Document byKLe69qrZNgkaGXqpRL8XNZO

P-1 "McCrea, Deborah" <mccrea@taftlaw.com> 03/15/2010 02:08 PM To NCIC OPPT@EPA cc "Bilott, Robert A." < bilott@taftlaw.com> bcc Subject 03/15/2010 Letter To EPA Docket Center Taft / Deborah McCrea / Legal Assistant Taft Stettinius & Hollister LLP 425 Walnut Street, Suite 1800 Cincinnati, Ohio 45202-3957 Tel: 513.381.2838 Fax: 513.381.0205 www.taftlaw.com / mccrea@taftlaw.com Internal Revenue Service Circular 230 Disclosure: As provided for in Treasury regulations, advice (if any) relating to federal taxes that is contained in this communication (including attachments) is not intended or written to be used, and cannot be used, for the purpose of (1) avoiding penalties under the Internal Revenue Code or (2) promoting, marketing or recommending to another party any transaction or matter addressed herein. This message may contain information that is attorney-client privileged, attorney work product or otherwise confidential. If you are not an intended recipient, use and disclosure of this message are prohibited. If you received this transmission in error, please notify the sender by reply e-mail and delete the message and any attachments. CONTAINS NO CBI 3 5 5 hM \n v ^ P-2 Taft Stettinius & Hollister LLP 425 W alnut Street. Suite 1800 / Cincinnati, OH 45202.-3957 /Tel: 513.381.2838 / Fax: 513.381.0205 / www.taftlaw.com Cincinnati / Cleveland / Columbus / Dayton 1Indianapolis / Northern Kentucky / Phoenix I Beijing Robert A. Bilott 513-357-9638 bilott@taftlaw.com March 15,2010 FEDERAL EXPRESS EPA Docket Center, MC 2822T U.S. Environmental Protection Agency EPA West, Room 3334 1301 Constitution Avenue, NW Washington, D.C. 20004 o 7* : ___ .i * tr'? S Re: Submission to IRIS and AR-226 Database For PFOA/PFOS: EPA-HQORD-2003-0016 To IRIS Database for PFOA/PFOS: In letters dated April 21,2004, June 2, 2004, January 7, 2005, and February 7, 2005, we submitted to USEPA preliminary data that had been made public during scientific seminars relating to a study of residents and workers exposed to PFOA. (Extra copies enclosed.) In our February 7, 2005, letter on this topic, we noted that an "article explaining the study and the cancer results in more detail has been peerreviewed and accepted for publication" and that the article "is expected to be published" during the summer of 2005. As five years have now passed since that letter and the final article has not been made available in published, peer-reviewed literature, we felt it appropriate to clarify the record on the status of that article. As indicated in our prior submissions, an article addressing the cancer results was peer-reviewed and accepted for publication in 2004. More specifically, the Archives of Environmental Health confirmed acceptance of the article for publication (following peer review) in October 2004 and confirmed in December of 2004 that the article was in-press and scheduled to appear in the sixth of the next six issues of that Journal. Following a seminar in October 2005 during which one of the article's authors revealed which journal was publishing the article, a new Editor was appointed for the Journal and the article was removed from the on-going publication process. Thus, the article was not published, as anticipated. ' 11705411.1 CONTAINS NO CBI P-4 March 15, 2010 Page 2 Although we recognize that, since submission of the article for publication, an independent Science Panel was created, which will be studying in more depth (among other things) cancer among many of these same residents and workers exposed to PFOA, we wanted to make sure the public record was complete as to the scientific basis for the preliminary data and results included with our prior letters referenced above. We are, therefore, attaching a copy of the final, peer-reviewed version of the article that had been approved for publication and was in-press in 2005 from which that preliminary data was derived. We have been informed by the lead author of this article that there is no longer any claim of confidentiality over the document. Robert A. Bilott RAB:mdm Enclosures cc: Gloria Post (NJDEP)(w/ end.) (via U.S. Mail) Helen Goeden (MDH)(w/ end.) (via U.S. Mail) Lora Werner (ATSDR)(w/ end.) (via U.S. Mail) <W1405808.1} P-5 ARCHIVES OF ENVIRONMENTAL HEALTH Bldg A7, #7401 1000 S. Fremont Ave/Unit #2 Alhambra, CA. 91803 AN INTERNA TIONAL JOURNAL Kaye H. Kilbum, Editor-in-Chief Tel: 626 457 4202 Fax: 626 457 4203 Email: Kilbum@usc.edu October 8, 2004 James G. Dahlgren MD 2811 Wilshire Blvd. #510 Santa Monica, C 90403 Dear Jim, The paper is now acceptable with your approval of the editorial changes that were made to simplify sentences and clarify meanings. Please go through these carefully and be sure they are all correct. Change then if necessary. Also, please make other changes you wish as you consider these. Then two copies and the corrected disk should be forwarded to me. Sincerely, Kaye H. Kilbum MD Editor-in-Chief, Archives o f Environmental Health P-6 PREVALENCE AND INCIDENCE OF CANCER IN POPULATIONS EXPOSED TO PERFLUOROOCTANOATE (PFOA) James Dahlgren MDl, Pamela Anderson-Mahoney PhD2, Jenny Kotlerman MS3, Harpreet Takhar MPH4, Alex Lee4,Toby Robinson4, Marilyn Zwass MD4, Ayman Ibrahim MD1'4, Raphael Warshaw4 1. UCLA School o f Medicine 2. Health Research Association 3. UCLA School of Public Health 4. Comprehensive Health Screening Services Please address correspondence to: James Dahlgren, MD 2811 Wilshire Blvd. Santa Monica, CA 90403 Voice: 310-449-5525 e x t 226 FAX: 310-449-5526 dahlgren@envirotoxicologv.com Page 1 o f 38 P-7 Short Title: CANCER PREVALENCE AND INCIDENCE GIVEN PFOA EXPOSURE Page 2 o f 38 p.8 Abstract: PFOA is a bio-persistent man-made chemical that is widely used and widely spread in the environment. Previous worker studies have suggested increased rates o f prostate, kidney, bladder and other cancers. This study examines the cancer prevalence rates in a cross-sectional sample o f residentially PFOA-exposed adults (578 subjects). There were 50/578 (8.65 %) cancers other than skin cancer in this population compared to 3.43% expected using age-adjusted US population prevalence rates for Whites. The all cancer age-standardized prevalence morbidity rate ratio (PR) ranged from small or none in the highest age categories and increased in each decreasing age category for both genders with the exception of 30 - 44 year old males where there were no reported cancers in the study population. Statistically significantly increased PRs for all cancer (2.58), uterine/cervical (33.12), multiple myeloma (15.71), lung (7.89), nonHodgkin's lymphoma (6.67) and bladder (5.30) were found comparing the residentially PFOA- exposed population to national figures. Increased rates o f colon/rectal and prostate cancer was also suggested with a PR o f 2.65; Cl = 0.99; 7.11) and 1.96; Cl = (0.98; 3.92), respectively. Cancer incidence from an occupationally exposed population o f 3394 adults is also considered; and the test for trend o f increasing cancer with increasing exposure time was statistically significant with p-values all less than 0.05 (bladder, kidney and prostate). PFOA appears to increase cancer in humans. Key words*, perfluoroalkanes, C8, PFOA, cancer, environmental, questionnaire, incidence, prevalence Page 3 o f 38 P-9 Introduction: Perfluorooctanoic acid (PFOA or C8) is a man-made chemical with numerous industrial and consumer uses. Many stain resistant treatments o f upholstery, carpet and textiles release PFOA into the environment.1Although PFOA is not an intended component o f these