergency Response; A Guide on Remedial Actions at Superfund Sites With PCB Contamination; Directive 9355.4-01 FS; August 1990.
- DJ Paustenbach, BL Finley, and TF Long; The critical role of house dust in understanding the hazards posed by contaminated soils; Int J Toxicol; 16 339-362 (1997).
- JH Shirai and JC Kissel; Uncertainty in estimated half-lives of PCBs in humans: impact on exposure assessment; Science of the Total Environment 187 199-210 (1996).
- JD Sahl et al; Polychlorinated biphenyls in the blood of personnel from an electric utility; J Occup Med 27 639-643 (1985).
- MS Wolf et al; Blood levels of organochlorine residues and risk of breast cancer; J Nat Cancer Inst 85 648-652 (1993).
- ME Hovinga et al; Historical changes in serum PCB and DDT levels in an environmentally -exposed cohort; Arch Environ Contam Toxicol 22 362-366 (1992).
- DJ Hunter et al; Plasma organochlorine levels and the risk of breast cancer; New Eng J Med; 337 1253-1258 (1997).
- HEB Humphrey et al; PCB congener profile in the serum of humans consuming great lakes fish; Environ Health Perspec 108 167-172 (2000).
- LP Hanrahan et al; Serum PCB and DDE levels of frequent Great Lakes sport fish consumers - A first look; Environ Research Section A 80 S26-S37 (1999).
- JL Jacobson et al; Effects of exposure to PCBs and related compounds on growth and activity in children; Neurotoxicology and Teratology 12 319-326 (1990).
- A Schecter et al; Polychlorinated biphenyl levels in the tissues of exposed and nonexposed humans; Environ Health Perspect 102 Suppl 1: 149-158 (1994).
Date of testing
|5||4||738||1982-1984||California||pre-employment screening||Sahl et al |
|5.8||3.9||840||1985-1986||Massachusetts||random sample - New Bedford, MA||Miller et al |
|6.7||-||171||1985-1991||New York City||breast cancer controls||Wolff et al |
|6.8||-||90||1989||Michigan||controls for fish eaters||Hovinga et al |
|5.16||4.68||230||1989-1990||US||women - median age of 59||Hunter et al |
|4.56||-||78||1993-1995||Michigan||>= 50 years old||Humphrey et al |
|(geometric mean-males)||1.5||57||1994-1995||Great Lakes||infrequent fish eaters||Hanrahan et al |
|(geometric mean - females)||.9||42|
|3.7||-||66||1997||Great Lakes||Ojibwa Indians||Gerstenberger et al |
Date of testing
|2.1||0-23.3||285||4-5||1984-1985||Michigan||Jacobson et al |
|4.3||-||11||-||1984||US||Schecter et al |
Figures 1 and 2 were not available in electronic format for conversion to HTML at the time of the preparation of this document. To obtain a hard copy of these figures, please contact:
Agency for Toxic Substances and Disease Registry
Division of Health Assessment and Consultation
Attn: Chief, Program Evaluation, Records, and Information Services Branch E-56
1600 Clifton Road NE, Atlanta, Georgia 30333