Document rp7ddw163ak6K7yvzx5rRgvEa

NEW SOLUTIONS. Vol. 18(2) 129-143.2008 PiR - y 4 4 ?1<? RECEIVED OP?T CS!C 08 OCT 29 W 9 C 0 7 Scientific Solutions SELF-REPORTED HEALTH EFFECTS AMONG COMMUNITY RESIDENTS EXPOSED TO PERFLUOROOCTANOATE* PAMELA ANDERSON-MAHONEY JENNY KOTLERMAN HARPREET TAKHAR DAVID GRAY JAMES DAHLGREN ABSTRACT Serious health effects chic to perfluorooctanoate (PFOA) exposure are sus pected. The aim o f this study was to evaluate the health status o f nearby residents, with prolonged exposure to PFOA in their drinking water. A population o f 566 white residents who were plaintiffs or potential plaintiffs in a lawsuit was evaluated by questionnaire for health history and sym p toms. Standardized Prevalence Ratios were estimated using National Health and Examination Survey (NHANES) data files for comparison rates. The exposed subjects reported statistically significant greater prevalence o f angina, myocardial infarction, and stroke (SPR = 8.07, 95% C.l. = 6.54 9.95; SPR = 1.9 1.9 5 % C.l. = 1.40 - 2.62, and SPR = 2.17,95% C.l. = 1.47 3 .2 1. respectively), chronic bronchitis, shortness o f breath on stairs, asthma (SPR = 3.60, 95% C.l. = 2.92 - 4.44; SPR = 2.05, 95% C.l. = 1.70 - 2.46; SPR = 1.82, 95% C.l. = |.47 - 2.25. respectively), and other serious health problems. The increased prevalence o f adverse health effects may be due to PFOA. Further study is needed. This study was supported by The Law Finns o f Winter Johnson and Hill PLLC, Law Finn o f Taft. Stettmius and Hollister LLP. Law Finn oT Hitt. Peterson, Carper, Bee and Deitzler. PLLC. The law firms were not involved with data analysis, data interpretation, or writing o f the report. The legal case was settled prior to submission o f this manuscript. The corresponding author had full access to all the data in the study and had final responsibility for the decision to submit for publication. 2008, Baywood Publishing Co.. Inc. doi; 10.2190/NS.18.2.d h ttp://bayw oo d.co m 129 130 / ANOERSON-MAHONEYETAL. Organic fluorinatcd chemicals have been the focus o f scientific and public health debate for some time. Most of the studies on these compounds have perfhiorooctyl sulfonate (PFOS) and perfluorooctanoic acid (PFOA). In addition, PFOS and PFOA are commonly present and persist in the environment [1], PFOA is produced as an emulsifier in the manufacturing process for fluoro polymers [2]. Since the 1980s, there has been a steady increase in the use of fluoropolymers due to their many useful properties [3]. Because o f their specific chemical and physical properties, fluoropolymers are used in electrical insula tion, fire foam, floor polish, insecticides. Teflon, stain-resistant treatments for upholstery, carpet, textiles, and oil-resistant treatments for paper and plastic [4], Several sources o f human exposure have been suggested, including environ mental releases and some consumer products, but due to a dearth o f research, specific pathways responsible for human exposure are not well understood [5]. Potential pathways for human exposure include food, water, leaching from commercial products such as food packaging, contact with products such as clothing, and inhalation of dust or vapor phase precursors coming off o f house hold products such as carpet [6, 7-9,10]. Perfluoroalkylated substances (PFAS) are eliminated slowly from the human body {11J. The biological half-life of PFOA is approximately 4V4 years [12], PFOA is persistent in the environment. It does not hydrolyse, photolyse or biodegrade under environmental conditions f13]. Bioaccumulation [14] and ubiquitous exposure to U.S. citizens heightens concern about adverse health effects [15,16]. Although a number of studies have been conducted to determine the toxicity associated with PFAS, the relative toxicides of the different chemical structures like PFOA and PFOS are not clearly understood. In rodent studies, PFAS cause multiple adverse health effects [ 17]. Endocrine disruption is observed with elevated estrogen and decreased testosterone in animal studies [18, 19], Elevated Thyroid Stimulating Hormone (TSH) and