treatments; fluorotelomer-based products like these degrade to PFOA and similar compounds. Fluorocarbon chemicals are also used in paper and plastic oil-resistant treatments, as well as in electrical insulation, fire foam, floor polish, insecticides and Teflon.2 PFOA does not readily degrade in the environment3,4 but instead accumulates in air, soil and water.5,6 Potential pathways for human exposure include food, water and leaching from commercial products such as food packaging, contact with products such as clothing, and inhalation o f dust or vapor phase precursors coming off o f household products, such as carpet.79,10,11 PFOA is slowly eliminated from the human body.11 Bioaccumulation heightens concern about adverse health effects. In rodent studies PFOA and related compounds cause multiple adverse health effects,12 including neoplasms o f the liver, testes, pancreas, and mammary glands.13 In humans PFOA increases cancer rates.14 Human epidemiological studies of PFOA exposed workers have reported statistically significant elevations in prevalence o f cancer in the prostate,15 kidney,16 bladder,16,17colon,16testes,16and other cancer types.16Also there have been excesses of lymphoma, multiple myeloma, breast cancer and melanoma reported.18 Page 4 o f 38 We report the cancer prevalence o f a largely White residentially PFOA-exposed population using a self-administered questionnaire and compare that to the cancer prevalence in the U.S. population o f Whites. Incidence data from an occupationally exposed population followed for over 50 years is also presented. Methods Residential data We administered a questionnaire to volunteers from a population o f approximately 23,900 households near a manufacturing plant located along the Ohio River in Wood County West Virginia (Table 1). PFOA has been used at this plant since the early 1950s. The Plant uses PFOA to manufacture Teflon and other materials and has consistently released the substance in the local surrounding areas. According to the Environmental Working Group (EWG), in 1999 alone, the Plant released over 40 tons (86,806 pounds) o f PFOA into the air and the Ohio River.19 EWG also reports that the Plant reports it has reduced emissions to 10 tons (20,168 pounds) in 2002.19PFOA has been present in the Plant's drinking water at 1-5 parts per billion (ppb) (Figure 1). PFOA levels above 0.05 ppb 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 of a neighboring manufacturing plant (Figure 1). Study participants were recruited through public invitation via TV, radio, and newspaper advertisements inviting all users of the PFOA-contaminated public and private drinking water to participate in a study by filling out a questionnaire. Over a period o f three days in August of Page 5 o f 38 2003, five hundred and ninety-nine (599) volunteers (2.5%) from the targeted population participated in die study. Each person who filled out a questionnaire reported exposure to PFOAcontaminated water for at least a year. Although this could include subjects who used water with PFOA levels as low as 0.05 ppb, die 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 (Table 1). Some study subjects worked in the Plant where PFOA was used and had residential and occupational exposures. All participants between the ages o f 20 and 80 years o f age are included in this analysis. Cancer and U.S. population statistics are available in 5-year categories, with the "adult" category beginning at age 20. Only 4 persons older than 80 were surveyed. For these reasons, we restrict all analyses to those between the ages o f 20 and 80. Because a mandatory non-opt-out class action was certified against the Plant on behalf o f all persons whose drinking water was contaminated with PFOA (>0.05 ppb), all of our study participants were mandatorily included in a law suit regardless o f their individual choice to be included. A sample question from the health questionnaire is set forth in Figure 1. Questionnaire responses were machine-readable,20 scanned on-site and verified before the subjects left the test site. All subjects who reported cancer were contacted through a follow-up phone conversation to Page 6 o f 38 verify the cancer information. Medical record confirmation is underway but not yet completed. Occupational data We also report on the incidence o f cancer mortality among a historical cohort o f workers at the Plant. The occupationally PFOA-exposed cancer data were obtained through discovery in the above-mentioned litigation. These data are publicly available through the Environmental Protection Agency.16 Cancer mortality is reported from 1959 through June 2003 among the cohort. Many o f the older persons included did not have vital status data even though they would be well into their hundreds (years old). For this reason, we only include persons hired between 1950 and 1990 m our analyses. This maximizes the potential that, for those included in the analysis, some attempt was made to document their disease experience. Even in this restricted cohort, there are many subjects for whom no outcome data is recorded even though their current age if still living would be well over 100. We retain these subjects in our analysis with the understanding that the lack o f follow-up data will result in measures o f effect biased toward the null. This provides the reader with the most conservative measures o f effect. While working, all Plant employees had access to the same PFOA-contaminated drinking water, however, workers in the chemical division were frequently exposed to higher PFOA air levels while others at the plant were not.21 For this reason, we compared the cancer incidence of those working in the chemical division to those working in another manufacturing department where Page 7 o f 38 there was no direct work with PFOA performed. We also repeated the dose-response analysis including all workers hired between 1950 and 1990 who worked at the company for at least 6 months. The results from the restricted cohort were more conservative and are, therefore, presented in this paper. Statistical Methods: Residential data Frequencies and percents for demographic, social, behavioral and physical characteristics are presented. For analyses where all cancers are grouped together, we counted only thefirst prim ary malignancy reported. For analyses where cancer types are reported separately, we included all prim ary malignancies. Unadjusted odds ratios (OR) and confidence intervals were estimated using logistic regression for each variable using primary cancer other than skin as the outcome variable: (cancer: yes/no). Test for trends were estimated for all ordinal variables with greater than two categories. Epidemiological cancer morbidity prevalence rates for the U.S. population o f Whites were obtained from the SEER 2000 website.18 SEER data provides an estimate o f overall cancer prevalence and incidence o f all types o f cancer, other than skin cancer (except melanoma), by type, age and gender. Cancers represented in the SEER data are classified according to their primary site or origin regardless o f where in the body they may eventually spread. For example, a lung cancer that spreads to the lymph nodes is still classified as lung cancer and not as a Page 8 o f 38 lymphoma (cancer o f the lymph nodes). The SEER Registries routinely collect data on cancer , patient demographics, primary tumor site, and follow-up for survival status. We calculated internally standardized morbidity prevalence ratios (PR) for all cancers.22 These rates were compared with the