49938 Federal Register / Vol. 82, No. 207 / Friday, October 27, 2017 / Rules and Regulations 

1The Commission voted 3–2 to publish this final 

rule in the Federal Register. Commissioners Robert 

S. Adler, Marietta S. Robinson, and Elliot F. Kaye 

voted to publish this final rule. Acting Chairman 

Anne Marie Buerkle and Commissioner Joseph 

Mohorovic voted against publication of this final 

rule. 

CONSUMER PRODUCT SAFETY 

COMMISSION 

16 CFR Part 1307 

[Docket No. CPSC–2014–0033] 

Prohibition of Children’s Toys and 

Child Care Articles Containing 

Specified Phthalates 

AGENCY: Consumer Product Safety 

Commission. 

ACTION: Final rule. 

SUMMARY: The United States Consumer 

Product Safety Commission 

(Commission or CPSC) issues this final 

rule prohibiting children’s toys and 

child care articles that contain 

concentrations of more than 0.1 percent 

of diisononyl phthalate (DINP), 

diisobutyl phthalate (DIBP), di-n-pentyl 

phthalate (DPENP), di-n-hexyl phthalate 

(DHEXP), and dicyclohexyl phthalate 

(DCHP). Section 108 of the Consumer 

Product Safety Improvement Act of 

2008 (CPSIA) established permanent 

and interim prohibitions on the sale of 

certain consumer products containing 

specific phthalates. That provision also 

directed the CPSC to convene a Chronic 

Hazard Advisory Panel (CHAP) to study 

the effects on children’s health of all 

phthalates and phthalate alternatives as 

used in children’s toys and child care 

articles and to provide 

recommendations to the Commission 

regarding whether any phthalates or 

phthalate alternatives, other than those 

already permanently prohibited, should 

be prohibited. The CPSIA requires the 

Commission to promulgate a final rule 

after receiving the final CHAP report. 

This rule fulfills that requirement. 

DATES: The rule will become effective 

on April 25, 2018. 

FOR FURTHER INFORMATION CONTACT: For 

information related to the phthalates 

prohibitions, contact: Carol L. 

Afflerbach, Compliance Officer, Office 

of Compliance and Field Operations, 

Consumer Product Safety Commission, 

4330 East West Highway, Bethesda, MD 

20814–4408; telephone: 301–504–7529; 

email: cafflerbach@cpsc.gov. 

SUPPLEMENTARY INFORMATION: 

Outline. The information in this 

preamble is organized as follows: 

I. Background 

A. Consumer Product Safety Improvement 

Act 

1. Statutory Prohibitions 

2. Chronic Hazard Advisory Panel 

3. Rulemaking 

B. The Proposed Rule 

C. Additional NHANES Analysis 

D. Public Comments 

E. Final Rule 

II. Legal Authority 

A. Summary of Legal Authority 

B. Comments Regarding Legal Authority 

1. The Information Quality Act 

2. CPSIA Requirements for the CHAP 

3. CPSIA’s Requirements for the 

Rulemaking 

4. The APA’s Requirements 

III. The CHAP 

A. CPSIA Direction 

B. The CHAP’s Process 

C. The CHAP Report 

1. Health Effects 

2. Exposure 

3. Phthalates Risk Assessment 

4. CHAP’s Recommendations to the 

Commission 

D. Comments Regarding the CHAP 

1. Peer Review 

2. CHAP’s Transparency and Openness 

3. Weight of Evidence and Completeness of 

CHAP’s Review 

IV. Final Rule and Rationale 

A. Hazard: Phthalates’ Effect on Male 

Reproductive Development 

1. Summary 

2. Comments Concerning MRDE 

B. Exposure to Phthalates 

1. Human Biomonitoring Data 

2. Scenario-Based Exposure Assessment 

C. Risk Assessment 

1. Cumulative Risk Assessment 

2. Risk in Isolation 

D. Assessments/Determination for Each 

Phthalate 

1. Phthalates Subject to the Interim 

Prohibition 

2. Phthalates Subject to the Rule But Not 

Currently Prohibited Under the CPSIA 

E. The Concentration Limit 

F. International and Other Countries’ 

Requirements for Children’s Toys and 

Child Care Articles Containing 

Phthalates 

1. Summary of Requirements 

2. Comments Concerning Other Countries’ 

and International Requirements 

G. Description of the Final Rule 

H. Effective Date 

V. Regulatory Flexibility Act 

A. Certification 

B. Comments Concerning Impact on Small 

Business 

VI. Notice of Requirements 

VII. Paperwork Reduction Act 

VIII. Preemption 

IX. Environmental Considerations 

X. List of References 

I. Background 

A. Consumer Product Safety 

Improvement Act 

In accordance with the Consumer 

Product Safety Improvement Act of 

2008 (CPSIA), the Commission issues 

this final rule prohibiting children’s 

toys and child care articles containing 

concentrations of more than 0.1 percent 

of certain phthalates.1

1. Statutory Prohibitions 

Section 108 of the CPSIA establishes 

requirements concerning phthalates. 

Section 108(a) of the CPSIA 

permanently prohibits the manufacture 

for sale, offer for sale, distribution in 

commerce, or importation into the 

United States of any ‘‘children’s toy or 

child care article’’ that contains 

concentrations of more than 0.1 percent 

of di(2-ethylhexyl) phthalate (DEHP), 

dibutyl phthalate (DBP), or butyl benzyl 

phthalate (BBP). 15 U.S.C. 2057c(a). In 

addition, section 108(b)(1) prohibits on 

an interim basis (i.e., until the 

Commission promulgates a final rule), 

the manufacture for sale, offer for sale, 

distribution in commerce, or 

importation into the United States of 

‘‘any children’s toy that can be placed 

in a child’s mouth’’ or ‘‘child care 

article’’ containing concentrations of 

more than 0.1 percent of diisononyl 

phthalate (DINP), diisodecyl phthalate 

(DIDP), or di-n-octyl phthalate (DNOP). 

Id. 2057c(b)(1). The CPSIA provides the 

following definitions: 

• ‘‘Children’s toy’’ is ‘‘a consumer 

product designed or intended by the 

manufacturer for a child 12 years of age 

or younger for use by the child when the 

child plays.’’ 

• ‘‘child care article’’ is ‘‘a consumer 

product designed or intended by the 

manufacturer to facilitate sleep or the 

feeding of children age 3 and younger, 

or to help such children with sucking or 

teething.’’ 

• A ‘‘toy can be place in a child’s 

mouth if any part of the toy can actually 

be brought to the mouth and kept in the 

mouth by a child so that it can be 

sucked and chewed. If the children’s 

product can only be licked, it is not 

regarded as able to be placed in the 

mouth. If a toy or part of a toy in one 

dimension is smaller than 5 centimeters, 

it can be placed in the mouth.’’ 

Id. 2057c(g). These statutory 

prohibitions became effective in 

February 2009. The interim prohibitions 

remain in effect until the Commission 

issues a final rule determining whether 

to make the interim prohibitions 

permanent. Id. 2057c(b)(1). 

2. Chronic Hazard Advisory Panel 

The CPSIA directs the CPSC to 

convene a Chronic Hazard Advisory 

Panel (CHAP) ‘‘to study the effects on 

children’s health of all phthalates and 

phthalate alternatives as used in 

children’s toys and child care articles.’’ 

Id. 2057c(b)(2). A ‘‘phthalate 

alternative’’ is ‘‘any common substitute 

to a phthalate, alternative material to a 

phthalate, or alternative plasticizer.’’ Id. 

2057c(g). The CHAP is to recommend to 


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the Commission whether any phthalates 

or phthalate alternatives other than 

those permanently prohibited should be 

declared banned hazardous substances. 

Id. 2057c(b)(2)(C). 

3. Rulemaking 

The CPSIA requires the Commission 

to promulgate a final rule, pursuant to 

section 553 of the Administrative 

Procedure Act (APA), not later than 180 

days after the Commission receives the 

final CHAP report. The Commission 

must ‘‘determine, based on such report, 

whether to continue in effect the 

[interim] prohibition . . . , in order to 

ensure a reasonable certainty of no harm 

to children, pregnant women, or other 

susceptible individuals with an 

adequate margin of safety. . . .’’ 15 

U.S.C. 2057c(b)(3)(A). Additionally, the 

Commission must ‘‘evaluate the 

findings and recommendations of the 

Chronic Hazard Advisory Panel and 

declare any children’s product 

containing any phthalates to be a 

banned hazardous product under 

section 8 of the Consumer Product 

Safety Act (15 U.S.C. 2057), as the 

Commission determines necessary to 

protect the health of children.’’ Id. 

(b)(3)(B). 

B. The Proposed Rule 

On December 30, 2014, the 

Commission published a notice of 

proposed rulemaking (NPR) in the 

Federal Register. 79 FR 78324. The 

preamble to the NPR summarized the 

CHAP report, explaining the CHAP’s 

review of potential health effects of 

phthalates in animals and humans, the 

CHAP’s assessment of human exposure 

to phthalates, the CHAP’s assessment of 

risk (both cumulative and in isolation) 

of various phthalates, and the CHAP’s 

recommendations to the Commission. 

The preamble to the NPR then provided 

CPSC staff’s assessment of the CHAP 

report and stated the Commission’s 

description of the proposed rule and its 

explanation of the rationale for the 

proposal. 

The NPR generally followed the 

recommendations of the CHAP report. 

As explained further in section III of 

this preamble, the CHAP focused on 

certain phthalates’ effect on male 

reproductive development. After 

reviewing relevant studies, the CHAP 

found that certain phthalates (which the 

CHAP called active or antiandrogenic) 

cause adverse effects on the developing 

male reproductive tract. The CHAP 

determined that these phthalates act in 

a cumulative fashion. The CHAP 

concluded that DINP is an active 

(antiandrogenic) phthalate. Based on the 

cumulative risk assessment conducted 

by the CHAP, the Commission 

determined that ‘‘to ensure a reasonable 

certainty of no harm to children, 

pregnant women, or other susceptible 

individuals with an adequate margin of 

safety,’’ the Commission proposed to 

permanently prohibit children’s toys 

and child care articles containing 

concentrations of more than 0.1 percent 

of DINP. The Commission proposed 

making the interim prohibition 

concerning DINP permanent because the 

Commission concluded that allowing 

the use of DINP in children’s toys and 

child care articles would further 

increase the cumulative risk to male 

reproductive development. Although 

the interim prohibition applies to 

children’s toys that can be placed in a 

child’s mouth and child care articles, 

the NPR proposed permanently 

prohibiting DINP in all children’s toys 

and child care articles. 79 FR at 78334– 

35. 

The Commission proposed lifting the 

interim prohibitions regarding DIDP and 

DNOP. The Commission agreed with the 

CHAP that DIDP and DNOP are not 

antiandrogenic, and therefore, they do 

not contribute to the cumulative risk 

from antiandrogenic phthalates. The 

CHAP determined that neither phthalate 

poses a risk in isolation. Therefore, the 

Commission concluded that continuing 

the prohibitions regarding DIDP and 

DNOP is not necessary to ensure a 

reasonable certainty of no harm to 

children, pregnant women, or other 

susceptible individuals with an 

adequate margin of safety. Id. at 78334– 

78336. 

In addition, the Commission 

determined that DIBP, DPENP, DHEXP, 

and DCHP are associated with adverse 

effects on male reproductive 

development and contribute to the 

cumulative risk from antiandrogenic 

phthalates. The Commission agreed 

with the CHAP’s recommendation and 

proposed to prohibit children’s toys and 

child care articles containing 

concentrations of more than 0.1 percent 

of DIBP, DPENP, DHEXP, and DCHP. 79 

FR at 78326–38. The Commission 

proposed that the rule would take effect 

180 days after publication of a final rule 

in the Federal Register. Id. at 78339. 

C. Additional NHANES Analysis 

As explained further in section III.C.2 

of this preamble, the CHAP based its 

analysis, in part, on human 

biomonitoring data from the Centers for 

Disease Control and Prevention’s (CDC) 

National Health and Nutrition 

Examination Survey (NHANES). The 

CHAP analyzed data from NHANES’ 

2005/2006 data cycle. That data set had 

a larger number of pregnant women 

than is usual for NHANES data sets. 

Since publication of the NPR, CPSC staff 

has reviewed and analyzed the 

NHANES data cycles released by the 

CDC after the 2005/2006 data cycle. 

CPSC staff issued a report in June 2015 

concerning the NHANES data sets that 

had been released up to that point: 

‘‘Estimated Phthalate Exposure and Risk 

to Pregnant Women and Women of 

Reproductive Age as Assessed Using 

Four NHANES Biomonitoring Data Sets 

(2005/2006, 2007/2008, 2009/2010, 

2011/2012).’’ See https://www.cpsc.gov/ 

s3fs-public/NHANES-Biomonitoringanalysis-for-Commission.pdf . The June 

2015 staff analysis reviewed the 2005/ 

2006 NHANES data set to replicate the 

CHAP’s methodology and reviewed the 

subsequent NHANES data sets through 

2011/2012. Staff’s analysis used women 

of reproductive age (WORA; 15–45 year 

of age) as the population of interest, 

because NHANES data sets after 2005/ 

2006 did not have sufficient numbers of 

pregnant women to be statistically 

relevant. The Commission published a 

notice of availability in the Federal 

Register seeking comment on the CPSC 

staff document. 80 FR 35939 (June 23, 

2015). 

In December 2016, the CDC released 

the NHANES 2013/14 data cycle. CPSC 

staff prepared a document with staff’s 

analysis of the NHANES 2013/14 data 

cycle titled, ‘‘Estimated Phthalate 

Exposure and Risk to Women of 

Reproductive Age as Assessed Using 

2013/2014 NHANES Biomonitoring 

Data.’’ See https://www.cpsc.gov/s3fspublic/Estimated%20Phthalate

%20Exposure%20and%20Risk

%20to%20Women

%20of%20Reproductive

%20Age%20as%20Assessed%20Using

%202013%202014%20NHANES

%20Biomonitoring%20Data.pdf. The 

Commission published a notice of 

availability in the Federal Register 

seeking comments on CPSC staff’s 

February 2017 analysis of the NHANES 

2013/14 data cycle. 82 FR 11348 

(February 22, 2017). 

D. Public Comments 

The NPR, which published in the 

Federal Register on December 30, 2014, 

requested comments by March 16, 2015. 

79 FR 78324 (Dec. 30, 2014). The 

Commission extended the comment 

period for an additional 30 days to April 

15, 2015. 80 FR 14880 (March 20, 2015). 

Additionally, the Commission requested 

comments on each of the staff’s analyses 

of more recent NHANES data. 80 FR 

35939 (June 23, 2015); 82 FR 11348 

(February 22, 2017). The Commission 

received 91 comments on the NPR and 

an additional 18 comments on CPSC 


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staff’s reports on more recent NHANES 

data cycles. The comments are available 

on regulations.gov under the docket: 

CPSC–2014–0033. Throughout this 

preamble, we discuss significant issues 

raised by these comments and CPSC’s 

responses to those issues. As part of the 

briefing package that CPSC staff 

prepared for the Commission’s 

consideration of this final rule, staff 

developed a more detailed summary of 

the public comments and staff’s 

responses. These may be found at Tab 

B of the staff’s briefing package: https:// 

www.cpsc.gov/s3fs-public/ 

Final%20Rule%20-%20Phthalates%20- 

%20September%2013%202017.pdf At 

the end of each comment summary in 

this preamble, we provide, in 

parentheses, the number of the relevant 

and more detailed comment/response in 

Tab B of the staff’s briefing package. 

E. Final Rule 

The Commission has considered the 

CHAP report, CPSC staff’s analyses, and 

comments submitted on the NPR and 

staff’s reports concerning later NHANES 

data cycles. CPSC staff prepared a 

briefing package for the Commission 

that provides staff’s analysis of these 

materials and gives staff’s 

recommendations for the final rule. 

Staff’s briefing package is available at: 

https://www.cpsc.gov/s3fs-public/ 

Final%20Rule%20-%20Phthalates%20- 

%20September%2013%202017.pdf 

Based on consideration of these 

materials, the Commission issues this 

final rule, which is substantially the 

same as the proposed rule. 

In the interest of clarity, the final rule 

restates the CPSIA’s permanent 

prohibition on the manufacture for sale, 

offer for sale, distribution in commerce, 

or importation into the United States of 

any children’s toys and child care 

articles that contain concentrations of 

more than 0.1 percent of DEHP, DIBP, 

or BBP. 

The final rule continues the interim 

prohibition concerning DINP and 

expands that restriction to prohibit all 

children’s toys (not just those that can 

be place in a child’s mouth) and child 

care articles that contain concentrations 

of more than 0.1 percent of DINP. After 

reviewing the information presented by 

the CHAP, CPSC staff, and commenters, 

the Commission concludes that 

continuing the interim prohibition 

regarding DINP will ensure a reasonable 

certainty of no harm to children, 

pregnant women, or other susceptible 

individuals with an adequate margin of 

safety. The Commission also determines 

that expanding the prohibition 

regarding DINP to cover all children’s 

toys, not just those that can be placed 

in a child’s mouth, is necessary to 

protect the health of children. 

The final rule also prohibits 

children’s toys and child care articles 

that contain concentrations of more than 

0.1 percent of DIBP, DPENP, DHEXP, 

and DCHP. After reviewing the 

information presented by the CHAP, 

CPSC staff, and commenters, the 

Commission concludes that this 

restriction on the four additional 

phthalates is necessary to protect the 

health of children. 

The final rule adds a paragraph, not 

in the proposed rule, that repeats the 

statutory provision stating that the 

phthalates prohibitions apply to 

plasticized component parts of 

children’s toys and child care articles, 

or other component parts of those 

products that are made of materials that 

may contain phthalates. See 15 U.S.C. 

2057c(c). This addition does not make 

any substantive change, but it provides 

clarity by placing this statutory language 

in the regulation. 

As was proposed, the final rule will 

take effect 180 days after publication in 

the Federal Register and will apply to 

products manufactured or imported on 

or after that date. The Commission’s 

rationale for the final rule is explained 

in the following sections of this 

preamble. 

II. Legal Authority 

A. Summary of Legal Authority 

Section 108 of the CPSIA provides the 

legal authority for this rule. As directed 

by section 108(b)(2), the Commission 

convened a CHAP to study the effects 

on children’s health of phthalates and 

phthalate alternatives. The CPSIA 

directs the CHAP to examine ‘‘the full 

range of phthalates that are used in 

products for children,’’ and to consider 

numerous issues specified in the statute 

(discussed further in section III.A of this 

preamble). As required by section 

108(b)(2)(C), the CHAP prepared a 

report for the Commission that included 

recommendations to the Commission 

concerning any phthalates not already 

subject to the permanent prohibition or 

phthalate alternatives that should be 

prohibited. 15 U.S.C. 2057c(b)(2)(C). 

The CPSIA further directs that, within 

180 days of receiving the CHAP’s report, 

the Commission shall promulgate a final 

rule in accordance with section 553 of 

the APA. The Commission must 

‘‘determine, based on such report, 

whether to continue in effect the 

[interim] prohibition . . ., in order to 

ensure a reasonable certainty of no harm 

to children, pregnant women, or other 

susceptible individuals with an 

adequate margin of safety.’’ Id. 

2057c(b)(3)(A). Additionally, the 

Commission must ‘‘evaluate the 

findings and recommendations of the 

Chronic Hazard Advisory Panel and 

declare any children’s product 

containing any phthalates to be a 

banned hazardous product under 

section 8 of the Consumer Product 

Safety Act (15 U.S.C. 2057), as the 

Commission determines necessary to 

protect the health of children.’’ Id. 

2057c(b)(3)(B). 

A violation of the permanent or 

interim prohibitions or any rule the 

Commission subsequently issues under 

section 108(b)(3) ‘‘shall be treated as a 

violation of section 19(a)(1) of the 

Consumer Product Safety Act.’’ Id. 

2057c(e). Additionally, section 108(f), 

concerning preemption, states that the 

permanent and interim prohibitions and 

the Commission’s phthalates rule ‘‘shall 

be considered consumer product safety 

standards under the Consumer Product 

Safety Act.’’ Id. 2057c(f). 

Section 108 of the CPSIA sets out the 

criteria for the Commission’s 

determinations in this rulemaking. 

Regarding phthalates subject to the 

interim prohibition, the Commission is 

to determine, based on the CHAP report, 

whether their continued regulation is 

needed ‘‘to ensure a reasonable certainty 

of no harm . . . with an adequate 

margin of safety.’’ Regarding other 

children’s products and other 

phthalates, the Commission is to 

evaluate the CHAP report and determine 

whether additional restrictions are 

‘‘necessary to protect the health of 

children.’’ 15 U.S.C. 2057c(b)(3). 

Congress required the Commission to 

use these criteria for the phthalates 

rulemaking. 

B. Comments Regarding Legal Authority 

Comments raised various issues 

concerning the Commission’s legal 

authority for this rulemaking. These 

comments focused primarily on: The 

CPSIA’s requirements for the CHAP, the 

CPSIA’s requirements for the 

rulemaking, relevance of (and 

compliance with) the Information 

Quality Act (IQA), and compliance with 

requirements of the Administrative 

Procedure Act (APA). This section 

summarizes and responds to key issues 

raised by comments related to the 

Commission’s legal authority. Tab B of 

staff’s briefing package provides a more 

detailed discussion of the comments 

and responses. https://www.cpsc.gov/ 

s3fs-public/Final%20Rule%20-

%20Phthalates%20-%20September

%2013%202017.pdf?nArsRDzq81e90

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2CPSC Information Quality Guidelines. Available 

at: https://www.cpsc.gov/en/Research--Statistics/ 

Information-Quality-Guidelines/. 3NRC (2008). 

1. The Information Quality Act 

Comment: IQA Applicability: Several 

commenters asserted that the CHAP 

report and the phthalates rulemaking 

must comply with the Office of 

Management and Budget’s (OMB’s) 

Guidelines issued under the IQA and 

CPSC’s guidelines. The commenters 

stated that the OMB’s IQA Guidelines 

require that agencies’ disseminations 

meet a basic standard of quality for 

objectivity, utility and integrity, and 

that these requirements apply to the 

CHAP report and to CPSC’s rulemaking. 

The commenters also asserted that the 

CHAP report is ‘‘influential’’ under the 

IQA Guidelines because it meets the 

OMB standard for influential, i.e., has 

‘‘a clear and substantial impact on 

important public policies or private 

sector decisions.’’ 

Response: The IQA, Public Law 106– 

554, required OMB to draft guidelines 

regarding ‘‘the quality, objectivity, 

utility, and integrity of information . . . 

disseminated by Federal agencies’’ and 

required each agency to issue its own 

guidelines. OMB issued ‘‘Guidelines for 

Ensuring and Maximizing the Quality, 

Objectivity, Utility, and Integration of 

Information Disseminated by Federal 

Agencies’’ (OMB Guidelines), 67 FR 

8452. The CPSC issued its Information 

Quality Guidelines (CPSC Guidelines) 

in October 2002, which substantially 

follow OMB’s Guidelines.2 As provided 

in CPSC’s Guidelines, we are 

responding to comments on the NPR to 

address a commenter’s request for 

correction under the IQA. 

OMB’s Guidelines apply to federal 

agencies that are subject to the 

Paperwork Reduction Act (PRA), 42 

U.S.C. chapter 35. 67 FR 8453. This 

includes the CPSC. Both OMB’s and 

CPSC’s Guidelines apply to information 

that the agency ‘‘disseminates.’’ OMB’s 

Guidelines define the term 

‘‘dissemination’’ to mean ‘‘agency 

initiated or sponsored distribution of 

information to the public,’’ with several 

exclusions. Under OMB’s Guidelines, if 

an agency releases information prepared 

by an outside party, but the agency then 

distributes the information ‘‘in a manner 

that reasonably suggests that the agency 

agrees with the information, this 

appearance of having the information 

represent agency views makes agency 

dissemination of the information subject 

to the guidelines.’’ 67 FR 8454. As the 

commenters noted, the CHAP report 

was not prepared by CPSC but by a third 

party. However, in the NPR, CPSC based 

its recommendations on the CHAP 

report as required by section 108 of the 

CPSIA. Thus, we agree that OMB’s and 

CPSC’s Guidelines apply to the CHAP 

report. 

As discussed in the following 

comments/responses, OMB’s Guidelines 

require agencies to adopt a basic 

standard of information quality that 

includes ‘‘objectivity, utility, and 

integrity.’’ 

OMB’s Guidelines define 

‘‘influential’’ as: 

‘‘Influential’’, when used in the phrase 

‘‘influential scientific, financial, or statistical 

information’’, means that the agency can 

reasonably determine that dissemination of 

the information will have or does have a 

clear and substantial impact on important 

public policies or important private sector 

decisions. Each agency is authorized to 

define ‘‘influential’’ in ways appropriate for 

it given the nature and multiplicity of issues 

for which the agency is responsible. 

67 FR 8460. The definition of 

‘‘influential’’ places significant 

emphasis on the agency’s discretion to 

determine what information is 

influential. The OMB Guidelines state 

that influential information is held to a 

higher standard and must have a high 

degree of transparency. Even if the 

CHAP report is considered 

‘‘influential,’’ it met the OMB 

Guidelines’ provisions for such 

documents. As explained throughout 

this document, the CHAP was 

transparent about its data sources and 

processes. See the following comments 

and responses. (Comments 8.1 and 8.2). 

Comment: Objectivity of CHAP report. 

Commenters asserted that the CHAP 

Report (and by extension, the 

rulemaking) does not meet the IQA 

Guidelines’ standard of ‘‘objectivity.’’ In 

addition, the commenters argued that, 

because the CHAP Report is influential 

information regarding risks to health, 

safety, or the environment, it ‘‘must be 

based on requirements drawn from the 

Safe Drinking Water Act (SDWA), to use 

‘the best available, peer-reviewed 

science and supporting studies 

conducted in accordance with sound 

and objective scientific practices; and 

. . . data collected by accepted methods 

or best available methods . . . .’ ’’ 

(Comment 8.3). 

