March 23, 2020Leah J. SmithDistrict and Business Support ProgramDivision of Waste ManagementFlorida Department of Environmental Protection2600 Blair Stone RoadTallahassee, FL 32399-2400Re: Update on PFAS criteria development in other statesDear Ms. Smith:At your request, we have reviewed the development of perfluoroalkyl (PFAS) criteria fordrinking water and groundwater by the federal government and states. This documentrepresents an attempt to summarize the current PFAS drinking water and groundwater criteriain the United States and the methods used to calculate them. The summary includes bothpromulgated values and values that are in various stages of an approval process, and isintended to facilitate comparison of approaches for deriving PFAS drinking water andgroundwater criteria by various environmental agencies. We found that transparency inmethods for deriving these criteria varied substantially. For some, there was thoroughdocumentation from the source agency and clear explanations for choices made in approachand assumptions. For others, details regarding the basis for the values were not found or wereobtained indirectly from secondary sources (e.g., documents from other agencies).In 2016, the United States Environmental Protection Agency (USEPA) developed healthadvisory levels (HALs) for perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid(PFOS) in drinking water. A number of states have adopted formally or informally these values(70 ng/L for PFOA, 70 ng/L for PFOS, and 70 ng/L for the sum of PFOA and PFOS) forassessment of PFAS contamination of drinking water and/or groundwater (Table 1). As noted inTable 1, Connecticut has applied the 70 ng/L limit to the sum of a number of specific PFASbeyond PFOA and PFOS, in effect assuming that the toxicity of these additional PFAS is similarto PFOA and PFOS and that their effects are additive.In 2018, the Agency for Toxic Substances and Disease Registry (ATSDR) derivedMinimal Risk Levels (MRLs) for PFOA and PFOS, and from these Environmental MediaEvaluation Guidelines (EMEGs) for drinking water were developed, including values for children.The EMEGs for children were substantially lower than the USEPA HALs — 21 ng/L for PFOAand 14 ng/L for PFOS (Table 2). Several states have also derived their own criteria for PFOA

and PFOS that are different from USEPA HALs, as well as drinking water and/or groundwatercriteria for a number of other PFAS. These criteria are summarized in Table 2. Like the ATSDREMEGs, all of the PFOA and PFOS drinking water criteria developed by states except Nevadaare lower than the USEPA HALs. Explanations for the differences in criteria from the USEPAHALs, and from each other, for most states can be found in Tables 3-5 for PFOA and 6-8 forPFOS. The proposed PFOA and PFOS criteria for Illinois are identical to the ATSDR childEMEGs, and it can be speculated that the intent is for Illinois to adopt the ATSDR values.However, we were unable to confirm this at the time of this report, so the basis for these valuesis not included in Tables 3-8. Also, the proposed New York criteria of 10 ng/L for PFOA andPFOS were not based directly on a specific approach or set of assumptions, but rather reflect amanagement approach given the range of options available. This approach is explained furtherlater in this report, but for purposes of comparisons in Tables 3-8, New York is also notincluded.All of the criteria in Table 2 are based upon non-cancer effects of the various PFAS. Inaddition to non-cancer effects, California also developed drinking water limits based uponcarcinogenicity for PFOA and PFOS, which are lower (see footnote in Table 2). To facilitatecomparison with other states, the criteria shown in Table 2 for California are their non-cancernumbers. Criteria based upon carcinogenicity are discussed later in this report.PFOAThe critical effects used to derive PFOA references are listed in Table 3. A range ofcritical effects were identified by the different states. The USEPA, Massachusetts, Minnesota,Nevada, Vermont, and Wisconsin chose the reduced ossification of phalanges and acceleratedpuberty in mice as the critical effect. The ATSDR, Michigan, and Washington identifiedneurodevelopmental as well as skeletal effects in mice. New Hampshire and New Jersey listedaltered