elevated prolactin have been observed in humans [20,21]. Increased liver weight has been documented in rats [22] and in monkeys [23]. Dose-dependent hepatic enzyme elevations have been seen in PFOA-cxposed workers [24] and recently a small sample o f PFOA workers in Trissino, Italy, was found to have slightly increased levels o f non-HDL cholesterol and total cholesterol with increasing blood levels o f PFOA [25]. In addition, a study in January 2005 reported statis tically significant increases in cholesterol fractions (total and LDL) and increases in triglycerides in the highest serum PFOA exposure group [26]. Rat studies have shown liver and pancreatic neoplasms [19]. Studies o f PFOA-exposed workers have shown increased rates of cancer, including prostate [27], kidney [28], bladder [28,29], colon, testes, and other cancer types [28]. This article reports on the results of a cross-sectional comparison study of self-reported health history and symptoms. A separate manuscript reports an increase o f cancer prevalence among this PFOA-exposed population [30], SELF-REPORTED HEALTH EFFECTS / 131 MATERIALS AND METHODS Study Subjects We administered a questionnaire to volunteers from a population o f approxi mately 23,900 households (approximately 70,010 individuals) near a Teflon manufacturing plant located along the Ohio River in Wood County, West Virginia. All o f our study participants were mandatorily included in a law suit, regardless o f their individual choice to be included, because a non-opt-out class action was certified against the local plant on behalf o f all persons whose drinking water was contaminated with PFOA {>0.05 parts per billion (ppb)}. PFAS has been used at this plant since the early 1950s. The plant uses PFAS to manufacture Teflon and other materials and has consistently released perfluoroalkylated substances into the surrounding areas. According to the Environmental Working Group (EWG), in 1999 alone, the plant released more than 40 tons (86,806 pounds) o f PFOA into the air and the Ohio River. The plant reports it reduced emissions to 10 tons (20,168 pounds) in 2002 (EWG). PFOA has been present in the plant's drinking water at 1-5 parts per billion (ppb). PFOA levels above 0.05 parts per billion have also been detected in public and private drinking water supplies in communities on both the Ohio and West Virginia sides o f the Ohio River near the plant, including the water supply o f the neighboring manufacturing plant. Study participants were recruited through a public invitation via TV, radio, and newspaper advertisements inviting all users of the PFOA-contaminated public and private drinking water sources to participate in a study by filling out a questionnaire. Over a period o f three days in August 2003, five hundred and ninety-nine (599) volunteers or 2.5% from the targeted population participated in the study. Most were white. Each person who filled out a questionnaire reported exposure to PFOA-contaminated water for at least a year. They included subjects who used water with PFOA levels as low as 0.05 parts per billion (ppb), such as from Pomeroy, Ohio, and Mason, West Virginia, which is similar to levels measured elsewhere in the greater region. However, the majority (65%) who participated were exposed to water provided by the Lubeck Public Service District in West Virginia where PFOA ranged from 0.4-3.9 ppb and the Little Hocking Water Association in Ohio where PFOA ranged from 1.7-4.3 ppb. Each water district in the area reported PFOA levels including well testing data, and company records have released information on PFOA in the company drinking water (see Table I). Some study subjects worked in the plant where PFAS were used and therefore had both residential and occupational exposures. Data Collection and Questionnaire We collected data on 599 adults exposed to PFOA in their drinking water from a nearby manufacturing plant. Trained and experienced proctors administered 132 / ANDERSON-MAHONEY ET A L Table 1. PFOA Levels by Water District/Source and Percent of Study Subjects Reporting Water Consumption from Each