Document ppGkEpxk47yMOx1NpvrVd07Gj

"McCrea, Deborah" <mccrea@taftlaw .com> 03/15/2010 02 :08 PM p. 1 Alezze-3f3/ To NCIC OPPT@EPA cc "Bilott, Robert A." <bilott@taftlaw.com> bcc Subject 03/15/2010 Letter To EPA Docket Center Taft I Deborah McCrea / Legal Assistant Taft Stettinius & Hollister LLP t; Y 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 . CONTAII~ ~~ CBI p. 3 A'` u` "I's/- - aft/ TaftStettinius & HoAisterLLP 425 Walnut Street, Suite 1800 /Cincinnati, OH 45202-3957 /Tel : 513 .381 .2838 / Fax: 513 .381 .0205 / www.taftlaw.com Cincinnati / Cleveland / Columbus / Dayton 7 Indianapolis / Northern Kentucky / Phoenix / Beijing ROBERT A. B1LOT! 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 Re: Submission to IRIS and AR-226 Database For PFOAIPFOS : EPA-HQORD-2003-0016 To IRIS Database for PFOAIPFOS : 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 aA 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 . RAB :mdm Enclosures cc: Gloria Post (NJDEP)(wl encl.) (via U.S. Mail) Helen Goeden (MDH)(wl encl .) (via U .S. Mail) Lora Werner (ATSDR)(wl encl.) (via U.S. Mail) wY1405808 .1} ARCHIVES OF ENVIRONMENTAL HEALTH Bldg A7, #7401 1000 S. Fremont Ave/Unit #2 Alhambra, CA. 91803 AN INTERNATIONAL JOURNAL Kaye H . Kilburn, Editor-in-Chief Tel: 626 457 4202 Fax: 626 457 4203 Fanail: Ki}burn(u?usc.rdu October 8, 2004 James G. Dahlgren MD 2811 Wilshire Blvd . #510 Santa Monica, CA 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 ifnecessary. Also, please make other changes you wish as you consider these. Then two copies and the corrected disk should be forwarded to me. Sincerely, Kave H. Kiibum MD Editor-in-Chief Archives of Environmental Health PREVALENCE AND INCIDENCE OF CANCER IN POPULATIONS EXPOSED TO PERFLUOROOCTANOATE (PFOA) James Dahlgren MD', Pamela Anderson-Mahoney PhDZ, Jenny Kotlerman MS3, Harpreet Takhar MPH4, Alex Lee4,Toby Robinson4, Marilyn Zwass MD4, Ayman Ibrahim MD''d, Raphael Warshaw4 1 . UCLA School ofMedicine 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 ext. 226 FAX: 310-449-5526 dahlQrennenvirotoxicolop,y .com Page 1 of 38 Short Title: CANCER PREVALENCE AND INMENCE GIVEN PFOA EXPOSURE Page 2 of 38 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 of prostate, kidney, bladder and other cancers. This study examines the cancer prevalence rates in a cross-sectional sample of 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 of colon/rectal and prostate cancer was also suggested with a PR of 2.65; C1= 0.99; 7.11) and 1 .96; C1= (0 .98; 3.92), respectively. Cancer incidence from an occupationally exposed population of3394 adults is also considered ; and the test for trend of 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 of 38 Introduction : Perfluorooctanoic acid (PFOA or C8) is a man-made chemical with numerous industrial and consumer uses . Many stain resistant treatments of upholstery, carpet and textiles release PFOA into the environment.' Although PFOA is not an intended component of 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? 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 of dust or vapor phase precursors coming off of household products, such as carpet .'~8-9''o''t PFOA is slowly eliminated from the human body." Bioaccumulation heightens concern about adverse health effects. In rodent studies PFOA and related compounds cause multiple adverse health effects, 12 including neoplasms ofthe liver, testes, pancreas, and mammary glands . 13 In humans PFOA increases cancer rates. 14 Human epidemiological studies o PFOA exposed workers have reported statistically significant elevations in prevalence of cancer in the prostate, 15 kidney,' 6 bladder, l6"l' colon, 16 testes, 16 and other cancer types. 16 Also there have been excesses of lymphoma, multiple myeloma, breast cancer and melanoma reported. 