liver function as the critical effect. Finally, California listed increased oxidative DNAdamage and changes in mitochondrial membrane potential in liver as the specific critical effect.Point of departures (PODs), uncertainty factors (UFs), and reference doses (RfDs) forPFOA are listed in Table 4. Using the NOAEL or LOAEL for the critical effect chosen byATSDR or the state, a POD was identified. These PODs are expressed as the humanequivalent dose (HED) for the NOAEL or LOAEL observed in the animal study and range from0.00014 to 0.0053 mg/kg-d. Conversion of the animal dose to an equivalent human doserequires a Dosimetric Adjustment Factor (DAF), which is based upon assumptions regarding thevolume of distribution and half-life of PFOA. Most states used a DAF of 1.4 x 10-4 L/kg-d, butATSDR used 9.9 x 10-5 and New Jersey used 1.6 x 10-4. Differences in DAF help explain, forexample, how ATSDR and Michigan derive somewhat different POD HED values from the samecritical effect in the same animal study.These PODs were divided by the total UF to derive a RfD for PFOA. [Note: Technically,the ATSDR value is termed a Minimal Risk Level, or MRL). States chose a total UF rangingfrom 100 to 1000 (individual UFs are identified in Table 4). Reference doses for PFOA rangefrom 0.45 to 20 ng/kg-d. Drinking water exposure assumptions for PFOA are listed in Table 5.The USEPA and Massachusetts chose the lactating woman as the receptor of concern forPFOA exposure. New Jersey and Nevada chose an adult as the receptor of concern.Wisconsin, Vermont, and the ATSDR chose a child less than a year old (infant) as the receptorof concern. The ATSDR also calculated criteria for an adult receptor. California used a lifetimeaverage normalized drinking water intake rate. Minnesota modeled lifetime intake throughbreastmilk for 1 year of breast feeding followed by continuous exposure in drinking water. Thismodel was also used by Michigan, New Hampshire, and Washington. Relative source2

contributions (RSCs) for PFOA ranged from 0.2 to 1. Several states referenced the USEPAdecision tree for selecting a RSC value. In some cases, the 0.2 value was based on therecommended USEPA default.In other instances, states used information on bloodconcentrations of PFOA in the population and a target blood concentration limit (correspondingto the RfD) to determine an RSC. The calculated drinking water limit was used as thepromulgated or proposed drinking water criteria for PFOA for all states except California. Theydetermined that the calculated value (2 ng/L; Table 5)) was below the detection limit for PFOA inwater, and chose instead a detection limit of 5.1 ng/L for their criterion (Table 2).The USEPA also considered potential carcinogenic effects of PFOA. Based uponLeydig cell testicular tumors in rats in a rodent bioassay and findings of a possible link betweenPFOA exposure and testicular and renal tumors in humans, the USEPA has determined thatthere is Suggestive Evidence of Carcinogenic Potential of PFOA in humans. The USEPA alsonoted that the International Agency for Research on Cancer has classified PFOA as PossiblyCarcinogenic in Humans. USEPA benchmark dose modeling of Leydig cell tumor data in ratsresulted in a BMDL04 (the 95% lower confidence limit on a 4% excess probability of response) of1.99 mg/kg-day, which corresponded to a HED of 0.58 mg/kg-d and resulted in a cancer slopefactor of 0.07 (mg/kg-d)-1. Using this cancer slope factor, the USEPA calculated drinking waterconcentration corresponding to a 1 E-06 excess cancer risk assuming a drinking water ingestionrate of 2.5 L/day and a default adult body weight of 80 kg. The drinking water HAL derivedusing the cancer slope factor was 500 ng/L, compared with 70 ng/L based upon non-cancereffects of PFOA. Because the value was higher than the non-cancer value, the latter was usedas the basis for the USEPA HAL. With the exception of California, other states have explicitly orimplicitly accepted the conclusion that a risk-based criterion for PFOA is driven by non-cancereffects.Recently, California derived a cancer slope factor (CSF) for PFOA using hepatic andpancreatic tumors in male rats as the critical effect. For each tumor site, California’s Office ofEnvironmental Health Hazard Assessment (OEHHA) derived a point of