Source PFOA levels3 (PPb) Location Total population6 Study sam ple Households (% total pop) (% study sample) 1.7-4.3 Little Hocking, Ohio 0.4-3.9 Lubeck, WV 0.25-0.37 Tuppers Plains. Ohio 0.08-0.13 Belpre, Ohio 0.06-0.1 Mason, WV 0.06-0.07 Pomeroy, Ohio 0.165 Blennerhassett 1.0-5.0 Dupont, Washington Works0 1.75-1.87 GE Plastics0 0.05-8.6 68 Private Weds WVA &Ohio 4200 3700 4800 6000 4200 1000 71 N/A N/A 68 11.760(17%) 10,360(15%) 13,440 (19%) 16,800 (24%) 11,760(17%) 2,800 (4%) 200 (0%) 2,200 (3%) 700 (1%) 190 (0%) 70,010 161 (27%) 219 (37%) 19 (3%) 45 (8%) 4 (0.7%) 1 (0.2%) 6 (1%) 90(15% ) 43(7% ) 11 (2%) 599 aAII PFOA levels were reported by their respective water dstricts and are available via the Internet. ^Estimated as 2.8 people per household. cCom pany employment reports. Note: N/A not applicable. the questionnaire in groups of 30 to 40 persons or individually by telephone interview. In the group sessions, all subjects were given the same instruction and proctors were available to answer questions. The questionnaire explores demographics, including age, gender, occupa tional and residential history as well as medical, social, and behavioral history. We asked about health symptoms, diseases, surgeries, medications, family history, income, chemical exposures, and lifestyle measures including smoking and drinking. One unlikely symptom question is designed to test for the veracity o f the responses provided. Questionnaire responses are machine-readable, scanned on-site, and verified before subjects leave. This basic questionnaire has been used in prior studies of exposed and unexposed groups [31J. SELF-REPORTED HEALTH EFFECTS / 133 Comparison Databases The Centers for Disease Control and Prevention's (CDC) National Center for Health Statistics (NCHS), Division o f Health Examination Statistics (DHES) has conducted health and nutrition surveys since the early 1960s and is designed to obtain a nationally representative sample of the health and nutritional status o f the U.S. population. Details for each survey in addition to the public use data files are available online (CDC). The most recent National Health and Nutrition Examination Survey (NHANES) began in 2001. Every year, approximately 7,000 civilian, noninstitutionalized U.S. citizens of all ages are interviewed; o f these citizens, approximately 5,000 complete the health examination component o f the survey. NHANES 2001-2002 over-samples low-income persons, adolescents 12-19 years, persons 60+ years of age, African Americans and Mexican Americans. Statistical Methods Frequencies and percents for demographic, social, behavioral and physical characteristics are presented. Standardized Prevalence Ratios (SPRs) for certain disease endpoints were calculated using the NHANES 2001-2002 data files for comparison rates. SPRs are simply observed to expected ratios, (number o f cases in exposed population/total number exposed) divided by (number o f cases in the comparison population/total in the comparison population). A value o f one represents the null or an equal value in both the observed population (survey data) and the expected population (NHANES). Values greater than one indi cate higher prevalence in the observed population compared to expected and values less than one indicated lower prevalence in the observed compared to expected. Statistical significance is demonstrated with either /?-values, confidence limits, or both. Other studies have used the NHANES data files for similar analyses [33]. NHANES data was restricted to non-Hispanic whites 18 and older to be comparable to the exposed population. Only whites were included in the analysis because the number of non-white participants was too small to yield robust results. Rates were calculated for each medical condition using sampling weights developed specifically for the NHANES data source, controlling for age and gender. The sampling weights account for the sampling methods as well as the non-response rates, and they render the data representative of the total U.S. population. The weights also provide for accurate assessment of the sampling error o f statistics based on these survey data [34). Exposed subjects were restricted to those who had lived in the area for a minimum of one year. The health effects of participants who were diagnosed prior to the time o f residence were excluded from the analysis. 