rates in the U.S. population o f Whites using the age distribution in the exposed population.23'24 Similar estimates are constructed for each cancer type comparing the exposed population to the U.S. population. The internal standardization takes into consideration the differences in the age distribution between the exposed study population and the comparison population (in this case, the US population of Whites) where we derive our expected number of cancers. In effect, this measure is the number o f cases that actually occurred in the exposed population (standard) divided by the number o f cases that would have occurred in the absence o f exposure. The latter number is estimated by assuming that the exposed group would have experienced, in the absence o f exposure, the same stratum-specific risks experienced by the unexposed group. Occupational data Frequencies and percents for demographic and work characteristics are presented. For cancerspecific and all cancers analyses, we included all primary malignancies. Proportional hazards models for selected cancers were used to compare survival times between workers directly using PFOA compared to those who did not directly work with PFOA. Hazard ratios, confidence intervals and p-values are presented. Page 9 o f 38 PFOA dose-response relationships were assessed for each cancer type using logistic regression to adjust for age at hire while estimating odds ratios for increased rate of cancer comparing those who worked less than 21 years with those who worked between 2 1 - 2 9 years and those who worked greater than 29 years at the company. Test for trend is reported. The "years o f exposure" variable was calculated by counting the years between hire date and cancer date, if cancer happened before termination. If cancer was after termination, we added years from date of hire to date of termination. If the person had no date o f termination, but has a date o f death, we add the years between date o f hire and date o f death. If date o f termination is not missing and there is no cancer, we add from date o f hire to date of termination. If there is no date o f death and no date o f termination we add from date o f hire to July 1, 2003, the last documented date for follow-up in this cohort. All statistical analysis was performed using SAS 8.0.25 Results Residential data The questionnaire was administered to 599 subjects. Fifteen (15) o f the subjects were less than 20 years old and 4 were greater than 80, two (2) subjects were missing age and were therefore excluded from the analyses. O f the 578 subjects between the ages o f 20 and 80, 77 subjects answered yes to the question "Have you ever been told by a doctor that you have cancer?" One o f the 77 respondent's cancer diagnosis was not present on medical record verification. O f the Page 10 o f 38 p. 16 remaining 76 subjects, 4 1 reported one primary malignant cancer other than non-melanoma skin cancer, 8 individuals reported two primary malignancies that included at least one primary malignancy other than non-melanoma skin cancer, one person reported 3 malignancies that included one primary malignancy other than non-melanoma skin cancer and 23 reported skin cancer only. Four primary malignancies were diagnosed prior to reported exposure and were therefore excluded from the numerator and included in the denominator. In total, there were 50 primary malignancies other than skin cancer in the residentially PFOA-exposed population for an all cancer prevalence rate of 50/578 or 8.65 % compared to 3.43 % that were expected to occur in this residential population had they experienced the same age- and gender-specific rates as in the U.S. population o f Whites. Each subject's cancer status was confirmed with the respondent by telephone. Medical record confirmation o f the 50 primary malignancies other than skin reports is in progress. To date, 26 (52%) requested medical records have been obtained, all confirmed the self-reported cancer diagnosis for primary malignancies other than skin. Table 1 shows the water source distribution o f the cross-sectional study population compared to the total population in the area. A greater percentage o f study subjects consumed water from Little Hocking and Lubeck compared to the total population in the area. Those who consumed water from either or both of the two plants in the area also appear to be over-represented, however, the number o f workers in the table represents current workers and the number o f study participants is computed by counting all the participants who responded that they had ever Page 11 o f 38 consumed water from either o f the plants so this may be a fair representation o f the proportion of people who have ever worked at one o f the plants in the area. Table 2 presents the demographic, social, behavioral and physical characteristics o f the exposed population. The age distribution was about equal in one 15-year and three 10-year categories ranging from age 20 to 64. Fewer participants contributed to the oldest age category. The average age o f the PFOA-exposed residents was 49 +/-14.5 years. Gender was evenly split and nearly all o f the participants were White. The majority o f participants were high school graduates or had some college or vocational school. Nearly half o f the study sample was overweight with a body mass index greater than 28 meters per kilograms squared. Sixty (60) percent o f the sample never smoked and roughly 20 percent were represented in each o f the two smoker categories: less than 15 years, greater than 15 years. Ten percent (10%) worked at plant 1 at some point in their life. Table 3 presents the number and percent o f all cancers in each demographic sub-category excluding skin cancers and including only the first reported primary malignant cancer for the 50 subjects who reported having cancer other than skin. Unadjusted odds ratios and 95% confidence intervals for each variable is presented comparing all cancer rates within each category (Table 3). The referent categories were chosen with the assumption o f least risk. As expected, increasing age is associated with increased risk o f cancer (test for trend: p = 0.0002). Increasing years smoking appears to be associated with increased risk o f cancer (test for trend: p = 0.16). The lowest education level, less than 9th grade, is associated with the greatest risk o f cancer. There is Page 12 o f 38 no effect o f body mass index on the all cancer rate in this group. The association between working in the Plant or the neighboring manufacturing facility and increased risk o f all cancer did not reach the level o f statistical significance, however, the Plant employees had a nearly 2 fold odds o f cancer compared to those who never worked at either location, p-value = 0.13. Next, Table 4 compares the all cancer prevalence in the PFOA-exposed residents to the cancer prevalence in the U.S. population of Whites by age and gender. The ratios in each age category for both males and females increase with decreasing age category culminating in the youngest age categories showing the largest effects with the exception o f males aged 3 5 - 4 4 where there were no cancer cases reported in the exposed population. Table 5 presents the age-standardized morbidity prevalence ratio (PR) calculated from the observed and expected rates for each cancer type reported in the exposed population. The U.S. population rates for Whites are used to generate the expected age-adjusted rate per 100,000 using the age distribution in the exposed residents. The all cancer PR is