18 Page 4of38 We report the cancer prevalence of a largely White residentially PFOA-exposed population using a self-administered questionnaire and compare that to the cancer prevalence in the U.S. population of 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 of 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) of 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 .19 PFOA 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 of 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 of three days in August of Page 5 of 38 2003, five hundred and ninety-nine (599) volunteers (2 .5%) from the targeted population participated in the 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, the majority (65%) who participated were exposed to water provided by the Lubeck Public Service District in West Virginia where PFOA ranged from 0_43 .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 of 20 and 80 years of 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 of20 and 80. Because a mandatory non-opt-out class action was certified against the Plant on behalf of 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 of their individual choice to be included . A sample question from the health questionnaire is set forth in Figure 1. Questionnaire responses were machine-readable, Z 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 of 38 verify the cancer information. Medical record confirmation is underway but not yet completed. Occupational data We also report on the incidence of cancer mortality among a historical cohort of 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 of the older persons included did not have vital status data even though they would he well into their hundreds (years old) . For this reason, we only include persons hired between 1950 and 1990 in 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 of follow-up data will result in measures of effect biased toward the null. This provides the reader with the most conservative measures of 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.z1 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 of 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 primary malignancy reported . For analyses where cancer types are reported separately, we included all primary 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 of Whites were obtained from the SEER 2000 website.'$ SEER data provides an estimate ofoverall cancer prevalence and incidence of all types of 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 of 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 8of38 lymphoma (cancer ofthe 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." These rates were compared with the rates in the U.S. population ofWhites 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 of cases that actually occurred in the exposed population (standard) divided by the number of cases that would have occurred in the absence of exposure . The latter number is estimated by assuming that the exposed group would have experienced, in the absence of 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 of 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 21 - 29 years and those who worked greater than 29 years at the company. Test for trend is reported. The "years of exposure" variable was calculated by counting the years between hire date and cancer date, if cancer happened before termination. Ifcancer was after termination, we added years from date of hire to date of termination. If the person had no date of termination, but has a date of death, we add the years between date of hire and date of death. If date of termination is not missing and there is no cancer, we add from date of hire to date of termination. Ifthere is no date of death and no date of termination we add from date of hire to July 1, 2003, the last documented date for follow-up in this cohort. All statistical analysis was performed using SAS 8.0.Z5 Results Residential data The questionnaire was administered to 599 subjects. Fifteen (15) of 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. Of the 578 subjects between the ages of 20 and 80, 77 subjects answered yes to the question "Have you ever been told by a doctor that you have cancer?" One of the 77 respondent's cancer diagnosis was not present on medical record verification. Of the Page 10 of 38 remaining 76 subjects, 41 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 of Whites . Each subject's cancer status was confirmed with the respondent by telephone. Medical record confirmation