Response: The OMB Guidelines state: 

‘‘ ‘Objectivity’ includes whether 

disseminated information is being 

presented in an accurate, clear, 

complete, and unbiased manner.’’ 67 FR 

8459. According to the OMB Guidelines, 

this involves presenting the information 

within a proper context and identifying 

the sources of the information. Id. The 

OMB Guidelines further state: ‘‘In 

addition, ‘objectivity’ involves a focus 

on ensuring accurate, reliable, and 

unbiased information.’’ In a scientific 

context, this means ‘‘using sound 

statistical and research methods.’’ Id. 

The CHAP report met the 

‘‘objectivity’’ standard enunciated in the 

OMB Guidelines. The fact that the 

commenters might have conducted the 

analysis differently does not mean that 

the CHAP’s analysis was not 

‘‘objective.’’ The CHAP report clearly set 

forth its data sources and noted that to 

assess studies, it used the criteria of 

reliability, relevance, and adequacy 

established by the Organisation for 

Economic Cooperation and 

Development. CHAP report at pp. 13– 

14. The CHAP held open meetings 

during the process of developing its 

analysis, inviting experts to present 

their latest research findings and taking 

submissions of a large volume of written 

material. The CHAP members were 

selected in accordance with section 28 

of the CPSA through a process to ensure 

their independence from bias (e.g., 

nominated by National Academy of 

Sciences; free from compensation by or 

substantial financial interest in a 

manufacturer, distributor or retailer of a 

consumer product; not employed by the 

federal government, with certain 

scientific/research related exceptions). 

The CHAP explained its choices, such 

as the decision to focus on the effects on 

male reproductive development, and the 

CHAP noted that this approach was 

consistent with a National Research 

Council (NRC) report.3 Similarly, the 

CHAP explained its decision to conduct 

a cumulative risk assessment and 

explained the methodology that it used 

which, again, was consistent with one of 

the methods discussed in the NRC 

report. 

For an analysis of risks to human 

health, safety, and the environment that 

an agency disseminates, OMB’s 

Guidelines direct agencies to ‘‘adapt or 

adopt’’ the information quality 

principles of the SDWA. 67 FR 8460. 

The SDWA directs agencies to use: ‘‘ (i) 

The best available, peer-reviewed 

science and supporting studies 

conducted in accordance with sound 

and objective scientific practices; and 

(ii) data collected by accepted methods 

or best available methods (if the 

reliability of the method and the nature 

of the decision justifies use of the 

data).’’ Id. at 8457. The SDWA direction 

is very similar to the charge to the 

CHAP in section 108, which states, 

among other things, that the CHAP is to 

‘‘review all relevant data, including the 

most recent best available, peer 

reviewed, scientific studies of these 

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that employ objective data collection 

practices or employ other objective 

methods.’’ 15 U.S.C. 2057c(b)(2)(B)(v). 

As our discussion in section III of this 

preamble demonstrates, the CHAP 

report met this direction. 

Comment: IQA deficiencies as basis to 

invalidate rule. A commenter asserted 

that the CHAP report had numerous 

methodological flaws that violated the 

IQA and that these deficiencies would 

invalidate the phthalates rulemaking 

unless they are corrected because the 

proposed rule was premised almost 

entirely on the CHAP report. The 

commenter further asserted that OMB’s 

IQA Guidelines are ‘‘binding’’ on 

agencies. (Comment 8.4). 

Response: Elsewhere in this 

document and in Tab B of staff’s 

briefing package, staff responds to the 

specific methodological ‘‘flaws’’ the 

commenter identifies. Regarding the 

legal point, we note that OMB’s 

Guidelines are not legally enforceable 

requirements—guidelines, which are 

essentially interpretive rules, by their 

nature do not establish binding 

requirements. See, e.g., U.S. Iowa 

League of Cities v. EPA, 711 F.3d 844, 

873 (8th Cir., 2013) (‘‘interpretive rules 

do not have the force of law’’). Notably, 

the IQA directed OMB to ‘‘issue 

guidelines . . . that provide policy and 

procedural guidance to Federal 

agencies.’’ The IQA did not direct OMB 

or agencies to undertake substantive 

legislative rulemaking. Consolidated 

Appropriations Act of 2001, Public Law 

06–554, 515 (codified at 44 U.S.C. 3516 

Note). OMB’s Guidelines repeatedly 

stress their flexibility, noting that they 

are not intended to be ‘‘prescriptive, 

‘one-size-fits-all’ ’’ and that OMB 

intends for agencies to ‘‘apply them in 

a common-sense and workable 

manner.’’ 67 FR at 8452–53. The IQA 

established a binding requirement that 

OMB issue guidelines and that each 

agency that is subject to the PRA must 

issue its own guidelines, but the 

guidelines themselves do not bind 

agencies. Courts that have examined the 

question of the legal status of the IQA 

have found that the IQA (and thus 

necessarily, OMB’s guidelines) ‘‘creates 

no legal rights in any third parties.’’ Salt 

Inst. v. Leavitt, 440 F.3d 156, 159 (4th 

Cir. 2006). See Mississippi Comm. on 

Environmental Quality v. EPA, 790 F.3d 

138 (D.C. Cir. 2015) (dismissing 

argument that IQA created a legal 

requirement for EPA to use ‘‘best 

available science and supporting 

studies’’). 

2. CPSIA Requirements for the CHAP 

Comment: Review of all relevant data. 

Several commenters noted that the 

CPSIA directed the CHAP to ‘‘review all 

relevant data, including the most recent, 

best available . . . scientific studies 

. . . that employ objective data 

collection practices.’’ A commenter 

asserted that the CHAP’s ‘‘selective use 

and systematic mischaracterization of 

the data’’ did not meet this requirement. 

Commenters argued that the CHAP’s 

reliance on the 2005/2006 NHANES 

data set, rather than later data sets that 

were available to the CHAP before the 

CHAP’s stopping point (2007/2008, 

2009/2010 and 2011/2012 data sets), 

violated the CPSIA’s direction to review 

‘‘all relevant data’’ and to include ‘‘the 

most recent’’ studies. The commenters 

asserted that the CHAP’s failure to rely 

on later data sets is particularly 

important because, due to the drop in 

DEHP exposures, there has been a 

significant decline in total risk. One 

commenter asserted that the CHAP had 

ignored 32 relevant publications on 

phthalates. Other commenters stated 

that the CHAP’s analysis ‘‘represents the 

cutting edge and most current and best 

available science,’’ a significant 

improvement over methodologies 

currently used for government review of 

chemical risk that considered one 

chemical at a time. (Comments 7.8, 8.17, 

and 10.2). 

Response: The CHAP used 2005/2006 

NHANES data on pregnant women to 

assess phthalate exposure as part of the 

CHAP’s cumulative risk analysis, to 

satisfy the CPSIA’s charge to ‘‘examine 

the likely levels of children’s, pregnant 

women’s, and others’ exposure to 

phthalates . . . ’’ 15 U.S.C. 

2057c(b)(2)(B)(iii). This data set was the 

most recent data on pregnant women 

available at the time the CHAP 

completed its analysis in July 2012, 

CHAP report at p. 31, and it was the last 

data set to include a larger sample of 

pregnant women. CPSC staff 

subsequently analyzed NHANES WORA 

data from 2007/2008 through 2013/2014 

using the CHAP’s analytical 

methodology. 

The CHAP considered new scientific 

information published up to the end of 

2012, and used standard and acceptable 

methods for study review, conducting 

an unbiased literature search and 

publication identification and in-depth 

review and reporting of the most 

important publications. Specifically, the 

CHAP included many elements of 

systematic review methods in its work. 

The CHAP used a defined literature 

search strategy and limited the search to 

studies published through 2012. The 

CHAP considered the quality, relevance, 

and weight of evidence (WOE) of 

individual studies. The CHAP described 

criteria for evaluating published studies, 

CHAP report at pp. 19–23, and the 

CHAP ensured that all studies and data 

were publicly available. The CHAP also 

described the criteria used to formulate 

its recommendations on individual 

phthalates and phthalate alternatives. 

Id. at p. 79. The CHAP criteria included 

review of animal and human data, 

weight of evidence, study replication, 

human exposure, hazard, and risk. Id. at 

pp. 82–142. The CHAP conducted a 

thorough review of a large body of 

literature on a complex environmental 

health question using appropriate 

methods. 

All current scientific publications and 

NHANES data sets have been analyzed 

by the CHAP and CPSC staff in 

preparation for the final rule. This 

fulfills the CPSIA’s directive to review 

‘‘all relevant data’’ and to include ‘‘the 

most recent’’ studies. 

Regarding the assertion that the CHAP 

ignored 32 relevant publications, CPSC 

staff reviewed this claim. The CHAP 

cited approximately 250 articles using a 

systematic approach to select the most 

relevant and informative articles. Five of 

the 32 articles the commenter identified 

are not relevant because they considered 

effects that are not relevant to the 

CHAP’s focus on male reproductive 

development (e.g., onset of puberty in 

girls, estrogenic effects); they measured 

exposure, but not health effects; or did 

not accurately reflect exposure. The 

other 27 articles were review articles 

(which are considered secondary 

sources), several of which covered broad 

topics such as environmental chemicals. 

Staff’s more detailed assessment of these 

publications is provided in the response 

to comment 7.8 at Tab B of the staff’s 

briefing package. 

Comment: Foreseeable use and likely 

exposure. Several commenters noted 

that the CPSIA required the CHAP to 

‘‘examine the likely levels of children’s, 

pregnant women’s, and others’ exposure 

to phthalates, based on a reasonable 

estimation of normal and foreseeable 

use and abuse of such products.’’ 

Commenters asserted that the CHAP 

failed to meet this requirement because 

the CHAP ignored the more recent data 

that shows a significant drop in DEHP 

exposure and the CHAP included 

permanent prohibitions involving 

phthalates in the analysis. (Comment 

8.18). 

Response: As explained, the 2005/ 

2006 NHANES dataset that the CHAP 

used was the most recent data on 

pregnant women available at the time 

the CHAP completed its analysis in July 

2012, CHAP report at p. 31, and 

included a larger sample of pregnant 

women. CPSC staff has since analyzed 

more recent NHANES data using the 


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same methodology used by the CHAP 

and using WORA as a surrogate for 

pregnant women because an insufficient 

number of pregnant women were 

sampled in the later data sets. The final 

rule considers the most recent NHANES 

data, as well as the CHAP report. 

In accordance with the CPSIA’s 

direction to the CHAP, the CHAP’s 

cumulative risk analysis estimated 

phthalate exposure from all phthalates 

and all sources, not only toys and child 

care articles. Because the CPSIA 

prohibition covers only children’s toys 

and child care articles, exposures to 

DEHP, DBP, and BBP still occur from 

other sources. Thus, the CHAP and 

subsequent staff analyses provide a 

robust assessment of the ‘‘likely levels’’ 

of current exposures to phthalates. 

Comment: CPSIA direction to CHAP 

to conduct a cumulative risk 

assessment. One commenter stated that 

the CPSIA did not require the CHAP to 

conduct a cumulative risk assessment; 

the CHAP could have considered 

cumulative effects in a more general 

(qualitative) way. Other commenters 

asserted that a cumulative risk 

assessment was well within the CPSIA’s 

direction to the CHAP, noting that the 

CPSIA provided a clear mandate to 

‘‘review the toxicity of phthalates 

cumulatively’’ and to consider ‘‘the 

exposure to all sources of these 

chemicals.’’ One comment from a group 

of commenters stated Congress 

specifically required the cumulative risk 

analysis. (Comment 8.19). 

Response: Several provisions in 

section 108(b)(2) called on the CHAP to 

consider cumulative effects of 

phthalates. Specifically, the statute 

directed the CHAP to: 

• ‘‘Study the effects on children’s 

health of all phthalates and phthalate 

alternatives as used in children’s toys 

and child care articles’’; 

• ‘‘consider the potential health 

effects of each of these phthalates both 

in isolation and in combination with 

other phthalates’’; and 

• ‘‘consider the cumulative effects of 

total exposure to phthalates, both from 

children’s products and from other 

sources, such as personal care 

products.’’ 

Thus, the CPSIA required the CHAP to 

use some method to evaluate the health 

effects of multiple phthalates from 

multiple products. The statute did not 

specify that the only way to do this was 

through a cumulative risk assessment. 

However, nothing in the statute 

prohibited the CHAP from conducting a 

cumulative risk assessment. As 

explained in the CHAP report, and in 

the NPR, based on the CHAP’s 

knowledge and expertise, the CHAP 

decided that a cumulative risk 

assessment was the most appropriate 

method to fulfill the direction given to 

the CHAP. Furthermore, the CHAP used 

a cumulative risk assessment approach 

that was consistent with 

recommendations from a National 

Academy of Sciences committee that 

was convened specifically to consider 

methods for assessing the cumulative 

risks from phthalates. Thus, the CHAP 

used its judgment and provided an 

explanation for its reasonable choice. 

Comment: Applicability of the 

Federal Hazardous Substances Act. A 

commenter argued that the CPSIA 

required the CHAP to present its 

analysis in terms of the criteria stated in 

the FHSA, and the commenter asserted 

that the CHAP failed to do so. Similarly, 

a commenter asserted that the CHAP’s 

risk assessment improperly included 

consideration of exposures to 

substances that are excluded from the 

FHSA’s definition of ‘‘hazardous 

substance,’’ such as foods and drugs. 15 

U.S.C. 1261(f)(2). (Comments 8.27 

through 8.29). 

Response: The commenter bases its 

argument that the CHAP should have 

followed FHSA criteria on a phrase in 

CPSIA section 108 that also appears in 

the FHSA. However, neither section 108 

nor the legislative history of that 

provision mentions the FHSA. Rather, 

section 108(b)(2)(B) provides detailed 

direction to the CHAP about the criteria 

that the CHAP is to consider in its 

examination. Moreover, section 108(f) 

states clearly that the statutory 

prohibitions and the Commission’s 

future phthalates rule ‘‘shall be 

considered consumer product safety 

standards under the Consumer Product 

Safety Act.’’ It is not logical that 

Congress would expect the CHAP to 

apply FHSA criteria (without 

mentioning that statute) to provide a 

report to the Commission for a rule that 

is to be treated as a rule under the 

CPSA. In fact, section 108 established a 

unique procedure for phthalates, 

making it clear that Congress did not 

intend for the Commission to undertake 

rulemaking under the FHSA. The CHAP 

and the Commission followed the 

specific process and criteria set forth in 

section 108. The direction to the CHAP 

explicitly requires the CHAP to consider 

phthalates that are in products outside 

the CPSC’s jurisdiction, directing the 

CHAP to consider effects ‘‘both from 

children’s products and from other 

sources, such as personal care 

products.’’ 15 U.S.C. 2057c(b)(2)(B)(iv). 

Many personal care products are 

considered cosmetics and are under the 

jurisdiction of the U.S. Food and Drug 

Administration (FDA). Congress thus 

intended for the CHAP’s examination to 

be broader than just products under 

CPSC’s authority, even though CPSC’s 

rulemaking applies only to products 

under CPSC’s jurisdiction. 

3. CPSIA’s Requirements for the 

Rulemaking 

Comment: Commission’s role 

regarding the CHAP report. Comments 

questioned the Commission’s reliance 

on the CHAP report in the NPR. 

Commenters asserted that the 

Commission cannot merely codify or 

‘‘rigidly adhere’’ to the CHAP report 

without applying the Commission’s own 

judgment. To do so, they argued, would 

raise serious Constitutional questions by 

vesting government powers in a private 

entity and would also conflict with the 

CPSIA and sections 28 and 31 of the 

CPSA (e.g., the word ‘‘advisory’’ in the 

CHAP). Another commenter stated that 

CPSC acted appropriately on the CHAP 

report, noting that ‘‘CPSC made its own 

decision, issued its own proposed rule, 

and solicited public comment from 

industry and others on its proposed 

rule.’’ (Comment 8.20). 

Response: Section 108(b)(3) of the 

CPSIA requires that the Commission’s 

rule concerning the interim prohibition 

be ‘‘based on’’ the CHAP report and 

requires the Commission to evaluate the 

findings and recommendations of the 

CHAP to determine whether to prohibit 

any other children’s products 

containing any other phthalates. We 

agree that the statutory language does 

not require rigid adherence to the CHAP 

report and that the Commission cannot 

simply ‘‘rubber-stamp’’ the CHAP’s 

recommendations. Rather, the CHAP 

report is advisory, and the Commission 

must use its judgment to decide on 

appropriate regulatory action in 

accordance with the specific criteria 

stated in section 108(b)(3)(A) and (B) 

and must consider public comments 

that the Commission received. This is 

exactly the process the Commission 

followed. The NPR summarized the 

CHAP report, including the CHAP’s 

recommendations. 79 FR 78326–78330. 

The NPR presented CPSC staff’s 

evaluation of the CHAP report and the 

Commission’s assessment of the CHAP’s 

recommendations. Id. 78330–78338. 

Additionally, CPSC staff reviewed more 

recent NHANES data and conducted an 

analysis of the CHAP’s evaluation of 

exposure data. Staff reviewed and 

considered the comments submitted in 

response to the NPR and the NHANES 

data analysis to develop 

recommendations to the Commission. 

All of this information provides the 


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basis for the Commission’s decision on 

the final rule. 

Comment: Meaning of ‘‘reasonable 

certainty of no harm.’’ Several 

commenters addressed the meaning of 

the phrase ‘‘reasonable certainty of no 

harm.’’ Some commenters asserted that 

the standard must be interpreted in the 

context of CPSC’s other statutes and 

case law. In this view, the phrase 

essentially means ‘‘reasonably necessary 

to prevent or reduce an unreasonable 

risk of injury,’’ as would be required for 

a consumer product safety rule the 

Commission issues under sections 7, 8 

and 9 of the CPSA. Commenters also 

discussed the level of certainty required 

for a ‘‘reasonable certainty of no harm.’’ 

One commenter noted that the FDA uses 

a similar standard for food additives. 

One commenter stated that in the NPR, 

the CPSC has applied the standard 

essentially to require absolute certainty. 

In contrast, another commenter 

emphasized that the CPSIA calls for 

ensuring a ‘‘‘reasonable certainty of no 

harm’ (emphasis added).’’ (Comments 

8.14, 8.22, 8.23, and 8.25). 

Response: The requirements stated in 

section 108(b)(3) of the CPSIA, rather 

than sections 7, 8 and 9 of the CPSA, 

apply to this rulemaking. For the 

Commission to issue a consumer 

product safety rule under sections 7, 8 

and 9 of the CPSA, the Commission 

must determine that the product 

presents an unreasonable risk of injury 

and that a rule is necessary to reduce or 

prevent the unreasonable risk. The term 

‘‘unreasonable risk’’ does not appear 

anywhere in the criteria stated in 

section 108(b)(3) that the Commission is 

to use to determine appropriate 

phthalate regulations. Nothing in the 

legislative history of section 108 

indicates that Congress intended the 

Commission to make ‘‘unreasonable 

risk’’ determinations. Nor is there any 

indication that Congress intended that 

the case law related to the Commission’s 

rules issued under sections 7, 8 and 9 

of the CPSA would apply to the 

phthalates rulemaking. 

We are aware of two other statutory 

schemes that use somewhat similar 

language. The Food Quality Protection 

Act (FPQA) uses a similar phrase 

regarding tolerance levels for pesticide 

residue on food. That provision requires 

the U.S. Environmental Protection 

Agency (EPA) to ‘‘ensure that there is a 

reasonable certainty that no harm will 

result to infants and children from 

aggregate exposure to the pesticide 

chemical residue.’’ 21 U.S.C. 

346a(b)(2)(A)(ii)(I). Under the Federal 

Food, Drug, and Cosmetic Act (FDCA), 

food additives must be ‘‘safe.’’ 21 U.S.C. 

348. FDA has issued regulations that 

define ‘‘safe or safety’’ to mean ‘‘that 

there is a reasonable certainty in the 

minds of competent scientists that the 

substance is not harmful under the 

intended conditions or use.’’ In a very 

general sense, CPSC’s approach on 

phthalates is consistent with FDA and 

EPA in that CPSC’s evaluation is based 

on expert scientific opinion (the CHAP), 

takes into account the cumulative effect 

of the substance at issue (phthalates), 

and provides appropriate safety factors 

(e.g., for inter- and intra-species 

uncertainties). However, because the 

pesticide tolerance and food additive 

schemes differ significantly from the 

CPSIA’s phthalates provision, FDA’s 

and EPA’s approaches do not provide 

CPSC with more specific guidance on 

‘‘reasonable certainty of no harm.’’ 

Regarding the level of certainty 

required, the language ‘‘ensure a 

reasonable certainty of no harm . . . 

with an adequate margin of safety’’ calls 

for a highly protective standard, but not 

100 percent certainty of no harm. 

Congress required ‘‘a reasonable 

certainty of no harm,’’ not an absolute 

certainty of no harm. 

4. The APA’s Requirements 

Comment: Data and the CPSC’s 

obligation under the APA. Some 

commenters argued that the 

Commission’s reliance on certain data 

violated the APA. One commenter 

asserted that the NPR’s reliance on 

‘‘decade-old data’’ is not reasonable, and 

therefore, violates the APA. Some 

commenters stated that because the NPR 

‘‘rests on outdated data,’’ CPSC should 

withdraw the NPR, conduct a reanalysis 

with current exposure data, and repropose the rule with a new comment 

period. In comments on CPSC staff’s 

analysis of recent NHANES data, a 

commenter asserted that under the APA, 

‘‘the Commission has an obligation to 

disregard the CHAP’s report to the 

extent it is incorrect, unreasonable, 

inconsistent with existing CPSC policy, 

practice, regulations or governing 

statutes, or is based on data that is 

outdated or of poor quality.’’ The 

commenter set out the minimum 

requirements of informal rulemaking: 

Adequate notice, sufficient opportunity 

for public to comment, and a final rule 

that is not arbitrary and capricious. 

(Comments 8.12 and 8.13). 

Response: The NPR’s reliance on the 

CHAP report and the data the CHAP 

used did not violate the APA. Rather, 

the Commission followed the CPSIA’s 

direction to base the rulemaking on the 

CHAP report. As commenters requested, 

staff subsequently considered updated 

exposure data. As the CPSIA requires, 

the Commission’s proposal regarding 

the interim prohibition was ‘‘based on 

the CHAP report,’’ and in addition, the 

Commission evaluated the CHAP report 

to determine whether to prohibit any 

children’s products containing any 

other phthalates. Additionally, as 

required by the CPSIA, the Commission 

followed the notice and comment 

procedures of the APA. For the final 

rule staff considered more recent 

exposure data than the CHAP used. 

Several commenters asked the 

Commission to do this additional work. 

Staff conducted two analyses of more 

recent NHANES biomonitoring data 

sets, posted reports of staff analyses on 

the CPSC Web site, and the Commission 

requested public comment on each 

analysis. 80 FR 35938 (June 23, 2015) 

and 82 FR 11348 (February 22, 2017). 

We agree that under section 553 of the 

APA, the Commission must evaluate the 

CHAP report along with comments 

submitted in response to the proposed 

rule and engage in reasoned decision 

making to issue a final rule. This is the 

approach the agency has taken. The 

Commission provided adequate notice 

in the NPR (describing the CHAP report, 

providing staff’s evaluation of the CHAP 

report and explanation of, and reasons 

for, the proposed rule); provided 

sufficient opportunity for the public to 

comment (even extending the comment 

period and obtaining comment on the 

two staff reanalysis documents); and the 

Commission explains its reasoning for 

the final rule in this preamble and 

supporting documents. 

Comment: Restriction involving DINP 

and compliance with APA: A 

commenter asserted that continuing the 

interim prohibition involving DINP is 

arbitrary and capricious (in violation of 

the APA) because: 

• There is a reasonable certainty of no 

harm without such a prohibition (due to 

permanent prohibition involving 

DEHP); 

• DINP contributes only a small 

fraction to overall risk; 

• the endpoint of antiandrogenicity is 

likely inappropriate; 

• it is questionable that DINP should 

be included in a cumulative risk 

assessment; 

• it is questionable that a cumulative 

risk assessment provides a reasonable 

basis for a regulatory decision; 

• DEHP levels have dropped so that 

the Hazard Index (HI) is now well below 

one; and 

• even using the 2005/2006 NHANES 

data, the contribution of DINP to the 

overall HI is minimal and the major 

source of exposures is diet—children’s 

products account for only a small 

fraction of overall HI. 


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4The CHAP met in one closed meeting as part of 

the peer review process, January 28–29, 2015. 

5http://www.cpsc.gov/chap. 

6Peer reviewers were nominated by the National 

Academy of Sciences. Peer reviewers did not 

receive compensation from, nor did they have a 

substantial financial interest in, any of the 

manufacturers of the products under consideration. 

In addition, the peer reviewers were not employed 

by the federal government, except the National 

Institutes of Health, the National Toxicology 

Program, or the National Center for Toxicological 

Research. 

7NRC recommended, for example, that it is 

appropriate to perform a phthalate cumulative risk 

assessment for MRDE (phthalate syndrome); the 

cumulative risk assessment should consider all 

endpoints associated with MRDE or, alternatively, 

one sensitive endpoint such as reductions in 

testosterone. NRC also recommended using dose 

addition, a hazard index approach, assuming that 

mixture effects occur at low-doses, and including 

other (non-phthalate) antiandrogens. 

8Nipple retention does not normally occur in 

rodents, as it does in humans. 

In contrast, another commenter stated 

that the CHAP’s recommendation and 

the Commission’s proposal to 

permanently prohibit children’s toys 

and child care articles containing more 

than 0.1 percent of DINP are justified. 

The commenter stated that data 

indicating that DINP is a potential 

health risk have gotten stronger since 

release of the CHAP report. (Comment 

8.16). 

Response: In general, the APA 

requires that agencies’ rulemaking be 

based on reasoned decision making. 

