50 California St. | Suite 1500 | San Francisco CA 94111 | T: 415-463-5186 | F: 415-358-4467 ann.grimaldi@grimaldilawoffices.com | www.grimaldilawoffices.com

November 16, 2016

VIA EMAIL(P65PUBLIC.COMMENTS@OEHHA.CA.GOV)AND FACSIMILE (916-323-2265)

Michelle Ramirez Office of Environmental Health Hazard Assessment P.O. Box 4010, MS-12B Sacramento, California 95812-4010

Re: Notice of Intent to List PFOA

Dear Ms. Ramirez:

On behalf of 3M Company, I am pleased to submit comments on the Notice of Intent to List perfluorooctanoic acid (“PFOA”). 3M Company also separately is submitting comments on the Notice of Intent to list perfluorooctane sulfonate (“PFOS”). Although some of 3M’s comments on these two chemicals overlap, we believe it is appropriate to submit separate comments on these two separate chemicals to avoid their inadvertent conflation.

The California Office of Health Hazard Assessment (“OEHHA”) proposes to list perfluorooctanoic acid (“PFOA”) as a reproductive toxicant pursuant to the Proposition 65 authoritative bodies mechanism. OEHHA bases the proposed listing on two United States Environmental Protection Agency (“EPA”) documents, the Drinking Water Heath Advisory for Perfluorooctanoic Acid (PFOA) and Health Effects Support Document for Perfluorooctanoic Acid (“EPA PFOA Documents”). As explained below, these documents do not meet the procedural criteria for the Proposition 65 authoritative bodies mechanism set forth in Title 27, California Code of Regulations, Section 25306(d) because EPA did not “formally identify” PFOA as a reproductive toxicant. In addition, the proposed listing does not meet the substantive criteria for listing reproductive toxicants under the authoritative bodies mechanism set forth in Section 25306(g). Therefore, PFOA should not be listed as a reproductive toxicant under this mechanism. If OEHHA proceeds with any further consideration of this substance for listing, it should do so under the State’s Qualified Expert’s (“SQE”) mechanism process initiated in August 2015.

I. EXECUTIVE SUMMARY

OEHHA relies on the EPA PFOA Documents to provide the support required for listing PFOA as a reproductive toxicant under the authoritative body mechanism. Specifically, OEHHA claims that EPA (the authoritative body) formally identified PFOA as causing reproductive toxicity under 25306(d) and that the evidence considered by EPA meets the sufficiency criteria under 25306(g). However, the EPA PFOA assessment documents fail on both counts.

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First, the EPA PFOA Documents do not formally identify PFOA as causing reproductive toxicity. The EPA PFOA Documents neither conclude that PFOA is a reproductive toxicant, nor indicate that EPA has taken final action. Therefore, the listing fails procedurally under 25306(d)(1). Section 25306(d)(2) establishes additional criteria for documents in which substances purportedly are “formally identified” as causing reproductive harm, including review of the document by an advisory committee in a public meeting or public review. EPA did not make the 2016 EPA PFOA Documents available for public review and comment before they were issued. Nor were the 2016 EPA PFOA Documents reviewed by an advisory committee. These failures are fatal to OEHHA’s attempted use herein.

Second, the EPA PFOA Documents also fail the sufficiency criteria prong of the authoritative body mechanism, under 25306(g). This section requires that studies in humans indicate that there is a causal relationship between the chemical and reproductive toxicity, or that studies in experimental animals provide sufficient data to support the biological plausibility of an association between adverse reproductive effects in humans and the toxic agent. The EPA PFOA Documents do not use human studies for dose response quantification. Instead they use animal studies to suggest adverse reproductive effects which might occur in humans. The toxicological weight-of-evidence does not support a causal relationship between PFOA and reproductive toxicity in humans for three reasons. First, the rodent studies referenced by EPA provide strong evidence that many of the developmental outcomes reported are the consequence of maternal toxicity as opposed to developmental toxicity of PFOA. Additionally, PFOA levels in rodents were several orders of magnitude higher than PFOA levels in the general human population and are, therefore, of limited relevance to humans. Finally, mode-of-action data suggest that rodents are not the most appropriate species for the hazard assessment of PFOA toxicity in humans.