departure using thelinear multistage cancer model from USEPA’s BMD software. The 95% lower confidence limiton the dose associated with a 5% increased risk of developing a tumor was identified as thePOD. Body weight scaling to the ¾ power was used to calculate a human equivalent POD of3.5 E-04 mg/kg-d and a cancer slope factor of 143 (mg/kg-d)-1. Because the toxicity datasuggest early-life exposures to PFOA do not significantly increase tumor formation later in life,OEHHA did not apply age sensitivity factors for the derivation of the cancer slope factor. Alifetime average drinking water rate of 0.053 L/kg-d was used to calculate a one in a millioncancer risk criterion of 0.1 ng/L PFOA. As with the non-cancer criterion described above, thisvalue is below the detection limit for PFOA determined by California, and a detection limit of 5.1ng/L is used as their PFOA criterion (Table 2).PFOSThree critical effects were identified in the derivation of reference doses for PFOS (Table6). The USEPA, ATSDR, Massachusetts, Michigan, Nevada, Vermont, and Wisconsin all listedreduced pup body weight from the Luebker et al. study as a critical effect. The ATSDR,Michigan, and Wisconsin also listed delayed eye opening from this study as a critical effect.California, Minnesota, New Hampshire, New Jersey, and Washington chose suppressedimmune response in mice from Dong et al. 2009 or Dong et al. 2011. PODs, UFs, and RfDs forPFOS are listed in Table 7. PODs range from 0.0000546 to 0.000515 mg/kg-d. To obtain theseHEDs, a variety of DAFs were used, reflecting different interpretation of the data regarding thetoxicokinetics of PFOS. A DAF of 1.3 (or 1.28) x 10-4 L/kg-d was used by Minnesota, NewHampshire, and Michigan, while the USEPA, Massachusetts, and New Jersey used 8.1 or 8.2 x3

10-5 L/kg-d. PODs were divided by a UFs ranging from 30 to 300, with ATSDR, Michigan, andWisconsin applying an additional Modifying Factor (MF) of 10 (individual UFs and MFs areidentified in Table 7). Reference doses for PFOS range from 1.8 to 20 ng/kg-d. Drinking waterexposure assumptions from PFOS are listed in Table 8. Receptors of concern for PFOS indrinking water, exposure assumptions, and RSCs are identical to those chosen for PFOA. Aswith PFOA, RSC values range from 0.2 to 1, with some based on the USEPA default of 0.2,while others were developed based upon serum concentrations in the population intended torepresent background exposure and a target serum concentration limit based upon the RfD.Minnesota and Washington used two age-dependent RSC values — 0.5 for infants and children(or young children) and 0.2 for older receptors.The USEPA determined that there is Suggestive Evidence of Carcinogenic Potential forPFOS based upon liver and thyroid tumors observed in rats. However, they concluded thatthere was a lack of dose-response relationship for these tumors and did not develop a cancerslope factor. California recently derived a cancer slope factor for PFOS using hepatocellularadenomas in male rats and hepatocellular adenomas/carcinomas in female rats as the criticaleffects. OEHHA derived a POD using the linear multistage cancer model from USEPA’s BMDsoftware. The 95% lower confidence limit on the dose associated with a 5% increased risk ofdeveloping a tumor was identified as the POD. Body weight scaling to the 1/8th power(adjustment for pharmacodynamics differences between animals) was used to calculate ahuman equivalent POD of 0.0011 mg/kg-d. These PODs result in cancer slope factors forPFOS of 45.5 (mg/kg-d)-1 for males and 35.7 (mg/kg-d)-1 for females. The higher cancer slopefactor was used to drive a drinking water criterion corresponding to a 1 E-06 excess cancer risk.Because the toxicity data suggest early-life exposures to PFOS do not significantly increasetumor formation later in life, OEHHA did not apply age sensitivity factors for the derivation of thecancer slope factors. A lifetime average drinking water rate of 0.053 L/kg-d was used tocalculate a one in a million cancer risk criterion of 0.4 ng/L PFOS. As with the non-cancercriterion developed by California described above, this value is below the detection limit forPFOS determined by California, and a detection limit of 6.5 ng/L is used as their PFOS criterion(Table 2).New York Management Approach for