of 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 of the cross-sectional study population compared to the total population in the area. A greater percentage of 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 of workers in the table represents current workers and the number of study participants is computed by counting all the participants who responded that they had ever Page i 1 of 38 consumed water from either of the plants so this may be a fair representation of the proportion of people who have ever worked at one of the plants in the area. Table 2 presents the demographic, social, behavioral and physical characteristics of the exposed population. The age distribution was about equal in one 15-year and three l0-year categories ranging from age 20 to 64. Fewer participants contributed to the oldest age category. The average age ofthe PFOA-exposed residents was 49 +/- 14 .5 years. Gender was evenly split and nearly all of the participants were White. The majority of participants were high school graduates or had some college or vocational school. Nearly half of the study sample was overweight with a body mass index greater than 28 meters per kilograms squared. Sixty (60) percent of the sample never smoked and roughly 20 percent were represented in each of 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 of 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 of least risk. As expected, increasing age is associated with increased risk ofcancer (test for trend: p = 0.0002) . Increasing years smoking appears to be associated with increased risk of cancer (test for trend: p = 0.16). The lowest education level, less than 9`h grade, is associated with the greatest risk of cancer. There is Page 12 of 38 no effect of 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 of all cancer did not reach the level of statistical significance, however, the Plant employees had a nearly 2fold odds of 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 of males aged 35 - 44 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 of 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 of 1 .96 and confidence limits that just include 1 .00 at the 0.05 significance level (CI; 0.98 - 3 .92). Page 13 of 38 Occupational data In Table 6, we introduce the occupational data from a cohort of 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 ofworkers was largely born 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 of 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 of 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 of 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 of 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 of PFOA in his/her blood.26, 27,28 Many studies in animals and humans suggest an increased risk ofcancer 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 of prostate, ls kidney, " bladder, 16,17 colon' 6 and testesl6 cancers. 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 of cancer was elevated for Page 15 of 38 almost every age category compared to the U.S. population of Whites . Ofparticular 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 of the cancers previously identified in the literature as suspected outcomes of 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 of the association. It is the consistency of 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 ofdust or vapor is a potential pathway for human PFOA exposure.' Could it be that PFOA causes lung and other respiratory cancers? Given the dramatic rise in incidence of non-Hodgkin's lymphomal S over the past several decades any research question regarding causation is worth pursuing . Could ubiquitous bioaccumulation of PFOA be adding to the increased risk of 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 of 38 but not bladder cancer . Respiratory cancer has a strong hazard ratio and 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 b months all the 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 of the data from the residential study include small sample sizes for rare cancers, lack of a true unexposed comparison group and potential self-selection bias of study participants . We