In October 2015, 3M submitted comments to OEHHA as OEHHA was pursuing listing PFOA as a reproductive toxicant under the SQE Mechanism. OEHHA has not responded to 3M’s submitted comments, all of which remain valid, relevant and applicable. In those comments 3M explains that there have been significant efforts in the United States to restrict manufacture, import, and use of PFOA and PFOA-Precursors, and that the production of PFOA completely ceased by the end of 2015. Accordingly, there is an unmistakable downward trend in the levels of PFOA found in the U.S. general population in the last decade. Based on the Centers for Disease Control and Prevention (“CDCs”) National Health and Nutrition Examination Survey (NHANES) data, mean blood levels of PFOA in the general population have declined by approximately 60% between 1999-2000 and 2011-2012. Most importantly, 3M explains that there is an absence of data that supports reproductive toxicity.

II. INTRODUCTION

In May 2000, 3M announced that it would voluntarily phase out the production and use of perfluorooctanyl chemistries, including PFOA. The goal was reached by 2004 in the U.S. In 2006, EPA invited eight major fluoropolymer and telomere manufacturers (Arkema, Asahi, BASF (successor to Ciba), Clairant, Daikin, 3M/Dyneon, DuPont, and Solvay Solexis) to join in a global stewardship program with two goals: 1) To commit to achieve, no later than 2010, a 95 percent reduction, measured from a year 2000 baseline, in both facility emissions to all media of PFOA, precursor chemicals that can break down to PFOA, and related higher homologue

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chemicals, and product content levels of these chemicals; and 2) To commit to working toward the elimination of these chemicals from emissions and products by 2015. In 2016, EPA announced that all participants met the program goals. Furthermore, EPA has promulgated several Federal Regulations (Significant New Use Rules) that effectively preclude the reintroduction of long-chain poly- and perfluoroalkyl substances into commerce in the U.S.

III. THE EPA PFOA DOCUMENTS DO NOT MEET THE REQUIREMENTS OF SECTION 25306(d).

A. The EPA PFOA Documents Do Not Meet The Requirements Of Section 25306(d)(1).

For a chemical to be “formally identified,” Section 25306(d)(1) requires that at least one of the following three requirements be met:

• The chemical has been included on a list of chemicals causing cancer or reproductive toxicity issued by the authoritative body; or

• The chemical is the subject of a report which is published by the authoritative body and which concludes that the chemical causes cancer or reproductive toxicity; or

• The chemical has otherwise been identified as causing cancer or reproductive toxicity by the authoritative body in a document that indicates that such identification is a final action.

OEHHA implicitly acknowledges in its Notice of Intent to List that EPA did not issue a “list of chemicals” identifying PFOA as causing reproductive harm. Instead, OEHHA relies on the remaining two prongs of Section 25306(d)(1). However, neither of these two prongs is met.

One prong requires that the chemical be the subject of a report which is published by the authoritative body and which concludes that the chemical causes cancer or reproductive toxicity. The discussion below explains that EPA’s “published report” itself is suspect due to the deeply flawed regulatory process which led to its publication. Beyond that, the EPA PFOA Documents published by EPA do not “conclude” that PFOA causes reproductive toxicity. In this regard, Section 25306(g), establishing how human and animal studies are to be evaluated for listing, has significant bearing on the issue of whether the EPA PFOA Documents “conclude” that PFOA causes reproductive toxicity.

Under Section 25306 (g)(1), a chemical may be listed as a reproductive toxicant if human studies “indicate that there is a causal relationship between the chemical and reproductive toxicity.” (Emphasis added.) The Final Statement of Reasons for Section 25306 (“FSOR”) further explains the requirement that “sufficient evidence [of causation] exist from such studies.”1 But the EPA PFOA Documents merely summarize associations, not causal relationships supported by sufficient evidence, in human epidemiology studies between PFOA and reproductive toxicity.