significantly elevated at 2.58. Statistically significant increases in PRs were found for uterine/cervical cancer in women (33.12), lung (7.89), non-Hodgkins lymphoma (6.67) and bladder (5.30) cancers. We also found excess morbidity for several different cancer types among the residentially PFOA-exposed population although several o f the estimates are based on small numbers including colon/rectal (4), multiple myeloma (2), melanoma (3) and kidney (1). Prostate in men was also nearly significant with a PR o f 1.96 and confidence limits that just include 1.00 at the 0.05 significance level (CI: 0.98 - 3.92). Page 13 o f 38 O ccupational data In Table 6, we introduce the occupational data from a cohort o f PFOA-exposed workers who were hired between 1950 and 1990. There were 451 identification numbers in the data set with no other associated data. The remaining data set had 6105 workers with some occupational and health related data. From this total, we excluded 409 who were hired prior to January 1, 1950; 1442 who were hired after December 31, 1990; 160 who worked for company less than 6 months and 700 who were in divisions other than the two divisions that we know either did or did not work directly with PFOA. This left 3394 subjects who are represented in tables 7 and 8. This cohort o f workers was largely bom between 1950 and 1969 (51.79%). The next largest birth cohort was between 1920 and 1959. Most were male (84.23%) and had direct exposure to PFOA (60.85%). The cohort was equally divided among the three "years o f exposure" categories (less than 21 years, between 21 and 29 years and 30 - 50 years). Insufficient information on smoking status, body mass index, race or education level was available. Table 7 uses proportional hazards models to control for age at hire while examining type-specific cancer rates among workers directly exposed to PFOA through their work compared to workers at the same plant who did not directly work with PFOA. In this survival analysis, pancreatic, respiratory, kidney, colon/rectal and prostate cancers were all significantly associated with direct PFOA exposure: hazard ratios ranging between 2.51 and 4.46. Breast, non-Hodgkin's Page 14 o f 38 lymphoma, bladder and liver cancers did not show association with PFOA exposure in this analysis. Table 8 examines these same data using logistic regression to explore a dose-response relationship between increased exposure and increased risk o f cancer. Age at hire and division are included in the model to control for confounding. Prostate, kidney and respiratory (nearly) cancers have a dose response relationship with number o f years exposed. Although bladder and pancreatic cancers show increasing odds ratios with years worked, the p-value exceeds 0.05. When we reran the analysis for table 8, including all who worked at least 6 months in any department hired between 1950 and 1990; every cancer-exposure relationship except for respiratory cancer was strengthened. We present the more conservative estimates. Discussion: Almost every person in the U.S. has measurable quantities o f PFOA in his/her blood.26,27,28 Many studies in animals and humans suggest an increased risk o f cancer with PFOA exposure. In particular, rodent studies indicated neoplasms in the liver,29 testes, pancreas and mammary glands.13 Human studies have suggested increased rates o f prostate,15 kidney,16bladder,16,17 colon16 and testes16cancers. The data presented in this paper are consistent with the prior findings. Residential data Similarly for both men and women, we found that the prevalence o f cancer was elevated for Page 15 o f 38 almost every age category compared to the U.S. population o f Whites. O f particular interest and importance, the rate ratios were higher for the younger age categories suggesting that PFOA exposure not only caused more cancer but did so preferentially in younger populations. Many o f the cancers previously identified in the literature as suspected outcomes o f PFOA exposure were also represented in this residential sample including uterine/cervical, bladder, prostate and colon/rectal cancers. We interpret these PRs as indicators of potential increased risk and not as effect measures describing the strength o f the association. It is the consistency o f these findings with previous animal and human studies that strengthens the conclusion that there is a measurable and important relationship between PFOA exposure and these cancer outcomes. Lung cancer and non-Hodgkin's lymphoma also show large PRs (7.98; 6.67, respectively), each with confidence intervals that show significance at the 0.05 level. These two findings clearly call for additional research. We know that inhalation o f dust or vapor is a potential pathway for human PFOA exposure.10Could it be that PFOA causes lung and other respiratory cancers? Given the dramatic rise in incidence o f non-Hodgkin's lymphoma18over the past several decades any research question regarding causation is worth pursuing. Could ubiquitous bioaccumulation of PFOA be adding to the increased risk o f non-Hodgkin's lymphoma? Occupational data The occupational data support the residential data, especially for males. Kidney, prostate and colon/rectal cancers were elevated in the proportional hazards models with significant p-values Page 16 o f 38 but not bladder cancer. Respiratory cancer has a strong hazard ratio aid very small p-value. The dose-response analysis also indicates that the odds of prostate and kidney cancers increase with increasing years exposed at the company. Again, respiratory cancer approaches significance. The reported analysis is done with a restricted data set. When repeated including all workers in any department hired between 1950 and 1990 who worked at least 6 months all die odds ratios increase and the p-values decrease with the exception of respiratory. Conservatively, a causal association between PFOA and prostate and kidney cancers is supported with these data from an occupationally exposed cohort. Despite varying methods for data collection and analysis, increased cancer rates (both prevalence and incidence) were similar for PFOA exposed residents and workers for prostate and colon/rectal cancers. Kidney cancer is also indicated in both data sets but based on only 1 case in the residential. Increased rates of respiratory cancer are a new finding in both data sets that demands further investigation. The limitations o f the data from the residential study include small sample sizes for rare cancers, 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 the risk o f all cancers and limiting interpretation to common cancers. National statistics estimated using SEER 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. Possible selection bias Page 17 o f 38 was examined by evaluating the effect on ail cancer prevalence o f commonly known and wellunderstood risk factors: age, gender, smoking status and educational attainment. The all cancer rate increased with increasing age, increased smoking and for those in the lowest category o f educational attainment. If these data reflected self-selection bias or reporting bias we would expect one or more o f these variables to behave outside the norm. Furthermore, the distribution o f cancer types parallels that seen in PFOA exposed workers. Even if there were a selection bias with a disproportionate number o f patients with cancers, there is no reason to assume that only patients with certain types o f cancers would be more likely to volunteer for the study. Our study results are consistent