reduce the limitation of the small sample size by analyzing the risk of 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 of 38 was examined by evaluating the effect on all cancer prevalence of 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 of educational attainment . Ifthese data reflected self-selection bias or reporting bias we would expect one or more of these variables to behave outside the norm . Furthermore, the distribution of cancer types parallels that seen in PFOA exposed workers. Even if there were a selection bias with a disproportionate number of patients with cancers, there is no reason to assume that only patients with certain types of cancers would be more likely to volunteer for the study. Our study results are consistent with the literature on PFOA that suggests increased rates of 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 of 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 of "litigation bias" among subjects being followed for health effects from trichloroethylene in their drinking water" 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 of 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 ofthe medical records received all of 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 ofa 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 of reproductive cancers (i.e. cervical/uterine and prostate) is also consistent with the observation of altered reproductive hormones among PFOA exposed workers. 15 Animal studies with ingested PFOA support the findings in this study. 16 The increased risk of respiratory cancer in the residential data with a PR of 7.96 is similar to the occupational data with a hazard ratio of 4.65 for direct PFOA exposure . And there is a doseresponse p-value of 0.08 for increasing odds of respiratory cancer with increasing categories of years exposed at the company. No published worker studies have reported increased risk of respiratory cancers. However, extensive animal data on PFOA toxicity through inhalation supports and strengthens this finding.13 These data show an association between increased cancer prevalence in a human population and exposure to PFOA . Because of wide spread human Page 19 of 38 exposure to this compound these findings are important for public health Page 20 of 38 References : 1 .Doering C. EPA Steps up Study of Teflon Chemical Risk to Humans. Reuters 2003 ; April 14. 2.Shabilina 1G, Panaretakis T, Bergstrand A, DePierre JW. Ca.rcinogenesis 1999; 20(12) :22372246 . 3.Hatfield T. 2001 . Screening studies on aqueous photolytic degradation of perfluorooctanoic acid . St Paul, MN:3M Environmental Laboratory. Lab Request Number E00-2192 . 4.Reiner EA . 1978 . Fate of Fluorochemicals in the Environment. St Paul, MN:3M Environmental Laboratory. Project Number 9970612613 . 5 .GiesyJP, Kannan K. Global Distribution ofPerfluorooctane Sulfonate in Wildlife . Environ Sci Technoi 2001 ; 35 :1339-1342 . 6.Kannan K, Koistinen J, Beckman K, Evans T, Gorzelany JF, Hansen KJ, Jones PD, Helie E, Nyman M, Giesy J. Accumulation of Perfluorooctane Sulfonate in Marine Mammals. Environ Sci Techno12001, 35 ;1593-1598 . 7.Taniyasu S, Kanna K, Horri Y, Hanari N, Yamashita N. A Survey of Perfluorooctane Sulfonate and Related Perfluorinated Organic Compounds in Water, Fish, Birds, and Humans from Japan. Environ Sci Techno12003, 37;2634-2639 . Page 21 of 38 8. Taniyasu SM, Kannan K, Horii Y, Hanari N, Yamnashita N. 2002. The first environmental survey of 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. lO.Moriwaki H, Takata Y, Arakawa R. Concentrations of PerfluorooctaneSulfonate (PFOS) and Perfluoroocatanoic Acid (PFOA) in vacuum cleaner dust collected in Japanese homes. J. Environ. Monit. 2003 ; 5 . 11 .Ubel FA, Sorenseon SD, Roach DE. Health Status of Plant Workers Exposed to fluorochemicals - A Preliminary Report . American Industrial Hygiene Association. 1980, 41(8);584-589 . 12 .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 of Perfluorooctanoic Acid and Its Salts. USEPA. OPPT, Risk Assessment Division. Washington DC. (AR226-1136). Page 22 of 38 14.Gilliland F, Mandel J. Mortality among Employees of a Perfuorooctanoic 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 ofOccupationally Exposed Men. American Journal of Industrial Medicine 1996 ; 29 :560 - 568. 