1 FSOR at p.21.

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Section 25306 (g)(2) allows the consideration of animal studies to support a listing, if “there are sufficient data, taking into account the adequacy of the experimental design and other parameters such as, but not limited to, route of administration, frequency and duration of exposure, numbers of test animals, choice of species, choice of dosage levels, and consideration of maternal toxicity, indicating that an association between adverse reproductive effects in humans and the toxic agent in question is biologically plausible.” “Sufficient evidence” of such biologically plausible association also is required.2 The EPA PFOA Documents also rely on animal studies for their conclusions; however, the association between PFOA and developmental effects has not been established as biologically plausible by sufficient evidence. Developmental observations in laboratory rodents exposed to PFOA are not appropriate for hazard assessment of the developmental toxicity in humans for various reasons, including differences in mode of action across species. Importantly, biologically relevant developmental findings in laboratory rodents for PFOA were primarily mediated by maternal toxicity. Moreover, developmental observations in rodents occurred at PFOA much higher than those experienced by the general human population. The EPA PFOA Documents do not properly address these issues and therefore, no definitive conclusion can be reached regarding reproductive toxicity.

Thus, the requirement of Section 25306 (d)(1) is not met. Indeed, evaluating this question in its broadest sense, in the absence of causation supported by sufficient evidence, the chemical cannot meet the statutory standard of being “known to the State to cause” reproductive toxicity.

The term “final action” as used in the third prong has been interpreted to have a broader meaning than the formal, administrative law meaning of the term. In explaining this broader meaning, the Final Statement of Reasons for Section 25306 acknowledges that regulatory agencies “do not treat the identification of chemical hazards as a regulatory endpoint.”3 That is certainly the case here: EPA explains in its Fact Sheet for the PFOA & PFOS Drinking Water Health Advisories that its health advisory is not a final action. First, EPA acknowledges the advisory is to provide information and is non-enforceable and non-regulatory.4 Second, EPA admits that they are continuing to monitor the chemicals.5 Third, EPA has admitted that they are still evaluating PFOA and that they have not established national primary drinking water regulations for PFOA because the chemical has not met the minimal requirements for regulation. Therefore, final action, in the usual legal sense, has not taken place.6

2 FSOR at p. 22. 3 FSOR at p 11. 4 “The EPA develops health advisories to provide information on contaminants that can cause human health effects and are known or anticipated to occur in drinking water. EPA’s health advisories are non-enforceable and non-regulatory and provided technical information to states agencies and other public health officials on health effects, analytical methodologies, and treatment technologies associated with drinking water contamination.” EPA Fact Sheet PFOA & PFOS Drinking Water Health Advisories. 5 “As science on health effects of these chemicals evolves, EPA will continue to evaluate new evidence.” EPA Fact Sheet PFOA & PFOS Drinking Water Health Advisories. 6 “EPA has not established national primary drinking water regulations for PFOA and PFOS. EPA is evaluating PFOA and PFOS as drinking water contaminants in accordance with the process required by the Safe Drinking Water Act (SDWA). To regulate a contaminant under SDWA, EPA must find that it: (1) may have adverse health effects; (2) occurs frequently (or there is a substantial likelihood that it occurs frequently) at levels of public health

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But even if “final action” has a broader meaning under Proposition 65, this prong of Section 25306 (d)(1) fails. As the Final Statement of Reasons explains, this term is “intended to prevent the listing of chemicals on the basis of preliminary discussions as to whether a chemical should be considered a cancer or a reproductive hazard, or draft documents dealing with the identification of a chemical hazard.”7 Here, the actual events constituting the EPA regulatory process demonstrate that EPA’s statement should in fact be considered “preliminary discussions.” In the 2014 proceeding and draft documents, EPA focused on liver weight effects, not developmental effects. The 2016 EPA PFOA documents raised, for the first time, developmental effects in a regulatory process which denied input by the public and the scientific community. In this regard, EPA’s conclusions are properly deemed “preliminary discussions.” Therefore, no “final action” exists to meet this prong of Section 25306(d)(1).

B. The EPA PFOA Documents Do Not Meet The Requirements Of Section 25306(d)(2).

Section 25306(d)(2) establishes additional criteria for documents in which substances purportedly are “formally identified” as causing cancer or reproductive harm. OEHHA relies on three of them:8

• The document was reviewed by an advisory committee in a public meeting, if a public meeting is required, or

• The document was made subject to public review and comment prior to its issuance, or

• The document was published by the authoritative body in a publication, such as,

but not limited to, the federal register for an authoritative body which is a federal agency.

