Document 7LqpNX2YZMx8gbdq0pozx8bE

FINAL REPORT Epidemiology, 220-6W-08 Medical Department 3M Company St. Paul, MIN 55144 Date: June 14,2013 Title: Perfluoroalkyl Biomonitoring Assessment of the 3M Decatur 304 Remediation Project Study Start Date: October 29, 2012 Protocol Number N/A IRB Approval N/A Principal Investigator: Co-investigators: Geary W. Olsen, D.V.M,, PhD. Betsy D. Buehrer, D.O., MPH." DavidJ. Ehresman, B.S., MT (ASCP) Study Director Carol A. Ley, MD, MPH. 1. Corporate Occupational Medicine, Medical Department, 220-6W-08, St. Paul, MN 55144 2. Toxicology Laboratory, Tox Assmt & Compl Assurance, Medical Department, Mail Stop 236-1B-22, St. Paul, MN 55144 Summary "The purpose of this report is to provide a descriptive analysisof the perfluorooctanoate (PFOA) and perfluorooctanesulfonate (PFOS) serum concentrations (ng/mL) measured at baseline and end-of-project time periods for workers involved in the 3M Decatur 304 project Atthe end of 2012, a remediation project was performed on process piping and vessels associated with the 304 reactor system in Building 3 at 3M Decatur. A total of 34 workers (33 contract workers and 1 3M employee) participated in the biomonitoring assessment for this remediation project. Overall, these workers had a statistically significant increase in the mean matched-pairserum concentrations for PFOA [20.1 ng/mL (95% C1 10.8 - 29.5) ] and PFOS [67.7 ng/mL (95% C1 39.0 ~96.3)]. These increased PFOA and PFOS concentrations were not significantly associated with the changes measured in total cholesterol, non-HDL, HDL, and the totalcholesterol HDL ratio during the same time period. Introduction Several 3M remediation projects have been completed regarding legacy perfluoroalkyls. In Minnesota, these projects have included the 3M Cottage Grove Building 15/73 demolition and disposal project, the 3M Woodbury landfill remediation project, the 3M Oakdale landfill remediation project, the 3M Cottage Grove Building25 re-roof project, the 3M Cottage Grove DI/D2 and DO projects, and the East Cove remediation projects. Also finalized was the biomonitoring assessment of SKB Environmental employees who hauled waste material from these projects and subsequently deposited it in the SKB Environmental licensed industrial landfill operations located in Rosemount, Minnesota. Atthe 3M Decatur (Alabama) facilities, remediation activities focused on the demolition and disposalofthe Buildings 2/48/49 (Olsen et al. 2011). Recently completed was the work on the Decatur 304 project within Building 3 at Decatur. For allofthese 3M projects in Minnesota and Alabama, baseline and end-of-project assessments were required of 3M employees and contractor workers who entered specified work zones where potential exposure to legacy perfluorochemicals (PFOA and PFOS) was possible but due to the uniquenessofthe work the magnitudeof exposure wasunknown. Both baseline and end-of-project assessments required response to a medical questionnaire and blood (serum) measurements of PFOS, PFOA, and several clinical chemistries. "The purpose of this report is to provide a descriptive analyosftihse PFOA and PFOS. serum concentrations (ng/mL) at baseline and end-of-project time periods for the 3M Decatur 304 project. At the end of 2012, demolition was performed on process piping and vessels associated with the 304 reactor system in Building 3 at 3M Decatur. In addition, the flaker that was located in close proximity10 the 304 Area, had to be temporarily relocated until the demolition in the 304 Area was completed. Once relocated, the flaker was repositioned in close proximity to its original location and new duct work was run from the main exhaust duct in the area back to the flaker. Historically, the flaker was utilized to flake and packagesome C8-based materials. It should be noted that when the section of duct work was removed from the flaker to the main exhaust duct tie-in in the area, there was approximately 0.75 inches of residual material `which had accumulated over time in the bottom of the removed