with the literature on PFOA that suggests increased rates o f uterine/cervical, prostate, bladder and colon/rectal cancers. The only unexpected result was for the respiratory that mirrored occupational data and is biologically plausible. Some researchers question whether reliable data can be obtained from participants in a class action lawsuit. While it is claimed that litigants exaggerate their symptoms we know o f no evidence that this is true, particularly when examining averaged group responses. A study by the Agency for Toxic Substance and Disease Registry (ATSDR) revealed no evidence o f "litigation bias" among subjects being followed for health effects from trichloroethylene in their drinking water30 with no statistically significant difference in the validity of the survey responses from litigant versus non-litigant populations. They also report "litigants are no more likely than nonlitigant(s) to provide inaccurate or exaggerated responses." Page 18 o f 38 Observational bias is unlikely to influence these results because the techniques used to collect the data do not require interpretation and all cancers were verified by telephone interview. Medical records are being pursued to compare to questionnaire responses. With nearly half o f the medical records received all o f the reported primary malignancies have been confirmed. The questionnaires were filled out in a neutral environment supervised by trained proctors. All subjects were given the same instructions. Moreover, the study participants are members o f a mandatory, non-opt-out class action where their participation in the lawsuit is not voluntary. Recall bias is also unlikely to affect the results, particularly when it comes to cancer. Increased prevalence rates of reproductive, kidney and bladder cancer are also seen in PFOA exposed workers. The excess o f reproductive cancers (i.e. cervical/uterine and prostate) is also consistent with the observation of altered reproductive hormones among PFOA exposed workers.15Animal studies with ingested PFOA support the findings in this study.16 The increased risk o f respiratory cancer in the residential data with a PR o f 7.96 is similar to the occupational data with a hazard ratio o f 4.65 for direct PFOA exposure. And there is a doseresponse p-value o f 0.08 for increasing odds of respiratory cancer with increasing categories o f years exposed at the company. No published worker studies have reported increased risk o f respiratory cancers. However, extensive animal data on PFOA toxicity through inhalation supports and strengthens this finding.13These data show an association between increased cancer prevalence in a human population and exposure to PFOA. Because o f wide spread human Page 19 o f 38 exposure to this compound these findings are important for public health Page 20 o f 38 References: 1.Doering C. EPA Steps up Study o f Teflon Chemical Risk to Humans. Reuters 2003; April 14. 2.Shabilina IG, Panaretakis T, Bergstrand A, DePierre JW. Carcinogenesis 1999; 20(12):22372246. 3.Hatfield T. 2001. Screening studies on aqueous photolytic degradation o f perfluorooctanoic acid. St Paul, MN:3M Environmental Laboratory. Lab Request Number E00-2192. 4.Reiner EA. 1978. Fate o f Fluorochemicals in the Environment. St Paul, MN:3M Environmental Laboratory. Project Number 9970612613. 5.Giesy JP, Kannan K. Global Distribution o f Perfluorooctane Sulfonate in Wildlife. Environ Sci Technol 2001; 35:1339-1342. 6. Kannan K, Koistinen J, Beckman K, Evans T, Gorzelany JF, Hansen KJ, Jones PD, Helle E, Nyman M, Giesy J. Accumulation o f Perfluorooctane Sulfonate in Marine Mammals. Environ Sci Technol 2001, 35;1593-1598. 7. Taniyasu S, Kanna K, Horri Y, Hanari N, Yamashita N. A Survey o f Perfluorooctane Sulfonate and Related Perfluorinated Organic Compounds in Water, Fish, Birds, and Humans from Japan. Environ Sci Technol 2003, 37;2634-2639. Page 21 o f 38 8. Taniyasu SM, ftannan KL, Horii Y, Hanari N, Yamnashita N. 2002. The first environmental survey o f perfluorooctane sulfonate and related compounds in Japan. Barcelona, Spain:Dioxin 11-16 August 2002. 9.3M. Sulfonated Perfluorochemicals in the Environment: Sources, Dispersion, Fate and Effects. 3M Environmental Laboratory, 2001. USEPA AR OPTT-2002-0043-005. 10.Moriwaki H, Takata Y, Arakawa R. Concentrations o f Perfluorooctane Sulfonate (PFOS) and Perfluoroocatanoic Acid (PFOA) in vacuum cleaner dust collected in Japanese homes. J. Environ. Monit. 2003, 5. 1l.Ubel FA, Sorenseon SD, Roach DE. Health Status o f Plant Workers Exposed to fluorochemicals - A Preliminary Report. American Industrial Hygiene Association. 1980, 41(8);584-589. H.Griffith FD, Long JE. Animal Toxicity studies with ammonium Perfluorooctanoate. Am. Ind Hyg Associt J 1980; 41:576-582. 13.EPA. 2002. Revised Draft Hazard Assessment o f Perfluorooctanoic Acid and Its Salts. USEPA. OPPT, Risk Assessment Division. Washington DC. (AR226-1136). 14. Gilliland F, Mandel J. Mortality among Employees o f a Perfiiorooctanoic Acid Production Plant. JOM 1993; 35(9):950-954. 15. Gilliland F, Mandel J. Serum Perfluorooctanoic Acid and Hepatic Enzymes, Lipoproteins, and Cholesterol: A Study o f Occupationally Exposed Men. American Journal of Industrial Medicine 1996; 29:560 - 568. l.Leonard RC. Epidemiology Surveillance Report Cancer Incidence for Washington Works Site 1959-2001. Haskell Laboratory for Health a id Environmental Sciences. E.I. du Pont de Nemours and Company. 2003. USEPA AR OPTT-226-1307. 17.Alexander B, Olsen G, Burris J, et al. Mortality o f employees of a Perfluorooctanesulphonyl fluoride manufacturing facility. Occupational and Environmental Medicine 2003; 60:722-729. 18.SEER. http://seer.cancer.gov/ 19. Environmental Working Group. Web Page rhttp://www.ewg.org/reports/pfcworld/partl.phpl 20. Cardiff Software (1991). Teleform standard user guide, version 8.2 San Marcos, CA:Cardiff Software Inc 21. Dupont. Internal Final Report. "A Case-Control Study o f Leukemia At the Washington Page 23 o f 38 Wortes Site." (12/3/91). USEPA AR OPTT226-1308. 22. Checkoway H, Pearce NE, Crawford-Brown DJ. Research Methods in Occupational Epidemiology. Oxford University Press; 1989. page 215 - 218. 23. Miettinen. Standardization o f Risk Ratios. Am. J. Epidemiol. 1972;96(6): 383-388. 24. Rothman KJ, Greenland S. Modem Epidemiology. Philadelphia: Lippincott-Raven; 1998. 25. SAS. Version 8.0. Cary, NC: SAS Institute Inc; 2002. 26,Olsen GW, Burris JM, Burlew MM, Mandel JH. Epidemoiological Assessment o f Worker Serum Perflurooctanesulfonate (PFOS) and Perfluorooctanoate (PFOA) Concentrations and Medical Surveillance Examinations. JOEM. 2003, 45(3); 260-270. 27.01sen G, Hansen K, Stevenson LA, Burris J, Mandel J. Human Donor Liver and Serum Concentrations o f Perfluorooctanesulfonate and Other Perflurochemicals. Environ. Sei Technol. 2003, 37; 888-891. 28.01sen GW, Church TR, Larson EB, Belle GV, Lundberg JK, Hansen KJ, Burris JM, Mandel JH, Zobel LR. Serum Concentrations of Perfluorooctanesulfonate and other Fluorochemicals in an Elderly Population from Seattle, Washington. Chemosphere 2004, 54; 1599-1611. Page 24 o f 38 29.Abdeilatif A, Al-Tonsy AH, Awad ME, Roberfiroid M, Khan MN. Perixosomal enzymes and 8-hydroxyguanosine in rat liver treated with perfluorooctanoic acid. Dis Markers. 2003 04,19(1): 19-25. 