Staff’s briefing package explains the 

reasons for staff’s recommendations, 

satisfying this threshold requirement. 

The specific issues the commenter 

raised about regulation of DINP and the 

apparent reductions over time in 

exposure to DEHP are addressed in 

detail in section IV.D.1.a. of this 

preamble. 

III. The CHAP 

A. CPSIA Direction 

The CPSIA directed the Commission 

to convene a CHAP ‘‘to study the effects 

on children’s health of all phthalates 

and phthalate alternatives as used in 

children’s toys and child care articles.’’ 

15 U.S.C. 2057c (b)(2). The statute 

provides very specific direction to the 

CHAP regarding its work. The CHAP 

must: 

Complete an examination of the full 

range of phthalates that are used in 

products for children and shall— 

• examine all of the potential health 

effects (including endocrine disrupting 

effects) of the full range of phthalates; 

• consider the potential health effects 

of each of these phthalates both in 

isolation and in combination with other 

phthalates; 

• examine the likely levels of 

children’s, pregnant women’s, and 

others’ exposure to phthalates, based on 

a reasonable estimation of normal and 

foreseeable use and abuse of such 

products; 

• consider the cumulative effect of 

total exposure to phthalates, both from 

children’s products and from other 

sources, such as personal care products; 

• review all relevant data, including 

the most recent, best-available, peerreviewed, scientific studies of these 

phthalates and phthalate alternatives 

that employ objective data collection 

practices or employ other objective 

methods; 

• consider the health effects of 

phthalates not only from ingestion but 

also as a result of dermal, hand-tomouth, or other exposure; 

• consider the level at which there is 

a reasonable certainty of no harm to 

children, pregnant women, or other 

susceptible individuals and their 

offspring, considering the best available 

science, and using sufficient safety 

factors to account for uncertainties 

regarding exposure and susceptibility of 

children, pregnant women, and other 

potentially susceptible individuals; and 

• consider possible similar health 

effects of phthalate alternatives used in 

children’s toys and child care articles. 

Id. 2057c(b)(2)(B). In its final report, the 

CHAP is required to recommend to the 

Commission whether any ‘‘phthalates 

(or combinations of phthalates)’’ in 

addition to those permanently 

prohibited, including the phthalates 

covered by the interim prohibition or 

phthalate alternatives, should be 

declared banned hazardous substances. 

Id. 2057c(b)(2)(C). 

B. The CHAP’s Process 

The CHAP’s process was open and 

transparent. The CHAP met in public 

session (and webcast) seven times and 

met via teleconference (also open to the 

public) six times.4 A record of the 

CHAP’s public meetings, including 

video recordings and information 

submitted to the CHAP, as well as the 

final CHAP report, are available on the 

CPSC Web site.5

At a meeting on July 26–28, 2010, the 

CHAP heard testimony from the public, 

including testimony from federal agency 

representatives, who discussed federal 

activities on phthalates. The CHAP also 

invited experts to present their latest 

research findings at the meeting in July 

2010 and during subsequent meetings. 

Members of the public who presented 

testimony to the CHAP at the July 2010 

meeting included manufacturers of 

phthalates and phthalate substitutes, as 

well as representatives of nongovernmental organizations. In addition 

to oral testimony, the manufacturers and 

other interested parties submitted an 

extensive volume of toxicity and other 

information to the CHAP and the CPSC 

staff. All submissions given to CPSC 

staff were provided to the CHAP. 

Although the CPSIA did not require 

peer review of the CHAP’s work, at the 

CHAP’s request, four independent 

scientists peer reviewed the draft CHAP 

report. CPSC staff applied the same 

criteria for selecting the peer reviewers 

as is required for the CHAP members.6

The CHAP report was due to the 

Commission on April 8, 2012. The 

CHAP submitted the final report to the 

Commission on July 18, 2014. 

C. The CHAP Report 

1. Health Effects 

The CHAP reviewed all of the 

potential health effects of phthalates. 

The CHAP explained that, although 

phthalates cause a wide range of 

toxicities, the CHAP focused on male 

reproductive developmental effects 

(MRDE) in part because this is the most 

sensitive and extensively studied 

endpoint for phthalates. The CHAP 

noted that this focus was consistent 

with a 2008 report from the National 

Research Council.7 The CHAP 

systematically reviewed literature on 

phthalate developmental and 

reproductive toxicology. CHAP report, 

at pp. 1–2 and 12–13. The CHAP found 

that ‘‘[s]tudies conducted over the past 

20 years have shown that phthalates 

produce a syndrome of abnormalities in 

male offspring when administered to 

pregnant rats during the later stages of 

pregnancy.’’ Id. at p. 15. The CHAP 

explained its approach to selection of 

data so that its analysis would be based 

on the most appropriate and reliable 

toxicological data. Id. at pp. 19–22. The 

CHAP stated that this collection of 

interrelated abnormalities, known as the 

‘‘rat phthalate syndrome,’’ is 

characterized by various effects on the 

male reproductive system: 

Malformations of the testes, prostate, 

and penis (hypospadias); undescended 

testes; reduced anogenital distance 

(AGD), and retention of nipples.8 Male 

pups also have reduced fertility as 

adults. The CHAP noted that only 

certain phthalates produce these 

abnormalities, phthalates with certain 

structural characteristics (three to seven, 

or eight, carbon atoms in the backbone 

of the alkyl side chain). The CHAP 

referred to these phthalates as ‘‘active’’ 

or ‘‘antiandrogenic’’ phthalates. Id. at 

pp. 15–16. 

The CHAP noted that, although there 

is a great deal of information on 


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9A malformation of the penis. 

10 Distance between the anus and genitals, which 

is greater in males than in females. 

phthalate syndrome in rats, there is 

relatively little on the phthalate 

syndrome in other animal species. The 

CHAP reviewed the existing dataexposing species, such as rabbits, mice, 

and marmosets, to phthalates. The 

CHAP concluded that these studies with 

animals other than rats show that most 

animals tested are more resistant to 

phthalates than rats, but due to the 

limitations on these studies (e.g., small 

number of animals exposed, only one 

phthalate, only one dose, high 

experimental variation), the CHAP 

found that ‘‘studies in rats currently 

offer the best available data for assessing 

human risk.’’ Id. at p. 18. 

The CHAP reviewed, and discussed in 

its report, studies examining the 

mechanism by which phthalates 

produce adverse effects. The CHAP 

concluded that the phthalate syndrome 

effects are largely due to the 

suppression of testosterone production, 

as well as reduced expression of the 

insulin-like hormone 3 gene. Id. at pp. 

18–19. 

In addition to studies on animals, the 

CHAP also reviewed studies on the 

effect that exposure to phthalates has on 

human health (epidemiological studies). 

The CHAP noted that rat phthalate 

syndrome resembles testicular 

dysgenesis syndrome (TDS) in humans. 

TDS includes poor semen quality, 

reduced fertility, testicular cancer, 

undescended testes, and hypospadias.9

CHAP report at p. 2. The CHAP 

concluded that studies provide human 

data linking prenatal exposure to 

phthalates with certain effects on male 

reproductive development (such as 

reduced anogenital distance,10 reduced 

sperm quality and infertility in male 

infants). In addition, the CHAP 

discussed studies that found 

associations between prenatal or 

neonatal exposure to phthalates and 

reductions in mental and psychomotor 

development and increases in attention 

deficits and behavioral symptoms in 

children. Id. at pp. 27–33; Appendix C. 

2. Exposure 

The CHAP assessed human exposure 

to phthalates by two different, but 

complementary, methods: Human 

biomonitoring (HBM) and exposurescenario analysis. HBM relies on 

measurements of phthalate metabolites 

in human urine to estimate exposure to 

phthalates. Id. at pp. 34–48; Appendix 

D. The CHAP used two data sources for 

HBM: NHANES and the Study for 

Future Families (SFF). NHANES is 

conducted by the CDC, and measures 

phthalates and other chemicals in 

human urine and blood in a statistically 

representative sample of thousands of 

U.S. residents. The CHAP used data 

from NHANES to estimate phthalate 

exposures in pregnant women and 

women of reproductive age (WORA). 

Because NHANES does not measure 

phthalate metabolites in children 

younger than 6 years old, the CHAP 

used measurements from the SFF to 

obtain exposure estimates for infants. 

SFF is a study of mother-child pairs, 

funded by the National Institutes of 

Health (NIH) and the EPA. The CHAP 

used this HBM data to derive daily 

intake (DI) estimates to use in its risk 

assessment calculations. The CHAP 

used the 2005/2006 NHANES data cycle 

in its analysis. The SFF data are from 

1999 to 2005. From the HBM data, the 

CHAP concluded that ‘‘exposure to 

phthalates in the United States (as 

worldwide) is omnipresent. The U.S. 

population is co-exposed to many 

phthalates simultaneously.’’ Id. at p. 37. 

The CHAP also noted that, because the 

data indicate that sources and routes of 

exposure among high- and lowmolecular weight phthalates are similar, 

it is highly likely that substitution of 

one phthalate will lead to increased 

exposure to another similar phthalate. 

Id. 

The HBM data do not measure the 

sources of people’s exposure to 

phthalates. For this, the CHAP used a 

scenario-based exposure assessment. Id. 

at pp. 49–60; Appendix E. The CHAP 

used estimations of phthalate 

concentrations in various sources to 

predict exposures to subpopulations 

(pregnant women/WORA, infants, 

toddlers, and children). For the 

scenario-based exposure assessment, the 

CHAP estimated the DINP exposure that 

would occur if DINP were allowed in 

children’s toys and child care articles. 

The CHAP found that for most 

phthalates, food, rather than children’s 

toys or child care articles, is the primary 

source of exposure for women and 

children. The CHAP examined 

exposures to various phthalates from 

these sources. The CHAP found that 

infants, toddlers, and children were 

primarily exposed to DINP, DEHP, and 

DIDP. For infants, exposure to DINP was 

primarily from diet, but exposure was 

also due to DINP in teethers and toys. 

Id. at pp. 50–51. 

3. Phthalates Risk Assessment 

a. Cumulative Risk Assessment 

In accordance with the CPSIA’s 

direction, the CHAP considered health 

effects of phthalates ‘‘in combination 

with other phthalates.’’ 15 U.S.C. 

2057c(b)(2)(B)(ii). The CHAP found, 

based on published studies, that active 

phthalates act in an additive fashion. 

That is, exposures to multiple 

phthalates at lower doses act in concert 

to produce the same effect as a higher 

dose of a single phthalate. The CHAP 

stated: ‘‘Experimental data on 

combination of effects of phthalates 

from multiple studies (e.g., Howdeshell 

et al. (2008)) provide strong evidence 

that dose addition can produce good 

approximations of mixture effects when 

the effects of all components are 

known.’’ Id. at p. 61. The CHAP also 

noted that, in addition to phthalates, 

other chemicals, including certain 

pesticides and preservatives, add to the 

male reproductive effects of phthalates. 

CHAP report at pp. 26–27. Due to the 

additive effects of certain phthalates, the 

CHAP determined that it is appropriate 

to conduct a cumulative risk analysis to 

assess the antiandrogenic phthalates the 

CHAP identified. Id. 

For its cumulative risk assessment, 

the CHAP used a Hazard Index (HI) 

approach which, the CHAP noted, is 

widely used in cumulative risk 

assessments of chemical mixtures. Id. 

To determine the HI, one first calculates 

the hazard quotient (HQ) for each 

chemical and then adds the HQs 

together. The ‘‘HQ’’ is generally defined 

as the ratio of the potential exposure to 

a substance and the level at which no 

adverse effects are expected. If the HQ 

is less than one, the expectation is that 

no adverse effects will result from 

exposure; but if the HQ is greater than 

one, adverse effects are possible. Rather 

than use acceptable daily intakes (ADI) 

or reference doses (RfDs) as the 

denominator of HQs, the CHAP used 

‘‘potency estimates for 

antiandrogenicity’’ (PEAAs). The PEAA 

is an estimate of the level of exposure 

at which the risk of antiandrogenic 

effects is considered negligible. The 

CHAP estimated a PEAA for each 

phthalate by dividing the MRDE 

‘‘antiandrogenic’’ point of departure 

(POD; toxicity endpoint) by an 

uncertainty factor (UF). The CHAP used 

three sets of PEAAs (the CHAP refers to 

these as Cases) to evaluate the impact of 

assumptions in calculating the HI. Id. at 

pp. 61–65. 

The CHAP calculated the HI per 

woman and infant, using the NHANES 

data on pregnant women (representing 

exposure to the fetus) and the SFF data 

on children. The CHAP found that 

roughly 10 percent of pregnant women 

in the U.S. population have HI values 

that exceed 1.0 (pregnant women had 

median HIs of about 0.1 (0.09 to 0.14), 

while the 95th percentile HIs were 


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about 5, depending on which set of 

PEAAs was used. The CHAP found that 

4–5 percent of infants have HI values 

that exceed 1.0 (infants had median HIs 

about 0.2, while the 95th percentiles 

were between 0.5 and 1.0). Id. at p. 65 

and Table 2.16. Based on this 

cumulative risk assessment, the CHAP 

recommended that phthalates that 

induce antiandrogenic effects (DINP, 

DIDP, DPENP, DHEXP, and DCHP 

should be permanently banned from use 

in children’s toys and child care articles 

at levels greater than 0.1 percent. Id. at 

pp. 7–8. 

Regarding the HQs for the individual 

phthalates, the CHAP found that DEHP 

dominated, ‘‘with high exposure levels 

and one of the lowest PEAAs.’’ Id. at p. 

65. HQ values were similar for three 

phthalates (DBP, BBP, and DINP), while 

DIBP had the smallest HQs. Id. 

b. Risks in Isolation 

In accordance with the CPSIA’s 

direction, the CHAP also considered the 

risks of phthalates in isolation. 15 

U.S.C. 2057c(b)(2)(B)(ii). The CHAP 

used a margin of exposure (MOE) 

approach to assess the risks in isolation. 

CHAP report at p. 69. The MOE is the 

‘‘no observed adverse effect level’’ 

(NOAEL) of the most sensitive endpoint 

in animal studies divided by the 

estimated exposure in humans. Higher 

MOEs indicate lower risks. Generally, 

MOEs greater than 100 to 1,000 are 

adequate to protect public health. Id. 

The CHAP found that, with the 

exception of DEHP, for all phthalates 

that it evaluated in isolation, the MOEs 

were within acceptable ranges. Id. at pp. 

82–121. 

4. CHAP’s Recommendations to the 

Commission 

a. Phthalates Subject to the Interim 

Prohibition 

Diisononyl phthalate (DINP) 

The CHAP recommended that the 

Commission permanently prohibit the 

use of DINP in children’s toys and child 

care articles at levels greater than 0.1 

percent. The CHAP explained that, 

although DINP is less potent than other 

active phthalates, it induces 

antiandrogenic effects in animals, and 

therefore, DINP can contribute to the 

cumulative risk from other 

antiandrogenic phthalates. Id. at pp. 95– 

99. 

The CHAP explained that studies 

exposing rats to DINP during the critical 

period of fetal development showed 

effects on male reproductive 

development. The CHAP stated: ‘‘Five 

such studies have shown that DINP 

exposure in rats during the perinatal 

period is associated with increased 

incidence of male pups with areolae and 

other malformations of androgendependent organs and testes (Gray et al., 

2000), reduced testis weights before 

puberty (Matsutomi et al., 2003), 

reduced AGD (Lee et al., 2006), 

increased incidence of multinucleated 

gonocytes, increased nipple retention, 

decreased sperm mobility, decreased 

male AGD, and decreased testicular 

testosterone (Boberg et al., (2011)), and 

reduced fetal testicular testosterone 

production and decreased StAR and 

Cyp11a mRNA levels (Adamson et 

al.,2009; Hannas et al., 2011b).’’ Id. at 

pp. 96–97. 

The CHAP report discussed the 

CHAP’s determination of a NOAEL for 

DINP. Id. at pp. 97–98. The CHAP 

stated: 

Taken together, the data from Boberg et al. 

(2011), Hannas et al. (2011b), and Clewell et 

al. (2013a; 2013b) indicate that the 

developmental NOAEL, based on 

antiandrogenic endpoints (nipple retention, 

fetal testosterone production, and MNGs) is 

between 50 and 300 mg/kg–day. Taking a 

conservative approach, the CHAP assigns the 

NOAEL for DINP at 50 mg/kg–day. However, 

the CHAP also wants to point out that a 

simple extrapolation based upon relative 

potencies (as described in Hannas et al., 

2011b) with 2.3-fold lesser potency of DINP 

than DEHP (in terms of fetal testicular T 

reduction) would lead to a NOAEL of 

11.5mg/kg–d for DINP. This scenario is 

reflected in case 2 of the HI approach. 

Id. at p. 98. Regarding exposure, the 

CHAP observed: ‘‘DINP has been used 

in children’s toys and child care articles 

in the past.’’ Id. The CHAP noted that 

metabolites of DINP have been detected 

in urine samples in NHANES surveys. 

Id. 

Considering risk in isolation 

(following the MOE approach), the 

CHAP found MOEs that are generally 

considered adequate for public health. 

For male developmental effects, in 

infants (using the SFF study) the CHAP 

stated that the total exposure ranged 

from 640 to 42,000, using 95th 

percentile estimates of exposure. For 

pregnant women (using NHANES data), 

the CHAP stated that the MOE for total 

DINP exposure ranged from 1000 to 

68,000. The CHAP stated: ‘‘Typically, 

MOEs exceeding 100–1000 are 

considered adequate for public health; 

however, the cumulative risk of DINP 

with other antiandrogens should also be 

considered.’’ Id. at p. 99. The CHAP also 

considered the effects of DINP on the 

liver, and it found that the MOEs were 

within an acceptable range. 

In making its recommendation to the 

CPSC concerning DINP, the CHAP 

stated: ‘‘The CHAP recommends that the 

interim ban on the use of DINP in 

children’s toys and child care articles at 

levels greater than 0.1% be made 

permanent. This recommendation is 

made because DINP does induce 

antiandrogenic effects in animals, 

although at levels below that for other 

active phthalates, and therefore can 

contribute to the cumulative risk from 

other antiandrogenic phthalates.’’ Id. 

Di-n-octyl phthalate (DNOP) 

The CHAP reviewed data on DNOP. 

Id. at pp. 91–95. The CHAP found that, 

although DNOP is a potential 

developmental toxicant (causing 

supernumerary ribs) and a potential 

systemic toxicant (causing adverse 

effects on the liver, thyroid, immune 

system and kidney), ‘‘DNOP does not 

appear to possess antiandrogenic 

potential.’’ The CHAP estimated that 

MOEs for DNOP for infants and toddlers 

ranged from 2,300 to 8,200. The CHAP 

concluded: ‘‘because the MOE in 

humans are likely to be very high, the 

CHAP does not find compelling data to 

justify maintaining the current interim 

ban on the use of DNOP in children’s 

toys and child care articles.’’ The CHAP 

recommended that the Commission lift 

the interim prohibition with regard to 

DNOP, but also recommended that 

‘‘agencies responsible for dealing with 

DNOP exposures from food and child 

care products conduct the necessary risk 

assessments with a view to supporting 

risk management steps.’’ Id. at p. 95. 

Diisodecyl phthalate (DIDP) 

The CHAP reviewed data on DIDP. Id. 

at pp. 100–105. The CHAP found that, 

although DIDP is a potential 

developmental toxicant (causing 

supernumerary ribs) and a potential 

systemic toxicant (causing adverse 

effects on the liver and kidney), ‘‘DIDP 

does not appear to possess 

antiandrogenic potential.’’ The CHAP 

estimated the MOEs for DIDP range from 

2,500 to 10,000 for median intakes and 

from 586 to 33,000 for 9th percentile 

intakes. Id. at p. 104. The CHAP found 

that DIDP’s MOEs in humans are likely 

to be relatively high. The CHAP stated: 

‘‘The CHAP does not find compelling 

data to justify maintaining the current 

interim ban on the use of DIDP in 

children’s toys and child care articles.’’ 

The CHAP recommended that the 

Commission lift the interim prohibition 

with regard to DIDP, but suggested that 

‘‘agencies responsible for dealing with 

DIDP exposures from food and child 

care products conduct the necessary risk 

assessments with a view to supporting 

risk management steps.’’ Id. at pp. 104– 

105. 


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b. Other Phthalates 

Due to their adverse effect on male 

reproductive development (and thus 

their contribution to the cumulative risk 

from other antiandrogenic phthalates), 

the CHAP recommended that the 

Commission permanently prohibit the 

use of four additional phthalates at 

levels greater than 0.1 percent in 

children’s toys and child care articles. 

Diisobutyl phthalate (DIBP) 

The CHAP found that DIBP is similar 

in toxicity to DBP, one of the phthalates 

subject to the CPSIA’s permanent 

prohibition. The CHAP reviewed 

studies that found that exposure to DIBP 

had effects on male reproductive 

development. The CHAP stated: ‘‘Six 

studies in which rats were exposed to 

DIBP by gavage during late gestation 

showed that this phthalate reduced 

AGD in male pups, decreased testicular 

testosterone production, increased 

nipple retention, increased the 

incidence of male fetuses with 

undescended testes, increased the 

incidence of hypospadias, and reduced 

the expression of P450scc, ins13, genes 

related to steroidogenesis, and StAR 

protein (Saillenfait et al., 2006; Borch et 

al., 2006a; Boberg et al., 2008; 

Howdeshell et al., 2008; Saillenfait et 

al., 2008; Hannas et al., 2011b).’’ Id. at 

p. 110. 

Regarding exposure, the CHAP noted 

that DIBP has been detected in some 

toys during routine CPSC compliance 

testing. The CHAP stated: ‘‘DIBP is too 

volatile to be used in PVC but is a 

component in nail polish, personal care 

products, lubricants, printing inks, and 

many other products.’’ Id. at 111. 

Metabolites of DIBP have been detected 

in human urine in NHANES surveys 

and in Germany. 

Assessing risk, the CHAP found: ‘‘The 

margins of exposure (95th percentile 

total DIBP exposure) for pregnant 

women in the NHANES study ranged 

from 5,000 to 125,000. For infants in the 

SFF study, the MOE (95th percentile 

total DIBP exposure) ranged from 3,600 

to 89,000.’’ Id. Although these MOEs are 

within an acceptable range, the CHAP 

stated that the cumulative risk should 

be considered. Id. Explaining its 

recommendation concerning DIBP, the 

CHAP stated: 

Current exposures to DIBP alone do not 

indicate a high level of concern. DIBP is not 

widely used in toys and child care articles. 

However, CPSC has recently detected DIBP 

in some children’s toys. Furthermore, the 

toxicological profile of DIBP is very similar 

to that of DBP, and DIBP exposure 

contributes to the cumulative risk from other 

antiandrogenic phthalates. The CHAP 

recommends that DIBP should be 

permanently banned from use in children’s 

toys and child care articles at levels greater 

than 0.1%. 

Id. at pp. 111–112. 

Di-n-pentyl phthalate (DPENP) 

Although DPENP is not widely used, 

the CHAP found that it is the most 

potent phthalate with respect to 

developmental toxicity. According to 

the CHAP, two studies (Howdeshell et 

al. (2008) and Hannas et al. (2011a)) 

found that DPENP exposure reduced 

fetal testicular testosterone production, 

StAR Cyp11a, and ins13 gene 

expression, and increased nipple 

retention. Id. at p. 112. The CHAP stated 

that DPENP is not currently found in 

children’s toys or child care articles and 

is not widely found in the environment. 

Id. at p. 113. In its recommendation, the 

CHAP stated: ‘‘The CHAP recommends 

that DPENP should be permanently 

banned from use in children’s toys and 

child care articles at levels greater than 

0.1%. The toxicological profile of 

DPENP is very similar to that of the 

other antiandrogenic phthalates, and 

DPENP exposure contributes to the 

cumulative risk.’’ Id. 

Di-n-hexyl phthalate (DHEXP) 

According to the CHAP, a National 

Toxicology Program review of DHEXP 

in 2003 reported that based on the 

limited data available at that time, 

DHEXP is a developmental toxicant at 

high doses (9900 mg/kg-d), but the data 

were not adequate to determine an 

NOAEL or LOAEL. The CHAP stated 

that since then, ‘‘one developmental 

toxicity study has reported that DHEXP 

exposure reduced the AGD in male pups 

in a dose-related fashion and increased 

the incidence of male fetuses with 

undescended testes (Saillenfait et al., 

2009a).’’ Id. at p. 114. The CHAP report 

stated: ‘‘Saillenfait et al. observed 

reproductive tract malformations, 

including hypospadias, undeveloped 

testes, and undescended testes, in young 

adult male rats exposed prenatally to 

doses of 125 mg/kg-d DHEXP or greater 

(Saillenfait et al., 2009b).’’ Id. at p. 115. 

The CHAP stated that DHEXP is 

currently not found in children’s toys or 

child care articles and is not widely 

found in the environment. It is 

primarily used in the manufacture of 

PVC and screen printing inks and is also 

used ‘‘as a partial replacement for 

DEHP.’’ Id. at p. 116. Regarding risk, the 

CHAP stated: ‘‘DHEXP is believed to 

induce developmental effects similar to 

those induced by other active 

phthalates. Due to low exposure, current 

risk levels are believed to be low.’’ Id. 

The CHAP recommended that DHEXP 

be permanently banned from use in 

children’s toys and child care articles at 

levels greater than 0.1%. The CHAP 

stated: ‘‘The toxicological profile of 

DHEXP is very similar to that of the 

other antiandrogenic phthalates, and 

DHEXP exposure contributes to the 

cumulative risk.’’ Id. 