16.Leonard RC. Epidemiology Surveillance Report Cancer Incidence for Washington Works Site 1959-2001 . Haskell Laboratory for Health and Environmental Sciences . E.I. du Pont de Nemours and Company. 2003. USEPA AR OPTT-226-1307. 17 .Aiexander B, Olsen G, Burris J, et al . Mortality of employees of a Perfluorooctanesulphonyl fluoride manufacturing facility. Occupational and Environmental Medicine 2003 ; 60:722-729. iB.SEER. httn ://seer.cancer.gov/ 19. Environmental Working Group. Web Page (htty://www.ewg.org/renorts/pfcworld/partl .phpl 20. Cardiff Software (1991). Teleform standard user guide, version &.2 San Marcos, CA:Cardiff Software Inc 21 .Dupont. Internal Final Report. "A Case-Control Study ofLeukemia At the Washington Page 23 of 38 Works 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 of Risk Ratios . Am. J. Epidemiol. 1972;96(6) : 383-388 . 24.Rothman KJ, Greenland S. Modern 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 of Worker Serum Perflurooctanesulfonate (PFOS) and Perfluorooctanoate (PFOA) Concentrations and Medical Surveillance Examinations . JOEM. 2003, 45(3); 260-270. 27.Olsen G, Hansen K, Stevenson LA, Burris J, Mandel J. Human Donor Liver and Serum Concentrations of Perfluorooctanesulfonate and Other Perflurochemicals. Environ. Sci Technol. 2003, 37; 888-891 . 28 .Olsen 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 of 38 29 .Abdellatif A, Al-Tonsy AH, Awad ME, Roberfroid M, Khan MN . Perixosomal enzymes and 8-hydroxyguanosine in rat liver treated with perfluorooctanoic acid. Dis Markers. 2003 04,19( i ):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 of 38 Acknowledgements : The Law Firm of Winter Johnson & Hill PLLC, Law Firm of Taft, Stettinius & Hollister LLP, Law Firm of Hill, Peterson, Carper, Bee & Deitzler, PLLC . Human Subjects : The study was conducted in accordance with institutional guidelines for the protection of human subjects . Conflict of Interest : The above-mentioned law firms funded this study; the first author of this manuscript is sometimes invited as an expert witness. Page 26 of 38 Table Legend: Table 1 . PFOA levels by Water District/source and percent ofstudy 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) ofcancer (yes/no) and 95% confidence intervals (CI) 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 ofthe U.S. population for Whites and the age distribution of 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 (CI) for selected cancers in an occupationally PFOA-exposed cohort hired between 1950 and 1990 : results of 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 of 38 a department with direct exposure versus those in a department with no direct exposure . Figure Legend: Figure 1 : Example of the Questionnaire Section Pertaining to Cancer Prevalence . Page 28 of 38 Table 1. PFOA levels by water district/source and percent of study subjects reporting water consumption from each source PFOA Levels b 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 Luheck, WV Tuppers Plains, Ohio Belpre, Ohio Mason, WV Pomeroy, Ohio Blennerhassett Oupont, Washington Works" GE Plastics" 68 Private Wells WVA & Ohio Households 4200 3700 4800 6000 4200 1000 71 NIA NIA 68 Estimated as 2.8 people per household bCompany employment reports Abbreviations: NIA Not Applicable Total Population" % total o 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 % stud sample) 161 (27%) 219(37%) 19(3%) 45(8%) 4(0.7%) 1 (0.29'0) 6(1%) 90(15%) 43(7%) 11(2%) 599 Page 29 of 38 Table 2. Frequencies and percents for demographic, social, behavioral and physical characteristics in a residentially PFOA-ex osed population. e Category No. % 20-34 35-44 45-54 105 18 .17 104 17 .99 135 23 .36 55-64 154 26 .64 65-80 80 13 .84 Gender Male Female 284 49 .13 294 50.87 RaceJEthnici White African American Others 558 97 .38 6 1.05 9 1.57 Education Level Less than 9 grade 17 9 -11 grade 59 12 Nocational/Some College 430 College Graduate 65 2.98 10_33 75 .31 11 .38 Body Mass Index Underwei t (<23) Ave e 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 ears 