30.Allred SL, Burg JR. Environmental personal injury litigation as one source of response effects: Findings from the National Exposure Registry. Toxicology and Industrial Health 1995; 11(2): 217-230. Page 25 o f 38 Acknowledgements: The Law Firm o f Winter Johnson & Hill PLLC, Law Firm o f Taft, Stettinius & Hollister LLP, Law Firm o f Hill, Peterson, Carper, Bee & Deitzler, PLLC. Human Subjects: The study was conducted in accordance with institutional guidelines for the protection o f human subjects. Conflict o f Interest: The above-mentioned law firms funded this study; the first author o f this manuscript is sometimes invited as an expert witness. Page 26 o f 38 Table Legend: Table 1. PFOA levels by Water District/source and percent o f study subjects reporting water consumption from each source. Table 2. Numbers and percents for demographic, social, behavioral and physical characteristics in a residentially PFOA-exposed population. Table 3. Estimated unadjusted odds ratios (OR) o f cancer (yes/no) and 95% confidence intervals (Cl) for demographic, social, behavioral and physical characteristics in a residentially PFOAexposed population. Table 4. All cancer prevalence rates per 100,000 in PFOA-exposed residents by age and gender compared to U.S. population rates for Whites. Table 5. Standardized Morbidity Prevalence Ratio (PR) comparing observed cancer rate per 100,000 among a residentially PFOA-exposed population to the expected cancer rate using the age-specific rates o f the U.S. population for Whites and the age distribution o f the exposed population. Table 6. Numbers and percents for demographic and work characteristics in an occupationally PFOA-exposed population. Table 7. Estimated test for trend of cancer incidence with increasing years worked at the company using adjusted odds ratios (OR) and 95% confidence intervals (Cl) for selected cancers in an occupationally PFOA-exposed cohort hired between 1950 and 1990: results o f a logistic regression analysis controlling for age at hire and department. Table 8. Proportional Hazards models for selected cancers in an occupationally PFOA-exposed cohort hired between 1950 and 1990 adjusted for age-at-hire, gender comparing those workers in Page 27 o f 38 a department with direct exposure versus those in a department with no direct exposure. Figure Legend: Figure 1: Example o f the Questionnaire Section Pertaining to Cancer Prevalence. Page 28 o f 38 T able 1. PFOA levels by water district/source and percent o f study subjects reporting water consumption from each source PFOA Levels (ppb) 1.7-4.3 0.4-3.9 0.25-0.37 0.08-0.13 0.06-0.1 0.06-0.07 0.165 1.0-5.0 1.75-1.87 0.05-8.6 Location Little Hocking, Ohio Lbeck, WV Tuppers Plains, Ohio Belpre, Ohio Mason, WV Pomeroy, Ohio Blennerhassett Dupont, Washington Works0 GE Plastics" 68 Private Wells WVA & Ohio 4 Estimated as 2.S people per household bCompany employment reports Abbreviations: N/A Not Applicable Households 4200 3700 4800 6000 4200 1000 71 N/A N/A 68 Total Population4 (% total pop) 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 Study Sample (% study sample) 161 (27%) 219 (37%) 19 (3%) 45 (8%) 4 (0.7%) 1 (0.2%) 6 (1%) 90 (15%) 43 (7%) 11 (2%) 599 Page 29 o f 38 T able 2. Frequencies and percents for demographic, social, behavioral and physical characteristics in a residentially PFOA-exposed population._____________ Age Category No. % 20-34 35-44 45-54 55-64 6 5 -8 0 105 18.17 104 17.99 135 23.36 154 26.64 80 13.84 Gender M ale Female 284 49.13 294 50.87 Race/Ethnicity White African American Others 558 97.38 6 1.05 9 1.57 Education Level Less than 9mgrade 9 - 1 1 " grade 12mA^ocational/Some College College Graduate 17 59 430 65 2.98 10.33 75.31 11.38 Body Mass Index Underweight (<23) Average (23 - 28) Overweight (> 28) 106 18.53 190 33.22 276 48.25 Smoking Status Never smoked Smoked less than 15 years Smoked more than 15 years 252 60.58 72 17.31 92 22.12 W ork History Plant 1 Plant 2 No plant work 54 9.42 19 3.32 500 87.26 Page 30 o f 38 T able 3. Estimated unadjusted odds ratios (OR) o f cancer (yes/no) and 95% confidence intervals (Cl) for demographic, social, behavioral and physical characteristics in a residentially PFOA-exposed population.________________________ _______ ________________________ No. * (% )b OR 95% Cl P-valuec Gender Male Female (ref.) 25 (8.80%) 25 (8.50%) 1.04 (0.58 - 1.86) 1.00 - 0.90 - Age Category 20 - 34 (ref.) 35-44 45-54 55-64 6 5 -8 0 5 (4.76%) 4(3.88%) 9(6.67%) 16 (10.39%) 16 (20.00%) 1.00 0.80 (0.21-3.07) 1.43 (0.46 - 4.40) 2.32 (0.82-6.54) 5.00 (1.75-14..32) 0.0002 - 0.74 0.53 0.11 0.003 Education Level Less than 9ra grade 9th grade or higher 8 (47.06%) 42 (7.58%) 10.84 1.00 3.97-29.53 - <0.0001 - Body Mass Index Underweight (<23) Average (23 - 28) (ref) Overweight (>28 ) 8 (7.55%) 18 (9.47%) 23 (8.33%) 0.78 (0.33 -1 .8 6 ) 1.00 - ' 0.87 (0.46-1.66) 0.93 0.58 - 0.67 Smoking Status Never smoked (ref) Smoked less than 15 years Smoked more than 15 years 20 (7.94%) 7 (9.72%) 12 (13.04%) 1.0 1.25 (0.51-3.08) 1.74 (0.81-3.72) 0.16 - 0.63 0.15 W ork Site Plant 1 Plant 2 No plant employment (ref) 8 (14.81%) 1 (5.26%) 41 (8.20%) 1.87 (0.83-4.22) 0.48 (0.06-3.62) 1.0 - 0.13 0.47 - "Number o f cancer observations considered in the logistic procedure b% w ith cancer in each category. c Bolded p-value refers to the p-value for a test for trend Page 31 o f 38 Table 4. All cancer prevalence rates per 100,000 in PFOA-exposed residents compared to the US popu ation rates for Whites i>yage and gender. ' Males Females Prevalence Ratio Age Group 20-34 Age Specific Rates (u s `) 338 Age Specific Rates (EP*) 1,923 Age Specific Rates (US) 451 Age Specific Rates (EP) 7,547 35-44 799 - 1,447 7,547 45-54 1,722 4,839 3,167 8,219 55-64 5,080 9,211 5,390 11,538 65+ 15,661 32,558 9,173 5,405 aUS = United States population (Whites only) EP = Residentially PFOA-exposed population EP/US Males 5.69 . 2.81 1.81 2.08 P 0.16 0.09 0.10 0.009 EP/US females 16.75 5.21 2.59 2.14 0.59 P 0.0001 0.008 0.03 0.03 0.85 Page 32 o f 38 T able 5. Standardized Morbidity Prevalence Ratio (PR) comparing observed cancer rate per 100,000 among a residential^ PFOA-exposed population to the expected cancer rate using die age-specific rates o f the general U.S. population and the age distribution o f the exposed population._______________________________________________ CANCER TYPE All Cancer Number of Cancers 50 Observed Rates* (per 100,000) 8,651 Expected Ratesb (per 100,000) 3,426 PR 2.58 CIC 1.91 -3.47* Uterine/Cervicald 9 3,061 96 33.12 17.03-64.41* M. Myeloma 2 346 22 15.71 3.91-63.14* Lung 7 1,211 153 7.89 3.72 - 16.74* Non-Hodgkins 5 865 130 6.67 2.76-16.13* Bladder 5 865 163 5.30 2.19-12.87* Colon/Rectal 4 692 261 2.65 0.99-7.11 Kidney 1 173 79 2.20 0.31 - 15.63 Prostate 9 3,169 1633 1.96 0.98 - 3.92 Melanoma 3 519 214 2.42 0.78 - 7.54 Breast 5 1,701 1,579 1.12 0.46 - 2.71 a Observed cancer rates per 100,000 in the exposed population bInternally standardized rates per 100,000, age adjusted using the distribution in the PFOA exposed residents, SEER 2000. c Confidence Interval d7 women reported cervical and 6 reported uterine cancer, 3 women reported both * Confidence interval excludes the null value Page 33 o f 38 T able 6. Numbers and percents for demographic and work characteristics in an occupationally 0OJ 1 o Birth Cohort 1900-1919 1920 - 1939 1940 - 1959 1960 - 1989 Gender Male Female Years of Occupational Exposure <21 years 21 - 2 9 D epartm ent No direct PFOA exposure Direct PFOA exposure No. 160 1209 2203 682 3583 671 1266 1462 1366 2157 1388 % 3.76 28.42 51.79 16.03 84.23 15.77 30.92 35.71 33.37 60.85 39.15 Page 34 o f 38 p. 40 T able 7. Proportional Hazards models for selected cancers in an occupationally PFOA-exposed cohort hired between 1950 and 1990 adjusted for age at hire comparing those working in a department with direct PFOA exposure compared to those in a department with no direct exposure.