Dicyclohexyl phthalate (DCHP) 

The CHAP found that studies on 

DCHP showed effects on male 

reproductive development. The CHAP 

report states: ‘‘Two studies in rats 

exposed to DCHP by gavage during late 

gestation showed that this phthalate 

prolonged preputial separation, reduced 

AGD, increased nipple retention, and 

increased hypospadias in male offspring 

(Sallenfait et al, 2009a; Yamasaki et al., 

2009). One study in rats exposed to 

DCHP in the diet showed that DCHP 

decreased the AGD and increased 

nipple retention in F1 males (Hoshino et 

al., 2005).’’ Id. at pp. 116–117. The 

CHAP stated that DCHP is currently not 

found in children’s toys or child care 

articles and is not widely found in the 

environment. FDA has approved it ‘‘for 

use in the manufacture of various 

articles associated with food handling 

and contact.’’ DCHP is also a component 

of hot melt adhesives. Id. at p. 117. The 

CHAP stated: ‘‘DCHP induces 

developmental effects similar to other 

active phthalates. Due to low exposure, 

current risk levels are believed to be 

low.’’ The CHAP recommended that 

DCHP be permanently banned from use 

in children’s toys and child care articles 

at levels greater than 0.1%. Id. at p. 118. 

c. Phthalate Alternatives 

The CPSIA also directed the CHAP to 

consider health effects of phthalate 

alternatives and to include in its report 

to the Commission recommendations for 

any phthalate alternatives that should 

be banned. 15 U.S.C. 2057c(b)(2)(B)(viii) 

and 2057c(b)(2)(C). The CPSIA defines 

‘‘phthalate alternative’’ as ‘‘any common 

substitute to a phthalate, alternative 

material to a phthalate, or alternative 

plasticizer.’’ Id. 2057c(g)(2)(A). 

Accordingly, the CHAP also reviewed 

phthalate alternatives. CHAP report at 

pp. 121–142. The CHAP did not 

recommend banning any phthalate 

alternatives. We also note that the 

Commission’s rulemaking authority 

under section 108 of the CPSIA does not 

extend to phthalate alternatives. 15 

U.S.C. 2057c(b)(3). 

D. Comments Regarding the CHAP 

Comments concerning the substance 

of the CHAP’s analysis are discussed in 

section IV of this preamble. This section 

covers comments concerning the 

CHAP’s process. 


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11See https://www.cpsc.gov/chap. 

1. Peer Review 

Comment: Applicability of OMB Peer 

Review Bulletin. Commenters asserted 

that the CHAP report was subject to 

OMB’s peer review bulletin, that it 

qualifies as a ‘‘highly influential’’ 

scientific assessment, and that it should 

be subject to a peer review that 

comports with the highest standards for 

transparency, openness, and objectivity, 

as outlined in the OMB’s peer review 

bulletin. (Comments 8.6 and 8.7). 

Response: The OMB’s bulletin, Final 

Information Quality Bulletin for Peer 

Review (70 FR 2664 (Jan. 14, 2005)) 

(OMB Bulletin), requires ‘‘to the extent 

permitted by law,’’ that agencies 

conduct peer review on all influential 

scientific information that the agency 

intends to disseminate. The OMB 

Bulletin defines ‘‘influential scientific 

information’’ as ‘‘scientific information 

the agency reasonably can determine 

will have or does have a clear and 

substantial impact on important public 

policies or private sector decisions.’’ Id. 

at 2675. We believe that the CHAP 

report could be considered ‘‘influential’’ 

under this definition. According to the 

OMB Bulletin, ‘‘dissemination’’ means 

‘‘agency initiated or sponsored 

distribution of information to the 

public.’’ Id. at 2674. The preamble to the 

OMB Bulletin notes that the OMB 

Bulletin ‘‘does not directly cover 

information supplied by third parties 

(e.g., studies by private consultants, 

companies and private, non-profit 

organizations, or research institutions 

such as universities). However, if an 

agency plans to disseminate information 

supplied by a third party (e.g., using this 

information as the basis for an agency’s 

factual determination that a particular 

behavior causes a disease), the 

requirements of the OMB Bulletin 

apply, if the dissemination is 

‘influential.’ ’’ Id. at 26676. Although the 

CHAP report was written by a third 

party, we believe that by relying on the 

CHAP report in support of the NPR, the 

Commission disseminated the CHAP 

report. Under the Bulletin, additional 

requirements apply to ‘‘highly 

influential scientific assessments,’’ 

which the Bulletin defines as a 

scientific assessment that: 

(1) Could have a potential impact of 

more than $500 million in any year, or 

(2) is novel, controversial, or 

precedent-setting or has significant 

interagency interest. 

One might consider the CHAP report 

to be a ‘‘novel, controversial, or 

precedent-setting’’ report that it could 

be of ‘‘significant interagency interest’’ 

because, as the CHAP report indicates, 

many of the products that contain 

phthalates (e.g., food and cosmetics) fall 

under other agencies’ jurisdiction. 

Comment: Compliance with OMB 

Peer Review Bulletin. Some commenters 

asserted that the CHAP failed to adhere 

to the OMB Bulletin requirements for 

the peer review of a highly influential 

scientific assessment. In contrast, other 

commenters supported the peer review 

process used for the CHAP report, 

stating that the peer review was part of 

an open and transparent process. 

(Comment 8.7). 

Response: The peer review process 

used for the draft CHAP report complied 

with the additional requirements for 

highly influential scientific assessments. 

For example, as noted by some 

commenters, the peer review of the draft 

report was conducted by four 

independent scientists, using the same 

criteria for selecting the peer reviewers 

(by nomination of the National 

Academy of Sciences) required for 

selecting the CHAP members. The peer 

reviewers were not employed by 

manufacturers of the products under 

consideration or by the federal 

government, except the National 

Institutes of Health, the National 

Toxicology Program, or the National 

Center for Toxicological Research. 

Additionally, the CPSC made public: 

The identity of the peer reviewers, the 

charge to the peer reviewers, the draft 

report that was reviewed, and the peer 

reviewers’ comments. CPSC posted all 

of the information on the CPSC Web site 

at the same time the final CHAP report 

was released to the public; and the 

information is available on the CPSC’s 

Web site, in accordance with the 

additional requirements for a highly 

influential scientific assessment.11

Thus, the public would have ample 

opportunity to see the concerns 

reviewers raised and how the CHAP 

addressed the concerns. 

Finally, regarding public comment, as 

discussed in the next response, the peer 

review process used by CPSC complied 

with the OMB Bulletin. 

Comment: Peer review and public 

comment. Commenters asserted that as 

a ‘‘highly influential’’ assessment, the 

CHAP report should have been subject 

to an open public comment period, as 

set forth in the OMB Bulletin. 

Commenters asserted that the Bulletin 

establishes strict minimum 

requirements for the peer review of 

highly influential scientific assessments, 

including a requirement that an agency 

‘‘make the draft scientific assessment 

available to the public for comment at 

the same time it is submitted for peer 

review . . . and sponsor a public 

meeting where oral presentations on 

scientific issues can be made to the peer 

reviewers by interested members of the 

public.’’ Commenters asserted that this 

would have allowed for comment on 

flaws in the CHAP’s analysis. (Comment 

8.8). 

Response: The OMB Bulletin states: 

‘‘The selection of an appropriate peer 

review mechanism for scientific 

information is left to the agency’s 

discretion.’’ Id. at 2665. It also advises: 

‘‘[a]gencies are directed to choose a peer 

review mechanism that is adequate, 

giving due consideration to the novelty 

and complexity of the science to be 

reviewed, the relevance of the 

information to decision making, the 

extent of prior peer reviews, and the 

expected benefits and costs of 

additional review.’’ Id. at 2668. We also 

note that CPSC staff consulted with 

OMB staff before finalizing the peer 

review plan for the CHAP report, as 

recommended by the OMB Bulletin. 

Although the OMB Bulletin uses the 

term ‘‘requirements,’’ the document 

emphasizes the intent to allow agencies 

flexibility in determining appropriate 

methods of peer review, id. at 2665, and 

the OMB Bulletin is a guidance 

document. The OMB Bulletin states that 

it ‘‘is not intended to, and does not, 

create any right or benefit, substantive 

or procedural, enforceable at law or in 

equity.’’ Id. at 2677. See Family Farm 

Alliance v. Salazar, 749 F. Supp. 2d 

1083 (E.D. Cal. 2010) (finding that a 

claim that the U.S. Fish and Wildlife 

Service had not conducted appropriate 

peer review was not judicially 

reviewable). Although the draft CHAP 

report was not provided to the public 

for comment at the time that the CHAP 

submitted the report for peer review, the 

agency was not required to do so, nor 

was the agency required to sponsor a 

public meeting on the peer review. 

CPSC staff and the CHAP members 

reasonably desired that the report 

should achieve a high level of quality 

before it was released to the public. 

Moreover, as explained in the next 

response, the CHAP report was 

developed through a very open public 

process that provided for public input 

as the CHAP was developing its report. 

2. CHAP’s Transparency and Openness 

Comment: Transparency and 

openness of CHAP’s process. Several 

commenters stated generally that the 

process for the CHAP report was not 

open and transparent, but had been 

conducted behind closed doors. Other 

commenters questioned the 

transparency of particular aspects of the 

CHAP report, such as the methods used 

to review the scientific health evidence 


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12Underdeveloped gubernacular cords lead to 

undescended testes. 

13Foster (2006); Foster et al. (2001); Howdeshell 

et al. (2016); Howdeshell et al. (2008). 

14The CHAP referred to phthalates that cause 

phthalate syndrome as ‘‘antiandrogenic,’’ due to the 

importance of testosterone inhibition in causing 

phthalate syndrome. Antiandrogenic also serves to 

distinguish phthalates from other chemicals that act 

through the androgen receptor, which phthalates do 

not. 

15 Guinea pigs (Gray et al. (1982)), mice, (Gray et 

al. (1982); Moody et al. (2013); Ward et al. (1998)), 

rabbits (Higuchi et al. (2003)), and ferrets (Lake et 

al. (1976)). 

16Clewell et al. (2011) and Ding et al. (2011). 

and assess cumulative risk. In contrast, 

other commenters asserted that the 

CHAP process was a sound and fair 

process, adding that the process was 

highly public, and that the CHAP 

considered public comments and 

written submissions (including from 

industry representatives who charged 

that the process was not open). 

(Comments 8.8 and 10.3). 

Response: The CHAP’s process for 

developing its report was open and 

transparent throughout. The CHAP 

developed its approach in public during 

seven public meetings and six public 

teleconference calls. During these public 

meetings, the CHAP discussed the 

methods that the CHAP would use to 

conduct the cumulative risk assessment. 

CPSC provided a page on its Web site 

to post all CHAP-related information. 

All of the data submitted to the CHAP, 

CPSC contractors’ reports, and peerreviewed staff reports used by the CHAP 

were posted on the CPSC’s public Web 

site. The CPSC’s Web site also included 

correspondence submitted to CPSC 

concerning the CHAP’s work. In fact, 

the CHAP elected not to use industry 

studies on DINX and DPHP, for the very 

reason that the manufacturer would not 

make the toxicology studies available to 

the public. NHANES data (which the 

CHAP relied on) are available to the 

public from the CDC. Once the CHAP 

transmitted its final report to the 

Commission, CPSC posted the final 

report, the draft report that had been 

submitted for peer review, and peer 

reviewers’ comments. The CHAP 

considered all subject matter expert 

comments from the peer review of the 

CHAP draft report. The initial pages of 

the CHAP report outlined changes to the 

CHAP report resulting from the peer 

reviewers’ comments. 

3. Weight of Evidence and 

Completeness of CHAP’s Review 

Comment: Nature of CHAP’s review. 

Some commenters stated that the CHAP 

did not, but should have, conducted a 

systematic review and/or followed a 

weight of evidence (WOE) approach. 

Various commenters asserted that the 

CHAP should have: Employed a 

consistent WOE framework; 

demonstrated how the CHAP graded, 

rated, and interpreted the epidemiology 

studies; and specified a clear and 

systematic approach for addressing the 

uncertainties of the data equally. 

(Comment 10.1). 

Response: The CHAP used the WOE 

approach in two different manners. 

First, the CHAP wrote a ‘‘Weight of 

Evidence’’ section for each 

recommendation for each phthalate and 

phthalate alternative. The CHAP also 

used WOE more broadly when 

developing overall recommendations for 

each phthalate or phthalate alternative. 

The CHAP explicitly stated factors it 

considered relevant to making its 

recommendations. CHAP report at p. 79. 

The CHAP stated, however, that 

‘‘Because of the nature of the subject 

matter and the charge questions, which 

involve different streams of evidence 

and information, the CHAP concluded 

that its review was not amenable to the 

systematic review methodology.’’ Id. at 

p. 12. This does not mean that the 

CHAP’s review was unsystematic and 

biased. Rather, the CHAP, which began 

in 2010, did not have all of the 

systematic review methods that are 

available today. However, the CHAP 

incorporated many of the elements that 

are now included in systematic review 

methods in their work. (See Response 

10.1 of Tab B of staff’s briefing package 

for more detailed response.) 

IV. Final Rule and Rationale 

This section presents the final rule 

and explains the Commission’s rationale 

for the rule. The Commission has 

considered the CHAP report, staff’s 

analysis of the CHAP report, staff’s 

analysis of recent NHANES data, and 

the public comments submitted in 

response to the proposed rule and staff’s 

NHANES reports. More specifically, we 

present the Commission’s rationale for 

the rule by explaining the Commission’s 

consideration of: Phthalates’ effects on 

male reproductive development, human 

exposure to phthalates, assessment of 

phthalates’ cumulative risk and risks in 

isolation, and assessment of risk for 

each phthalate that the CHAP 

considered. In addition, the 

Commission considered the appropriate 

concentration limit for the phthalates 

restrictions and the appropriate effective 

date for the rule. In this section, we also 

discuss phthalate requirements 

established by international standards 

and other countries. 

A. Hazard: Phthalates’ Effect on Male 

Reproductive Development 

1. Summary 

In accordance with the CPSIA’s 

direction, the CHAP reviewed all 

available toxicity data on phthalates. 

The CHAP determined that the critical 

endpoint for its analysis was adverse 

effects on male reproductive 

development (MRDE) and other adverse 

effects on male fertility. This focus was 

consistent with the NRC’s 2008 

assessment. As noted in the NPR, CPSC 

staff supports the CHAP’s choice to 

focus on this endpoint because: MRDE 

in animals is associated with many of 

the most common phthalates; for most 

active phthalates, these effects are the 

most sensitive health effect; and 

phthalate syndrome in animals 

resembles testicular dysgenesis 

syndrome (TDS) in humans. Moreover, 

phthalates’ effects on male reproductive 

development are well studied. 79 FR 

78331–32. 

As the CHAP reported, ‘‘Studies 

conducted over the past 20 plus years 

have shown that phthalates produce a 

syndrome of reproductive abnormalities 

in male offspring when administered to 

pregnant rats during the later stages of 

pregnancy.’’ CHAP report at p. 15. 

These effects include: Reduced 

testosterone synthesis, reduced 

anogenital distance (AGD), nipple 

retention (normally does not occur in 

male rats), undescended testes, 

testicular atrophy, testicular 

histopathology, multi-nuclear gonocytes 

(MNGs), reduced production of insulinlike hormone 3 (insl3), underdeveloped 

gubernacular cords,12 undescended 

testes, and genital malformations 

(hypospadias).13 Effects may differ 

depending on the dose. The CHAP 

noted: ‘‘the highest incidence of 

reproductive tract malformations is 

observed at higher phthalate dose levels, 

whereas changes in AGD and nipple/ 

areolae retention are frequently 

observed at lower phthalate does 

levels.’’ CHAP report at p. 15. These 

effects persist into adulthood and lead 

to reduced or absent reproductive 

ability. Many, but not all, phthalates 

cause phthalate syndrome.14 The CHAP 

identified five phthalates (DBP, BBP, 

DINP, DIBP, and DEHP) that cause 

phthalate syndrome and for which 

human biomonitoring data were 

available to assess exposure. 

As discussed in the CHAP report, 

studies have reported similar effects in 

species other than rats, such as guinea 

pigs, mice, rabbits, and ferrets.15 The 

evidence of phthalate syndrome in mice 

is even stronger now than when the 

CHAP developed its analysis.16 In 

addition, as the CHAP noted, ‘‘there is 

a rapidly growing body of 


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17Scott et al. (2007); Skakkebaek et al. (2001). 

18 Doyle et al. (2013) and Ge et al. (2015). 

19Barnes and Dourson (1988); CPSC (1992); EPA 

(1991). 

20 Desdoits-Lethimonier et al. (2012); Lambrot et 

al. (2009). 

epidemiological studies on the potential 

association of exposure to phthalates 

with human health.’’ CHAP report at p. 

27. For example, the CHAP discussed 

two human studies linking prenatal 

phthalate exposure to effects such as 

reduced AGD in male infants. Id. at p. 

28. TDS in humans bears similarities to 

rat phthalate syndrome. Id. at p. 2. The 

effects of TDS (e.g., hypospadias, 

cryptorchidism, testicular cancer, 

impaired fertility) are observed with 

regularity in the U.S. population. 

Phthalates have been proposed as 

possible contributors to TDS.17

2. Comments Concerning Male 

Reproductive Developmental Effects 

Several commenters raised issues 

concerning phthalates’ effects on male 

reproductive development (MRDE). 

They asserted that studies do not 

support a determination that phthalates 

have the same effects on male 

reproductive development in humans 

(and other animals) as they do in rats. 

Commenters also asserted that, even if 

phthalates have some effect, humans are 

less sensitive and the CHAP failed to 

take this into account, especially 

through appropriate uncertainty factors. 

Additionally, commenters raised 

questions about the epidemiology 

studies the CHAP discussed, i.e., studies 

concerning phthalates’ effects on human 

populations. Commenters also asserted 

that, because MRDE would affect the 

developing fetus, this was not an 

appropriate endpoint for CPSC’s 

consideration of a regulation on 

children’s toys and child care articles. 

Commenters raised questions 

specifically about DINP’s association 

with MRDE. A summary of key 

comments/responses concerning MRDE 

appears in this section. Comments/ 

responses concerning DINP, in 

particular, are provided in section 

IV.D.1.a. of this preamble. 

a. Animal Studies and Their Relevance 

to Humans 

Comment: Studies on effects of 

phthalates on animals other than rats. 

Several commenters questioned the 

relevance of studies on rat phthalate 

syndrome in assessing effects on 

humans. Commenters asserted that 

studies involving animals other than 

rats (e.g., hamsters and marmosets,) 

indicate that phthalates are not likely to 

have the same adverse effects in people 

that they have in rats. Commenters 

argued that marmosets, being primates 

and having reproductive organ 

development that is similar to humans, 

were more closely related to humans 

than rats and, therefore, are a better 

model for estimating human risk. 

Commenters focused particularly on one 

study (McKinnell et al. (2009)) that 

reported no observed effects for several 

relevant endpoints. Some commenters 

asserted that studies involving mice 

indicate that humans, who are more 

similar to mice than rats, are likely less 

sensitive to phthalates than rats. 

Commenters also cited xenograft studies 

(i.e., transplanting human fetal 

testicular tissue into rats or mice) as 

supporting the conclusion that exposure 

to phthalates does not result in MRDE 

in humans, or at the least, humans are 

less sensitive than rats. (Comments 1.1 

through 1.5). 

Response: Phthalate syndrome has 

been reported to occur in multiple 

mammalian species, including guinea 

pigs, mice, rabbits, and ferrets. Although 

studies indicate that hamsters were 

resistant to the effects of phthalates due 

to their slow metabolism to the active 

metabolite, a study by Gray et al. (1982) 

shows that giving the active metabolite 

to hamsters causes phthalate syndrome. 

Regarding mice, the CHAP discussed 

studies that found some effects in mice 

(e.g., disruptions in seminiferous cord 

formation, the appearance of 

multinucleated gonocytes, and 

suppression of insulin-like factor 3 

(insl3)). CHAP report at p. 6. Some 

studies published after the CHAP 

completed its analysis provide 

additional evidence of phthalate 

syndrome effects in mice, including 

reduced testosterone levels, reduced 

testosterone production, testicular 

damage, reduced sperm count and 

quality, reduced AGD, delayed pubertal 

onset, and increased nipple retention.18

Thus, there is now even stronger 

evidence of phthalate syndrome in mice 

than was available to the CHAP. The 

CHAP cautioned that differences in 

methodology could cloud the issue of 

which species is more sensitive. CHAP 

report at pp. 17 and 72. Even if mice or 

other species are less sensitive than rats, 

it is not possible to make a direct 

comparison to humans without doseresponse information in humans. 

Furthermore, the most sensitive 

species is generally used in assessing 

risks to humans.19 The CHAP 

concluded that rats provide the most 

sensitive and most extensive studies in 

male developmental toxicity. CHAP 

report at pp. 1, 15, 16, 76. Phthalate 

syndrome in rats resembles the TDS in 

humans. Id. at pp. 2, 75. For these 

reasons, the CHAP concluded that 

studies in rats currently offer the best 

available data for assessing human risk. 

Id. at pp. 18, 75. 

Regarding the marmoset studies, the 

CHAP paid particular attention to these 

studies and invited Richard Sharpe, the 

principal investigator of the Hallmark 

and McKinnell studies, to present his 

findings at the CHAP meeting in 

November 2011. Dr. Sharpe agreed with 

the CHAP that both studies were limited 

by the small numbers of animals used 

and the brief duration of exposure. Dr. 

Sharpe added that his studies were very 

preliminary and that it would be 

premature to use his studies’ results to 

support public health decisions. Even 

though limited, the published studies 

do show that the phthalate metabolite 

suppressed steroidogenesis in neonatal 

marmosets. 

Regarding the xenograft studies, 

commenters cited two studies in which 

rat fetal testes or human fetal testicular 

tissue were transplanted (xenografted) 

into rats (Heger et al. (2012)) or mice 

(Mitchell et al. (2012)). As discussed by 

the CHAP, these studies are subject to 

a number of limitations. CHAP report at 

p. 17. Most of the human fetal tissue 

samples were obtained after the human 

window of maximum susceptibility to 

phthalates, meaning that the tissues 

were less susceptible to MRDE induced 

by phthalates. In contrast, constant 

exposure to phthalates in the womb 

would always expose the fetal tissue to 

phthalates at their time of maximum 

sensitivity. Staff provides more detailed 

responses concerning these studies on 

animals other than rats in comment/ 

responses 1.1 through 1.5. 

Comment: Implications of in vitro 

studies and studies involving chemicals 

other than phthalates. Some 

commenters discussed studies in which 

human testicular tissue or cells were 

cultured in vitro and then exposed to 

phthalates.20 Commenters asserted that 

these studies raise questions about 

whether phthalate-induced testosterone 

reduction in rats is relevant to humans. 

Commenters also asserted that studies 

(which were not cited by the CHAP) of 

chemicals with the same mode of action 

as phthalates, DES and finasteride, show 

that humans are resistant to phthalates. 

(Comments 1.6 and 1.7). 

Response: In vitro studies use 

techniques that are performed in a 

controlled environment outside of a 

living cell or organism, while in vivo 

studies are performed inside living cells 

or organisms. CPSC staff reviewed the 

studies and concludes that the in vitro 

studies with human fetal testicular 


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21Barnes and Dourson (1988); CPSC (1992); 

Dankovic et al. (2015); EPA (1991); Pohl and 

Abadin (1995). 

22EPA (1991). 

23 Klaassen (2001), p. 703. 

24Pohl and Abadin (1995). 

25Barnes and Dourson (1988); CPSC (1992); 

Dankovic et al. (2015); EPA (1991). 

tissue are still preliminary and are 

generally not sufficient, by themselves, 

to support public health decisions. In 

vivo animal studies are generally given 

greater weight in risk assessment. As the 

CHAP noted, there is also a growing 

body of evidence in humans that shows 

associations between phthalate 

exposure and MRDE endpoints that are 

consistent with the rat data. 

Regarding DES and finasteride, the 

CHAP assessed each phthalate based on 

the best available data for each 

individual chemical, and based its 

recommendations on those assessments. 

The CHAP did not base its conclusions 

on an assumption that all phthalates 

will behave the same way as DES or 

finasteride. The DES and finasteride 

publication cited by commenters 

implies that humans are less sensitive 

than rats to these two chemicals. 

However, this assertion does not mean 

that all phthalates will produce similar 

biological effects as DES or finasteride; 

phthalates do not have a similar 

chemical structure, are not metabolized 

or detoxified in the same way, and will 

not have similar dose-response curves to 

those of DES or finasteride. 

b. Uncertainty Factors 

Comment: Adjusting uncertainty 

factors. Some commenters asserted that, 

even if one accepts that studies on rats 

demonstrate that phthalates have some 

effect on humans, humans are less 

sensitive than rats, and one must adjust 

the interspecies uncertainty factor to 

avoid overestimating the risk to 

humans. Some commenters suggested 

that instead of an interspecies 

uncertainty factor of 10, which the 

CHAP used, the uncertainty factor 

should be 0.1 (i.e., humans are 10x less 

sensitive than rodents) to 1 (humans are 

equally sensitive as rodents).’’ Other 

commenters asserted that the CHAP 

should have used a different 

intraspecies uncertainty factor. They 

argued that the intraspecies uncertainty 

factor of 10 used by the CHAP is overly 

conservative because the PEAAs are 

already based on a sensitive population. 

Commenters on both types of 

uncertainty factors asserted that 

following their recommendations would 

have reduced the HI in the CHAP’s 

cumulative risk analysis so that it would 

be less than one. (Comments 1.8 and 

1.9). 

Response: An uncertainty factor is 

used in risk assessments to account for 

differences among different species. An 

interspecies uncertainty factor of 10 is 

consistent with the general practice 

used by CPSC, EPA, and others in risk 

assessment, to account for interspecies 

differences.21

Humans are frequently more sensitive 

to reproductive and developmental 

effects than animals,22 and human 

males are considered more vulnerable 

than other mammals.23 Commenters 

cited xenograft studies to support the 

assertion that humans are less sensitive 

than rats to phthalates effects. As 

discussed in the response above, these 

preliminary studies do not provide 

sufficient support for reducing the 

interspecies uncertainty factor. 