252 60.58 72 17 .31 92 22,12 Work History Plant 1 Plant 2 No plant work - 54 19 500 9.42 i 3.32 i 8726 Page 30 of 38 Table 3. Estimated unadjusted odds ratios (OR) of cancer (yes/no) and 95% confidence intervals (CI) for demographic, social, behavioral and physical characteristics in a residentially PFOA-ex sed population. No.' (%)b OR 95% Cl P-valuec Gender We 25 (8.80%) 1.04 0.58 - 1 .86) 0.90 Female ref, 25 (8.50%) 1 .00 - - Age Category 20 - 34 ref.) 35-44 45-54 55-64 65-80 5(4.76%) 4 (3.88%) 9 (0.67%) 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 9 e 9 grade or hi gher 8(47 .06%) 42 (7.58%) 10.84 1 .00 3.97-29.53 - <0.0001 - Body Mass Index Underwei ght <23) Average (23 - 28) (ref.) Overweight (>28 ) 0.93 8 (7.55%) 0.78 0.33 -1.86) 0.58 18(9 .47%) 1 .00 - - 23 (8.33%) 0.87 0.46 -1 .66) 0.67 Smoking Status Never smoked (ref. Smoked less than 15 ears Smoked more than 15 years 0.16 20 (7.94%) 1 .0 - - 7(9.720/.) 1 .25 0.51 - 3.08) 0.63 12 (13 .04%) 1.74 (0.81- 3.72) 0.15 Work Site Plant 1 Plant 2 No plant em lo ent (ref) 8 14.810%) 1 .87 0.83 -4.22) 0.13 1 5.26%) 0.48 (0 .06 -3.62) 0.47 41 (8.20%) 1 .0 - - 'Number of cancer observations considered in the logistic procedure b % with cancer in each category. Bolded p-value refers to the p-value for a test for trend Table 4. All cancer prevalence rates per 100,000 in PFOA-exposed residents compared to the US population rates for Whites by age and gender Males Females Prevalence Ratio Age Group Age Specific Rates USs Age Specific Rates P" Age Specific Rates US) Age Specific Rates (EP) 20-34 338 1,923 451 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) bEP = Residentially PFOA-exposed population EPIUS 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 of 38 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 of the general U.S . population and the age distribution of the exposed ulation. Number Observed Expected CANCER TYPE of Rates' Ratesb Cl ~ Cancers (per 100,000) (per 100,000) PR All Cancer 50 8,651 3,426 2.58 1 .91 - 3 .47* UterinelCervical d 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 bInternaliy standardized rates per 100,000, age adjusted using the distribution in the PFOA exposed residents, SEER 2000 . ` Confidence Interval d 7 women reported cervical and 6 reported uterine cancer, 3 women reported both * Confidence interval excludes the null value Page 33 of 38 Table 6. Numbers and percents for demographic and work characteristics in an occupationally PFOA-exposed population. Birth Cohort 1900-1919 1920-1939 1940-1959 1960-1989 No. 160 1209 2203 682 % 3.76 28_42 51 .79 16 .03 Gender Male Female 3583 84 .23 671 15 .77 Years of Occu pational Ex posure <21 years 1266 21-29 1462 30-50 1366 30.92 35 .71 33 .37 Department No direct PFOA ex osure Direct PFOA exposure 2157 1388 60 .85 39 .15 Page 34 of 38 Table 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 azard wlcancer Ratio l -value Pancreatic cancer No direct exposure 2(0.09%) 1 .00 Direct PFOAexposure 6(0.48%) 4.46 (0.87,22 .91) 0.07 Respiratory cancer Nodirect exposure 11(0 .51%) 1 .00 Direct PFOA exposure 26(2.10%) 4.41 (2 .13,9 .13) <0 .0001 Kidney cancer No direct exposure 6(0.28%) 1 .00 Direct PFOA exposure 11(0 .89%) 3.14 (1 .10,8.95) 0.03 Colon/rectal cancer No direct exposure 9(0.42%) 1 .00 Direct PFOA exposure 11(0 .89%) 2.96 (1 .15,7.64) 0.02 Prostate cancer" No direct exposure 14(0 .65%) 1 .00 Direct PFOA exposure 23(1 .86%) 2.51 (1 .24,5.08) 0.01 Non-Hodgkin's Lymph No direct exposure 3(0.14%) 1 .00 Direct PFOA exposure 3(0.24"/0) 2.44 (0.47, 12 .73) 0.29 Bladder cancer No direct exposure 10(0.46%) 1 .00 Direct PFOA exposure 10(0.81%) 1 .46 (0 .59,3 .54) 0.41 Liver cancer No direct exposure 1(0.05%) 1 .00 Direct PFOA exposure 1(0.08%) 1 .13 (0.06.23.07) 0.94 - Page 35 of 38 No. (1/6) of all those in category w/cancer Breast cancer No direct exposure S(0.23%) Direct PFOA exposure 1(0.08%) a Women excluded from analyses Hazard Ratio 1.00 0.21 C1 (0.02, 1 .88) P-value 0.16 Page 36 of 38 Table 8. Dose response for cancer incidence with increasing years of occupational exposure using adjusted odds ratios (OR) and 95% confidence intervals (CI) for selected cancers in an