134 I ANDERSONM AHONEY ET AL. The 76 subjects who had worked at the Teflon plant were compared to the general population o f the exposed area. They were subsequently included in the exposed group because no worker-exposed differences were found. RESULTS The questionnaire was administered to 599 subjects. Ten o f the subjects were less than 18 years old and 21 were non-white, and two subjects were missing age and were therefore excluded from the analyses. The remaining group o f 566 residentially PFOA-exposed adults are middle aged (49.9 years with a standard deviation (SD) o f 14.43 years), a balanced proportion o f males and females, with slightly more than high school attainment o f education (12.76 years o f school, SD 2.18). The average body mass index is 28.36 kg/ra2with a large SD (+ /- 6.41). Almost half (48.25%) o f the sample can be classified as over-weight (BMI > 28), one-third (33.22%) as average (BMI = 23 - 28), and the remaining (18.53%) as underweight (BMI < 23). Table 2 shows the Standardized Prevalence Ratios (SPRs) comparing the exposed group and NHANES 2001-2002 data while controlling for age and gender. The significantly elevated SPR for cardiovascular problems was 4.29 (95% C.I. = 3.47 - 5.29), and included is that of angina (SPR = 8.07; 95% C.I. = 6.54 - 9.95), myocardial infarction (SPR = 1.91; 95% C.I. = 1.40 - 2.62), and stroke (SPR = 2.17; 95% C.I. 1.47 - 3.21). Respiratory health effects were elevated for chronic bronchitis (SPR = 3.60; 95% C.I. = 2.92 - 4.44) and asthma (SPR 1.82; 95% C.I. = 1.47 - 3.21). The prevalence rate for shortness o f breath was also elevated (SPR = 2.05; 95% C.I. = 1.70 - 2.46). Thyroid prob lems and diabetes were marginally elevated in this PFOA-exposed group (SPR = 1.56; 95% C.I. = 0.22 - 1.98 and SPR = 1.54; 95% C.I. = 1.16 - 2.05, respectively). The overall rate o f liver disease was not significantly elevated. The prevalence of liver problems was 3.4% (18 persons) with liver disease diagnosed by their doctors and 10.6% (59 persons) reporting elevated liver enzymes. Table 3 examines selected outcomes by age and gender. The effect o f exposure appears to be exaggerated in young adulthood for several of the listed outcomes: high blood pressure, cardiovascular problems, and liver problems. By age 65 and over, the effect measure is either at the null (liver, kidney, and thyroid disease in males) or greatly reduced (cardiovascular problems). However, the exposed population (EP)/US ratios for the older population remain high for asthma and chronic bronchitis, and are slightly elevated for high blood pressure, shortness o f breath, and cardiovascular problems. DISCUSSION The U.S. EPA pressured perfluorooctane sulfonic acid (PFOS) off the market in 2000 because o f its persistence in the environment and human body, concerns SELFREPORTED HEALTH EFFECTS / 135 Table 2. Standardized Prevalence Ratio (SPR) Comparing Observed Disease Rate Per 100,000 among a Residentialty PFOA-Exposed Population to the Expected Disease Rate of the General U.S. Population Controlling for Age and Gender Disease of symptom type Cartfiovascutar problems0 Number diseased in exposed Observed rates (per 100.000) Expected rates9 (per 100,000) SPR 170 30.088 7,019 4 .2 9 C fi 3 .4 7 -5 .2 9 * Chronic bronchitis Kidney disease Shortness of breath on stairs 113 21 323 22,114 3.757 57,270 6 .1 4 5 1.665 27.994 3 .6 0 2 .2 6 2 .0 5 2 .9 2 -4 .4 4 * 1 .4 5-3 .5 1 * 1 .7 0-2 .4 6 * A sthm a 105 20,669 11.369 1.82 1 .4 7-2 .2 5 * Thyroid problems 82 15.589 10.019 1.56 1 .2 2-1 .9 8 * D iab etes 56 9.947 6 ,4 5 7 1.54 1.1 6-2 .0 5 * High blood pressure 186 33.096 28,077 1.18 0 .9 7 -1 .4 3 Liver problems 19 3.754 3 .7 2 8 1.01 0 .6 4 -1 .5 9 aExpected rates are from NHANES 2001-2002 using sampling weights to calculate an unbiased estimate of national rates while