___________________________________ No. (% ) of all those in category Hazard w/cancer Ratio Cl P-value Pancreatic cancer No direct exposure 2(0.09%) 1.00 Direct PFOA exposure 6(0.48%) 4.46 (0.87,22.91) 0.07 Respiratory cancer No direct exposure Direct PFOA exposure 11(0.51%) 26(2.10%) 1.00 4.41 (2.13,9.13) <0.0001 Kidney cancer No direct exposure Direct PFOA exposure 6(0.28%) 11(0.89%) 1.00 3.14 (1.10,8.95) 0.03 Colon/rectal cancer No direct exposure Direct PFOA exposure 9(0.42%) 11(0.89%) 1.00 2.96 (1.15,7.64) 0.02 Prostate cancer* No direct exposure Direct PFOA exposure 14(0.65%) 23(1.86%) 1.00 2.51 (1.24,5.08) 0.01 N on-Hodgkin's Lymph No direct exposure 3(0.14%) 1.00 Direct PFOA exposure 3(0.24%) 2.44 (0.47,12.73) 0.29 Bladder cancer No direct exposure Direct PFOA exposure 10(0.46%) 10(0.81%) 1.00 1.46 (0.59,3.54) 0.41 Liver cancer No direct exposure Direct PFOA exposure 1(0.05%) 1(0.08%) 1.00 1.13 (0.06.23.07) 0.94 Page 35 o f 38 p. 41 No. (% ) of all those in category w/cancer Breast cancer No direct exposure 5(0.23%) Direct PFOA exposure 1(0.08%) a WI T r omen excl1 u4ded/ from analyses Hazard Ratio 1.00 0.21 Cl (0.02, 1.88) P-value 0.16 Page 36 o f 38 p. 42 T able 8. Dose response for cancer incidence with increasing years o f occupational exposure using adjusted odds ratios (OR) and 95% confidence intervals (Cl) for selected cancers in an occupationally PFOA-exposed cohort hired between 1950 and 1990: results o f a logistic Cancer Type OR 95% Cl P-Value b Prostate <21 years* 21-29 30-50 0.0002 1.0 - - 2.68 0.82 - 8.79 0.10 8.71 2.63-28.83 0.0004 Kidney <21 years 21-29 30-50 1.0 6.28 11.57 - 0.75 - 52.89 1.38 - 97.32 0.03 - 0.09 0.02 Respiratory <21 years 21 - 2 9 30-50 1.0 1.42 0.61 - 3.30 1.47 0 .6 3 -3 .4 3 0.07 - 0.42 0.37 B lad d er <21 years 21-29 30-50 1.0 1.30 0 .4 0 -4 .2 4 2.09 0 .5 9 -7 .4 0 0.17 . 0.66 0.29 Colon/Rectal <21 years 21-29 30-50 1.0 - 0.38 0 .1 0 -1 .5 0 1.41 0 .5 0 -4 .0 0 0.24 - 0.17 0.52 Pancreatic <21 years 21 - 2 9 30-50 1.0 1.71 0.28 - 10.49 1.92 0 .2 8 -1 3 .2 0 0.35 - 0.56 0.51 'Bolded p-value refers to the p-value for a test for trend Page 37 o f 38 p. 43 Figure 1: Questionnaire Have you ever been told by a doctor that you have cancer? o Yes 0 No If you were diagnosed with cancer, are you still receiving medical treatment? O Yes O No If you answered yes to the previous cancer questions, please indicate which cancels) and when you were diagnosed. Yes No Year Yes No Year O O Hodgkin's 0 OLung O O Non-Hodgkin's O O Other Lymphoma O O Leukemia O O Bone O O Stomach O O Liver O O Multiple Myeloma O O Kidney O O Thyroid O O Pancreas O O Testicular O O Colon O O Breast O O Rectal O O Uterine O O Prostate O O Cervical O O Ovarian O O Brain O O Mouth,Nose,Throat O O Skin O O Melanoma O O Bladder O O Gall Bladder Other Cancer Type O O Other Page 38 o f 38 NORTHERN KENTUCKY OFFICE SUITE 340 1717 OUUE HIGHWAY COVINGTON. KENTUCKY 41011-4704 006-331 2038 513-301-2130 FAX: 613-3314613 DAYTON. O HIO OFFICE SUITE 960 110 NORTH M AM STREET DAYTON. O HIO 45402-1706 937-228-2038 FAX: 937-221-2810 ..FT, STETTINIUS & HOLLISTER L_ 425 WALNUT STREET, SUITE 1800 CINCINNATI, OHIO 45202-3957 513-381-2838 FAX: 513-381-0205 w w w .tafttaw .co m Ro b e r t a . B ilott (513) 357-9638 bilott@taft!aw.corn April 21, 2004 TELECOPY AND FEDERAL EXPRESS CLEVELAND, OHIO OFFICE 3900 DP TOWER 200 PUBUC SQUARE CLEVELAND, OHK3 44114-2302 216-241-2030 FAX: 210-241-3707 COLUMBUS. OHIO OFFICE 21 EAST STATE STREET COLUMBUS. OHIO 43216-4221 614-221-2030 F A X :614-221-2007 Dr. Charles M. Auer Chemical Control Division Office o f Prevention, Pesticides and Toxic Substances United States Environmental Protection Agency 1201 Constitution Avenue, N.W. Room 3166A Washington, DC 20004 Richard H. Hefter, Chief United States Environmental Protection Agency High Production Volume Chemicals Branch Office of Pollution Prevention and Toxics 1201 Constitution Avenue, N.W. Room 6334AA Washington, DC 20004 Mary Ellen Weber Chemical Control Division United States Environmental Protection Agency 1201 Constitution Avenue, N.W. Room 5124A Washington, DC 20004 Oscar Hernandez Director, Risk Assessment Division Office of Prevention, Pesticides and Toxic Substances United States Environmental Protection Agency 1201 Constitution Avenue, N.W. Room 6220A Washington, DC 20004 Jennifer Seed United States Environmental Protection Agency 1201 Constitution Avenue, N.W. Room 6334A Washington, DC 20004 Mary Dominiak Chemical Control Division Office of Prevention, Pesticides and Toxic Substances United States Environmental Protection Agency 1201 Constitution Avenue, N.W. Room 441 OS Washington, DC 20004 Re: PFOA Human Health Effects Study: Cancer Data W0162920 l Dr. Charles M. Auer Oscar Hernandez Richard H. Hefter. Chief Jennifer Seed Mary Ellen Weber Mary Dominiak April 21,2004 Page 2 Ladies and Gentlemen: In response to USEPA's prior requests for available information regarding the potential threat to human health or the environment from PFOA, we have attached a copy of an abstract presented this week during the annual Society o f Environmental Toxicology and Chemistry (SETAC) meeting in Prague, Czechoslovakia referencing cancer rates among individuals exposed to PFOA-contaminated drinking water in communities near E.L duPont de Nemours and Company's ("DuPont's") Washington Works Plant in Wood County, West Virginia. In view of the nature of the potential public health threat at issue and DuPont's failure to respond to our requests for confirmation that it has submitted the results o f this study to USEPA under Section 8(e) o f TSCA, we are forwarding this information to you directly to make sure that USEPA has access to the information. The abstract and related poster information also is available on-line through SETAC. Please include this information in AR-226, OPPT-2003-0012, and the appropriate IRIS database for PFOA. RAB/mdm Attachment cc: IRIS Submission Desk (w/ attachment) Mark Garvey, Esq. (USEPA) (w/ attachment) R. Edison Hill, Esq. (w/ attachment) Larry A. Winter, Esq. (w/ attachment) Gerald J. Rapien, Esq. (w/ attachment) W016Z920.1 p. 46 NORTHERN KENTUCKY OFFICE SUITE 340 1717 DIXIE HIGHWAY OVWGTON, KENTUCKY 41011-4704 606*331-2838 $13*381*2838 FAX: $13-381-6813 DAYTON. OHIO OFFICE SUITE 900 110 NO RTH MAIN STREET DAYTON. OHIO 45402*1786 937-226*2838 FAX: 937*228*2816 TAFT, STETTINIUS & HOLLISTER LLP 425 WALNUT STREET, SUITE 1800 CINCINNATI, OHIO 45202-3957 513-381-2838 FAX: 513-381-0205 w w w .taftlaw .co m Ro b e r t a . B ilott (513) 357-9638 bitott@taftlaw.com June 2, 2004 TELECOPY AND FEDERAL EXPRESS CLEVELAND. OHIO OFFICE 3500 BP TOWER 200 PUBLIC SQUARE CLEVELAND, OHIO 44114 2302 216*241*2838 FAX: 216-241-3707 CO LUM 8US, OHIO OFFICE 21 EAST STATE STREET COLUMBUS. OHIO 43215-4221 614-221*2838 F A X :614-221-2007 Dr. Charles M. Auer Chemical Control Division Office o f Prevention, Pesticides and Toxic Substances United States Environmental Protection Agency 1201 Constitution Avenue, N.W. Room 3166A Washington, DC 20004 Richard H. Hefter, Chief United States Environmental Protection Agency High Production Volume Chemicals Branch Office o f Pollution Prevention and Toxics 1201 Constitution Avenue, N.W. Room 6334AA Washington, DC 20004 Mary Ellen Weber Chemical Control Division United States Environmental Protection Agency 1201 Constitution Avenue, N.W. Room 5 124A Washington, DC 20004 Oscar Hernandez Director, Risk Assessment Division Office o f Prevention, Pesticides and Toxic Substances United