duct. Contractors involved in this remediation providedjob safety analyses. As an example, ajob safety analysis (SA) for the performanceofthe 304 demolition work provided three levelsofpersonal protective equipment (PPE) requirements based on the natureof the task being performed associated with the project. `These levels were identified as being Level | PPE, Level Il PPE, and Level 111 PPE. Level I PPE, corresponded to most stringentofthe PPE requirements and was utilized for tasks which were expected to have the highest exposure potential to residual materials in the process equipment. An example ofa task with Level 1 PPE requirements would be the sawing and removal of process piping. Other tasks which were performed as partofthe project withlesserexposure potential have the corresponding task-specific level of PPE requirements Methods 1. Informed consent "The purpose of the project was explained in an Informed Consent. Subjects read and signed this informed consent at both baseline and end-of-project assessments. Subjects were informed they could not work on this specific project without such compliance. 2. Clinical chemistries Unlike previous biomonitoring assessments, clinical chemistries for the Decatur 304 project involved only a lipid panel profile. This was an inadvertent orderingmistakeby the nurse who requested this panel. Not included, therefore, were blood glucose, BUN, creatinine, serum electrolytes, and liver enzyme tests (including alkaline phosphatase, AST, ALT, and total bilirubin). Fasting was not a requirement becauseof the logisticsofcollecting blood samples during various times ofthe day. The lipid clinical chemistries were analyzed by Quest Diagnostics. Lipid analyses at baseline and at end-of-project were medically reviewed by Dr. Buehrer. Subjects were informed in writing that this examination program was nota full medical "check-up." Values out of reference range were indicated with a notation for the subjects to follow up with their primary care physicianifthey had abnormal test results. However, questions could be directed to Dr. Buehrer regarding their ipid test results should the subject so desire. 3. Analytical measurements ofPFOA and PFOS Serum samples were analyzed for PFOA and PFOS by state-of-the-art high performance Tiquid chromatography mass spectrometry methods by the 3M Medical Department's Toxicology Laboratory under the direction of Dave Ehresman Medical Department personnel collected blood samples that were processed to provide serum samples for analysis. These samples were assigned unique identification numbers prior to the samples being delivered for analysis. The 3M Medical Department's Toxicology Laboratory was "blinded" to the identityofall samples received for analysis Sample extractions were performed using solid phase extraction (SPE) technique. The extraction and sample clean-up was based on a 100 uL sample size and utilized Waters (Milford, MA) Oasis hydrophilic-lipophilic balance (HLB) 3.0mL cartridges (Eresman et al. 2007) `The method used two stable labeled intemal standards for quantitation. The intemal standards used were a dual labeled PFOS where two '*0 molecules were included in the sulfonate group (intemal standard, >99% purity, synthesized by Research Triangle Institute, Research Triangle Park, NC) and a dual labeled PFOA molecule, where the carboxyl and alpha carbons were labeled with "C stable isotope (greater than 97%, provided by DuPont, Wilmington, DE). All quantitations were based on matrix matched extracted standard curves. AS ul injectionof the sample eluate was introduced into the High Pressure Liquid Chromatograph (HPLC) which was directly interfaced into the triple quadrupole mass spectrometer (Applied Biosystems/MDS-Sciex Instrument Corporation, Forest City, CA). Standard curves covered the range from 1.0- 150 ng/mL. Standard curves were evaluated usinag quadratic regression model where the standards were weighted at 1/x, and each curve had an **R" value equal to or greater than 0.9998. Matrix spiked controls (QC samples) evaluated during this study all had acceptable results "within" their previously established ranges. Matrixmatched dilutions were used for samples requiring dilution to bring the samples into the linear rangeofthe assay. Extracted serum and aqueous blanks remained below the lower limit of quantitation established at 1.0 ng/mL. (lowest standard fied on the standard curve used for this project). 