The discussion below, which describes the EPA proceedings which culminated in the publication of EPA PFOA Documents, demonstrates that those documents do not meet the above criteria. Therefore, EPA did not “formally identify” PFOA as a reproductive toxicant. Rather, the facts demonstrate that the EPA proceedings occurred without adequate opportunity for review and comment being given to the participating stakeholders, which deprived each of the protections otherwise afforded to them by law.

EPA presented the 2014 Draft Health Effects Document on February 28, 2014 for a limited 60-day public comment period that ran until April 29, 2014. Thereafter, in August, 2014, EPA hosted a peer review panel.

In May 2016, EPA released the final EPA PFOA Documents. Unfortunately, what EPA released was substantially different than that which the public reviewed in 2014 and what the

concern; and (3) there is a meaningful opportunity for health risk reduction for people served by public water systems.” EPA Fact Sheet. 7 FSOR at p. 11. 8 OEHHA implicitly acknowledges that the remaining three criteria are inapplicable.

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peer review panel discussed in its 2014 meeting. The 2016 PFOA Health Effects Support Document was significantly expanded from the 2014 PFOA Health Effects Support Document and was materially different from the 2014 document presented for public comment. It grew from 268 pages in length to 322 pages, with its references list nearly doubling in length from 21 pages to 39 pages. EPA also added more than 80 new epidemiological animal toxicity and toxicokinetic studies. Significantly, EPA changed the health effects end point from liver weight changes to an endpoint based on developmental effects, using a different study from the one used in the 2014 RfD.

None of these substantial revisions could have been anticipated from the 2014 draft documents – and certainly could not have been commented on by stakeholders in the 2014 public notice and comment period.

Nonetheless, EPA failed to specifically address these changes in 2016 Health Effects Support Document or in the PFOA Lifetime Health Advisory (“LHA”) document, and failed to explain in these documents why it moved from a critical end point based on liver weight change to one based on developmental effects.9

Most importantly, EPA made material changes to its conclusions in the EPA PFOA Documents, without allowing any review or comment by the public or the scientific community. In contrast to the process used for the 2014 document, EPA did not present the 2016 documents to a peer review panel, nor did it obtain input from the EPA’s Science Advisory Board. Similarly, EPA issued the PFOA LHA document, without any prior notice, public comment or review. EPA deviated from its own procedures in calculating LHAs, and failed to seek public or scientific comment before doing so.

Clearly, the documents upon which OEHHA relies for the proposed authoritative bodies listing reflect a brand new approach, which could not have been anticipated by stakeholders and which was not subject to public review. Thus, the EPA PFOA Documents do not meet the “public review” prong of Section 25306(d)(2).

OEHHA relies on another prong of Section 25306(d)(2), i.e., that the document was reviewed by an advisory committee in a public meeting. But the facts reveal otherwise: the advisory committee reviewed the 2014 draft, but had no opportunity to comment on or review EPA’s new approach set forth in the 2016 EPA PFOA Documents. Thus, the scientific community never validated EPA’s results and/or conclusions.10

Finally, OEHHA may decide to rely on the third prong, i.e., that the EPA PFOA Documents were published in the Federal Register. But, the Final Statement of Reasons for Section 25306(d)(2) reveals that this prong is based on the assumption that published reports “are subject to a thorough review prior to publication.”11 As the actual EPA regulatory proceedings

9 EPA failed to specifically address any of the 200 plus pages of public comments received from 3M and others in 2014. 10 See FSOR at p. 14 which explains that this prong of subsection(d)(2) is premised on the assumption that an advisory committee validates “the results and/or conclusions of a study or a scientific document, a process similar to that utilized by the Panel to evaluate chemicals for listing under the Act.” 11 FSOR at 14; emphasis added.

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amply demonstrate, there was no review at all of the 2016 documents. OEHHA’s reliance on this prong, in these circumstances where the EPA regulatory proceeding is so deeply flawed, contravenes the intent of this regulation and would risk long-term erosion of public confidence in the Proposition 65 listing process.