States Environmental Protection Agency 1201 Constitution Avenue, N.W. Room 6220A Washington, DC 20004 Jennifer Seed United States Environmental Protection Agency 1201 Constitution Avenue, N.W. Room 6334A Washington, DC 20004 Mary Dominiak Chemical Control Division Office o f Prevention, Pesticides and Toxic Substances United States Environmental Protection Agency 1201 Constitution Avenue, N.W. Room 441 OS Washington, DC 20004 Re: PFOA Human Health Effects Study: Cancer Data W184092.I p. 47 Dr. Charles M. Auer Oscar Hernandez Richard H. Hefter, Chief Jennifer Seed Mary Ellen Weber Mary Dominiak June 2, 2004 Page 2 Ladies and Gentlemen: In response to USEPA's prior requests for available information regarding the potential threat to human health or the environment from PFOA, we have attached copies o f two abstracts (LE5954-7) that have been submitted for presentation during the International Conference on Environmental and Public Health Management: Persistent Toxic Substances, which will be held in Hong Kong in November o f 2004. These abstracts reference some o f the age-adjusted data discussed more generally in the abstract that we forwarded to you on April 21, 2004. AH o f the abstracts refer to data generated in connection with the same study o f cancer rates among individuals exposed to PFOA-contaminated drinking water in communities near E.I. duPont de Nemours and Company's Washington Works Plant in Wood County, West Virginia. As with the prior abstract information, we request that you include this information in AR-226, OPPT-20030012, and the appropriate IRIS database for PFOA. RAB/mdm Attachments cc: IRIS Submission Desk (w/ attachments) Mark Garvey, Esq. (USEPA) (w/ attachments) R. Edison Hill, Esq. (w/ attachments) Larry A. Winter, Esq. (w/ attachments) Gerald J. Rapien, Esq. (w/ attachments) W0184092.1 p. 48 NORTHERN KENTUCKY OFFICE SUITE 3 *0 1717 O W E HIGHW AY COVINGTON. KENTUCKY 41011-4704 4 0 4 -0 3 1 -2 4 3 8 5 1 3 -3 8 1 -2 8 3 8 FAX: $13-381-813 DAYTO N, O HIO OFFICE SUITE 900 110 NORTH MAM STREET DAYTON. OHIO 43402-178 3 7 -2 2 8 -2 8 3 8 FA X: 37-228-281 R o b er t A . Bilott (513) 357-9638 bilott@taUlaw.com TA'rT, STETTINIUS & HOLLISTER LL. 425 WALNUT STREET, SUITE 1800 CINCINNATI, OHIO 45202-3957 513-381-2838 FAX: 513-381-0205 w w w .taftlaw .com CLEVELAND. OHIO OFFICE 3500 BP TOWER 200 PUBLIC SQUARE CLEVELAND, OHIO 44114-2302 218-241-2838 FAX: 21S-241-3707 COLUMBUS. OHIO OFFICE 21 EAST STATE STREET COLUMBUS. OHIO 43215-8221 614-221-2838 F A X :8 1 4 -2 2 1 -2 0 0 7 January 7, 2005 FEDERAL EXPRESS Dr. Charles M. Auer USEPA 1201 Constitution Avenue, N.W. Room 3 166A ) Washington, DC 20004 Mary Ellen Weber USEPA 1201 Constitution Avenue, N.W. Room 5124A Washington, DC 20004 Mary Dominiak USEPA 1201 Constitution Avenue, N.W. Room 441 OS Washington, DC 20004 Oscar Hernandez USEPA 1201 Constitution Avenue, N.W. Room 6220A Washington, DC 20004 Jennifer Seed USEPA 1201 Constitution Avenue, N.W. Room 6334A Washington, DC 20004 Re: PFOA Human Health Effects Studv: Cancer Data Ladies and Gentlemen: In response to USEPA's request for available information regarding the potential threat to human health or the environment from PFOA. we previously forwarded to you preliminary abstracts/summaries o f data generated in connection with a survey o f adverse health effects among individuals exposed to PFOA-contaminated drinking water in communities near E.I. duPont de Nemours and Company's Washington Work Plant in Wood County, West Virginia {see, e g.. OPPT-2003-0012-607. OPPT-2003-0012-677, and AR-226-1714-16). As a supplement to those previous submissions, we have enclosed a copy of several slides from a presentation that was made to the public in Hong Kong during the November 2004 international WG350205.1 p. 49 Dr. Charles M. Auer Oscar Hernandez Jennifer Seed Maiy Ellen Weber Mary Dominiak January 7, 2005 Page 2 - Conference on Environmental and Public Health Management: Persistent Toxic Substances. The slides summarize some of the reproductive effects data generated from the survey o f the community near DuPont's Washington Works Plant in West Virginia. As with the prior study fat? we request that you include this information in AR-226, OPT-2003-0012, and the appropriate IRIS database for PFOA. Robert A. Bilott RAB/mdm Enclosures cc: IRIS Submission Desk (w/ end s.) Mark J. Garvey, Esq. (USEPA) (w/ ends.) R. Edison Hill, Esq. (w/ ends.) Larry A. Winter, Esq. (w/ ends.) Gerald J. Rapien, Esq. (w/ ends.) W0350205.I NORTHERN KENTUCKY OFFICE SUITE 340 1717 O KIE HIGHW AY COVINGTON. KENTUCKY 41011-4704 606-331-2833 513-381-2838 FAX: S13-381-6613 DAYTON, OHIO OFFICE SUITE 900 110 NORTH MAIN STREET DAYTON, OHIO 45402-1786 937-228-2838 FAX: 937-223-2316 Ro b e r t A. B ilott <513)357-9638 bilott@taftiaw.com .-T, STETTINIUS & HOLLISTER LL 425 WALNUT STREET, SUITE 1800 CINCINNATI, OHIO 45202-3957 513-381-2838 FAX: 513-381-0205 w w w .taftlaw .com CLEVELAND. OHIO OFFICE 3500 BP TOWER 200 PUBUC SQUARE CLEVELAND, OHIO 44114-2302 216-241-2833 FAX: 216-241-3707 COLUM8US, OHIO OFFICE 21 EAST STATE STREET COLUMBUS, OHIO 43215-4221 614-221-2338 F A X ;614-221-2007 FEDERAL EXPRESS Dr. Charles M. Auer USEPA 1201 Constitution Avenue, N.W. Room 3166A Washington, DC 20004 Mary Ellen Weber USEPA 1201 Constitution Avenue, N.W. Room 5124A Washington, DC 20004 Mary Dominiak USEPA 1201 Constitution Avenue, N.W. Room 441 OS Washington, DC 20004 February 7, 2005 Oscar Hernandez USEPA 1201 Constitution Avenue, N.W. Room 6220A Washington, DC 20004 Jennifer Seed USEPA 1201 Constitution Avenue, N.W. Room 6334A Washington, DC 20004 Re: PFOA Human Health Effects Study: Cancer Data Ladies and Gentlemen: in response to USEPA's request for available information regarding the potential threat to human health or the environment from PFOA, we previously forwarded to you preliminary abstracts/summaries o f data generated in connection with a survey o f adverse health effects self reported among individuals exposed to PFOA-contaminated drinking water in communities near E.I. duPont de Nemours and Company's Washington Works Plant in Wood County, West Virginia (see, e.g., OPPT-2003-0012-607, OPPT-2003-0012-677, OPPT-2003-0012-836, AR226-1714-16, and AR-226-1893-94). As a supplement to those previous submissions, we have enclosed a copy of several tables providing more detailed summaries o f the age-adjusted, self- W0350203.I Dr. Charles M. Auer Oscar Hernandez Jennifer Seed Mary Ellen Weber Mary Dominiak February 7, 2005 Page 2 reported cancer data from the PFOA community health study. (Exhibit l) An article explaining the study and the cancer results in more detail has been peer reviewed and accepted for publication. The article is expected to be published this summer. Also enclosed are charts summarizing some o f the other adverse health effects reported in the same community study. (Exhibit 2). An article explaining these results has recently been completed and is being submitted for peer review and publication. In addition, we have enclosed documents recently released by one o f the public water suppliers to the community at issue, which discuss the increasing levels o f PFOA being detected in that particular public water supply. (Exhibit 3) As with the prior PFOA community study data, we request that you include this information in AR226, OPT-2003-0012, and the appropriate IRIS database for PFOA. RAB/mdm Enclosures cc: IRIS Submission Desk (w/ ends.) Mark J. Garvey, Esq. (USEPA) (w/ ends.) R. Edison Hill, Esq. (w/ ends.) Larry A. Winter, Esq. (w/ ends.) Gerald J. Rapien, Esq. (w/ ends.) W0350205.1