4. Data Analyses Because the data are paired samples, a matched-paired statistical analysis was performed where the mean value was determined for the average of the sum of the individual differences for the participants. See Equation | Equation 1. Mean Change = (end-3o4fp-apnriocjsec-t baseline)/34 `The mean `matched-pair" change was calculated for PFOA, POS, total cholesterol, nonHDL cholesterol, HDL cholesterol, and a total cholesterol/HDL ratio. Ninety-five percent confidence intervals were calculated for this mean `matched-pair' change. Linear regression analyses examined the change in the clinical parametbeyr the change in the perfluoroalkyl concentration. Crude and adjusted coefficients were calculated. Covariates. included in the adjusted analysis were 1) days between baseline and end-of-project measurements; and 2) thesubject's body mass index at baseline (BMI). 5. Communication After each blood collection, individual letters were sent to the participants describing their lipid results. In the baseline assessments, two letters were sent. One referred to the lipid chemistries and the other letter provided baseline PFOA and PFOS concentrations. At the endof-project, twa letters were again sent to each participant. The first letter provided the individual's lipid results. The second letter compared baseline to end-of-project serum PFOA and PFOS concentrations. Aggregate (non-identifying) results were communicated to supervisors representing the participating contractors identified immediately below as Contractor "A", Contractor "B", and Contractor * C." Results A totalof 34 workers involved in the Decatur 304 project had baseline and end-of- project biomonitoring assessments. Oneofthese workers was a 3M employee; the others were involved with contractor companies (number of workers in parenthesis): Contractor "A" (19); Contractor "B" (4); Contractor "C" (6); Contractor "D" (2); and Contractor "E" (2). There were 11 contract workers who participated in only a baseline assessment. Reasons for the nonparticipation at the end-of-project included: 1) some individuals never participated in the Decatur 304 project once it began; 2)others had left the contractor prior to completionof the project; and 3) others did not participate. Figure 1 and Figure 2 show the relationship between baseline and end-of project PFOA and PFOS concentrations, respectively, for the 34 workers who had paired measurements. Values above or below the diagonal line represent increased or decreased changes. The majority of individuals had their PFOA and PFOS concentrations increase whileworking on the Decatur 304 project (i ., their valueswereabove the diagonal line in these 2 figures). Overall, the 34 workers had statistically significant mean matched-pair increases of 20.1 ng/mL for PFOA and 67.7 ng/mL for POS while working on theDecatur 304 project (Table 1) `The mean amount of time between baseline and end-of-project blood collections was 103 days (95% C199 - 107; range 86 127). The median matched-pair changes for PFOA and PFOS were comparable to the mean matched-pair changes (Table 1). The largest changes occurred with `Contractor A where the mean matched-pair changes were 29.9 ng/mL. for PFOA and 106.0 ng/mL for PFOS (Table 2). Contractor A was directly involved with the demolition performed `on process piping and vessels associated with the 304 reactor system in Building 3: thus workers had the greatest potential for exposure. Results for contractors (D and E), who only had 2 workers each involved with the project, are not displayed in Table 2 to protect the confidentiality of the individual data (i.e. the