1. The EPA PFOA Documents Do Not “Formally Identify” PFOA as A Reproductive Toxicant

OEHHA proposes to list PFOA as a reproductive toxicant pursuant to the “authoritative bodies” listing mechanism, which requires an authoritative body – here, EPA – to “formally identify” the chemical causing an adverse reproductive effect. OEHHA relies on EPA regulatory proceedings initiated in 2014, which purported to include the opportunity for public review of EPA’s draft documents, as the basis for the required “formal” identification. However, as explained below, EPA finalized the EPA PFOA Documents with significant and substantial deviations from the earlier documents’ analyses and conclusions – with no opportunity for stakeholders to comment on EPA’s new scientific theories. EPA’s failure in this regard means that PFOA was not “formally identified” as a reproductive toxicant within the meaning of the relevant Proposition 65 regulations.

EPA’s actions precluded stakeholders from participating fully in the EPA proceeding, and thereby undermined the integrity of EPA’s scientific conclusions as well as the administrative process itself.

When EPA changed its course in 2016, it denied the public and other stakeholders any opportunity to address EPA’s revised scientific theories. This is no form over substance concern; this goes to the heart of the scientific and procedural integrity of the EPA’s decision, on which OEHHA intends to base its listing of PFOA. Should OEHHA proceed with this listing on these facts, it will infect the integrity of its own regulatory process with EPA’s flawed actions.

2. The History of the EPA Proceedings Underscores That EPA’s Decision to Focus on a Different Health Endpoint Occurred without Public Comment

On February 28, 2014, EPA announced that it prepared a draft Health Effects Documents for Perfluorooctanoic Acid (PFOA) “for purposes of public comment (scientific views) and peer review.” EPA stated that it “will consider any public comments submitted in accordance with this notice when finalizing the documents. Once the health effect documents are finalized, they will be utilized to develop lifetime health advisory values for each chemical.”

The draft Health Effects Document for PFOA summarized the findings of epidemiology studies that examined occupational and residential populations at or near large-scale PFOA production plants in the United States and reviewed existing animal studies. EPA found insufficient information from occupational and general population studies to establish a reference dose (RfD) for PFOA. Nonetheless, EPA said the animal studies showed “short-term and chronic exposure to PFOA resulted in an increase in liver weight as at least one of the critical effects with co-occurring effects which included changes in spleen, thymus, liver and/or developmental endpoints.” (Emphasis added.) Reflective of its focus on effects on liver weight,

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EPA selected a RfD “based on the consistency of the response and with recognition of the use of liver weight as a common denominator for loss of homeostasis and protection against co-occurring adverse effects.”

3M offered comments which, inter alia, objected to the selection of the RfD based on rodent liver weight as not based on reliable scientific evidence, pointing out that: 1) an increase in liver weight alone in response to PFOA exposure is an adaptive effect, not an adverse effect; 2) there is an established mode-of action for the liver hypertrophic effects in rodents from exposure to PFOA that was not considered in the selection of the RfD; 3) the experimental evidence shows the lack of a response, or a markedly reduced response, in human liver as compared to rodent liver; and 4) the large body of epidemiological evidence demonstrates a lack of evidence of liver toxicity (non-malignant or malignant) from exposure to PFOA.

3M requested the opportunity to comment on other aspects in anticipation of future drafts resulting from consideration of these comments and contractor managed external peer review. In addition, 3M stated that the full breadth and complexity of the epidemiological, toxicological and pharmacokinetic data related to PFOA exposure required a formal review by the USEPA Science Advisory Board.

Because EPA’s draft PFOA health assessment did not use developmental effects to develop the RfD, 3M’s comments did not address developmental concerns in any substantive manner. 3M was not alone in this regard; comments submitted by other stakeholders also did not address developmental effects.

It was, therefore, surprising when the final EPA PFOA Documents, released in May 2016, took an entirely different approach, one that no stakeholder could have anticipated based on the prior draft documents. The 2016 PFOA Health Effects Document was significantly expanded over the 2014 PFOA Health Effects Support Document. Not only did it grow from 268 pages in length to 322 pages, EPA added more than 80 new epidemiological, animal toxicity and toxicokinetic studies. Most significantly, EPA changed the health effects endpoint from liver weight changes to an endpoint based on developmental effects, using a different study from the one used in the 2014 RfD.