PFOA and PFOSNew York lists criteria of 10 ng/L for PFOA and PFOS. The derivation of their drinkingwater criteria differed from other states. Briefly, the New York State Drinking Water Councilreviewed other state and agency derivation of drinking water criteria. They identified the rangeof scientifically defensible criteria as 4 to 35 ppt. The Council then chose four possible drinkingwater criteria including the lowest value (4 ppt), 10 ppt, 20 ppt, and the highest value (35 ppt).Impacts for adopting each of the proposed criteria were discussed including number of watersystems that would be out of compliance, reporting limits, and monitoring and compliance costs.Based on this discussion, the council recommended the state adopt the PFOA and PFOScriteria of 10 ppt. The state of New York accepted the council’s recommendation and adopted aPFOA and PFOS criteria of 10 ppt.Other PFASThe ATSDR, Illinois, Massachusetts, Michigan, New Hampshire, New Jersey, Ohio,Vermont, and Washington also developed a drinking water criterion for PFNA. The criticaleffects identified for PFNA include reduced pup weight and developmental delays in mice andincreased liver weight in pups with prenatal exposure, all from the study of Das et al. (2015)(Table 9). Some states used benchmark dose modeling to determine a threshold dose from thisstudy, while others used a NOAEL (Table 10). The ATSDR, Michigan, New Hampshire, andNew Jersey each used a different DAF for PFNA. The POD HED values ranged from 0.000434

to 0.001 mg/kg-d. Total UFs ranged from 100 to 1000. The PFNA RfDs ranged from 0.74 to 4.3ng/kg-d PFNA. Table 11 lists the PFNA exposure assumptions. Receptors of concern include achild (0-1 year), an adult, or lifetime exposure beginning at birth. The ATSDR chose an RSC of1, while the other states used an RSC of 0.5. Massachusetts and Vermont did not calculate acriterion for PFNA using chemical-specific data, but instead applied their PFOA and PFOScriteria (20 ng/L for both PFAS in both states) to PFNA. We were unable to locate the basis forthe Ohio and Illinois PFNA criteria, so they are also absent from the comparisons in Tables 911.The ATSDR, Illinois, Massachusetts, Michigan, Minnesota, New Hampshire, Ohio,Vermont and Washington developed a drinking water criterion for PFHxS. Critical effects forPFHxS include thyroid follicular cell hypertrophy and hyperplasia in rats, reduced serumthyroxine in rats, decreased litter size and reproductive toxicity in mice, and increased liverweight and centrilobular hepatocellular hypertrophy in rats (Table 12). PFHxS reference dosesare summarized in Table 13. The ATSDR estimated the threshold dose for toxicity using aNOAEL while the states all used benchmark dose modeling. A variety of DAFs were used toobtain a HED: ATSDR used 6.42 x 10-5, Minnesota and Michigan used 9.0 x 10-5, and NewHampshire used 8.61 x 10-5 L/kg-d. PODs ranged from 0.0012 to 0.0047 mg/kg-d. Total UFswere consistently 300. Reference doses for PFHxS include 4, 9.7, and 20 ng/kg-d. Table 14lists the PFHxS exposure assumptions. Receptors of concern include an adult, a child, andlifetime exposure beginning at birth. The ATSDR chose an RSC of 1, while the other statesused an RSC of 0.5. Massachusetts and Vermont did not calculate a criterion for PFHxS usingchemical-specific data, but instead applied their PFOA and PFOS criteria (20 ng/L for bothPFAS in both states) to PFHxS. We were unable to locate the basis for the Ohio and IllinoisPFHxS criteria, so they are also absent from the comparisons in Tables 12-14.The states of Illinois, Massachusetts, Michigan, Minnesota, Nevada, Ohio, andWashington developed a drinking water criterion for PFBS. The USEPA developed an RfD forPFBS, but has not yet derived a HAL or other guidance value for PFBS in water. Critical effectsidentified included reduction in thyroid hormones in newborn offspring of mice dosed duringpregnancy from the Feng et al., 2017 study. Other critical effects were taken from two studiesby Lieder et al., (2009a,b) and include increased incidence of kidney hyperplasia in rats andkidney hyperplasia in parent and offspring in a 2-generational study in rats (Table 15). All of thethreshold dose estimates were based upon benchmark dose modeling of toxicity data from thecritical studies. PODs