range of data would have identified the 2 individual values for the contractor). The concentration changes were comparable to those reported for the ranges seen with Contractors B and C in Table 2 `Table 3 provides the distributionof pid clinical parameters at baseline and end of project for the 34 workers. There were no statistically significant mean matched-pair changes in total cholesterol, non-HDL, HDL, or total cholesterol/HDL ratio (Table 4). These nonsignificant mean matched-pair changes included lower total cholesterol, non-HDL, and HDL values. Excluding individuals who reported they did not take lipid lowering medications, the remaining 29 individuals' mean matched-pair changes for PFOA and PFOS (Table 5) were comparable to those reported for all workers (Table 1). These 20 individuals did not have significant changes in their lipid parameters (Tables 6 and 7). Including only workers (n = 21) who did not self-report taking cholesterol lowering medications and had end-of-project PFOA and PFOS concentrations higher than baseline levels, the findings resulted in somewhat higher mean matched pair changes of PFOA (30.9 ng/mL) and PFOS (100.9 ng/mL) (Table 8). Mean lipid changes trended nonsignificantly lower (Tables 9 and 10). Tables 11,12, and 13 provide the linear regression results for the 3 groupsof workers discussed above: all workers (n = 34); those not taking lipid lowering medications (n= 29); and those not taking lipid lowering medications with only increased PFOA and PFOS concentrations (n=21), respectively. The changes in total cholesterol, non-HDL, and total cholesterol/HDL ratio were not significantly associated with the changes in PFOA or PFOS in anyofthese analyses. The change in HDL was negatively associated with the change in PFOA and POS for all subjects (Table 11) but became less so with the more restricted worker categorizations and analyzing for adjusted coefficients (Tables 12 and 13). Covariates in the adjusted regression models included BMI [mean BMI = 30.6 (95% CI 28.5 - 32.7; range 20.7 - 49.2) and days between perfluoroalkyl blood collections (mean = 103 days)] Discussion Comparisonofbaseline and end-of-project serum concentrations of PFOA and PFOS. provided each workear method to assess his/her exposure experience in the Decatur 304 remediation project located in Building 3. Given the fact that exposure potential during the courseof the remediation project was unknown, the use of biomonitoring data allowed for an assessmentofthe actual exposure. These analyses indicated there were occupational exposures for the majority of workers involved with this project with average increases in serum PFOA and serum PFOS concentrations over baseline values of approximately 50%. Mean matched pair increases were approximately 20 ng/mL and 70 ng/mL, respectively. Because the biomonitoring data indicated there were increases in serum PFOA or PFOS concentrations, the clinical chemistry data were analyzed in relation to these changes. Potential exposure to any other material would not be known since only PFOA and PFOS were analyzed in the workers' serum. Total cholesterol, non-HDL cholesterol, and the total cholesterol/HDL ratio were not associated with the increased concentrations of PFOA and PFOS. A modest, nonsignfiicant inverse association was observed with changes in HDL and PFOA or PFOS although interpretation is difficult becauseofthe relatively few workers involved in this Decatur 304 project. `The increased PFOA and PFOS concentrations observed among the workers in the Decatur 304 project were lower than the PFOA increases reported for workers involved with the Cottage Grove Building 15 Phase I demolition project (Olsen et al. 2010). In this Cottage Grove project, 45 workers involved in the demolition of Building 15 had higher end-of-project PFOA concentrations than at baseline, indicating occupational exposure to PFOA. For these 45 workers, the mean number of days between their paired measurements was 96 days (range 23 251). The 45 subjects' mean matched-pair PFOA