In spite of all these changes, in the 2016 Health Effects Support Document for PFOA EPA failed to explain the differences between 2014 and 2016 PFOA documents. Nor did it state why it moved from a critical end point based on liver weight change to one based on developmental effects.

Most significantly for OEHHA’s proposed listing now, EPA failed to provide any opportunity for public comment on, or scientific validation of, what is a brand new proposal. Of course, this failure directly undermines EPA’s “formal identification” of PFOA – and, thus, goes to the heart of the integrity of OEHHA’s reliance on the EPA PFOA Documents herein.

C. OEHHA Should Not Proceed With This Listing Because The EPA PFOA Documents Do Not Meet The Requirements of Section 25306(d)

As a threshold matter, the Proposition 65 statutory obligations apply only to chemicals “known to the State” to cause reproductive harm. This principle is reflected in the use of the

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“known to the State” phrase throughout the statute, including at Health & Safety Code Section 25249.8, the section establishing the methods of adding chemicals to the Proposition 65 list. Indeed, this phrase is used throughout OEHHA’s Proposition 65 regulations, including in the Agency’s recently adopted warning regulations. This statutory “known to the State” requirement must inform any analysis of whether PFOA (or any other chemical) should be listed. Without establishing this statutory requirement, the listing of any chemical, including PFOA, would exceed OEHHA’s authority. 3M has previously discussed why the proposed listing fails to meet the regulatory listing criteria under Section 25306. That same discussion also establishes that PFOA is not “known to the State,” as required by the statute, to cause reproductive harm.

The authoritative bodies listing mechanism requires that an “authoritative body” – here, EPA – “formally identify” the chemical proposed for listing as causing cancer or reproductive toxicity. The requirement for formal identification goes directly to the statutory mandate that only chemicals “known to the State” to cause cancer or reproductive harm are the subject of the law’s obligations. In this proposed listing, OEHHA relies on EPA PFOA Documents. However, those materials do not meet the procedural criteria set forth in Section 25306(d). Therefore, PFOA was not “formally identified” as a reproductive toxicant – and cannot be deemed to be “known to the State” to cause reproductive toxicity.

IV. THE PROPOSED LISTING OF PFOA DOES NOT MEET THE SUBSTANTIVE CRITERIA FOR LISTING UNDER SECTION 25306(g)

The procedural deficiencies described above warrant the conclusion that PFOA must not be listed. However, even if the proposed listing meets the required procedural requirements it fails to meet the substantive criteria for listing because the data reviewed by US EPA do not support the identification of PFOA as a reproductive toxicant and do not meet the substantive listing criteria of Section 25306(g).

Section 25306(g) establishes the substantive criteria for listing under the authoritative bodies mechanism:

• Studies in humans indicate that there is a causal relationship between the chemical and reproductive toxicity, or

• Studies in experimental animals indicate that there are sufficient data, taking into account the adequacy of the experimental design and other parameters such as, but not limited to, route of administration, frequency and duration of exposure, numbers of test animals, choice of species, choice of dosage levels, and consideration of maternal toxicity, indicating that an association between adverse reproductive effects in humans and the toxic agent in question is biologically plausible.

Neither of these criteria is met here.

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A. Studies In Humans Indicate That There Is No Causal Relationship Between The Chemical And Reproductive Toxicity.

EPA has been unable to establish a causal relationship between PFOA and reproductive toxicity in humans. EPA issued its LHA for PFOA based on a RfD derived from a developmental toxicity study in mice. The PFOA RfDs are based on laboratory experiments on animals. RfDs can also be based on human data, where such data are adequate. The peer review and public comments include suggestions to use human data in the RfD development. In the peer review, “[a]ll reviewers generally agreed that the rationales provided for the exclusion of the human data were not actually appropriate” and opinions varied regarding whether or not human data would be useful. In particular, Matthew P. Longnecker and William L. Hayton of the peer review panel expressed support for the use of human health data.12 Public comments submitted by Gradient in April 2014 noted that “[t]here are many well-conducted PFOA and PFOS human studies available. Occupational cohorts have been followed since the 1970s with exposures well above those of the general population with no evidence of adverse effects. Overall, these studies do not provide evidence of adverse effects in humans.” The peer review and public comments on the 2014 draft had pointed out that the draft could benefit from considering published epidemiology data.