ranged from 0.089 to 18.9 mg/kg-d (Table 16). The POD used byNevada comes from a USEPA PPRTV developed in 2014. In that analysis, a DAF of 0.24 wasused based upon comparison of animal to human body weight. More recent analyses use aDAF derived from assumptions regarding the toxicokinetics of PFBS, which is consistent withDAFs for other PFAS used by the USEPA, ATSDR, and states. These DAFs are orders ofmagnitude lower and more accurately represent the difference in PFAS toxicokinetics betweenlaboratory animals and humans. Total UFs were either 300 or 1000, and the resulting RfDsranged from 230 to 20,000 ng/kg-d. Table 17 lists the PFBS exposure assumptions. Receptorsof concern include an adult, lactating women, and lifetime exposure beginning at birth. Theformula for calculating groundwater concentrations limits in Nevada does not have an RSCterm, so the value is, in effect, 1. The other states used a default RSC of 0.2. We were unableto locate the basis for the Illinois, Massachusetts, or Ohio PFBS criteria, so they are absent fromthe comparisons in Tables 15-17.Only one state, Michigan, was identified with a proposed drinking water limit for PFHxA.The critical effect selected by Michigan is renal tubular degeneration and renal papillarynecrosis in rats. Benchmark dose modeling of the data identified a BMDL10 of 90.4 mg/kg-d. In5

the absence of adequate toxicokinetic data for PFHxA, a HED of 24.8 mg/kg-d based uponextrapolation from rats to humans using body weight. A total UF of 300 was selected (UFH 10,UFA 3, UFs 1, UFL 1, UFD 10), yielding a RfD of 0.083 mg/kg/day (83,000 ng/kg-day). Based onan adult as the receptor, a drinking water ingestion rate of 3.353 L/d, a body weight of 80 kg,and an RSC of 0.2 were used to derive a drinking water concentration limit of 400,000 ng/L.North Carolina, Michigan, and Ohio have drinking water criteria for GenX (Table 2).North Carolina identified the critical effect for GenX exposure as liver toxicity. A NOAEL of 0.1mg/kg-d was used as the point of departure (POD). A total UF of 1000 was applied to the PODto derive a RfD of 1E-04 mg/kg-d, or 100 ng/kg-d. The receptor of concern is a bottle fed infantand the criterion of 140 ng/L was derived using a drinking water ingestion rate of 1.1 L/day, abody weight of 7.8 kg, and an RSC of 0.2. Michigan also identified liver toxicity as the criticaleffect (single cell necrosis in mice) and used benchmark dose modeling to obtain a BMDL10 of0.15 mg/kg-d. Using mouse and human body weight, a DAF of 0.15 was obtained, resulting in aPOD HED of 0.023 mg/kg-d. A total UF of 300 (UFH 10, UFA 3, UFS 3, UFL 1, UFD 3) wasapplied to the POD HED to calculate the RfD, 77 ng/kg-d. As with the PFHxA criterion,Michigan based the GenX criterion of 370 ng/L on an adult receptor, with a drinking wateringestion rate of 3.353 L/day, a body weight of 80 kg, and an RSC of 0.2. We were unable tolocate the basis for the Ohio GenX criterion of 700 ng/L.PFHpA and PFDA drinking water criteria in Table 2 for Massachusetts and PFHpA forVermont, were not based upon specific toxicity data for these chemicals, but rather anassumption that their toxicity would be similar to PFOA and PFOS. Thus, the same criteriadeveloped for PFOA and PFOS were used for these PFAS as well.While nearly all states have information about PFAS on a web page, most still do nothave clearly articulated drinking water criteria. Many without their own criteria mention theUSEPA HALs, but it is often not apparent from information presented whether or how they areusing those criteria. In preparing this report, we note that the toxicity and regulation of PFAS indrinking water is a rapidly evolving field. The information included in these tables is current asof the date of this letter, but it is reasonable to anticipate new or changing PFAS criteria fromstates in the near future.Please let us know if you have any questions regarding this review.Sincerely,Leah D. Stuchal, Ph.D.Stephen M. Roberts, Ph.D.References:Butenhoff JL, Chang S, Ehresman DJ, et al. 2009 Evaluation of potential reproductive anddevelopmental toxicity of potassium perfluorohexanesulfonate in Sprague Dawley rats.Reprod Toxicol 27:331-341.6