concentration increase was 133.7 ng/mL. (95% C1873 180.2; p<0.0001). The mean matched-pair difference for PFOS was 5.0 ng/mL (95% CI (-03)- 10.2; p= 0.07). The lack of any substantial changes for PFOS was due to the fact that, unlike PFOA, PFOS had not been manufactured in Building 15 for several decades `There were no statistically significant adverse changes among these 45 workers' serum lipids, renal function or liver clinical chemistries related to the change in serum PFOA concentration from baseline to end-of-project. A similar analysis was conductedof 47 workers at 3M Decatur who were involved in the demolitionof Buildings 2/48/49 (Olsen et al. 2011). Their end-of-project PFOA and PFOS. concentrations increased (or remained the same) and had mean matched-pair concentration increases of 10.3 ng/mL for PFOA and 12.0 ng/mL for PFOS, respectively (both p < 0.0001), For these 47 subjects, there were no statistically significant mean changes for total cholesterol (-1.4 mg/dL, p =0.70) or non-HDL (-4.2 mg/dL, p = 0.22). There was a statistically significant increase in the mean HDL (2.8 mg/dL,p = 0.006). Linear regression analyses did not result in statistically significant associations between changes total cholesterol, non-HDL, and HDL with the increased concentrations of PFOA and PFOS. As reviewed by Steenland etal. 2010) and Olsen et al. (2012) positive associations have been reported between PFOA concentrations and non-HDIL cholesterol levels in cross-sectional investigations of a random sample ofthe non-institutionalized United States general population (Nelson etal. 2010) via the National Health Nutrition Examination Survey (NHANES) and a mid-Ohio River community affected with contaminated drinking water (Steenland et al. 2009; Frisbee et al. 2010). Other large cross-sectional epidemiologic studies have (Eriksen etal. 2012) and have not (Patel etal. 2012;Fisher et al. 2013) observed such associations. The magnitude of the non-linear associations reported in cross-sectional studies has not been observed in crosssectional studies of perfluoroalkyl manufacturing workers (Sakr etal. 2007a; Olsen and Zobel 2007) or observed in longitudinal (Sakr et al. 2007; Olsen et al. 2012) investigationsofworkers (Sakr et al. 2007b; Olsen etal. 2012). The positive epidemiologic associations from crosssectional studies are contrary to well-established modes of action reported in toxicology studies that have demonstrated a hypolipidemic effect (Olsen et al. 2012). Nevertheless, Fletcher et al (2013) recently reported several associations between serum PFOA and PFOS levels and changes in the expression of human genes involved in either cholesterol transport or mobilization. Fletcher et al. suggested this led to a "hyperchoesterolemic environment". However, theirfindings have minimum diagnostic or predictive value because they only evaluated transcript concentrations in peripheral lymphocytes without other functional measures such as protein concentrations, free cholesterol and esterified cholesterol content of the cells, or enzyme activity. Conclusion A total of 34 workers participated in a biomonitoring assessment of the Decatur 304 project. The majorityofworkers had occupational exposure to PFOA and PFOS during the courseof the project. The mean change in concentration was 20.1 ng/mL and 67.7 ng/mL, respectively, that occurred over a mean duration of 103 days. Thefindings did not suggesta positive association between increasing cholesterol levels and PFOA/ PFOS concentrations. The study was limited because of its small sample size, the limited durationof follow-up, and the inadvertent omission to analyze for other clinical parameters. References Ehresman DJ, Froehlich JW, Olsen GW, Chang SC, ButenhoJfLf. 