adjusting for non-response, survey design, and sampling technique while giving an accurate estimate of sampling error. ^Confidence Interval clndudes M l. Stroke. Angina ` Statistically significant (p < 0.05) about its toxicity, and the fact that it is widely found in human populations and wildlife [ 3 ,11 ,14J. A short time later, one main producer, 3M, discontinued the perfluorooctanesulfonyl fluoride chemistry used to manufacture PFOS-based chemicals. Animal studies have confirmed that PFOA and PFOS are toxic [5, 35, 36J and worker studies indicate human health effects [29, 37]. To our knowledge, this is the first study evaluating the health status o f residents living near a Teflon production facility. The reported emissions from the production facility have contaminated the local water supply. Public drinking water delivered to those living near the plant contains more than 0.05 ppb PFOA as reported by the water districts in the area. Neighbors are exposed to much higher than background levels o f PFOA in drinking water and air [37, 38]. A recent study conducted by Edward Table 3. Prevalence Ratios (PR) Comparing Observed Disease Rate per 100,000 among a Residential^ PFOA-Exposed Population to the Expected Disease Rate of the General U.S. Population __________________ by Age Group and Gender for Various Disease Outcomes Age group A sthm a Males Age specific rates (USa) Age specific rates (EP6) Females Age specific rates (US) Age specific EP/US rates (EP)_____males_____ Prevalence ratio EP/US P females 18*34 35-49 50-64 85+ 12543.87 7895.13 9363.58 5694.06 Chronic Bronchitis 37209.30 14705.88 12903.23 19047.62 15209.92 15149.32 13065.51 10790.07 30000 21052.63 21568.63 18181.82 2.97 1.86 1.38 3.35 <0,0001 0.0005 0.002 <0.0001 1.97 1.39 1.65 1.69 18-34 35-49 50-64 65+ 4136.27 4716.72 2870.57 5000.83 High Blood Pressure 23255.81 20000 18750 15000 5867.84 8192.81 8022.41 11843.53 18000 25333.33 27884.62 25000 5.62 4.24 6.53 2.99 <0.0001 <0.0001 <0.0001 0.0006 3.07 3.09 3.48 2.11 18-34 35-49 50*64 65+ 9799.81 18366.59 32115.15 48057.77 22000 21250 37623.76 59090.91 Shortness of Breath Climbing Stairs 7359.86 17218.61 38440.91 60185.45 9090.91 13414.63 50877.19 57142.86 2.24 1.16 1.17 1.23 <0.0001 0.002 <0.0001 <0.0001 1.24 0.78 1.32 0.95 18-34 35-49 50-64 65 + -- 18804,02 33173.62 37010.25 45098.04 44444.44 51960.78 54545.45 32506.66 42327.80 49553.36 58181.62 56790.12 73684.21 71428.57 2.36 1.57 1.47 <0.0001 <0.0001 <0.0001 1.75 1.74 1.44 P <0.0001 0.0003 <0.0001 0.01 < 0.0001 <0.0001 <0.0001 0.0008 0.05 0.10 < 0.0001 0.006 <0.0001 <0.0001 <0.0001 S 8z 5 p 00 Cardiovascular Problems 18-34 35-49 50-64 65+ 647.54 3273.62 8524.01 26458.91 21568.63 28395.06 41176.47 40909.09 746.23 1775.02 7616.51 18080.36 21818.18 21951.22 32456.14 25714.29 33.31 8.67 4.83 1.55 <0.0001 <0.0001 <0.0001 <0.0001 29.24 12.37 4.26 1.42 <0.0001 <0.0001 <0.0001 0.005 Liver 18-34 35-49 50-64 65+ 424.68 6240.89 5221.11 3400.71 2325.58 2898.55 5376.34 2439.02 1696.30 2642.29 3983.46 3026.29 6122.45 4000 3921.57 -- 5.48 0.46 1.03 0.72 0.09 0.63 0.10 0.50 3.61 1.51 0.98 -- 0.009 0.08 0.15 -- Kidney Disease 18-34 35-49 50-64 65+ 342.84 965.12 1497.24 6177,16 2000.00 2500.00 6930.69 4545.45 267.94 2369.68 4083.52 3636.36 1234.57 1785.71 11428.57 5.83 2.59 4,63 0.74 0.08 0.06 <0.0001 0.39 4.61 0.75 2.80 0.10 0.38 0.006 Thyroid Disease 18-34 35-49 50-64 65+ -- 3551.87 4169.26 12164.48 5555.56 7216.49 11904.76 5761.79 10420.19 18424.43 28167.66 13725.49 20512.82 30188.68 32352.94 1.56 1.73 0.98 0.04 0.005 0.11 2.38 1.97 1.64 1.15 0.0008 <0.0001 <0.0001 0.1 'Expected rates are from NHANES 2001-2002 using sampling weights to calculate an unbiased estimate of national rates while adjusting for non-response, survey design, and sampling technique while giving an accurate estimate of sampling error, PFAS-exposed population (EP) MI, Stroke, Angina SELF-REPORTED HEALTH EFFECTS / 137 p to 138 / ANDERSO N-M AHO NEYETAL Emmett at die University o f Pennsylvania among community residents served by Little Hocking Water Association (LHWA) showed high levels o f scram periluonooctanoate [40). Dr. Emmett reported median residential blood levels o f327 ng/ml (interquartile range: 187-572) from a random sample o f 74 residents served by LHWA. Levels were high for all members o f the sampled group including children, adults, and the aged. Occupational exposure was restricted by limiting the study participants to those who had worked one year or less at the nearby chemical plant during the previous 10 years. Even so, the C8 blood levels approached and sometimes overlapped that o f reported worker levels. Dr. Emmett contends that the exposure source is the drinking water and not the air. Twenty-seven percent (27%) o f our study sample obtained their water from LHWA; our remaining subjects were served by other nearby water districts (see Table 1). This questionnaire study of the PFOA-exposed population in the Ohio and West Virginia communities near the plant suggests an increased prevalence o f several serious health problems. The interpretation o f these results depends, however, on several unknown factors. The assumption is that the Parkersburg sample is equivalent to the NHANES sample with regard to all factors that influence the health measures in this study, for example: smoking status, alcohol consumption, and genetic predisposition. If this is the case, the prevalence o f these problems is significantly increased compared to National rates. This study showed an increase in the reported prevalence o f respiratory and cardiovascular problems among the PFOA-exposed subjects. These findings are consistent with previous occupational studies o f exposed workers [25, 28, 41]. In addition, Gilliland found PFOA alteration in high-density lipoproteins (HDL) in a dose-dependent fashion among PFOA-exposed workers [27]. The alteration was observed only in moderate drinkers, and was considered non significant after adjusting for alcohol use, age, BMI, and cigarette use. Olsen reported a positive association between measured serum PFOS and total cholesterol although he claims that the finding is spurious [2]. He also reports a positive association between PFOA and triglycerides, but discounts the finding because it is inconsistent with previous research on rats. Costa reports a slight increase o f total cholesterol in workers exposed, which also showed an increasing trend associated with the highest blood PFOA levels [25], These findings are significant because now both PFOS and PFOA have been associated with an increase in cholesterol. Most recently, another report describes an inverse rela tionship between PFOA and HDL cholesterol coupled with a positive relation ship between PFOA and non-HDL cholesterol [26], These studies suggest a biological mechanism for increased cardiovascular disease in PFAS-exposed populations [25]. The increased prevalence of diabetes in the exposed subjects suggests an interference with insulin function. Studies of monkeys and rats exposed to PFOA revealed increased serum glucose levels [42.43]. SELF-REPORTED HEALTH EFFECTS / 139 Many studies o f PFAS-exposed populations found elevated liver enzymes [6,20,24,27,44,45], although most authors discount their findings. The current study was limited in its ability to evaluate the occurrence o f liver problems in this population. The reason is two-fold: 1. small sample size; and 2. the question asked o f the exposed residents is similar, but not precisely the same as that asked in NHANES. The question asked in NHANES is "Have you ever had liver problems?" and the question asked in the resident's survey was "Have you ever been told by a doctor that you had a liver disease?" Our question was more restrictive than the comparison question, introducing a definite bias toward the null value m alring jt harder to detect an effect. Nevertheless, we still see large prevalence ratios in the youngest age categories for both males and females demonstrating a potential effect o f PFAS exposure on liver function in this population. The limitations o f the data from the residential study include small numbers o f cases o f rare diseases, lack o f a true unexposed comparison group, and