An uncertainty factor is also used to 

account for differences in how members 

of the same species could react to a 

chemical (i.e., human variability). In 

deriving PEAAs, the CHAP applied an 

intraspecies UF of 10 to account for 

differences in sensitivity among 

individuals. CHAP report at pp. 63–66. 

CPSC staff expects that the population 

of infants and fetuses will have a broad 

range of sensitivity, because age, sex, 

genetic composition, nutritional status, 

and preexisting diseases may all alter 

susceptibility to toxic chemicals.24

Multiple federal agencies use an 

intraspecies uncertainty factor of 10.25

The CHAP used only the interspecies 

uncertainty factor and intraspecies 

uncertainty factor in its analyses. The 

CHAP did not apply an additional UF 

to protect infants. 

c. Epidemiology Studies 

Comment: Role of epidemiology 

studies in CHAP’s report and 

recommendations. Some commenters 

suggested that human epidemiological 

evidence for phthalate-induced effects 

was equivocal or inconsistent with 

results from animal studies, and did not 

support the CHAP’s conclusions and 

recommendations. Some commenters 

asserted that these studies did not show 

consistent results and have not 

established a cause and effect 

relationship between phthalate 

exposure and MRDE effects in humans. 

(Comment 7.1). 

Response: The CHAP’s assessment 

and recommendations to the 

Commission are based primarily on 

animal studies. However, the CHAP 

reviewed epidemiology studies as well. 

CPSC staff agrees with the CHAP that 

these epidemiology studies indicate an 

association of exposure to phthalates 

with human health. Under CPSC’s 

Chronic Hazard Guidelines and other 

agencies’ guidance, epidemiological 

studies establishing a causal 

relationship between exposure and 

effect are not required to conclude that 

a substance or mixture is ‘‘probably 

toxic to humans.’’ CPSC’s Chronic 

Hazard Guidelines, 57 FR 46626, 46641 

(Oct. 9, 1992). CPSC staff considers that 

there is sufficient evidence in animal 

studies to conclude that certain 

phthalates are probably toxic to 

humans. Epidemiological data provide 

supporting evidence for the animal data 

and also support the conclusion that the 

animal data are relevant to humans. In 

addition, staff states that the CHAP’s 

conclusion is consistent with a recent 

NAS (2017) report that also concluded 

that there is a ‘‘moderate level of 

evidence’’ from epidemiological studies 

that DEHP and DBP induce MRDE in 

humans (based on changes in AGD). The 

NAS report’s conclusions provide 

additional confidence that phthalates 

cause MRDE in humans. Although there 

are a few inconsistencies in the findings 

from epidemiological studies, 

inconsistencies among epidemiological 

studies are common, due to differences 

in study methods, characteristics of the 

study population, study size, and the 

statistical power of the study to detect 

associations. Establishing cause and 

effect in epidemiological studies is not 

required by federal and international 

agencies to conclude that a substance is 

likely to cause similar effects in 

humans. 

Comment: Studies on reduced 

anogenital distance (AGD). Several 

commenters raised questions about an 

association between phthalate exposure 

and reduced AGD in males. 

Commenters noted inconsistencies in 

results among published studies and 

noted that effects occurred sporadically 

and inconsistently, even when 

performed by the same laboratory. Some 

commenters pointed to inconsistencies 

between epidemiological and animal 

studies. Other commenters took a 

different view, noting that ‘‘these 

markers are linked with diminished 

reproductive health in males.’’ 

(Comments 7.3 and 7.7). 

Response: The CHAP considered and 

discussed the inconsistent 

epidemiological data, noting the need to 

evaluate carefully negative and positive 

findings. CHAP report at p. 21. The 

CHAP considered the available 

epidemiological evidence, along with 

the animal studies, and determined that 

human AGD is a relevant measure of the 

antiandrogenic mode of action of 

phthalates during fetal development. 

CPSC staff concludes that, with few 

exceptions, the epidemiology studies 


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26 e.g., Boberg et al. (2011); Clewell et al. (2013b). 

27Foster (2006). 

28Barnes and Dourson (1988); EPA (1991). 

29NAS (2017) Application of Systematic Review 

Methods in an Overall Strategy for Evaluating LowDose Toxicity from Endocrine Active Chemicals. 

National Academies of Sciences, Engineering, and 

Medicine, National Research Council. Washington, 

DC: The National Academies Press. doi: https://

doi.org/10.17226/24758. 

are generally consistent with one 

another and with the results of animal 

studies. 

Reduced AGD is one of many effects 

associated with phthalate syndrome. 

Studies demonstrate that phthalates 

cause permanent effects on male 

reproductive development.26 Jain and 

Singal (2013) reported that infants with 

undescended testis (cryptorchidism—an 

adverse clinical outcome) had a 

significantly shorter AGD and AGI when 

compared to infants with descended 

testis. Thankamony et al. (2014) 

reported the results of a comparative 

study involving AGD (and penile 

length) in infants that were normal and 

those with hypospadias or 

cryptorchidism. They determined that 

AGD was statistically reduced in boys 

with hypospadias or cryptorchidism 

when compared to boys without these 

pathologies. They concluded: ‘‘The 

findings support the use of AGD as a 

quantitative biomarker to examine the 

prenatal effects of exposure to endocrine 

disruptors on the development of the 

male reproductive tract.’’ 

Comment: DEHP exposure and 

medical procedures. One commenter 

stated that the lack of evidence showing 

effects occurring in adults and infants 

who are exposed to DEHP from 

intensive medical procedures makes it 

unlikely that less potent phthalates 

would induce adverse reproductive 

effects in humans. (Comment 7.4). 

Response: Few studies have 

specifically investigated possible health 

outcomes from phthalate exposures 

from medical equipment. The 

commenter cited two studies, one that 

the CHAP also discussed. Although this 

study did not find phthalate-related 

health effects, the CHAP concluded that 

the very small sample size limits its 

usefulness. CPSC staff concludes that 

because of the uncertainties in the 

existing data, no conclusions can be 

drawn from high exposures to DEHP in 

medical procedures. 

d. Relevance of Endpoint to Rulemaking 

Comment: Disconnect between risk 

assessment’s focus on fetus as target 

population and focus of rule. 

Commenters questioned how a rule 

restricting phthalates in children’s toys 

and child care articles could reduce the 

risk of phthalate syndrome when the 

fetus, not infants and children who use 

toys and child care products, is the 

population primarily at risk for adverse 

effects on male reproductive 

development. Commenters noted that 

the CHAP’s analysis shows that 

exposures of women to DINP from 

children’s toys and childcare articles are 

negligible. (Comment 1.11). 

Response: Although fetuses are 

considered to be the most sensitive 

population for MRDE, based on data 

from animal studies, the CHAP 

recognized that other populations such 

as infants, toddlers, and children also 

are susceptible to the effects of 

phthalates. CHAP report at p. 14. 

Testosterone production and other 

processes involved in reproduction 

remain critical throughout male 

development in animals and humans 

from the prenatal period through 

puberty. 

Testosterone production is required 

throughout a male’s lifetime to maintain 

the ability to reproduce.27 Moreover, 

CPSC, like other federal agencies, uses 

the most sensitive and appropriate 

human target population in risk 

assessments. The practice of selecting 

the most protective endpoints and 

potency estimates (i.e., PODs) based on 

the best available studies is consistent 

with the statutory mandate to provide a 

reasonable certainty of no harm with an 

adequate margin of safety. Using the 

lowest POD also is consistent with 

CPSC Chronic Hazard Guidelines, 57 FR 

46626 (Oct. 9, 1992), and other federal 

agency practices.28

3. National Academy of Sciences Report 

on Endocrine Disruptors 

In July 2017, the National Academies 

of Sciences, Engineering, and Medicine 

(NAS) released a report entitled, 

Application of Systematic Review 

Methods in an Overall Strategy for 

Evaluating Low-Dose Toxicity from 

Endocrine Active Chemicals (NAS 

2017).29 The study responds to EPA’s 

request that the NAS develop a strategy 

to evaluate the evidence for potential 

human health effects from endocrine 

active chemicals at low doses. The NAS 

selected phthalates as one of two 

chemicals to demonstrate the systematic 

review methods and integration of 

results. In a chapter titled, ‘‘Phthalates 

and Male Reproductive-Tract 

Development,’’ the NAS study evaluated 

three health effects (fetal testosterone, 

anogenital distance (AGD), and 

hypospadias). CPSC staff reviewed the 

NAS study. 

Unlike the CHAP report, the NAS 

study is not a risk assessment. Rather, 

the NAS study reviewed individual 

phthalates and three individual health 

effects, focusing on whether enough 

quality data existed to term the 

particular phthalates a reproductive 

hazard to humans. In contrast, the 

CHAP considered all phthalate 

syndrome effects. In spite of these 

differences, the NAS report’s 

conclusions are consistent with the 

CHAP and staff’s hazard conclusions. 

The phthalates section of the NAS 

report focused on DEHP, and provided 

a ‘‘final hazard conclusion’’ for each of 

the endpoints. Thus, for fetal 

testosterone and AGD, DEHP is 

presumed to be a reproductive hazard to 

humans; for hypospadias, DEHP is 

suspected to be a reproductive hazard to 

humans (NAS 2017, pp. 78–81). For the 

other assessed phthalates, including 

DINP, the NAS report did not conduct 

the final analysis step that results in a 

‘‘final hazard conclusion.’’ The report 

provides only the ‘‘initial hazard 

evaluations’’ for fetal testosterone, AGD, 

and hypospadias in humans. The report 

found for fetal testosterone, the 

phthalates BBP, DBP, DEP, DIBP, DINP, 

and DPP are presumed to be 

reproductive hazards to humans; DEP is 

not classifiable for this endpoint (NAS 

2017, Table 3–30). AGD, BBP, DBP, and 

DEP are presumed to be reproductive 

hazards to humans, while DIBP, DIDP, 

and DINP are not classifiable (NAS 

2017, Table 3–29). For hypospadias, 

BBP is suspected to be a reproductive 

hazard to humans and DBP is presumed 

to be a reproductive hazard to humans 

(NAS 2017, Table 3–31). The NAS 

committee did not evaluate DHEXP, 

DCHP, or DIOP. 

With regard to DINP, the NAS study 

concluded: 

• DINP effect on Fetal Testosterone: 

The NAS concluded: ‘‘there is a high 

level of evidence that fetal exposure to 

DINP is associated with a decrease in 

fetal testosterone in male rats,’’ and that 

there was ‘‘inadequate evidence to 

determine whether fetal exposure to 

. . . DINP, . . . is associated with a 

reduction in fetal testosterone in male 

humans.’’ Overall, the NAS’ initial 

hazard evaluation of DINP and fetal 

testosterone in humans was that DINP 

was a ‘‘presumed human hazard.’’ 

• DINP effect on AGD: The NAS 

concluded: ‘‘there is an inadequate level 

of evidence to assess whether fetal 

exposure to DINP is associated with a 

decrease in AGD in male rats,’’ and: 

‘‘the available studies do not support 

DINP exposure being associated with 

decreased AGD.’’ Overall, the NAS’ 

initial hazard evaluation of DINP and 

AGD in humans was ‘‘not classifiable.’’ 


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30Zota et al. (2014). 

31CHAP 2014; Sathyanarayana et al. (2008a); 

Swan (2008); Swan et al. (2005). 

32 Koch et al. (2004). 

CPSC staff provides a more detailed 

discussion of the NAS report in the final 

rule briefing package at section III.B. of 

the briefing memorandum. 

B. Exposure to Phthalates 

As noted, the CHAP considered 

exposure in two ways: Human 

biomonitoring studies that estimate total 

exposure to phthalates and the scenariobased assessment that estimates 

exposure to specific products and 

sources. 

1. Human Biomonitoring 

a. Summary 

The CHAP used data from NHANES 

to estimate phthalate exposures to 

pregnant women. The CHAP also used 

human biomonitoring data from the SFF 

study to estimate exposures to infants 

and their mothers because NHANES 

does not collect data on children under 

6 years old. The CHAP’s analysis of 

NHANES data was based on the 2005/ 

2006 data cycle. CPSC staff 

subsequently analyzed data from later 

NHANES data sets. Because the 2005/ 

2006 data set was the last to sample a 

sufficient number of pregnant women to 

make reliable exposure estimates for 

pregnant women, CPSC staff’s analyses 

are for women of reproductive age 

(WORA). Staff determined that WORA 

are a suitable surrogate for pregnant 

women. CPSC staff’s June 2015 report; 

Tab A of staff’s briefing package. CPSC 

staff then used the CHAP’s methodology 

and later NHANES data sets (2007/2008, 

2009/2010, 2011/2012) to estimate 

phthalate exposure, individual 

phthalate risk, and the cumulative risk 

(i.e, hazard index). Id. When CDC 

released another data set, 2013/2014, 

staff performed a similar analysis using 

that data. CPSC staff’s February 2017 

report; Tab A of staff’s briefing package. 

No more recent SFF data are available. 

In CPSC staff’s analysis of NHANES 

data published following the CHAP’s 

analysis, staff found that total phthalate 

exposures in WORA have changed. The 

median total exposure to the phthalates 

included in the CHAP’s cumulative risk 

assessment (DEHP, DINP, BBP, DBP, 

DIBP) has increased by 20 percent in 

WORA. In particular, the estimated 

median DEHP exposure in WORA has 

declined over time, while the estimated 

median DINP exposure in WORA has 

increased fivefold since 2005/2006.30

Although DEHP was the major 

contributor to the cumulative risk in 

2005/2006, DINP now contributes about 

as much as DEHP. See TAB A of staff’s 

briefing package, Figures 6 and 7, and 

Table 8. 

No new data on infants or pregnant 

women are available to quantify the 

effects of changing exposures. Given 

that the overall phthalate exposures to 

WORA have declined since 2005/2006, 

it is possible that exposures to infants 

and pregnant women have also 

declined. In general, studies indicate 

that infants’ and children’s exposures to 

chemicals tend to be greater than in 

adults.31 With regard to phthalates, 

daily intakes of the phthalates the CHAP 

examined in its cumulative risk 

assessment were generally twofold to 

threefold greater in SFF infants than in 

their mothers. CHAP report at Table 2.7. 

In the CHAP’s scenario-based exposure 

assessment, estimated daily intakes 

were twofold to fivefold greater in 

infants than in women. CHAP report, 

Appendix E1, Table E1–18. 

Additionally, a study of German nursery 

school children found they had roughly 

twice the DEHP exposure as their 

parents.32 Because CPSC does not have 

exposure data for children more recent 

than the SFF data used by the CHAP, 

staff can only make a qualitative 

assessment that infants and children 

could have greater exposure to 

phthalates than what the NHANES data 

indicate for WORA. In section IV.C.1. of 

this preamble, we discuss the effect of 

the more recent NHANES data on risk. 

b. Comments Concerning Biomonitoring 

Data 

i. Particular Data Sets 

Comment: CHAP’s use of 2005/2006 

NHANES data. Several commenters 

criticized the CHAP’s use of 2005/2006 

NHANES data. Commenters noted that 

the CHAP report states: ‘‘the stopping 

point for CHAP analysis and 

interpretation was information available 

by the end of 2012.’’ However, 

commenters stated, both 2007/2008 data 

and 2009/2010 data were available by 

then. A commenter noted that the 2009/ 

2010 data set was available in 

September 2012, nearly 2 full years 

before the final CHAP report was issued 

and before the CHAP cutoff date for 

consideration of new information (end 

of 2012). The commenter noted that the 

2011/2012 data set was available in 

November 2013, ahead of the meeting in 

January 2014 at which the CHAP 

discussed the peer review of its report. 

(Comment 3.1). 

Response: The CHAP used 2005/2006 

NHANES data on pregnant women to 

assess phthalate exposure as part of the 

cumulative risk assessment, to satisfy 

the CPSIA’s charge to ‘‘examine the 

likely levels of children’s, pregnant 

women’s, and others’ exposure to 

phthalates . . . .’’ 15 U.S.C. 

2057c(b)(2)(B)(iii) (emphasis added). 

This data set was the most recent data 

on pregnant women available at the 

time the CHAP completed its analysis in 

July 2012. CHAP report at p. 31. The 

2005/2006 NHANES study was the last 

data cycle to include a large sample of 

pregnant women. The CHAP included 

summary phthalate metabolite data from 

the 2007/2008 data cycle in its report, 

id. at Tables 2.5, 2.6., but did not 

calculate exposure and risk because this 

data set did not have sufficient numbers 

of pregnant women. Partial data for 

2009/2010 were first released in 

September 2012, after the CHAP 

completed its analysis in July 2012. 

Although the 2011/2012 data on 

phthalate metabolites were initially 

released in November 2013, the data 

were revised in October 2014, and other 

files that were needed to calculate 

exposure and risk were not published 

until January 2015, well after 

publication of the final CHAP report. 

Regarding the CHAP report’s statement 

about a cutoff date, read in context, the 

cutoff date clearly refers to the final 

update of the CHAP’s search of the 

biomedical literature for new peerreview publications in biomedical 

journals, specifically, National Library 

of Medicine databases. In any event, 

CPSC recognized that more recent 

NHANES data than the set on which the 

CHAP relied were available. 

Accordingly, CPSC staff analyzed the 

later NHANES data sets and used the 

most recent data in its analysis for the 

final rule. 

Comment: Pregnant women and 

women of reproductive age. Some 

commenters stated that the 2005/2006 

NHANES data on WORA were a 

reasonable surrogate for the data on 

pregnant women, and that the CHAP 

should have used WORA in its 

cumulative risk assessment because the 

WORA have an increased sample size in 

most NHANES datasets and phthalates 

exposures for both are statistically 

similar. Commenters asserted that the 

sample size for pregnant women in the 

CHAP’s analysis was too small to yield 

reliable risk estimates. In contrast, 

another commenter supported the 

CHAP’s decision to base its analysis on 

the 2005/2006 data that focused on 

pregnant women. (Comments 3.7 and 

3.10). 

Response: The CHAP stated that it 

chose to use biomonitoring data from 

the 2005/2006 NHANES and from the 

SFF ‘‘because of the CHAP’s task to 


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33Carruthers and Foster (2005); Creasy et al. 

(1987); Ferrara et al. (2006); Gray et al. (1999); 

Hannas et al. (2011); Jobling et al. (2011); Jones et 

al. (1993); Li et al. (2000); Parks et al. (2000); 

Saillenfait et al. (1998); Saitoh et al. (1997); Spade 

et al. (2015); Thompson et al. (2004); Thompson et 

al. (2005). 

34National Health and Nutrition Examination 

Survey, 2005–2006 Data Documentation, Codebook, 

and Frequencies. Available at: https://

wwwn.cdc.gov/Nchs/Nhanes/2005-2006/FASTQX_

D.htm. 

35National Health and Nutrition Examination 

Survey, 2003–2004 Data Documentation, Codebook, 

and Frequencies. Available at: http://

wwwn.cdc.gov/nchs/nhanes/2003-2004/PH_C.htm. 

investigate the likely levels of 

children’s, pregnant women’s, and 

others’ exposure to phthalates and to 

consider the cumulative effect of total 

exposure to phthalates both from 

children’s products and other sources.’’ 

CHAP report at p. 35. Although, as the 

CHAP stated, there are indications that 

exposures may be higher in pregnant 

women than in women in general, the 

CHAP stated: ‘‘the exposures were not 

found to be significantly different.’’ Id. 

at p. 36. CPSC staff compared estimates 

from the 2005/2006 NHANES data set to 

determine whether WORA had similar 

daily intake (DI) and Hazard Index as 

Pregnant Women. CPSC staff found that 

median and 95th percentile estimates of 

the DI for five phthalates were generally 

similar when comparing WORA to 

pregnant women. Regarding the sample 

size of pregnant women, CDC calculated 

the sample size necessary for statistical 

analysis of NHANES data. In the data 

sets after 2005/2006, NHANES no longer 

oversampled pregnant women. 

Therefore, the numbers of pregnant 

women in data sets after 2005/2006 

were too small to generate statistical 

estimates for pregnant women. See Tab 

A of staff’s briefing package. 

ii. Biomonitoring Methodology 

Commenters raised concerns about 

various technical aspects of the 

NHANES data (e.g., effects of fasting, 

spot sampling rather than averaging 

urine samples over time, using hydrolic 

metabolites for DINP and DIDP, and 

appropriate metabolite markers). Key 

points are discussed below. More details 

are provided in Tab B of the staff’s 

briefing package, particularly comments 

1.13, 3.6, 3.11, and comments 3.14 

through 3.17. 

Comment: Urinary spot sampling. 

Several commenters raised concerns 

about urinary spot sampling. They 

noted that biomonitoring studies (and 

NHANES in particular) take one spot 

urine sample as opposed to averaging 

urine samples collected over a longer 

period of time. Commenters claimed 

that spot sampling does not accurately 

reflect the duration of exposure 

necessary to develop MRDE. They stated 

that the exposure information should 

match the exposure scenario of that 

hazard data to which it is compared 

(e.g., chronic exposure to chronic 

hazard). They asserted that spot 

sampling would not capture the day-today variability in urinary concentration 

of most phthalates and would 

overestimate the risk. However, another 

commenter stated that spot samples are 

as predictive of urinary concentration as 

24-hour urinary samples. (Comments 

1.13 and 3.11). 

Response: The CHAP and CPSC staff 

estimated daily intake of each phthalate 

by modeling creatinine-related 

metabolite measurements across 

participants in NHANES. NHANES 

measured metabolites from one spot 

urine sample per individual in the 

study. Spot urine samples were 

collected at different sites and at various 

times of the day and days of the week. 

Additionally, because participants for 

each NHANES study cycle were 

randomly selected from civilian, noninstitutionalized individuals in the 

United States, according to a 

probability-based complex, multistage 

sample design, the estimated daily 

intakes are representative of the U.S. 

population. The estimated daily intakes 

and the resulting HQs and HIs represent 

estimated population per capita 

phthalate exposure across the 2-year 

NHANES cycle, not average daily 

estimates of an individual’s exposure 

across time. Thus, an estimated 

proportion of the population with an HI 

less than one, using HBM from 

NHANES, represents the estimated 

proportion of the population within that 

cycle that would have an HI less than 

one at any one given time of that cycle. 

Estimates based on NHANES HBM do 

not imply that individuals with HI less 

than one at a given time will continue 

to have an HI less than one for all 2 

years of a NHANES study cycle. 

CPSC staff notes that longer-term 

exposures are not necessarily required 

to cause MRDE. Numerous studies in 

animals have demonstrated that MRDE 

and related effects can occur after one 

or a few doses.33 Shorter-term elevated 

exposure could be related to adverse 

health outcomes in the fetus, if the 

exposure occurs during the window of 

susceptibility. Although human 

phthalate exposures may vary from dayto-day or during the course of a day, 

humans are exposed to phthalates every 

day. 

Comment: Fasting time differences. 

Some commenters discussed whether 

fasting times affected the concentration 

of phthalate metabolites in the urine in 

NHANES results and whether there 

were differences in fasting times in the 

data sets of different years. (Comment 

3.6). 

Response: The CHAP paid special 

attention to the possible effects of 

fasting on NHANES data. Staff reviewed 

NHANES documentation 34 35 and spoke 

with CDC staff regarding fasting 

protocol changes between cycles. No 

fasting requirements changed. 

Therefore, fasting requirements were not 

a factor in the decision not to combine 

data from subsequent NHANES cycles 

with the 2005/2006 data. CPSC staff 

concludes that fasting may have an 

impact on food-borne phthalates; but if 

anything, this would result in 

underestimation of risk. CPSC staff 

concludes that the major conclusion or 

the recommendation of the CHAP report 

would not change whether the CHAP 

included the early NHANES data or not. 

Comment: Urinary excretion rates and 

metabolites. Some commenters raised 

concerns about the urinary excretion 

rates and the metabolites used in the 

NHANES data. One commenter asserted 

that staff’s analysis in its June 2015 

report of the 2009/2010 and 2011/2012 

NHANES data sets overestimated 

exposures because it did not consider 

urinary excretion rates. Another 

commenter stated that the metabolites 

used for DINP and DIDP could lead to 

underestimation of phthalate risk when 

compared to other phthalates, such as 

DEP, DBP, DIBP, and BBP. Five 

commenters asked CPSC to re-evaluate 

exposure using additional metabolite 

biomarkers for DINP, DNOP, and other 

phthalates and also re-evaluate using 

later NHANES data. One of the 

commenters asserted that the 

quantitative estimates of DINP risk from 

the 2017 analysis provided by CPSC 

staff were calculated incorrectly and 

were 17 percent too high. The 

commenter requested that staff use 

multiple metabolites (e.g., MINP and 

MCOP) to estimate DINP exposure 

instead of just one (MCOP). The 

commenter noted that exposure 

estimated for DEHP used four 

metabolites. (Comments 3.14 through 

3.17). 

Response: Regarding staff’s 2015 

report and excretion rates, the 

additional information necessary to 

calculate directly urinary mass 

excretion rates was not collected during 

the 2005/2006 or 2007/2008 NHANES 

studies. Therefore, the extrapolation 

method was the only option available to 

the CHAP. Staff replicated the CHAP’s 

reported exposure and risk estimates 

using the 2005/2006 NHANES data and 


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36CHAP (2014); Sathyanarayana et al. (2008a); 

Swan (2008); Swan et al. (2005). 

applied the same methods to calculate 

estimates from the later NHANES 

studies. Regarding metabolite 

biomarkers, CPSC used MCOP to 

analyze phthalate exposure, as the 

CHAP did. This was appropriate 

because for exposed individuals, MCOP 

will be detected more frequently and at 

higher levels than other DINP 

metabolites. Regarding the use of both 

MINP and MCOP to estimate DINP 

exposures, staff does not agree that the 

estimated exposures for DINP in the 

2015 and 2017 analyses were incorrect. 

CPSC staff used one metabolite, MCOP, 

to estimate DINP exposure in order to be 

consistent with the CHAP methodology 

and previous staff exposure and risk 

documents. The CHAP recognized that 

there are multiple ways to estimate 

phthalate exposure using individual and 

combined phthalate metabolites, and 

the CHAP provided a table of potential 

metabolites and associated fraction of 

the urinary metabolite excreted factors. 