2007. Comparison of human `whole blood, plasma, and serum matrices for the determination of perfluorooctanesulfonate: (PFOS), perfluorooctanoate (PFOA), and other fluorochemicals. Environ Res 103:176-184, Eriksen KT, Raaschou-Nielsen O, McLaughlin JK, Lipworth L, Tionneland A, Overvad K, Sorensen M. 2013. Association between plasma PFOA and PFO levels and total cholesterol in a middle-aged Danish population. PLOS One. 2013;8:doi: 10.1371journal pone. 0056969. Fisher M, Arbuckle TE, Wade M, Haines DA. 2013. Do perfluoroalkyl substances affect metabolic function and plasma lipids? Analysis of the 2007-2009 Canadian Health Measures Survey (CHMS) Cycle 1. Environ Res 2013;121:95-103, Fletcher T, Galloway TS, Melzer D, Holcroft P, Cipelli R, Pilling LC, Mondal D, Luster M, Harries LW. 2013. Associations between PFOA, PFOS and changes in the expression of genes involved in cholesterol metabolism in humans. Environ Int 2013;57-58:2-10. Frisbee SJ, Shankar A, Knox SS, Steenland K, Fletcher T, Savitz DA. 2010. The C8 Health Project: associations between perfluorooctanoic acid and perfluorooctanesulfonic acid and serum lipids in children. Arch Pediatr Adolesc Med 2010;16:860-569. Nelson IW, Hatch EE, Webster TF. 2010. Exposure to polyfluoroalkyl chemicals and cholesterol, body weight, and insulin resistance in the general U.S. population. Environ Health Perspect 118:197-202. Olsen GW, Gibson BA, Ehresman DJ, Madsen DC. 2010. Biomonitoring Assessment of the 3M Cottage Grove Building 15 Demolition and Disposal Project: Phase1. 3M Company. August 20,2010. Olsen GW, Ehresman DJ, Buehrer BD. 2011. Biomonitoring Assessmentof the 3M Decatur Buildings 2, 48, and 49 Demolition and Disposal Project. 3M Company. May 1,201 Olsen GW, Ehresman DJ, Buehrer BD, Gibson BA,Butenhoff JL, Zobel LR. 2012 Longitudinal assessmentoflipid and hepatic clinical parameters in workers involved with the demolitionofperfluoroalkyl manufacturing facilities. J Occup Environ Med 2012;54:974-983 Olsen GW, Burris JM, Burlew MM, Mandel JH. 2003. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. J Occup Environ Med 45:260-270. Olsen GW, Zobel LR. 2007. Assessmentoflipid, hepatic, and thyroid parameters with serum perfluorooctanoate (PFOA) concentrations in fluorochemical production workers. Int Arch Occup Environ Health 81:231-246. Patel CJ, Cullen MR,loannidis JP, Butte AJ. Systematic evaluationofenvironmental factors: persistent pollutants and nutrients correlated with serum lipid levels. IntJ Epidemiol 2012;41:828-843. Sakr CJ, Kreckmann KH, Green JW, Gillies PJ, Reynolds JL, Leonard RC. 2007a. Crosssectional study of lipids and liver enzymes related to a serum biomoafrexkpoesurre (ammonium perfluorooctanoate or APFO) as part ofa general health survey in a cohortofoccupationally exposed workers. J Occup Environ Med 48:1088-1096. Sakr CJ, Leonard RC, Kreckmann KH, Slade MD, Cullen MR. 2007b. Longitudinal study of serum lipids and liver enzymes in workers with occupational exposure to ammonium perfluorooctanoate. J Occup Environ Med 49:1086-1096 Steenland K, Tinker S, Frisbee S, Ducatman A, Vaccarino A. 2009. Association of perfluorooctanoic acid (PFOA) and perfluorooctanesulfonate (PFOS) with serur lipids among adultsliving near a chemical plant. Am J Epidemiol 170:1268-1275. Steenland K, Fletcher T, Savitz DA. 2010. Epidemiologic evidence on the health effects of perfluorooctanoic acid (PFOA). Environ Health Perspect 118:1100-1108. Table 1. PFOA and PFOS Concentrations (ng/mL) at Baseline and End-of-Project with Matched-Pair Changes, All Subjects (N = 34) Baseline End-of-Project MatchedPair Change PEOA PEOS PFOA PEOS PFOA PEOS Mean 413 76 614 1452 201 6170 (95%CD) (155-671) (436-1116) (346-883) (1098-180.7)(108-29.5) (39.0963) Median 41 463 a7 1205 185 582 Range 18-3810 56-5130 43-442 86-4510 (260)-953 (:62)-3253 *Matched-paipr value <0.0001 Table 2. PFOA and PFOS Concentrations (ng/mL) for 3 Contractors Working on Decatur 304 Project at Baseline and End-of-Project with Matched-Pair Changes Table 2A (Contractor A) (N= 19) Baseline End-of-Project Matched-Pair Change Mean 95%Cl Median Ra*pn<g0e.0001 PFOA PEOS PFOA PEOS PFOA PFOS 16.1 414 46.0 147.4 299 106.0% (15-247) (238-590) (33.7-583) (162-1886) (170-428) (647-1472) 102 281 406 1420 233 723 18-736 56-1350 108-995 277-3370 (-155)-953 (:04)-3253 Table 28 (Contractor