Chang S, et al. 2018. Reproductive and developmental toxicity of potassiumperfluorohexanesulfonate in CD-1 mice. Reproductive Toxicology 78: 150-168.Das KP, Grey BE, Rosen MB, et al. (2015) Developmental toxicity of perfluorononanoic acid inmice. Reprod Toxicol 51:133-144. 10.1016/j.reprotox.2014.12.012.Dong GH, Zhang YH, Zheng L, Liu W, Jin YH, He QC (2009). Chronic effects ofperfluorooctanesulfonate exposure on immunotoxicity in adult male C57BL/6 mice. ArchToxicol 83(9): 805-815.Dong GH, Liu MM, Wang D, et al. (2011) Sub-chronic effect of perfluorooctanesulfonate (PFOS)on the balance of type 1 and type 2 cytokine in adult C57BL6 mice. Arch Toxicol85(10):1235-1244.Feng, X, Cao, X, Zhao, S, Wang, X, Hua, X, Chen, L, Chen, L (2017) Exposure of pregnantmice to perfluorobutanesulfonate causes hypothyroxinemia and developmentalabnormalities in female offspring. Toxicol Sci. 155(2): 409-419.Hoberman AM, York RG. (2003) Oral (gavage) combined repeated dose toxicity study of T-7706with the reproduction/developmental toxicity screening test. Argus Research.Koskela, A., Finnila, M.A., Korkalainen, M., Spulber, S., Koponen, J., Hakansson, H.,Tuukkanen, J, Viluksela, M. (2016) Effects of developmental exposure to perfluorooctanoicacid (PFOA) on long bone morphology and bone cell differentiation. Toxicol. Appl.Pharmacol. 301:14-21.Lau, C., JR Thibodeaux, RG Hanson, MG Narotsky, JM Rogers, AB Lindstrom, MJ Strynar.(2006). Effects of Perfluorooctanoic Acid Exposure during Pregnancy in the Mouse.Toxicological Sciences 90(2): 510-518.Li K, Sun J, Yang J, et al. (2017). Molecular Mechanisms of Perfluorooctanoate-InducedHepatocyte Apoptosis in Mice Using Proteomic Techniques. Environ Sci Technol 51(19):11380-11389.Lieder PH, York RG, Hakes DC, et al. 2009a. A two-generation oral gavage reproduction studywith potassium perfluorobutanesulfonate (K PFBS) in Sprague-Dawley rats. Toxicology259:33-45.Lieder PH, Chang SC, York RG, et al. 2009b. Toxicological evaluation of potassiumperfluorobutanesulfonate in a 90-day oral gavage study with Sprague-Dawley rats.Toxicology 255:45-52.Loveless SE, Finlay C, Everds NE, et al. (2006). Comparative responses of rats and miceexposed to linear/branched, linear, or branched ammonium perfluorooctanoate (APFO).Toxicology 220(2-3): 203-217.Luebker, D.J., M.T. Case, R.G. York, J.A. Moore, K.J. Hansen, and J.L. Butenhoff (2005) Twogeneration reproduction and cross-foster studies of perfluorooctanesulfonate (PFOS) inrats. Toxicology 215: 126-148.7

NTP (2018) National Toxicology Program. TOX-96: Toxicity Report Tables and Curves forShort-term Studies: Perfluorinated Compounds: Sulfonates. Retrieved n main.dataReview&bin id 3874 .Onishchenko, N., Fischer, C., Wan Ibrahim, W.N., Negri, S., Spulber, S., Cottica, D., Ceccatelli,S. (2011) Prenatal exposure to PFOS or PFOA alters motor function in mice in a sexrelated manner. Neurotox. Res., 19:452-461.State References:AlaskaADEC (October 2, 2019). Technical Memorandum: Action Levels for PFAS in Water andGuidance on Sampling Groundwater and Drinking Water. Alaska Department ofEnvironmental Conservation, Division of Spill Prevention and Response, ContaminatedSites Program and Division of Environmental Health, Drinking Water Program.CaliforniaOEHHA (August 2019) Notification Level Recommendations: Perfluorooctanoic Acid andPerfluorooctane Sulfonate in Drinking Water. Pesticide and Environmental ToxicologyBranch, Office of Environmental Health Hazard Assessment, California EnvironmentalProtection Agency.DelawareDNREC (July 2, 2018) Policy for Sampling and Evaluation of Per- and Poly- FluoroalkylSubstances (PFAS) in Surface Water and Groundwater. Department of Natural Resourcesand Environmental Control, Division of Waste and Hazardous Substances (DNRECDWHS).MaineMDER (October 19, 2018) Maine Remedial Action Guidelines (RAGS) for Sites Contaminatedwith Hazardous Substances. Maine Department of Environmental Protection, Augusta,Maine.MarylandMDOE (November 2019) Basic Information of PFAS. Maryland Department of the EnvironmentWater Supply Program.Massachusetts8