B. Studies In Experimental Animals Are Insufficient To Support An Association Between PFOA And Adverse Reproductive Effects In Humans.

The studies in experimental animals do not establish an association between PFOA and adverse reproductive effects in humans. For example, reference doses based upon animal studies are subject to uncertainty, including, but not limited to:

• Uncertainty in the relevance of the measured health endpoint in animals for

human health; • Uncertainty in sensitivity of humans vs. animals to chemical exposure; • Uncertainty in the sensitivity of human sub-populations versus the general human

population; • Uncertainty in the clearance rate (i.e., loss rate) of chemicals in humans versus

animals; and • Uncertainty in the extrapolation of limited-duration dosing in animals to lifetime

exposure in humans.

With respect to PFOA, findings from animal studies do not indicate that an association between PFOA and reproductive effects is biologically plausible. Reasons include evidence of maternal toxicity in the rodent studies, the presence of species-specific differences in response due to differences in nuclear receptors between humans and rodents, and the large difference between exposure levels in rodents treated with PFOA and human exposures to PFOA.

12 EPA Response to External Peer Review Comments on EPA Draft Documents, EPA May 2016.

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C. Absence Of Data That Would Support Reproductive Toxicity.

In October 2015, and in connection with the then-proposed prioritization of PFOA, 3M submitted comments to OEHHA. These comments discussed the scientific studies demonstrating that PFOA should not be prioritized for listing as a reproductive toxicant. These same comments also demonstrate that existing studies do not support the listing of PFOA under the authoritative bodies mechanism. 3M has attached its previous comments as Exhibit A hereto, and incorporates them by reference.

V. OEHHA STATE’S QUALIFIED EXPERTS (“SQE”) MECHANISM ACTION

In August 2015, OEHHA initiated the possible listing of PFOA via the SQE mechanism, by identifying PFOA for possible prioritization for listing as a reproductive toxicant. OEHHA ultimately did prioritize PFOA for possible listing and, in February 2016, the agency initiated the next step of the SQE process, the development of hazard identification materials for the chemical. This process remains ongoing and, absent listing under the authoritative bodies mechanism, will proceed. The issuance of EPA’s PFOA documents opened the door for an additional mechanism to list PFOA as a reproductive toxicant, “the authoritative bodies mechanism.”

Given the serious procedural infirmities in EPA’s issuance of the EPA PFOA

Documents, OEHHA cannot reasonably conclude that EPA “formally identified” PFOA as a reproductive toxicant. The 2016 EPA PFOA documents were not submitted for comment prior to issuance, and were substantially different from the original documents the EPA issued in 2014. The 2016 documents changed key study endpoints without explanation or the benefit of peer review comments.

For the reasons discussed above, OEHHA should refrain from listing PFOA under the

authoritative bodies mechanism. By doing so, OEHHA will preserve the integrity of its own regulatory process. And, by proceeding with the already-initiated SQE process, OEHHA may evaluate this substance for listing without the impediments created by the EPA proceedings.

VI. CONCLUSION

OEHHA’s efforts to list PFOA as known to the state to cause reproductive toxicity under the Safe Drinking Water and Toxic Enforcement Act of 1986 under the authoritative bodies listing mechanism should fail because the authoritative body that OEHHA relies on did not formally identify the chemical as causing reproductive toxicity section 25306 (d) and the evidence considered by the authoritative body does not meet the sufficiency criteria of section 25306(g).

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Thank you for your consideration of these comments.

Very truly yours,

Ann G. Grimaldi Counsel for 3M Company

cc: Carol Monahan-Cummings, OEHHA Chief Counsel (via email) Dr. Lauren Zeise, OEHHA Director (via email) William A. Brewer III (Brewer, Attorneys & Counselors, 1717 Main Street, Suite 5900, Dallas, Texas 75201)

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EXHIBIT A