CHAP report at Table D–1. 

Comment: SFF data. A commenter 

noted that SFF data were collected 

before the CPSIA was implemented, and 

before an asserted sharp decline in 

DEHP exposure. Thus, according to the 

commenter, basing the NPR on the SFF 

data (which was the exposure data used 

to determine that 5 percent of infants 

have an HI greater than one) is not 

supportable. (Comment 3.5). 

Response: Infants’ and children’s 

phthalate exposures tend to be greater 

than adults’ exposure.36 For the 

phthalates in the CHAP’s cumulative 

risk assessment, daily intakes were 

generally twofold to threefold greater in 

SFF infants than in their mothers. CHAP 

report at Table 2.7. No more recent 

information on infant exposures is 

available than the 1999/2005 SFF data, 

which was used by the CHAP (and 

subsequently by CPSC in the NPR). 

Infant exposures may have changed 

since 2005, but staff has no infant data 

to quantify any change. 

2. Scenario-Based Exposure Assessment 

a. Summary 

Because biomonitoring data do not 

provide any information about the 

sources of phthalate exposure, the 

CHAP also included a scenario-based 

exposure assessment in its report. CHAP 

report at pp. 49–60, Appendix E1. The 

exposure assessment evaluated 

exposure from individual sources, such 

as toys, personal care products, and 

household products. The assessment 

considered the exposure routes of 

inhalation, direct and indirect ingestion, 

and dermal contact. The CHAP stated 

that its goal was to determine the 

significance of exposure to phthalates in 

toys and to estimate exposure to 

toddlers and infants for all soft plastic 

articles, except pacifiers (because 

pacifiers do not contain phthalates). Id. 

at p. 49. For phthalates that are 

currently prohibited from being in 

children’s toys and child care articles, 

the CHAP report provides estimated 

exposures that would hypothetically 

occur if phthalates were allowed in 

those products. Id. at pp. 49–50. 

Scenario-based exposure estimates are 

developed using information about 

relevant sources of phthalate exposure 

(e.g., concentrations of phthalates in 

soil, dust, and in products); data on 

migration or leaching of phthalates from 

products; physiological information 

(e.g., body weight and skin surface area); 

and information about how the 

subpopulations use and interact with 

products, including frequency and 

duration of contact with products and 

environmental media. 

The exposure assessment considered 

seven categories of exposure sources 

and activities involving those sources: 

Diet, prescription drugs, personal care 

products, toys, child care articles, 

indoor environment, and outdoor 

environment. Id. at p. 50. For each 

subpopulation (pregnant women/ 

WORA, infants, toddlers, and children), 

the assessment provides estimated daily 

aggregate exposures to each of the eight 

phthalates included in the cumulative 

risk assessment. Id. at pp. 50–51 and 

Table 2.11. The relative contribution 

(percent of total exposure) for each 

activity was determined. The analysis 

found that for women, diet contributes 

more than 50 percent of the exposure to 

DIBP, DNOP, DEHP, DINP and DIDP. Id. 

at Appendix E1–26. For infants and 

toddlers, more than 50 percent of DIBP, 

DINP, and DIDP exposure and more 

than 40 percent of DEHP exposure 

comes from diet. 

Although certain phthalates had not 

been permitted in children’s toys and 

child care articles since 2008, the 

exposure assessment considered what 

contribution these products could make 

to overall phthalate exposure if those 

phthalates were allowed in children’s 

toys and child care articles. The 

exposure analysis showed that, on 

average, mouthing and dermal exposure 

to toys could contribute around 12.8 

percent to the overall DINP exposure of 

infants, if DINP were used in these 

products. CHAP report at Appendix E1, 

Table E–21. The same analysis shows 

that dermal contact with child care 

articles could contribute up to an 

additional 16.5 percent of the overall 

exposure to infants. Therefore, if DINP 

were used in all of the products that 

were included in the scenario-based 

exposure assessment, children’s toys 

and child care articles could account for 

around 29 percent of infants’ total 

exposure from all evaluated sources. Id. 

It is not possible to accurately 

quantify the number of toys that might 

have DINP in them if the interim 

prohibition were lifted or to quantify the 

effect that changes in DINP exposure 

would have on the percentage of the 

population (infants, pregnant women, or 

WORA) with HI less than or equal to 

one. 

b. Comments Concerning ScenarioBased Exposure Assessment 

Comment: Exposure through diet. 

Commenters noted that diet is the 

primary source of exposure to 

phthalates for infants and children and 

that children’s toys and child care 

articles contribute very little to overall 

phthalate exposures, especially for 

women of reproductive age and fetuses. 

They reasoned that, therefore, a 

prohibition on phthalate-containing 

children’s toys and child care articles 

would have little effect on overall risk. 

(Comment 5.3). 

Response: CPSC disagrees that the 

contribution from sources other than 

diet are negligible, especially for DINP. 

The scenario-based exposure assessment 

in the CHAP report shows that 

mouthing and dermal exposure to toys 

could contribute an average of 12.8 

percent, 5.4 percent, and 1 percent of 

the overall DINP exposure to infants, 

toddlers, and children, respectively, if 

DINP were used in these products. 

CHAP report at Appendix E1, Tables 

E1–21, E1–22 and E1–23. Mouthing and 

handling soft plastic teethers and toys 

could contribute 12.8 percent (mean 

exposure) or 16.6 percent (95th 

percentile exposures) of total DINP 

exposure in infants. Id. at Appendix E1, 

Tables E1–21. Dermal contact with the 

evaluated toys and child care articles 

may contribute up to an additional 16.5 

percent of exposures to infants. Id. 

Therefore, although infants’ DINP 

exposure was primarily from diet, up to 

29 percent may be due to the presence 

of DINP in the evaluated toys and child 

care articles (Id. Figure 2.1). 

Comment: Exposure through house 

dust. One commenter noted that house 

dust contributed to background 

exposure, that DEHP was in 100 percent 

of dust samples, that consumer products 

and building materials were the source 

of such dust, and that the EPA soil 

screening levels for DEHP were 

exceeded by the concentrations found. 

(Comment 5.4). 


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37Hannas et al. (2012); (2011); Howdeshell et al. 

(2007); (2016); (2008). 

38 Kortenkamp and Faust (2010). 

39Hannas et al. (2011). 

40Boberg et al. (2011). 

Response: The CHAP’s and staff’s 

analyses considered exposures to house 

dust. The CHAP’s exposure scenarios 

estimated theoretical exposures from 

house dust. The CHAP found that for 

infants and toddlers, incidental 

ingestion of household dust contributed 

roughly 25 percent to the total BBP 

exposure and 15 percent to total DEHP 

exposure. For children, the CHAP found 

that household dust contributed about 

18 percent to DEHP exposures. CHAP 

report at Appendix E1–35. Additionally, 

because NHANES includes exposures 

from all routes, the NHANES estimates 

would have included the survey 

individual’s exposures to household 

dust. 

C. Risk Assessment 

As the CPSIA directed, the CHAP 

considered risks of phthalates in 

combination and in isolation. The 

CHAP conducted a cumulative risk 

assessment to evaluate the effects of 

multiple phthalates, specifically 

phthalates known to cause MRDE and 

other adverse effects on male fertility. 

As explained in section III.C.3, the 

CHAP used information from toxicity 

studies concerning MRDE and human 

biomonitoring studies to determine a 

hazard quotient (HQ) for each phthalate 

and the hazard index (HI) for each 

individual in the two populations of 

interest (pregnant women and children). 

To assess risks of phthalates in 

isolation, the CHAP used a margin of 

exposure (MOE) approach. 

For reasons discussed in sections 

III.C.1 and IV.A.1. of this preamble, the 

CHAP and CPSC have focused on 

phthalates’ association with MRDE. The 

CHAP’s and CPSC’s determination of 

risk associated with the use of 

phthalates in children’s toys and child 

care articles is based on a cumulative 

risk assessment that considers the 

contribution that allowing 

antiandrogenic phthalates to be used in 

children’s toys and child care articles 

would have on the overall cumulative 

risk from phthalates. Relying on this 

cumulative risk assessment, the 

Commission determines that, to meet 

the CPSIA’s criteria of reasonable 

certainty of no harm and protection of 

the health of children, it is necessary to 

prohibit children’s toys and child care 

articles containing concentrations of 

more than 0.1 percent of the phthalates 

that can cause MRDE (DINP, DIBP, 

DPENP, DHEXP, and DCHP). In this 

section, we discuss the cumulative risk 

assessment and related comments. We 

discuss each phthalate in section IV.D of 

this preamble. 

1. Cumulative Risk Assessment 

a. Summary 

i. CHAP’s Analysis and NPR 

A cumulative risk assessment 

estimates the potential risk following 

exposure to multiple ‘‘stressors,’’ in this 

case, multiple phthalates. As discussed 

in section III.C of this preamble, the 

CHAP found, and CPSC agrees, that 

certain phthalates cause male 

reproductive developmental effects and 

may appropriately be considered in a 

cumulative risk assessment. CPSC 

concludes that a cumulative risk 

assessment is appropriate here because 

evidence indicates that phthalates are 

‘‘dose additive.’’ That is, for phthalates 

that cause MRDE, the chemicals will act 

together; the effects of one such 

phthalate will add to the effects of 

another such phthalate. As the CHAP 

report explained, experimental studies 

show the additive effects of phthalates 

on MRDE.37 The CHAP also 

demonstrated that the phthalates 

included in the CHAP’s cumulative risk 

assessment share a common mechanism 

of action (primarily antiandrogenicity) 

and affect the same target organ 

(primarily the testes). 

This rule is based on a cumulative 

risk assessment that uses the 

methodology employed by the CHAP, 

along with exposure data from the most 

recent NHANES data sets. The 

cumulative risk assessment follows a 

hazard index (HI) approach that is 

commonly used for cumulative risk 

assessments. The CHAP’s cumulative 

risk assessment was consistent with the 

recommendations of a National 

Academy of Sciences report on 

cumulative risk assessment of 

phthalates. Cumulative risk assessment 

of chemical mixtures has been an 

established practice since the 1980s. 

The CHAP introduced a minor 

modification to the standard 

methodology: The CHAP calculated 

hazard indices for each individual 

sampled in NHANES rather than the 

more common HI approach of using 

population percentiles from exposure 

studies on a per-chemical basis. This 

allowed the CHAP to calculate hazard 

quotients (HQs) for each phthalate and 

an HI for each individual in each study. 

This avoids overestimating the risk for 

individuals with higher than average 

exposures, such as those at the 90th and 

95th percentiles. 

The CHAP calculated an HQ for each 

phthalate using three sets of ‘‘potency 

estimates of antiandrogenicity’’ 

(PEAAs). The PEAA is an estimate of 

the exposure at which the risk of MRDE 

is negligible. The CHAP estimated a 

PEAA for each phthalate by dividing the 

MRDE ‘‘antiandrogenic’’ point of 

departure (POD; toxicity endpoint) by 

an uncertainty factor (UF). The POD is 

the lowest dose level at which an 

adverse effect was seen. A UF is a 

quantitative factor that is used to 

account for uncertainties associated 

with available data (e.g., interspecies, 

intraspecies, database, and toxicity 

uncertainties). The CHAP stated that it 

used three sets of PEAAs to explore the 

effect of different methodology (e.g., 

different uncertainty factors and PODs) 

on cumulative risk estimates to 

‘‘determine the sensitivity of the results 

to the assumptions for PEAAs and the 

total impact on the HI approach.’’ CHAP 

report at p. 4. Each case brings a 

different perspective to the risk 

assessment. The CHAP report discusses 

the three cases at pages 63–64. Case 1 

was based on published, peer-reviewed 

values using a study by Kortenkamp and 

Faust.38 Case 2 was based on a relative 

potency method with DEHP as the index 

chemical, using multiple-dose studies of 

in-vitro fetal testosterone production by 

Hannas et al. (2011).39 For Case 3, the 

CHAP derived new PEAA values after 

considering all the available literature, 

including studies such as Boberg et al. 

(2011).40 As explained in response to 

comments, CPSC staff concludes that 

each of the three cases has certain 

advantages, all three are appropriate, 

and the risks resulting from the three 

cases are quite similar. 

The CHAP calculated HQs for each 

phthalate by dividing the exposure by 

the PEAA. The CHAP then calculated 

the HI by summing the HQs for each 

phthalate. If the HI is greater than one, 

there may be concern for antiandrogenic 

effects in the exposed population due to 

cumulative effects of phthalates. As 

explained previously, the CHAP used 

2005/2006 NHANES data for exposure 

estimates for pregnant women and 

1999–2005 SFF data for exposure 

estimates for mothers and infants. CPSC 

staff subsequently repeated the CHAP’s 

analysis using more recent NHANES 

data. The CHAP found that pregnant 

women had median HIs of about 0.1 

(0.09 to 0.14), while the 95th percentile 

HIs were about 5, depending on which 

set of PEAAs was used. Roughly 10 

percent of pregnant women had HIs 

greater than one. CHAP report at Table 

2.16. Infants had median HIs about 0.2, 

while the 95th percentiles were between 


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41The median is the midpoint of the distribution, 

where one-half of the values are smaller than (i.e., 

below) the median value, and one-half of the values 

are larger than the median. The 95th percentile of 

the distribution is the value indicating 95 percent 

of values are smaller than this value, and 5 percent 

of values are larger. The median and 95th percentile 

values describe the data distribution, in this case 

the HI values estimated for the population of 

pregnant women or women of reproductive age who 

experience phthalate exposures. These values, by 

themselves, do not define acceptable risk levels. 

Rather, the acceptable risk level is a policy 

decision. 

0.5 and 1.0. About 5 percent of infants 

had HIs greater than one. Id. 

The CHAP characterized the 

distribution of the estimated HIs, by 

reporting the central tendency measure 

(statistical median 41) and the upper 

percentiles (95th, and 99th). CHAP 

report at Table 2.16. The CHAP’s 

analysis showed that the median HIs for 

NHANES pregnant women were less 

than one (HIs of 0.09 to 0.14), but the 

95th percentile HIs were greater than 

one (HIs of 3.6 to 6.1). Staff notes that 

the CHAP emphasized that an HI greater 

than one is the metric that defines 

excess exposure, relative to the 

acceptable exposure level; the CHAP 

did not indicate that the 95th percentile, 

or any other part of the cumulative risk 

distribution, should be used to establish 

unacceptable risk for risk management 

purposes. The CHAP, having 

determined that an HI greater than one 

was necessary to identify the population 

at risk, then used the distribution of HIs 

to identify the percentage of the 

population with an estimated HI greater 

than one. Staff notes that, while the 

CHAP presented the distribution 

statistics, described above, the CHAP 

focused on the proportion of the 

population with HIs exceeding one, not 

on any particular percentile of the 

distribution. To repeat, the CHAP 

neither used nor suggested a specific 

percentile as a threshold for 

recommendations or regulatory 

proposals. 

The CHAP’s HI approach is consistent 

with the CPSC’s chronic hazard 

guidelines (Chronic Guidelines). The 

Chronic Guidelines discuss a safety 

factor approach to determine acceptable 

risk for a reproductive or developmental 

toxicant. 57 FR 46626, 46656 (Oct. 9, 

1992). Under the safety factor approach, 

one determines the acceptable daily 

intake (ADI) for a substance by adding 

a safety factor to the lowest no observed 

effect level (NOEL) seen among relevant 

studies. The Chronic Guidelines state 

that if the hazard is ascertained from 

human data, a factor of 10 is applied to 

the NOEL, and if the hazard is 

ascertained from animal data, a factor of 

100 is applied. Id. Staff states that the 

safety factor approach is similar to the 

HI approach that the CHAP followed. 

The CHAP’s PEAA values are equivalent 

to an ADI, and the HI is the ratio of the 

daily exposure to the ADI. The Chronic 

Guidelines do not define the percentage 

of the population (i.e., number of 

individuals versus the sample 

population or entire population) that 

must have an HI less than one to ensure 

a ‘‘reasonable certainty of no harm . . . 

with an adequate margin of safety.’’ 

As discussed in the NPR preamble, 

based on the CHAP report, the 

Commission proposed to prohibit 

children’s toys and child care articles 

containing the antiandrogenic 

phthalates the CHAP had examined. 

The NPR stated that the Commission 

considers that an HI less than one is 

necessary to ensure a reasonable 

certainty of no harm to children, 

pregnant women, or other susceptible 

individuals with an adequate margin of 

safety and to protect the health of 

children. 79 FR at 78334. The NPR also 

stated that the Commission considers 

that an HI less than one is necessary to 

protect the health of children. Id. at 

78335. 

In the NPR, the Commission stated 

the CHAP’s determination that 

approximately 10 percent of pregnant 

women and 5 percent of infants had an 

HI greater than one. The Commission 

did not establish directly, however, that 

there was a specific proportion of the 

population that must have an HI less 

than or equal to one to ensure a 

‘‘reasonable certainty of no harm with 

an adequate margin of safety’’ or to 

‘‘protect the health of children.’’ 

ii. Analysis Using Most Recent Data 

After publication of the NPR, CPSC 

staff analyzed NHANES data for WORA 

(from 2007 through 2014). CPSC staff 

reports for 2015 and 2017; TAB A of 

CPSC staff’s briefing package: Staff’s 

analysis shows that the risk to WORA, 

as indicated by HI, has decreased. 

Median and 95th percentile HIs for 

WORA are both less than one. Staff 

estimates that between 98.8 and 99.6 

percent of WORA have HIs less than or 

equal to one. Out of a sample of 538 

WORA in the 2013/2014 cycle, 99.5 

percent of WORA have an HI less than 

or equal to one when considering PEAA 

Case 1 and 99.6 percent when 

considering Case 3. For PEAA Case 2, an 

estimated 98.85 percent of WORA have 

an HI less than or equal to one in the 

same cycle. See Tab A of staff’s briefing 

package. This means that some 

individual WORA in the NHANES 

sample have an HI greater than one for 

each PEAA case. Out of a sample of 538 

WORA, for PEAA Case 1, three WORA 

had an HI greater than one; for PEAA 

Case 2, nine WORA had an HI greater 

than one; and for PEAA Case 3, two 

WORA had an HI greater than one. 

However, the national population 

projection for HI greater than one is not 

estimable at the upper percentiles of the 

distribution due to sampling variability. 

Thus, staff is unable to estimate the 

percentage of WORA with an HI greater 

than one in the population of 

approximately 60 million WORA in the 

United States. 

As noted in Tab A of the staff’s 

briefing package, the decreases in HI are 

primarily due to decreases in DEHP 

exposures. The HQ for DINP is replacing 

the HQ for DEHP proportionally for 

contributions to the total HI. In each 

PEAA case, DINP has less potency than 

DEHP; thus, even though DINP’s 

proportion of contribution to total HI is 

increasing, the values of HI have still 

decreased overall across cycles. 

CPSC does not have exposure data for 

infants that is more recent than the SFF 

data on which the CHAP relied. Because 

the risk to WORA has declined since 

2005/2006, it is possible that exposures 

and risks to infants have also declined. 

However, because the routes of 

exposure (e.g., food, medicines, 

products) are different for each target 

population, it is not possible to quantify 

the changes in one population based on 

the other. As explained in section 

IV.B.1, infants’ exposures generally are 

two- to threefold greater than adults. 

Thus, CPSC concludes that phthalate 

exposures and risks in WORA probably 

underestimate the risks to infants and 

children. 

CPSC’s assessment of the risk (and the 

need for this rule) is also informed by 

the fact that, although the overall risk as 

portrayed in the cumulative risk 

assessment has decreased, DINP’s 

contribution to the cumulative risk has 

greatly increased. It is not possible to 

quantify accurately the number of toys 

expected to have DINP or the effect of 

changes in DINP exposure on the 

percentage of the population (infants, 

pregnant women, or WORA) with HI 

less than or equal to one. However, any 

increase in exposure due to resumed or 

increased use of DINP in products is 

likely to decrease the percentage of the 

population with HI less than or equal to 

one. Allowing DINP to be re-introduced 

into children’s toys and child care 

articles would open a pathway of 

exposure to a phthalate that studies 

have clearly demonstrated causes 

adverse effects on male reproductive 

development. Although DIBP, DPENP, 

DHEXP, and DCHP are not currently 

found in children’s toys and child care 

articles (or only rarely), these phthalates 


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42EPA (1986). EPA (2000b), ATSDR (2004), and 

WHO (Meek et al. 2011). 

43ATSDR (2017; EPA (2017); Howdeshell et al. 

(2016). 

44Christensen et al. (2014); Gallagher et al. 

(2015). 

45Hannas et al. (2012); (2011); Howdeshell et al. 

(2007); (2016); (2008). 

46Axelstad et al. (2014); Christiansen et al. 

(2009); Howdeshell et al. (2016); Levin et al. (1987); 

Rider et al. (2008; 2010; 2009). 

47Foster et al. (2001); Gray et al. (2000); 

Mylchreest et al. (1998); Parks et al. (2000). 

48Foster (2005); Howdeshell et al. (2016); NRC 

(2008); Wilson et al. (2004). 

49Axelstad et al. (2014); Christiansen et al. 

(2010); Hotchkiss et al. (2004); Howdeshell et al. 

(2007); (2016); Rider et al. (2010). 

50Conley et al. (2017). 

51Foster et al. (2001); Gray et al. (2000); 

Mylchreest et al. (1998); Parks et al. (2000). 

52Foster (2005), Howdeshell et al. (2016), NRC 

(2008), and Wilson et al. (2004). 

53Adamsson et al. (2009); Boberg et al. (2011); 

Clewell et al. (2013b); Gray et al. (2000); Hannas et 

al. (2011); Masutomi et al. (2003). 

also cause MRDE and contribute to the 

cumulative risk. 

b. Comments on Cumulative Risk 

i. Appropriateness of Conducting a 

Cumulative Risk Assessment 

Comment: General acceptance of 

cumulative risk assessment. 

Commenters asserted that cumulative 

risk assessment is not a generally 

accepted approach. They stated that 

cumulative risk assessment is not 

appropriate as a basis for regulatory 

action, but only as a screening analysis. 

However, another commenter noted that 

‘‘when multiple phthalates act on a 

similar biologic target, it is critical to 

understand and regulate based on their 

combined effect on human health.’’ 

(Comments 2.1 through 2.3). 

Response: Cumulative risk assessment 

is a well-established approach to 

evaluate risks posed by mixtures of 

multiple chemicals. EPA first issued 

guidelines for the risk assessment of 

chemical mixtures in 1986. 

Subsequently, ATSDR and the World 

Health Organization (WHO) issued 

guidance for cumulative risk assessment 

of chemical mixtures.42 EPA routinely 

uses cumulative risk assessment to 

assess risks from pesticides, as required 

by the Food Quality Protection Act of 

1996. Additionally, EPA and ATSDR 

use cumulative risk assessment to assess 

risks under Superfund.43 EPA also has 

performed cumulative risk assessments, 

to assess phthalates.44 The CHAP 

followed guidance issued by the 

National Academy of Science for 

conducting cumulative risk assessments 

with the one modification, explained 

above, that allowed the CHAP to 

calculate HQs for each phthalate and an 

HI for each individual in the NHANES 

and SFF studies. Regarding the assertion 

that the CHAP’s cumulative risk 

assessment was only a screening-level 

analysis, CPSC concludes that the 

CHAP’s analysis is a refined assessment 

that could be considered tier 3, the 

highest tier, under the framework 

established by the WHO. The CHAP’s 

CRA began with a comprehensive 

review of the toxicology and exposure 

literature. The primary exposure 

assessment for the CHAP report was 

based on measurements of phthalate 

metabolites in a statistically 

representative population (NHANES 

study) of actual people. As required for 

tier 3 assessments under the WHO 

framework, the CHAP’s analysis 

included probabilistic measurements of 

exposure and risk. 

Comment: Dose additivity. Several 

commenters asserted that there was not 

sufficient evidence of dose additivity, 

especially at low doses, to conduct a 

cumulative risk assessment for 

phthalates. Some commenters asserted 

that one needs a common mode or 

mechanism of action to support an 

assumption that phthalates are additive, 

and they stated that evidence of a 

common MOA was lacking. 

Commenters stated that the CHAP had 

not considered all the relevant papers 

on dose additivity. (Comments 2.4 

through 2.8). 

Response: The CHAP did not need to 

present evidence of a common MOA or 

mechanism of action to justify 

performing a cumulative risk 

assessment because data from laboratory 

studies by Hannas and Howdeshell 

show that phthalate mixtures, in fact, 

act in a cumulative, additive fashion.45

Thus, the CHAP did not have to make 

any assumptions about additivity. In 

fact, one of the reasons that the CHAP 

chose MRDE as the health effect for its 

CRA is that MRDE is the only health 

endpoint that was extensively studied 

in phthalate mixtures. CHAP report at p. 

2. Moreover, even without a common 

mechanism of action, chemicals can 

have cumulative effects in mixtures.46

Substances can act on the same process, 

but in different ways, to produce 

additive effects. In any event, CPSC 

concludes that evidence demonstrates 

that the phthalates in the CRA do have 

a common mechanism of action. As 

discussed, the phthalates all act on the 

male reproductive system. More 

specifically, they act by inhibiting 

testosterone production in the testis 

during a critical period in development 

by decreasing expression of genes 

involved in steroid synthesis.47

Additional factors, such as reduced 

expression of insulin-like hormone 3 

gene (insl3), also are at work.48

Regarding low doses, studies of 

phthalate mixtures at low doses do not 

exist, and the commenters did not 

present any evidence of a threshold for 

phthalate-induced MRDE. Although 

mixture studies at low (environmental) 

doses have not been performed, there 

are published studies in which the 

doses of the individual phthalates 

produced little or no effect, but the 

mixtures produced significant 

cumulative effects.49 In a recent study, 

rats were exposed to phthalates and 

other antiandrogens at doses well below 

the NOAEL. Although the individual 

phthalates had no observable effect, the 

mixture induced MRDE-related 

effects.50 Thus, additivity occurs even at 

doses where individual phthalates have 

no observable effect. As discussed in 

response to comments 2.6 and 2.7, CPSC 

concludes that the CHAP did consider 

all relevant papers and that dose 

addition is appropriate for assessing the 

cumulative effects of phthalates and 

other antiandrogens. 