occupationally PFOA-exposed cohort hired between 1950 and 1990 : results of a logistic regression analysis controIlin for age at hire and department. Cancer Type OR 95% CI P-Value Prostate <21 years' 21-29 30-50 _ 1 .0 2.68 8.71 0.82-8.79 2.63-28 .83 0.0002 - 0.10 0.0004 Kidney <21 ears 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 ears 21-29 30-50 _ 0.07 1.0 - - 1 .42 0-61-3 .30 0.42 1 .47 0.63-3.43 0.37 Bladder 0.17 <21 years 1.0 - - 21-29 1 .30 0.40-4.24 0.66 30-50 2.09 0.59-7.40 0.29 Colon/Rectal 0.24 <21 years 1 .0 - - 21-29 0.38 0.10-1.50 0.17 30-50 1 .41 0.50-4.00 0.52 Pancreatic 0.35 <21 ears 1 .0 - - 21-29 1.71 0.28-10.49 0.56 30 - 50 1.92 0.28-13.20 0.51 a Years of occupational exposure b Bolded p-value refers to the p-value for a test for trend Page 37 of 38 Figure 1 : Questionnaire Have you ever been told by a doctor that you have cancer'? O Yes O 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 canoer(s) and when you were diagnosed. Yes No Year Yes No Year O O Hodgkin's O O Non-Hodgkin's O O Other Lymphoma O Leukemia O O Multiple Myelorna O 0 Thyroid Il i I - O O Lung O O Bone O O Stomach O O Liver O O Kidney O O Pancreas 11111 11111 11111 11111 O 0 Testicular Ll I T] O OColon O O Breast O O Rectal O O Uterine O O Cervical O 0 Ovarian O O Brain O O Mouth,Nose,Throat UID Other Cancer Type O 0 Prostate O O Skin O O Melanoma O O Bladder O O Gall Bladder O O Other H I F1 Li I 1-111-1 11111 Pagc 38 of 38 p. 44 NORTHERN KENTUCKY OFFICE SUITE 340 1717 OWE HIGHWAY COVINGTON. KENTUCKY 41011-4704 606,as1-2+ae sts-3s1-2ea FAX: 5133a1-Oi13 DAYTON. OHIO OFFICE SUITE 900 110 NORTH MAIN STREET DAYTON. 0100 4W2 1736 937-220-26bD FAX: 937-221-2816 'i . .~T, STETTINIUS 8 HOLLISTER L-.- 425 WALNUT STREET, SUITE 1 800 CINCINNATI, OHIO 45202-3957 513-381-2838 FAX : 513-381-0205 1NVNW.Wh{ari.COT RoaERTA. SiioTr (513) 357-9638 bilott@taQlaw.corn April 21, 2004 TELECOPY AND FEDERAL EXPRESS CLEVELAND, OHIO OFFICE 7500 BP TOWER 200 PUBLIC SCtUARE CLEVELAND, OHIO 44114-2-102 216-241-2e3e FAY- 2141-241-3707 COLUMBUS . OHIO OFFICE 21 EAST STATE STREET COLUIRBVS, OHIO 432154121 614-221-2629 FAx:61e .221.2007 Dr. Charles M. Auer Chemical Control Division Office of 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 4410S Washington, DC 20004 Re: PFOA Human Health Effects Studv: Cancer Data WO i62920. t 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 of Environmental Toxicology and Chemistry (SETAC) meeting in Prague, Czechoslovakia referencing cancer rates among individuals exposed to PFOA-contaminated drinking water in communities near E.I . 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 of this study to USEPA under Section 8(e) of 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 lluS database for PFOA . ~--kobert A. ~Bilo'-tt 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 .1. Rapien, Esq. (w/ attachment) WD162920.1 p. 46 NORTHERN KENTUCKY OFFICE SUITE 340 1717 DI HIGHWAY OVINGTON, KENTUCKY 41011-4704 806-331-2838 St3-301-2838 FAX: 513-381-6613 DAYTON. OHIO OFRCE SUITE 900 110 NORTH MAIN STREET DAYTON. ONO }5402-1766 937-228-2.078 FAx: m-228-2e16 TAFT, STETTINIUS & HOLLISTER LLP 425 WALNUT STREET, SUITE 1800 CINCINNATI, OHIO 45202-3957 513-381-2838 FAX : 513-381-0205. www .taitlaw.cam ROBFRT A. BlLorr (513) 357-9638 bilott@taftlaw.com June 2, 2004 TELECOPY AND FEDERAL EXPRESS CLEVELAND, ONKIOFF= 5800 BP TOWER 200 PUBLIC SQUARE CLEVELAND, 01*0 44114-2302 216-241-2838 ' FAX : 2,6-241-3707 COLUMBUS, OHIO OFFICE 21 EAST STATE STREET COLUMBUS, OHIO 43215-M1 614-221-2638 FAX:614-221-2007 Dr. Charles M. Auer Chemical Control Division Office of Prevention, Pesticides and Toxic Substances United States Environmental Protection Agency 1201 Constitution Avenue, N. W. . Room 3166A 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 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 Jennifer Seed United States -Environmental Protection Agency 1201 Constitution Avenue, N. W. Room 6334A Washington, DC 20004 Mary Ellen Weber Chemical Control Division United States Environmental Protection Agency 1201 Constitution Avenue, N.W. Room 5124A 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 4410S Washington, DC 20004 Re : PFOA Human Health Effects Study: Cancer Data WQ184092 .1 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 US EPA's prior requests for available information regarding the potential threat to human health or the environment from PFOA, we have attached copies of 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 of 2004 . These abstracts reference some of the age-adjusted. data discussed more generally in the abstract that we forwarded to you on April 21, 2004 . All of the abstracts refer to data generated in connection with the same study of 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 (wl attachments) Mark Garvey, Esq. (USEPA) (w/ attachments) R. Edison Hill, Esq. (wl attachments) Larry A. Winter, Esq. (wl attachments) Gerald J. Rapien, Esq. (w/ attachments) Woisao92_ 1 p. 48 NORTHERN KENTUCKY OFFICE SUITE 340 1717 DOW HIGHWAY COVINGTON. KENTUCKY 41011-4704 i06J31-2636 513-3614l36 FAX: S13-U1-4613 DAYTON. OHIO OFFICE SUITS 900 110 NORTH MAIN STREET DAYTON. OHIO 43402-17II8 937-228-28.111 FAX: 937-226-2816 RosEa7 A. BiioTT (513) 357-9638 bilDttataPoaw.com T~.";T, STETTINIUS & HOLLISTER LL. 425 WALNUT STREET, SUITE 't800 CINCINNATI, OHIO 45202-3957 513-381-2838 FAX: 513-381-0205 1MWw.Wftlaw.COf11 CLEVELAND. OHIO OFFICE 3S00 BP TOWER 200 PUBLIC SQUARE CLEVELAND. ONO 44114-2302 216-241-2638 FAX: 216-241-3707 COLUMBUS. ONO OFFICE 21 EAST STATE STREET COLUMBUS. OHIO 43216-4221 614-221-2636 FAX: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 5~124A Washington, DC 20004 Mary Dominiak USEPA 1201 Constitution Avenue, N.W. Room 4410S Washington, DC 20004 January 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 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 of data generated in connection with a survey of adverse health effects among individuals exposed to PFOA-contaminated drinking water in communities near E .1. duPont de Nemouts 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 wo3so205.i Dr. Charles M. Auer Oscar Hernandez Jennifer Seed Mary 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 of the community near DuPont's Washington Works Plant in West Virginia. As with the prior study data, we request that you include this information in AR-226, OPT-2003-0012, and the appropriate IRIS database for PFOA . RAB/mdrn Enclosures cc: IRIS Submission Desk (w/ encls .) Mark J. Garvey, Esq. (USEPA) (w/ encls.) R. Edison Hill, Esq. (w/ encls.) Larry A. Winter . Esq. (w/ encis.) Gerald J . Rapien, Esq. (w/ encls.) W0350205 .1 p. 50 NORTHERN KENTUCKY OFFICE SUITE 340 1717 DIXIE HIGHWAY COVINGTON . KENTUCKY 41011-4704 606J31-2838 513-381-2838 FAX: S13-381-6613 DAYTON. 01410 OFFICE SUITE 900 110 NORTH MAIN STREET DAYTON. OHIO 45402-1786 437-228-7838 FAX ; 937-228-2816 ROBERT A- BIIOTT (513) 357-9638 bilott@tattlaw .tom ~ - .=T, STETTINIUS &HOLLISTER LL. 425 WALNUT STREET, SUITE 1800 CINCINNATI, OHIO 45202-3957 513-381-2838 FAX: 513-381-0205 www.taftlaw.com CLEVELAND. OHIO OFFICE 3500 BP TOWER 200 PUBLIC SQUARE CLEVELAND, OHIO 44114-2302 214-241-2838 FAX: 216-241-3707 COLUMBUS, OHIO OFFICE 21 EAST STATE STREET COLUMBUS, OHIO 43215-4221 614-221-2838 FAX: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 4410S 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 of data generated in connection with a survey of adverse health effects selfreported 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-i714-16, and AR-226-1893-94) . As a supplement to those previous submissions, we have enclosed a copy of several tables providing more detailed summaries of the age-adjusted, self- W0350205_1 Dr. Charles M. Auer Oscar Hernandex Jennifer Seed Mary Ellen Weber Mary Dominiak February 7, 2{}05 Page 2 reported cancer data from the PFOA community health study. (Exhibit 1) 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 of 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 of the public water suppliers to the community at issue, which discuss the increasing levels of 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: CRIS Submission Desk (w/ encls.) Mark J. Garvey, Esq. (USEPA) (w/ encls.) R Edison Hill, Esq. (w/ encls.) Larry A. Winter, Esq. (w/ encis.) Gerald J. Rapien, Esq. (w/ encls.) W0350205 . 1