B) (N= 4) Basline End-of-Project Matched-Pair Change PEOA Mean 298 SE 104 Median ~~ 294 Range 94-510 **p<005 * Standard Error. PEOS PFOA 827 491 197 122 75 563 446-1310 149-688 PEOS PFOA 1276 [CE 353 83 1255 189 433-2160 01-391 PEOS 44.9% 198 48.0 (-13)-850 Table 2C (Contractor ) (N= 6) Baseline End-of:Project Matched-Pair Change PFOA Mean 329 SE 178 Median 194 Rarnege=p 023, F2t6p-1=108200 * Standard Error PEOS 582 219 a1 95-1320 PFOA 366 165 27 43-1150 PEOS PFOA 732 380 432 1 822 [3 86-1160 (97)-201 PFOS 15.0%5%% 402 49 (:304)-709 Tale3DisbatLiipoCnlionicfalPaameers Bsnnd End Pct,A Sect=s4) TealCelW_PLNenTCiWNpDLL Men w w a sian aon amass een Ges e em2 i. M DSEL TCRIDL m 6 a" as Gaon anew Ga Gan [ saw so 6 2a. mes wens wen 2 Table 4. Matched-Pair Changes of Lipid Parameters, All Subjects (N = 34) Mean s%Ch Median "Total Chol 67 (147)-13) -5.0 Non:HDL HDL "Total Chol HDL 54 4 01 (130-23) (39-12) (04-02) -3.0 00 00 Table 5. Matched-Pair Changesof PFOA and PFOS Concentrations (ng/mL) for Subjects Who Self-Reported Not Taking Lipid Lowering Medications (N = 29) Baseline End-of:-Project Matched- Pair Change PFOA PFOS PFOA ~~ PFOS PFOA ~~ PFOS Mean 46.7 849 66.6 1549 19.8% 700% O5%CD) (167-768) (454-1244) 354-978) (1153-1945)(92-305) (71-1028) Median 196 586 ass 1240 177 556 Range 18-381 56-513 108-442 354-451 (:260)-953 (62)-3253 *p<0.001 ** p< 0.0001 Tale. DistroofLip CllPaces Bsn nd EfProje,SulNotTcilitngLispid LosingNicatons(+ 20) 2 SE TeslCel NewpL MDL TawmL ToiCll NewWDL MDL TCL TM i " " as n "w w" sian Gey naw san Go-sn 0 amen 0a Goman Metin i ws " as m w w " an swan wow pa 20. mo was ues dass Table 7. Matched-Pair Change of Lipid Parameters, Subjects Self-Reported Not Taking Lipid Lowering Medications (N = 29) Mean 5%CI) Median Range Total Chol 64 (143)-17) 30 -51)-37 Non-HDL 51 (126-24) -10 53)-30 HDL 13 (40)-15) 00 (200-8 Total Chol/HDL. 1 ((04)-02) 00 (25)-12 Table 8. PFOA and PFOS Concentrations (ng/mL) for Subjects Not Taking Lipid Lowering Yedcaiors `and Whose End-of-Project PFOA and PFOS Concentrations Were: Higher than Baseline: Baseline PFOA POS. Mean 340 88 S%CI) (0-709) (287-889) Median ~~ 99 247 Range 18-381 56-281 *p<0.0001 End-of-Project Matched-Pair Change PFOA PEOS PFOA PEOS 649 169.7 309 1009 (239-1059) (1269-303.6)19.6-42.1) (640-1378) as 1420 20 723 108-442 354-365 (28)-953 (107)-3253 "PTRaObSl0eC.onDcenitrsatitonrsoWfieLbirpiaHdiCtglhieonricntahlanPthe Ba asclionr feSubjemcts(e N =21r )Not Taking Lipid Lowering MedicationsandWhoseEndf-Prject PFOA and --- Mean ose Median Ran ToalChol mw Aen ws oom mew NewdiDL HDL 15 2 as G8an 1s w sow sew TChumpL a (9-50) as 24038 ToalClol m Aste m woos baefua NenHDL HDL TChaltDL 0 " 8 un Ea Gan w " 02 ew wes 2-63 Table 10. Matched-Pair Change of Lipid Parameters for Subjects Self-Reported Not Taking Lipid Lowering Medications and Whose End-of-Project PFOA and PFOS Concentrations Were Higher than Baseline Levels (N = 21) Mean 5%CI) Median Range Total Chol 83 (18.1)-16) 70 -51)-37 Non-HDL HDL 71 "1 ((160)-20) (46)-23) 0 10 (53)-30 (200-8 Total Chol/HDL 01 (04-02) 01 (16)-12 1. Rap ifChm 4dem)hs Reh FO HES) 5. S3 0) -- ee ams Coleee ee SshEaN ee oDwee sen OfToE aa a ame on anes or Meamimme ome ow ems ew Att incon ld hfdsi dn ft Pr a ems en ar oe sew ow 1Bop CofC in i ent Crs iois FF FRR, bitNT Li Lin eon) we an ane es oe po Chm Tethint ao TM om os ones a ann ox Cm oti maton OmslWOWDLES ame os am os own ow ES VA om oar sen o asi ew -- ns a oma aw ems an am on aun on ame on F1s3.Bop gCehBiatCnhae.yinLdet Chr iPenh FF FRR) fai Tog miNb JERSE ane I.EGoe sfWh ntFON at soMiim ees ow ems on A fottrin oted mfdsts tndbt ems en wen aw Figure 1. ScatterplotofBaseline and End-of-Project PFOA Concentrations (ng/mL) for the 3M Decatur 304. Project, N = 34 Subjects. Diagonal is the `identity line' 1000 100 PFOA End-of-Project 10 . 4 1 1 10 100 1000 PFOA Baseline FDiiggounr2aei.iSsthce iadenttiotefyBlapisneell.ineoantd End-of-Project PFOS Concentrations (ng/fmo Lth)e 3M Desstur 304 Project, N = 34 Subjects. 00 pros Ensatpriect 6 : CE They , ros taste