Comment: Mode or mechanism of 

action. Commenters asserted that the 

mechanism of action by which 

phthalates affect male reproductive 

development is not clear. They argued 

that, in the absence of clarity that 

phthalates share a common mechanism 

of action, the CHAP should not conduct 

a cumulative risk assessment. Some 

commenters focused particularly on 

DINP, asserting that DINP does not have 

the same mode or mechanism of action 

as other phthalates. (Comments 1.21 

through 1.25). 

Response: Knowledge of the mode or 

mechanism of action can help inform 

the risk assessment process. However, a 

detailed understanding of the mode/ 

mechanism of action is never required 

to perform a risk assessment. Several 

studies have shown that the phthalates 

act by inhibiting testosterone 

production in the testis during any 

critical period in development,51 by 

decreasing expression of genes involved 

in steroid synthesis. Reduced 

expression of insulin-like hormone 3 

gene (insl3) is an additional pathway.52

Furthermore, all of the phthalates in the 

cumulative risk assessment induce a 

similar spectrum of effects, known as 

the ‘‘phthalate syndrome,’’ and which is 

also described as ‘‘antiandrogenic’’ 

effects. DINP has been clearly 

established by multiple studies as 

causing the same pattern of effects 

(phthalate syndrome) 53 and by other 

studies as acting by the same MOA as 

other phthalates in the cumulative risk 


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54 Gray et al. (2000); Hannas et al. (2011). 

55Foster (2005); Howdeshell et al. (2016); NRC 

(2008). 

56Hannas et al. (2012); (2011); Howdeshell et al. 

(2007); (2016); (2008). 

57Clark (2009); Versar (2010). 

58Creasy et al. (1987); Jones et al. (1993); Saitoh 

et al. (1997); Saillenfait et al. (1998); Gray et al. 

(1999); Parks et al. (2000); Li et al. (2000); 

Thompson et al. (2004); Carruthers and Foster 

(2005); Thompson et al. (2005); Ferrara et al. (2006); 

Hannas et al. (2011); Jobling et al. (2011); Spade et 

al. (2015). 

assessment.54 Other experts agree that 

the phthalates in the CHAP’s 

cumulative risk assessment act by the 

same mechanism of action.55 Staff also 

notes that mixtures studies including 

DINP show that the effects of DINP and 

other phthalates are additive.56

Therefore, a common mechanism of 

action is not necessary to include DINP 

in the cumulative risk assessment. 

Comment: Inclusion of permanently 

prohibited phthalates in CRA. 

Commenters asserted that it was not 

appropriate for the CHAP to include 

DEHP and other phthalates that are 

subject to CPSIA’s permanent 

prohibition in the CHAP’s cumulative 

risk assessment. Commenters asserted 

that nearly all of the risk in the CHAP’s 

cumulative risk assessment is due to 

exposures to those phthalates, yet they 

can no longer contribute to the 

cumulative risk from exposure to 

children’s products. At least one 

commenter stated that if the cumulative 

risk assessment excluded phthalates 

subject to the CPSIA’s permanent 

prohibition, the HI would be less than 

one. The commenter reasoned that, 

therefore, there is a reasonable certainty 

of no harm from the use of any other 

phthalates in children’s products. Thus, 

the statutory requirement to ‘‘ensure a 

reasonable certainty of no harm to 

children, pregnant women, or other 

susceptible individuals with an 

adequate margin of safety’’ is satisfied 

without continuing the interim 

prohibition. Another commenter stated 

that a cumulative risk assessment is 

useful when exposure to each single 

substance is below the level of concern, 

but exposures to multiple chemicals 

with the same mechanism of action (or 

that affect the same endpoint) at the 

same time rise to levels of concern. 

However, the commenter asserted, with 

phthalates, only one chemical (DEHP) 

poses a risk in isolation. (Comments 2.9 

and 5.2). 

Response: In accordance with 

direction in the CPSIA, the CHAP 

examined phthalates in isolation and in 

combination with other phthalates. 15 

U.S.C. 2057c(b)(2)(B)(ii). Moreover, to 

accurately assess cumulative risk, it was 

appropriate for the CHAP to include 

DEHP (and other phthalate subject to 

CPSIA’s permanent prohibition). 

Although DEHP is not allowed in 

children’s toys and child care articles, it 

is permitted in other products. DEHP is 

found in drinking water, surface water, 

storm water, soil, and wildlife.57 It is 

found in indoor and outdoor air, 

household dust, and indoor surfaces. 

DEHP has been found in gloves, 

footwear, personal care products, 

medical devices, paints, adhesives, 

sealants, wallpaper, flooring and food. 

Thus, given the number and variety of 

sources of exposure, DEHP should be 

included in the cumulative risk 

assessment. The results of staff’s 

cumulative risk assessment using more 

recent NHANES data, show that, even 

though exposure to DEHP is decreasing, 

phthalate exposures are still high 

enough that some women in the data 

sample have HIs exceeding one. The 

CHAP’s and staff’s analyses indicate 

that risk is not entirely driven by DEHP. 

Considering 2013/2014 NHANES data, 

DINP contributes approximately 6 to 51 

percent (medians) or 18 to 76 percent 

(95th percentiles) of the overall risk. See 

TAB A of staff’s briefing package. 

ii. NHANES Data in the Cumulative 

Risk Assessment 

Comment: Using the CRA to assess 

individual’s risk. Some commenters 

asserted that calculating risk using 

NHANES data (that uses spot urine 

sampling rather than measurements 

over time) is not an accurate indication 

of a person’s real exposure to phthalates 

and thus the CHAP’s HI calculations do 

not show true risk. They asserted it is 

inappropriate and not scientifically 

supportable to report results as a 

proportion of the population with an HI 

over one (because the individual spot 

urine samples are too variable and do 

not represent chronic exposures over 

time). For example, one commenter 

stated that an individual’s HI from a 

spot urine sample ‘‘has essentially no 

bearing on risk to the individual’’ 

because it does not represent a repeat 

dose, longer term exposure is necessary 

to induce the adverse effects (phthalate 

syndrome) and that a few HIs (or HQs 

such as DINP) above one also are not 

representative of the population risk. 

Commenters thought that this approach 

was overly conservative and 

overestimated the risk. (Comments 3.11 

through 3.13). 

Response: Staff concurs that spot 

urine samples are variable and are not 

representative of long-term exposures, 

but also notes that numerous studies in 

animals have demonstrated that MRDE 

and related effects can occur after one 

or a few doses.58 It is impossible to 

know whether a particular spot urine 

sample is overpredicting or 

underpredicting the actual exposure. 

HBM data are a direct measure of 

human exposure and, therefore, 

superior to alternatives such as modeled 

exposures. NHANES is a high quality 

study and provided exposure data that 

are representative of the U.S. 

population. Similar data with 24-hour 

or longer sampling times are not 

available. 

Staff concludes that it is statistically 

appropriate to portray the individual 

NHANES data as a proportion of the 

NHANES sample population with an HI 

less than or equal to one. Staff notes that 

in the 2013/2014 NHANES sample of 

538 WORA (of approximately 60 million 

WORA in the U.S. population), there 

were from two to nine individuals with 

a HI greater than one (i.e., at risk), 

depending on the PEAA case. As 

described in section 5.4 of TAB A of 

staff’s briefing package, the 2013/2014 

NHANES data set cannot be used to 

estimate how many WORA in the U.S. 

population have HIs greater than one. 

Comment: Impact of more recent 

NHANES data on CRA. Several 

commenters stated that CPSC staff’s 

analysis of more recent NHANES data 

shows that the risk from phthalates has 

declined. Commenters noted that that 

even at the 95th percentile, the HI is 

uniformly less than one and has 

decreased further from the HI values 

calculated for the 2011/2012 data cycle. 

They concluded that the CRA using 

current exposure data shows that there 

is a reasonable certainty of no harm. 

Thus, the statutory requirement is 

satisfied without Commission action. 

(Comment 3.2). 

Response: The CRA using current 

exposure data indicates that at least 

some of the actual WORA in the 

NHANES data had HIs greater than one, 

showing that there is not a reasonable 

certainty of no harm with an adequate 

margin of safety. Moreover, the CHAP 

did not indicate that the 95th percentile, 

or any other part of the cumulative risk 

distribution, should be used to establish 

unacceptable risk. Therefore, 

discussions of acceptable risk should 

not be limited to the 95th or other 

percentile. Staff concurs with 

commenters that through the NHANES 

cycles, the population of WORA with an 

HI greater than one has decreased. In the 

2013/14 NHANES sample of 538 

WORA, there were from two to nine 

actual women from the NHANES 

sample with a HI greater than one (i.e., 

at risk), depending on the PEAA case. 


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The 2013/2014 NHANES data cannot be 

used to estimate how many WORA in 

the U.S. population have HIs greater 

than one. 

Comment: Use of values above the 

95th percentile. A commenter on the 

2017 staff report asserted that it is 

‘‘scientifically inappropriate to go above 

the 95th percentile in evaluating either 

individual or cumulative risks to the 

fetuses of women of reproductive age as 

indicated by the CRA.’’ The commenter 

stated that going above the 95th 

percentile values are too unstable to 

provide a basis for regulatory decisions. 

The commenter noted that EPA’s 2014 

paper on five phthalates reported the 

95th percentile from the calculations of 

HIs for three of the five phthalates (and 

the CHAP and CPSC’s previous analyses 

used the 95th percentile). (Comment 

3.21). 

Response: Neither the CHAP nor staff 

used the 95th percentile (or any other 

percentile) as a threshold for 

recommendations or regulatory 

proposals in evaluating individual or 

cumulative risks. The 95th percentile, as 

well as other measures such as the 

average, median, or 99th percentile, is a 

commonly used metric, included by the 

CHAP, to help characterize the 

distribution of exposure and risk in a 

population. The rule is not based on any 

particular percentile, but on the 

observation that actual women from the 

NHANES sample have HIs greater than 

one. 

For its cumulative risk assessment, 

the CHAP addressed the range of HI in 

representative populations—including 

but not limited to the 50th percentile, 

95th percentile, and 99th percentile. In 

all analyses of the updated NHANES 

data for WORA and in the rule, staff 

does not rely on any particular 

percentile as a threshold for 

recommendations or regulatory 

proposals, but on the fact that at least 

some of the actual WORA from the 

NHANES samples had HIs greater than 

one. Because at least some of the actual 

WORA from the NHANES samples had 

HIs greater than one in every NHANES 

data cycle analyzed, there is not a 

reasonable certainty of no harm with an 

adequate margin of safety. For example, 

for the 2013–14 NHANES data, between 

two and nine real women from the 

sample of 538 WORAs had an HI greater 

than one, depending on the case model 

used. The CHAP emphasized, and the 

Commission continues to agree, that an 

HI greater than one is the metric that 

defines excess exposure. 

CPSC disagrees with the blanket 

statement that it is scientifically 

inappropriate to go above the 95th 

percentile in interpreting a cumulative 

risk assessment. There is no scientific 

basis for an assertion that the 95th 

percentile of a distribution is the largest 

value that can be considered. The 

commenter specified that the values 

above the 95th percentile are unstable. 

In this case, staff agrees that the values 

associated with the upper tail of the 

distribution of HIs (e.g., above the 95th 

percentile) have large variance 

estimates, due to sample size (i.e., 

statistically unstable). The large 

variances mean that we are precluded 

from estimating the precise number of 

WORA with HIs greater than one in the 

larger population from which the 

sample was selected. However, as noted 

above, actual women with HIs greater 

than one were observed in every 

NHANES data cycle analyzed. As the 

commenter mentioned, EPA’s paper 

(Christensen et al. (2014)) states, ‘‘we 

present findings for the 95th percentile 

of estimated phthalate intake 

recognizing that there may be more 

variability in these values, because this 

information provides insight into the 

potential risk at the highest levels of 

exposure in a general population 

setting.’’ Staff considers EPA’s 

discussion to be consistent with the 

CHAP’s and staff’s presentation of 

results because the goal is to provide 

insight into the risks among the most 

highly exposed individuals. The 

CHAP’s and staff’s analyses are based on 

human biomonitoring, i.e., actual 

observations of people. These 

observations should be considered in 

risk management and decision-making. 

iii. The Three Cases 

Comment: Criticism of the three cases 

(PEAAs) the CHAP used. Commenters 

raised concerns about all three of the 

CHAP’s cases. Some commenters 

asserted that the cases inappropriately 

combined points of departure (PODs) for 

different types of endpoints (for 

example, reduced testosterone 

production, observation of MNGs, and 

retained nipples) for different effect 

measures. Commenters stated that the 

cases had treated transient, non-adverse 

biomarkers in the same way as adverse 

effects when selecting PODs. 

(Comments 4.1 through 4.3 and 4.6). 

Response: We discuss the major 

criticisms of the specific cases in the 

following comment/responses. As 

discussed in the section on MRDE, a 

wide variety of effects of different types 

and severities are included under the 

umbrella of phthalate syndrome. Staff 

disagrees with commenters’ assertions 

that these effects cannot be considered 

equal when selecting PODs. Any 

observed effect related to the male 

reproductive system is a marker of 

biological activity that could lead to a 

broad range of effects in the organism. 

Thus, such markers should be given 

equal weight in quantifying the 

biological activity. 

Comment: Case 1. Commenters 

criticized the study that was the basis 

for Case 1 (Kortenkamp and Faust), 

which calculated a potency estimate 

based on a lowest observed adverse 

effect level (LOAEL) rather than a no 

observed adverse effect level (NOAEL) 

which the commenters stated 

introduced greater uncertainties. 

Commenters also asserted that the 

publication of more robust studies since 

2010 (e.g., Boberg) indicating that the 

Case 1 PEAAs were overstated by a 

factor of 4 made Case 1 outdated. 

Commenters also criticized the use of 

larger uncertainty factors (UFs) for some 

phthalates. (Comments 4.7 and 4.8). 

Response: CPSC agrees that more 

recent literature has been published 

regarding the selection of PODs and UFs 

for phthalates that cause phthalate 

syndrome. However, this does not mean 

that Case 1 should be excluded. Rather, 

alternate approaches (such as Case 1) to 

POD selection are useful to understand 

the potential effects of POD and UF 

selection on risk. Notably, the CHAP 

considered all relevant hazard studies 

(including those cited by the 

commenters) in its de novo review of 

the literature for Case 3. 

Comment: Case 2. Commenters 

criticized various aspects of Case 2 and 

the study underlying it, (Hannas et al. 

(2011)). Several commenters asserted 

that CPSC should completely disregard 

Case 2. They asserted that Case 2 was 

based on a model that used a 

hypothetical NOEL for DINP and that 

the CHAP did not validate the 

assumptions in the model. The 

commenters stated that, because ‘‘real 

world data’’ exist that are more 

applicable and reliable, CPSC should 

not use Case 2. Commenters asserted 

that relative potency of DINP and DEHP 

was inappropriately estimated. For 

example, a commenter stated that an in 

vivo study (i.e., using live animals) by 

Gray et al. (2000) had previously 

estimated that DEHP is 10–20 times 

more active than DINP, so the CHAP 

should not have used Case 2’s estimate 

that DEHP is 2.3 times more active than 

DINP. A commenter asserted that the 

study underlying Case 2 (Hannas et al. 

(2011)) has several flaws and 

limitations, such as the rats were 

obtained from different labs, doseresponse curves for DINP and DEHP 

were different, and the study used a low 

number of animals per group. 

(Comments 4.9 through 4.13). 


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59Furr et al. (2014). 

60Benson (2009). 

61Barnes and Dourson (1988); CPSC (1992); EPA 

(1991). 

62NRC (2008), Howdeshell (2016), and Gaido 

(2007). 

63NRC (2009). 64 57 FR 46626 (Oct. 9, 1992). 

Response: The CHAP established 

alternate approaches (such as Case 2) to 

POD selection that are useful in 

understanding the potential effects of 

POD and UF selection on risk. By 

stating that Case 2 was based on a 

model, commenters imply that Hannas 

et al. (2011) was not an in vivo study. 

However, Hannas et al. did expose live 

animals to phthalates. Measurements of 

the rate of testosterone synthesis were, 

by necessity, made in a biochemical 

assay (in vitro study) using tissue 

obtained from the animals. The CHAP’s 

use of a study that included observation 

of effects from exposure both to DINP 

and DEHP allowed a direct comparison 

of the relative potencies of different 

phthalates because multiple phthalates 

were tested in the same laboratory using 

the same methods. This is the unique 

advantage of Case 2. Staff considers the 

estimation of relative potency in Hannas 

et al. (2011) to be valid and notes that 

substantially similar methods have been 

used in the estimation of relative 

potency.59 Moreover, a 2009 review 

study estimated that DINP is 2.6 times 

less potent than DEHP.60 This estimate 

is closer to the Hannas et al study 

underlying Case 2 than to the Gray 

study mentioned by commenters. 

Regarding other alleged flaws in the 

Hannas et al. study, staff agrees that the 

rats used to study DEHP and DINP were 

obtained from different suppliers (as 

noted by Hannas et al.) and that control 

testosterone production was different 

for each group of rats (also identified in 

the publication). However, the study 

adequately controlled for these 

differences. Staff also concludes that the 

number of animals per dose group was 

appropriate. 

Comment: Case 3. Commenters 

generally preferred Case 3. Some stated 

that the CHAP should have relied only 

on Case 3 in its cumulative risk 

assessment. However, some commenters 

had criticisms of Case 3. One 

commenter asserted that the POD for 

DINP was inadequately justified. A 

commenter characterized Case 3 as 

‘‘muddled’’ and noted inconsistencies 

in how the CHAP discussed the NOEL 

for DINP. Comments questioned 

whether multi-nucleated gonocytes 

(MNGs), which are the basis of Case 3’s 

point of departure for DINP, are relevant 

to antiandrogenicity and whether MNGs 

are an adverse effect. A comment 

questioned the choice of 50mg/kg/day 

as the POD for DINP, asserting that it is 

too conservative. (Comments 4.15 

through 4.17). 

Response: For Case 3, the CHAP 

derived PEAAs for each phthalate based 

on the CHAP’s own literature review 

considering all published peer reviewed 

studies on each phthalate. The CHAP 

considered studies by Clewell et al. 

(2013a, 2013b), Hannas et al. (2011), 

and Boberg et al. (2011) as most relevant 

and highest quality for identifying a 

NOAEL for DINP. CHAP report at pp. 

97–98. The CHAP found that the lowest 

no effect level seen in these studies was 

50 mg/kg-day based on observance of 

MNGs in the Clewell study. As the 

CHAP noted, this was a conservative 

estimate. It is common practice in risk 

assessment to select the most 

conservative health endpoint (from 

quality data sets) when performing a 

hazard assessment.61 Although MNG 

formation is not directly linked to 

changes in testosterone production, and 

not necessarily a direct antiandrogenic 

effect of phthalate exposure, MNGs are 

a characteristic effect routinely observed 

in phthalate syndrome.62 Thus, the 

observation of MNGs formed after DINP 

exposure is consistent with the 

occurrence of MNGs associated with 

exposure to other active phthalates and 

is a marker of phthalates’ effects in the 

developing male reproductive system. 

Although MNGs might not be an 

adverse effect, finding MNGs following 

DINP exposure supports that DINP has 

a biological effect similar to the other 

active phthalates. Staff concludes that 

the CHAP’s assignment of the NOAEL 

for DINP at 50 mg/kg-day based on the 

observation of MNGs, is reasonable. 

2. Risk in Isolation 

In accordance with the CPSIA’s 

direction, the CHAP also considered the 

risk of phthalates individually. 15 

U.S.C. 2057c(b)(2)(B)(ii). As discussed 

in section III.C.3.b, to do this, the CHAP 

used an MOE approach. The CHAP 

chose this approach, in part, due to the 

recommendation of a NRC report on risk 

assessment methodology.63 Like the HI 

approach, the MOE is also widely 

accepted. Id. The MOE is the ‘‘no 

observed adverse effect level’’ (NOAEL) 

of the most sensitive endpoint in animal 

studies divided by the estimated 

exposure in humans. Higher MOEs 

indicate lower risks. Generally, MoEs 

greater than 100 to 1,000 are adequate 

to protect public health. CHAP report at 

pp. 20 and 69. The MOE approach is 

conceptually similar to the CPSC staff’s 

default approach in CPSC’s Chronic 

Hazard Guidelines for assessing noncancer risks,64 and would lead to similar 

conclusions about risk. We discuss the 

MOE for each phthalate the CHAP 

examined in section IV.D of this 

preamble, and we discuss comments 

concerning risks in isolation in that 

section as well. 

D. Assessments/Determination for Each 

Phthalate 

The CHAP assessed and made 

recommendations concerning each of 

the phthalates that it examined. CHAP 

report at pp. 82–121. Based on the 

CHAP report, CPSC staff’s assessment, 

public comments on the NPR and staff’s 

NHANES reports, the Commission 

issues this rule prohibiting children’s 

toys and child care articles that contain 

concentrations of more than 0.1 percent 

of DINP, DIBP, DPENP, DHEXP, and 

DCHP. The Commission concludes that, 

based on the best available scientific 

data, all of these phthalates cause MRDE 

and all contribute to the cumulative 

risk. Previous sections of this preamble 

have discussed the health effect of 

MRDE, exposure to phthalates, and the 

risk assessment for these phthalates. 

This section presents the Commission’s 

evaluation of each of the phthalates 

covered under this regulation. 

1. Phthalates Subject to the Interim 

Prohibition 

The CPSIA established an interim 

prohibition on children’s toys that can 

be placed in a child’s mouth and child 

care articles that contain concentrations 

of more than 0.1 percent of DINP, DIDP, 

and DNOP. 15 U.S.C. 2057c (b)(1). The 

CPSIA directs the Commission to 

determine, based on the CHAP report, 

whether to continue in effect the interim 

prohibitions on children’s toys that can 

be placed in a child’s mouth and child 

care articles containing DINP, DIDP, and 

DNOP ‘‘to ensure a reasonable certainty 

of no harm to children, pregnant 

women, or other susceptible individuals 

with an adequate margin of safety.’’ 

Thus, for each of these phthalates, the 

Commission must decide whether it is 

appropriate to make the interim 

prohibitions permanent under the 

statutory criteria. 

As explained in the preamble to the 

NPR and above, for phthalates causing 

MRDE, the Commission considered the 

cumulative risk, which was based on 

the CHAP’s HI estimates. Consistent 

with the CHAP report, the Commission 

considers that the acceptable risk is 

exceeded when the HI is greater than 

one. This is also consistent with the 

CPSC’s chronic hazard guidelines. 57 


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65HI is the ratio of the daily exposure to the ADI. 

The CHAP’s PEAA values are equivalent to an ADI, 

EPA reference dose (RfD), ATSDR minimal risk 

level (MRL), or similar terms used by other 

agencies. 

66The NHANES data was analyzed using 3 

methods (Cases 1–3) For Case 1, three WORA had 

HIs greater than 1. For Case 2, nine WORA had HIs 

greater than 1. For Case 3, two WORA had HIs 

greater than 1. 

67 Gray et al. (2000); Hannas et al. (2011b). 

FR 46626 (Oct. 9, 1992). The CPSC’s 

chronic hazard guidelines consider the 

‘‘acceptable risk’’ for a reproductive or 

developmental toxicant to be equivalent 

to an exposure equal to or less than the 

‘‘acceptable daily intake’’ (ADI), that is, 

an HI 65 of less than or equal to one for 

the population affected by the toxicant. 

Thus, the Commission considers that an 

HI less than or equal to one is necessary 

‘‘to ensure a reasonable certainty of no 

harm to children, pregnant women, or 

other susceptible individuals with an 

adequate margin of safety.’’ The chronic 

hazard guidelines do not define the 

percentage of the population (i.e., 

number of individuals versus the 

sample population or entire population) 

that must have an HI less than one in 

order to ensure a ‘‘reasonable certainty 

of no harm . . . with an adequate margin 

of safety.’’ 

In the NPR, the Commission proposed 

to prohibit children’s toys and child 

care articles containing more than 0.1 

percent of DINP, DCHP, DHEXP, and 

DPENP based on the CHAP’s 

determination that approximately 10 

percent of pregnant women and 

5 percent of infants had an HI greater 

than one. 79 FR at 78334–35. Thus, in 

issuing the NPR, the Commission 

concluded that the proportion of 

populations not affected by cumulative 

exposure to phthalates (at least 90 

percent of pregnant women and 95 

percent of infants) did not meet the 

standard of ‘‘a reasonable certainty of no 

harm with an adequate margin of 

safety.’’ The Commission did not 

establish directly, however, that there 

was a specific proportion of the 

population that must have an HI less 

than or equal to one to ensure a 

‘‘reasonable certainty of no harm with 

an adequate margin of safety’’ or to 

‘‘protect the health of children.’’ 

Staff’s analysis of the most recent 

NHANES data showed that exposures to 

phthalates have changed. Using the 

CHAP’s cumulative risk assessment 

methodology and the most recent 

NHANES data, staff has determined that 

between 98.8 and 99.6 percent of WORA 

(2013/2014 NHANES) had an HI less 

than or equal to one. As in previous 

NHANES data cycles, some individuals 

in the 2013/2014 NHANES data set still 

have an HI greater than one. Depending 

on the PEAA case used for analysis, 

between two and nine of the 

approximately 538 WORA in the 

NHANES 2013/2014 data sample had an 

HI of greater than one.66 Thus, a portion 

of WORA is exposed to phthalates at 

levels that can induce MRDE or other 

phthalate syndrome effects. For nonantiandrogenic phthalates (i.e., those 

that do not cause MRDE), the 

Commission considered the MOE, as 

estimated by the CHAP to assess risk. As 

mentioned previously, MOEs greater 

than 100–1,000 are generally considered 

adequate to protect human health. Thus, 

the Commission considers a MOE of 100 

or greater to be necessary ‘‘to ensure a 

reasonable certainty of no harm to 

children, pregnant women, or other 

susceptible individuals with an 

adequate margin of safety’’ or to 

‘‘protect the health of children.’’ 

a. Diisononyl phthalate (DINP) 

i. Summary 

The CHAP recommended that ‘‘the 

interim prohibition on the use of DINP 

in children’s toys and child care articles 

at levels greater than 0.1 percent be 

made permanent.’’ CHAP report at p. 99. 