potential self-selection bias o f study participants. We reduce the limitation o f the small sample size by analyzing disease outcomes with relatively large numbers in our data se t National statistics estimated using NHANES data address the need for a comparison group, however, it is not possible to control for potential confounding from variables other than age and gender using these data, and some questions like liver problems or diseases were not strictly comparable to one another. Possible selection bias was examined by evaluating the effect o f all cancer prevalence in this group on commonly known and well-understood risk factors: age, gender, smoking status, and educational attainment, which are also reported in a companion paper examining cancer incidence and prevalence in this residential population [30J. The all-cancer rate increased with increasing age, increased smoking, and for those in the lowest category o f educational attainment. If one or more o f these variables behave outside the norm, we would surmise that this data reflected seif-selection bias or reporting bias. However, each category we examined behaved as expected. Furthermore, the diseases and symptoms identified in this analysis parallel those seen in PFAS-exposed workers. Even if there were selection bias with a disproportionate number of patients with various health problems, there is no reason to assume that only patients with certain types o f diseases would be more likely to volunteer for the study. Our study results are consistent with the literature on PFOA and simply support previously reported findings. The plant workers in this study were presumed to have larger exposures compared to those who did not work at the plant. Unexpectedly, we did not see a difference in health status. Although puzzling, we did not dismiss our findings in residents because o f the lack o f differential. Subsequently, we learn from Dr. Emmett's timely study that the residential blood levels in LHWA are 140 / ANDERSONM AHONEY ET AL remarkably similar to those o f workers, 60-80 times higher than expected, given commonly measured background levels of PFAS. Although these blood levels were not measured among our study participants, the measurements did come from residents in the same water district serving 27% o f our participants. We feel this adequately explains the lack of difference between worker and non-worker health effects in this study. Some observers have suggested that plaintiffs in a law suit create an inherent selection bias. The basis for this idea is that the subjects who volunteer to be plaintiffs exaggerate or lie about their symptoms. In addition, a study on the question o f selection bias reports that plaintiffs are not more likely to enhance their symptoms than is a normal population [46]. CONCLUSION In conclusion, living near this Teflon production facility appears to be associated with serious adverse health effects. Additional studies are needed to further delineate the extent and type of health problems associated with PFAS exposure. Such studies are also necessary to define safe levels for these environmental exposures so that governmental agencies can make recommendations and rules to ensure the public's health. The subjects o f this study are still living in the same conditions. The water is still contaminated and the plant still continues to dump tons of PFOA every year into the environment. Our findings indicate that chemical companies should reduce their emissions and discharges, and governmental agencies should ensure the public's health by limiting this exposure. AUTHORS' CONTRIBUTIONS PA and HT assisted in writing the manuscript, JK completed the analysis, DG reviewed drafts o f the manuscript, and JD conceived o f the study, supervised all aspects o f its implementation, and reviewed drafts o f the manuscript. ACKNOWLEDGMENTS We thank Richard Clapp, D.Sc., for comments on an earlier draft o f the manuscript. We wish to also thank Elaine Nitta and Evelyn Alvarez for their help in revising the manuscript. 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