MassDEP (December 26, 2019) Technical Support Document, Per- and PolyfluoroalkylSubstances (PFAS): An Updated Subgroup Approach to Groundwater and Drinking WaterValues. Massachusetts Department of Environmental Protection, Boston, MA.MassDEP (January 27, 2020) Per- and Polyfluoroalkyl Substances (PFAS) in Drinking Water:Questions and Answers for Consumers. Massachusetts Department of EnvironmentalProtection, Drinking Water Program, Boston, MA.MichiganMDHHS (February 22, 2019) Public heath drinking water screening levels for PFAS. MichiganDepartment of Health and Human Services, Division of Environmental Health, MichiganPFAS Action Response Team Human Health Workgroup.Michigan Science Advisory Workgroup (June 27, 2019) Health-based Drinking Water ValueRecommendations for PFAS in Michigan.MinnesotaMDOH (August 2018) Toxicological Summary for Perfluorooctanoate. Minnesota Department ofHealth, Health Based Guidance for Water, Health Risk Assessment Unit, EnvironmentalHealth Division.MDOH (April 2019) Toxicological Summary for Perfluorooctane sulfonate.MinnesotaDepartment of Health, Health Based Guidance for Water, Health Risk Assessment Unit,Environmental Health Division.MDOH (April 2019) Toxicological Summary for Perfluorohexane sulfonate.MinnesotaDepartment of Health, Health Based Guidance for Water, Health Risk Assessment Unit,Environmental Health Division.NevadaNDEP (July, 2017) User’s Guide and Background Technical Document for the Nevada Divisionof Environmental Protection (NDEP). Basic Comparison Levels (BCLs) for Human Healthfor the BMI Complex and Common Areas. Nevada Division of Environmental Protection,Bureau of Corrective Action, Special Projects Branch, Las Vegas, NVNew HampshireNHDES (June 28, 2019) Rules related to per- and polyfluoroalkyl substances (PFAS). NewHampshire Department of Environmental Services, Concord, NH.NDES (June 1, 2019) Technical Background for the June 2019 Proposed MaximumContaminant Levels (MCLs) for Perfluorooctanoate (PFOA), Perfluorooctane sulfonate(PFOS), Perfluorononanoate (PFNA) and Pefluorohexane sulfonate (PFHxS). NewHampshire Department of Environmental Services, Concord, NH.9

New JerseyNew Jersey Drinking Water Quality Institute (March 15, 2017) Maximum Contaminant LevelRecommendation for Perfluorooctanoic Acid in Drinking Water, Basis and Background.New Jersey Drinking Water Quality Institute.New Jersey Drinking Water Quality Institute (June 8, 2018) Maximum Contaminant LevelRecommendation for Perfluorooctane Sulfonate in Drinking Water, Basis and Background.New Jersey Drinking Water Quality Institute.New YorkNYDOH (December 18, 2018) Drinking Water Quality Council Meeting, December 18, 2018.New York State Department of Health. VOFF&id nysdoh&date 2018-12-18&seq 1North CarolinaNCDEQ (August 2018) Secretaries’ Science Advisory Board Review of the North CarolinaDrinking Water Provisional Health Goal for GenX. North Carolina Department ofEnvironmental Quality and North Carolina Department of Health and Human Services.OhioOhio EPA (December 2019) Ohio Per- and Polyfluoroalkyl Substances (PFAS) Action Plan forDrinking Water. Ohio Environmental Protection Agency and the Ohio Department ofHealth.VermontVDOH (July 10, 2018) Drinking Water Health Advisory for Five PFAS (per- and polyfluorinatedalkyl substances). State of Vermont, Department of Health, Agency of Human Services.WashingtonWDOH (November, 2019) Draft Recommended State Action Levels for Per- and PolyfluoroalkylSubstances (PFAS) in Drinking Water: Approach, Methods, and Supporting Information.Washington Department of Health, Office of Environmental Public Health Services.WisconsinWDOH (June 2019) Perfluorooctanoic acid (PFOA), 2019 Cycle 10. Wisconsin Department ofHealth Services.10

Table 1. States that Use the EPA HALs for PFOA and PFOS*StateAlaskaColoradoCommentConnecticutDrinking Water Action Level is based upon the EPA HAL expanded to include thesum of PFOA, PFOS, PFNA, PFHxS, PFHpA.DelawareFloridaMaineFlorida did not adopt the EPA HALs, but developed numbers that are numericallythe same using the EPA reference doses for PFOA and PFOSRemedial Action Guidelines listed as 0.4 µg/L for PFOA and PFOS in residentialwater, but recommends “that the EPA health advisory level be applied at siteswhere groundwater is currently being used, or may be used in the future, forhuman consu

Mar 23, 2020 · immune response in mice from Dong et al. 2009 or Dong et al. 2011. PODs, UFs, and RfDs for PFOS are listed in Table 7. PODs range from 0.0000546 to 0.000515 mg/kg-d. To obtain these HEDs, a variety of DAFs were used, reflecting different interpretation of the data regarding