The CHAP stated that it made this 

recommendation ‘‘because DINP does 

induce antiandrogenic effects in 

animals, although at levels below that 

for other active phthalates, and 

therefore, can contribute to the 

cumulative risk from other 

antiandrogenic phthalates.’’ Id. As 

discussed in section III.C.4.a. of this 

preamble, the CHAP cited multiple 

published studies that showed 

antiandrogenic effects after DINP 

exposure in rats. Id. at 96–97. DINP is 

less potent, by perhaps two- to 10-fold, 

than DEHP.67 However, DINP 

contributes to the cumulative risk from 

all antiandrogenic phthalates. The 

CHAP found that 10 percent of pregnant 

women and up to 5 percent of infants 

have a HI greater than one based on data 

at that time. 

CPSC staff examined more recent 

NHANES data than the dataset the 

CHAP considered. Using the CHAP’s 

methodology and the 2013/2014 

NHANES exposure data, CPSC staff 

determined that approximately 99 

percent of WORA in the U.S. population 

now have an HI less than or equal to one 

(using the 2005/2006 NHANES data, 97 

percent of WORA had an HI less than 

or equal to one). Additionally, CPSC 

staff’s evaluation of recent NHANES 

data shows that exposure to DINP has 

increased approximately five-fold since 

2005/2006. DINP now contributes as 

much to the cumulative risk as DEHP. 

As shown by the scenario-based 

exposure assessment included in 

Appendix E–1 of the CHAP report, 

lifting the interim prohibition on 

children’s toys that can be placed in the 

mouth and child care articles containing 

more than 0.1 percent DINP could 

increase exposure to DINP from these 

products, compared to exposures if 

DINP is not allowed in these products. 

If DINP were used in all of the products 

that were included in the scenario-based 

exposure assessment, DINP exposure 

from children’s toys and child care 

articles could account for up to about 29 

percent of infants’ total DINP exposure 

from all evaluated sources. Staff does 

not know the extent to which 

manufacturers would return to using 

DINP in children’s toys and child care 

articles if the interim prohibition were 

lifted. Staff is also unable to quantify the 

impact of increased DINP exposure on 

the percent of WORA or infants that 

have an HI less than or equal to one. 

However, staff notes that increased 

exposure will increase the MRDE risk to 

the population. 

The CHAP also assessed the risks of 

DINP in isolation and found that the 

MOEs ranged from 830 to 1,500. CHAP 

report at pp. 95–99. As discussed 

previously, MOEs of at least 100 are 

adequate to protect public health. CPSC 

agrees with the CHAP’s analysis that the 

MOEs for DINP in isolation, did not 

present a risk. However, DINP exposure 

has been increasing since the CHAP 

completed its analysis. Current analysis 

suggests that DINP MOEs, in isolation, 

(e.g., the MOE is now 220 to 14,000 at 

the 95th percentile) are below the upper 

limit, and are nearing the lower limit 

considered adequate for protecting 

public health. Based on the CHAP’s 

analysis and staff’s analysis of more 

recent NHANES data (and after 

consideration of the comments 

discussed below), the Commission 

determines that continuing the interim 

prohibition concerning DINP is 

necessary to ensure a reasonable 

certainty of no harm to children, 

pregnant women, or other susceptible 

individuals with an adequate margin of 

safety. 

The Commission proposed to expand 

the scope of the restriction on DINP’s 

use so that the rule would prohibit all 

children’s toys and child care articles 

containing DINP rather than only 

children’s toys that can be placed in a 

child’s mouth and child care articles. 79 

FR at 78335. Likewise, the final rule 

prohibits all children’s toys and child 

care articles containing concentrations 

of more than 0.1 percent of DINP. The 


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68Boberg et al. (2011); Borch et al. (2004); Clewell 

et al. (2013a); (2013b). 

69Hannas et al. (2011). 

70Hannas et al. (2011). 

71NAS (2017). 

Commission determines that this 

expansion of scope is necessary to 

protect the health of children. Covering 

all children’s toys means that the rule 

will protect against exposure to DINP 

through dermal contact (through the 

skin from handling toys), indirect oral 

exposure from children handling a toy 

and then placing their hands in their 

mouths, and all mouthing behavior. The 

CHAP’s estimates of oral exposure from 

mouthing toys included any behavior in 

which the toy contacts the mouth. 

CHAP report at Appendix E. However, 

the interim prohibition covers only toys 

that can be placed in a child’s mouth. 

The CPSIA provides the following 

definition of ‘‘toy that can be placed in 

a child’s mouth’’: 

For purposes of this section a toy can be 

placed in a child’s mouth if any part of the 

toy can actually be brought to the mouth and 

kept in the mouth by a child so that it can 

be sucked and chewed. If the children’s 

product can only be licked, it is not regarded 

as able to be placed in the mouth. If a toy 

or part of a toy in one dimension is smaller 

than 5 centimeters, it can be placed in the 

mouth. 

15 U.S.C. 2057c(g)(2)(B). Thus, 

continuing the interim prohibition with 

regard to DINP without expanding the 

scope would exclude toys that are 

5 centimeters or larger in one dimension 

(or have parts 5 centimeters or larger) 

even though children may be exposed to 

phthalates from licking or otherwise 

contacting the toy with the lips and 

tongue. Additionally, although staff 

does not have exposure estimates for 

indirect oral exposure from handling 

toys and normal hand-to-mouth 

behavior, staff concludes that exposures 

from handling toys will further 

contribute to the cumulative risk. Based 

on the analysis provided in Appendix E 

of the CHAP report, the Commission 

believes that the rule should encompass 

any behavior in which the toy contacts 

the mouth because this behavior 

provides a pathway of exposure to 

antiandrogenic phthalates. 

ii. Comments Concerning DINP 

As noted in section IV.A, commenters 

presented numerous arguments 

questioning whether phthalates are 

antiandrogenic, i.e., cause MRDE, and 

about the cumulative risk assessment. 

This section discusses the comments 

that focused on DINP. 

(a) Health Effects of DINP Exposure 

Comment: DINP and MRDE. 

Numerous commenters questioned 

whether DINP is antiandrogenic, that is, 

whether it causes MRDE. Commenters 

asserted that studies do not consistently 

show that DINP induces the effects 

associated with rat phthalate syndrome 

(e.g., decreased fetal testosterone, 

changes in anogenital distance, nipple 

retention, reproductive tract 

malformation, decreased sperm 

production). They cited numerous 

studies to support their assertions that 

DINP is not antiandrogenic and they 

stated that, for these reasons, the CHAP 

should not have included DINP in the 

cumulative risk assessment. However 

another commenter supported the 

inclusion of DINP in the cumulative risk 

assessment because DINP is 

antiandrogenic. (Comment 1.14). 

Response: The CHAP found, and 

CPSC agrees, that DINP-induced effects 

are consistent with phthalate syndrome 

in rats. Clewell et al. found changes in 

testosterone, nipple retention, and AGD, 

among other observations, by multiple 

laboratories, which indicate that DINP 

exposure is associated with outcomes 

similar to the effects of other phthalates 

such as DEHP and DBP that cause 

MRDE; these findings support the 

conclusion that DINP causes phthalate 

syndrome. CHAP report at pp. 97–98. 

CPSC’s conclusions are based on the 

weight of the evidence from review of 

multiple studies (discussed in comment 

responses 1.15 to 1.20). Phthalate 

syndrome is a spectrum of effects and 

thus one does not expect to observe all 

phthalate syndrome effects in all 

studies. The CHAP noted that effects of 

the phthalates it evaluated were doserelated. CHAP report at p. 2. 

Although DINP is less potent than 

other antiandrogenic phthalates, DINP 

can contribute to the cumulative risk 

from other phthalates. DINP has similar 

effects as other antiandrogenic 

phthalates, and thus is considered 

antiandrogenic in the context of the 

cumulative risk assessment. CPSC 

concludes that because DINP causes 

phthalate syndrome, it was appropriate 

for the CHAP to include DINP in its 

cumulative risk assessment and for the 

Commission to prohibit children’s toys 

and child care articles containing DINP. 

Comment: DINP and effects on 

testosterone production. Some 

commenters stated that studies showed 

inconsistent results regarding the effect 

of DINP on the production of 

testosterone and that this indicates 

DINP does not induce rat phthalate 

syndrome. (Comment 1.15). 

Response: As the commenters 

recognize, some studies do show 

reductions in testosterone following 

DINP exposure.68 CPSC staff agrees that 

some studies (e.g., Clewell et al. 

(2013a);(2013b)) involving repeated 

measurements over time have not 

shown permanent or persistent changes 

in testosterone. Sometimes this was due 

to differences in study design. However, 

permanent or persistent changes in 

testosterone are not required to have an 

adverse impact on male reproductive 

development; rather, transient 

reductions in the rate of testosterone 

synthesis at the critical period of 

development do have permanent effects 

(e.g., structural, functional) on male 

reproductive organs.69 Furthermore, 

staff agrees with the study by Hannas et 

al., showing that the rate of testosterone 

synthesis, rather than plasma or 

testicular levels, is the most relevant 

measure of phthalate-induced effects on 

testosterone.70 Additionally, 

testosterone measurements made after 

dosing lab animals with DINP has ended 

do not account for the possible effects 

of ongoing exposure, as could be 

expected for humans with exposures 

occurring after birth from food, water, or 

contact with consumer products. Staff 

notes that its conclusions are consistent 

with findings from a recent NAS 

systematic review of the DINP scientific 

literature.71 In that review study, the 

authors asserted with high confidence 

that DINP could be considered a 

‘‘presumed human hazard’’ because of 

its potential to reduce testosterone in 

male fetal rats. 

Comment: Effect of DINP on 

anogenital distance. Some commenters 

cited studies showing little or no effect 

on anogenital distance (AGD, i.e., the 

distance from the anus to the genitalia) 

after dosing with DINP. They asserted 

that these studies show DINP does not 

induce phthalate syndrome. A 

commenter questioned the results of one 

study where a significant decrease in 

AGD was observed, because of the very 

small differences between the treated 

and control groups. (Comment 1.16). 

Response: Reduced AGD is one of the 

abnormalities that characterizes rat 

phthalate syndrome. CHAP report at pp. 

1–2. The commenter questioned the 

AGD reductions observed in the Boberg 

et al. (2011) and Clewell et al. (2013b) 

studies; however, these results were 

actually larger than the magnitude 

considered by the commenter as 

unlikely to be biologically significant. 

Overall, the weight of evidence in the 

studies cited by the commenter 

demonstrates that DINP causes 

permanent effects on male reproduction. 

Thus, the commenter’s contention 

regarding a transient nature of DINP’s 

effects on AGD conflicts with the body 


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72Howdeshell et al. (2016). 

73Spade et al. (2015). 

74Ferrara et al. (2006). 

75The studies were (Joensen et al. (2012); 

Jurewicz et al. (2013); Main et al. (2006); Mieritz et 

al. (2012). 

76Bornehag et al. (2015). 

of evidence that DINP leads to phthalate 

syndrome. Furthermore, the animal 

studies, which involve short term 

exposures, do not reflect the continuous 

exposures that occur in humans. 

Comment: Nipple retention. 

Commenters questioned whether nipple 

retention is a relative endpoint when 

considering phthalates’ effects on 

humans and questioned the results of 

studies by Boberg et al. (2011) and Gray 

et al. (2000). Commenters also noted 

that Clewell et al. (2013b) reported no 

significant difference in nipples in male 

rats exposed to DINP. (Comment 1.17). 

Response: The CHAP specifically 

discussed nipple retention as a relevant 

endpoint for antiandrogenic activity, 

and concluded that nipple retention in 

male animals is consistent with 

phthalate-induced reductions in 

testosterone levels. CHAP report at p. 16 

and Appendix A–2. Staff notes that 

nipple retention is sensitive to exposure 

of the developing animal during key 

windows of susceptibility. Studies cited 

by the commenters that indicate the 

dosing ends during gestation or within 

the early part of the postnatal period do 

not consider possible effects of ongoing 

exposure, as could be expected for 

humans with exposures occurring after 

birth, but within early life periods of 

vulnerability from food, water, or 

contact with consumer products. As 

noted previously, phthalate syndrome is 

a spectrum of effects; all effects will not 

be present in every study.72 Although 

nipple retention in animals may not 

correspond to a specific endpoint in 

humans, nipple retention is an 

antiandrogenic effect that could 

manifest in different ways in humans. 

Comment: Reproductive tract 

malformations. Commenters noted that 

a number of animal studies involving 

DINP have not reported male 

reproductive tract malformations, such 

as cryptorchidism or hypospadias. For 

example, commenters stated that in the 

study by Gray et al. (2000), the 

significance of the changes after DINP 

exposure were unclear and 

questionable. (Comment 1.18). 

Response: Staff recognizes that the 

same specific male reproductive tract 

malformations have not been 

consistently observed following DINP 

exposure. As noted previously, 

phthalate syndrome is a spectrum of 

effects and not all effects will be 

observed in every study. As the CHAP 

recognized, the observation of effects 

depends on the dose level used in each 

study. CHAP report at p. 2. The three 

studies described by the commenter as 

‘‘definitive’’ studies (Hellwig et al., 

Hushka et al., and Waterman et al.) were 

not designed or intended to detect 

phthalate syndrome effects. In fact, one 

of the ‘‘definitive’’ studies (Hushka et 

al.) was on DIDP, which does not cause 

phthalate syndrome. Staff acknowledges 

that the Clewell study demonstrates that 

DINP induces limited or no phthalate 

syndrome effects following dietary 

dosing to rats. In spite of this, the 

authors themselves conclude that DINP 

has less potency than DEHP or DBP, but 

more than DEP when considering effects 

on the male reproductive tract. They 

additionally state ‘‘DINP is simply less 

potent than DBP and DEHP, i.e., it has 

lower potency in causing any adverse 

responses.’’ Staff also notes that this 

study involved oral dosing via feed, 

which is different than oral dosing using 

a tube inserted into the stomach (gavage 

dosing), which is used in typical 

developmental toxicity studies for 

determining phthalate syndrome effects. 

Different dosing strategies may account 

for the lack of effects seen in the Clewell 

study. Staff responds to commenters’ 

criticisms of other studies in comment/ 

response 1.18 in Tab B of the staff’s 

briefing package. 

Comment: DINP’s effects on sperm. 

Several commenters asserted that there 

is no strong evidence that DINP 

adversely affects sperm production or 

quality. They discussed a number of 

studies regarding DINP’s effects on 

sperm parameters, male mating 

behavior, and fertility. (Comment 1.19). 

Response: Three studies that 

commenters described as definitive 

were not actually designed or intended 

to detect phthalate syndrome effects. 

One of them was on DIDP, which does 

not cause phthalate syndrome. 

Inconsistencies could be due to study 

parameters or to the lower potency of 

DINP compared to other phthalates that 

have more consistent effects on sperm 

and fertility. Staff provides a more 

detailed response in comment/response 

1.19 in Tab B of the staff’s briefing 

package. 

Comment: Multi-nucleated gonocytes 

(MNGs). Several commenters disagreed 

with the CHAP’s use of MNG formation 

as a phthalate syndrome endpoint, and 

asserted that MNG formation is not a 

consequence of exposure to DINP. Some 

commenters asserted that MNG 

induction should not be considered an 

adverse effect because the MNGs are 

eliminated within a few weeks after 

birth. (Comment 1.20). 

Response: Although MNG formation 

is not linked directly to changes in 

testosterone production, and not 

necessarily a direct antiandrogenic 

effect of phthalate exposure, MNGs are 

a characteristic effect routinely observed 

after dosing with phthalates.73 Thus, the 

observation of MNGs formed after DINP 

exposure is consistent with results after 

exposure to other active phthalates, 

such as DBP, and is a marker of 

phthalates’ effects in the developing 

male reproductive system. Furthermore, 

one study suggests that the presence of 

MNGs may be linked to reduced fertility 

or testicular germ cell cancer in 

humans.74

Comment: Human epidemiology data 

and DINP antiandrogenicity. One 

commenter asserted that the available 

epidemiology data do not support the 

assertion that DINP is associated with 

reproductive effects in humans. The 

commenter presented a review of four 

studies that evaluated DINP’s 

association with adverse human 

reproductive effects.75 The review 

found lack of correlation or equivocal 

results in these studies. The commenter 

also found that a more recent study that 

reported slight reductions in AGD 

associated with DINP metabolites in 

mother’s urine was equivocal.76

Another commenter noted that 

statistical chance may have been 

responsible for some of the 

epidemiology studies’ positive 

association. The commenter concluded 

that the weight of the current 

information did not support that 

humans developed reproductive or 

developmental issues following 

exposure to phthalates. (Comment 7.5). 

Response: Of the four studies 

mentioned by the commenter, two were 

of adults and one was of boys aged 6– 

19 years. The CHAP concluded that 

studies in adult men were less relevant 

to the CHAP’s work because exposures 

measured during adulthood cannot be 

used to infer childhood or early life 

exposure. Observational epidemiology 

studies control for the possibility of 

random chance, bias, or confounding in 

their study design and analysis. The 

primary studies that commenters 

mentioned discuss the studies’ efforts to 

minimize these effects. Staff concludes 

that most of the studies cited by the 

commenters are not relevant to the 

current rulemaking on children’s toys 

and child care articles because they 

involved adults or older children. 

Because humans are simultaneously 

exposed to multiple phthalates, it is 

difficult to distinguish the effects of 

different phthalates in epidemiology 

studies. Staff concludes that the overall 


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weight of the evidence demonstrates an 

association between prenatal phthalate 

exposure and MRDE effects in infants. 

(b) DINP and Risk 

Comment: DINP’s contribution to risk. 

Several commenters asserted that DINP 

contributes little to the cumulative risk. 

They noted that the CHAP’s cumulative 

risk assessment showed that the 

estimated risks associated with 

phthalate exposure were driven by 

DEHP and DBP, and that DINP 

contributed only a small portion of the 

combined risk (less than one percent). A 

comment on CPSC staff’s 2017 report 

stated that as DINP continues to replace 

DEHP, the risk will continue to fall, thus 

increased replacement of phthalates by 

DINP will lower the cumulative risk 

further than it currently is. Along these 

lines, the commenter asserted that 

lifting the interim prohibition regarding 

DINP would have only an 

‘‘inconsequential effect’’ on cumulative 

risk. Some commenters asserted that, 

because DINP is less potent than DEHP, 

even if DINP entirely replaced DEHP, 

the 95th percentile HI would be far 

below one. (Comments 3.3, 3.4, and 5.1). 

Response: CPSC agrees that the 

median and 95th percentile HIs would 

be less than one if all CRA phthalate 

exposures were considered to be from 

DINP. However, a certain number of 

WORA in the 2013/2014 NHANES 

sample have HIs and DINP HQs greater 

than one. Any increase in DINP 

exposure could increase these 

individuals’ risk. In addition, there are 

a number of individuals that have HIs 

and DINP HQs near one. Additional 

DINP exposure to these individuals 

could increase the risk to greater than an 

HI of one (see comment response 3.2 

and TAB A). Based on the scenariobased exposure assessment, lifting the 

interim prohibition on children’s toys 

that can be placed in a child’s mouth 

and child care articles containing more 

than 0.1 percent of DINP could result in 

children’s toys and child care articles 

accounting for up to about 29 percent of 

total DINP exposure to infants. 

However, if DINP is not allowed in 

children’s toys and child care articles, 

such products would not contribute to 

total DINP exposure. Staff is unable to 

quantify the impact of changes in DINP 

exposure on the percent of WORA or 

infants that have an HI less than or 

equal to one, although staff notes that an 

increased exposure will increase the 

MRDE risk to the population. Staff does 

not consider that increasing MRDE risk 

to the population is ‘‘inconsequential,’’ 

particularly to those affected. 

As the commenter points out, in 

reality DINP would not replace all of the 

other phthalates because the differences 

in properties among the phthalates limit 

their use depending on the intended 

application. WORA with HQs greater 

than one were measured in each 

NHANES cycle despite the interim 

prohibition on children’s toys that can 

be placed in a child’s mouth and child 

care articles containing DINP. Any 

further increase in DINP exposure could 

increase the risk from DINP. 

Comment: ‘‘Reasonable certainty of no 

harm’’ and DINP. Some commenters 

asserted that the standard ‘‘reasonable 

certainty of no harm’’ is met without 

continuing the interim prohibition 

regarding DINP. They reasoned that, 

because the CPSIA permanently 

prohibited children’s toys and child 

care articles containing DEHP, DBP and 

BBP, those phthalates cannot contribute 

to any cumulative risk from these 

children’s products in the future; and 

without those phthalates, the HI clearly 

is less than one, so there is a reasonable 

certainty of no harm from use of DINP 

in these children’s products. In contrast, 

other commenters asserted that it ‘‘turns 

logic upside-down’’ to suggest that ‘‘as 

DEHP is replaced by less toxic 

phthalates, there is a reasonable 

certainty of no harm from increasing 

exposures to the remaining phthalates,’’ 

because the level of future replacement 

is unknown, but it is known that the 

replacement phthalates present hazards. 

Commenters on the staff’s analysis of 

more recent NHANES data asserted that 

CPSC staff’s analysis clearly 

demonstrates that the interim 

prohibition involving DINP can be lifted 

while meeting the ‘‘reasonable certainty 

of no harm’’ standard set forth in the 

CPSIA because the NHANES 2013/2014 

data show that cumulative risk for 

WORA continues to decline with the HI 

consistently below one for the 50th and 

95th percentiles. (Comment 3.20). 

Response: As explained, studies show 

that DINP contributes to the cumulative 

risk. The CPSIA’s permanent 

prohibition keeps DEHP, BBP, and DBP 

out of children’s toys and child care 

articles; however these phthalates 

continue to be used in other products 

and thus they contribute to the 

cumulative risk. The CRA demonstrates 

that HIs greater than one were observed 

in actual WORA sampled, in all 

NHANES data cycles, including the 

most recent (2013/2014). Thus, male 

children born to these women could be 

at risk for MRDE. Because a portion of 

the potentially sensitive population is 

still near the level of concern (HI greater 

than 1), permanently prohibiting 

children’s toys and child care articles 

containing DINP is still necessary to 

‘‘ensure a reasonable certainty of no 

harm’’ to children and pregnant women 

with an ‘‘adequate margin of safety.’’ 

Comment: Diet as source of exposure 

to DINP. Several commenters noted that 

diet is the primary source of exposure 

for DINP, as well as other phthalates, in 

infants and children. They asserted that 

DINP contributes so little to the 

combined risk from exposure to 

phthalates from all sources that a 

permanent prohibition on DINP’s use in 

children’s toys and child care articles 

would have little effect on the overall 

risk and, thus, the prohibition is not 

supported. (Comment 5.3). 

Response: The CHAP report does 

show that food, rather than children’s 

toys or child care articles, provides the 

primary source of phthalate exposure to 

women and children. CHAP report at 

pp. 49–53. The other main contributors 

were soft plastic toys and teethers (via 

mouthing), and personal care products 

such as lotions, creams, oils, soaps, and 

shampoos via dermal contact. Id. Figure 

2.1. 

The scenario-based exposure 

assessment included in the CHAP report 

shows that mouthing and dermal 

exposure to toys could contribute an 

average of 12.8 percent, 5.4 percent, and 

1 percent of the overall DINP exposure 

to infants, toddlers, and children, 

respectively, if DINP were used in these 

products. Id. at Appendix E1, Tables 

E1–21, E1–22, and E1–23. Mouthing and 

handling soft plastic toys and teethers 

could contribute 12.8 percent (mean 

exposure) or 16.6 percent (95th 

percentile exposures) of total DINP 

exposure in infants. Id. at Table E1–21. 

Dermal contact with the evaluated toys 

and child care articles may contribute 

up to an additional 16.5 percent of 

exposures to infants. Id. Therefore, 

although infants’ DINP exposure was 

primarily from diet, up to 29 percent 

may be due to the presence of DINP in 

the evaluated toys and child care 

articles. Id., Figure 2.1. 

Comment: DINP in isolation. 

Commenters asserted that the CHAP 

found no significant health risk from 

exposure to DINP by itself (considered 

in isolation), given the very large MOE 

estimates for median exposures, as well 

as for the 95th percentile of exposure. 

Commenters concluded that because of 

the high MOEs for DINP from all 

sources, the margins of safety must be 

even larger for the children’s products’ 

contribution to DINP exposure, and 

thus, there is no basis for a permanent 

prohibition on children’s toys and child 

care articles containing DINP. A 

commenter also stated that replacement 

of DEHP by DINP would not be 

expected to increase the risk because of 

DINP’s lower potency. A commenter 


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also asserted that even a doubling in 

DINP exposures would not increase the 

risk substantially, thus, restricting 

DINP’s use is unwarranted. (Comment 

5.5). 

Response: As discussed previously, 

the CHAP’s recommendations and the 

Commission’s rule are based on the 

cumulative risk from DINP in 

combination with other phthalates. We 

note, however, that due to the increased 

exposure to DINP (as seen in the 2013/ 

2014 NHANES data), DINP’s risk in 

isolation has increased. Thus, DINP 

alone may dominate the cumulative risk 

in the future, and DINP exposure in 

isolation may approach the level of 

concern, especially considering Case 2. 

Using the most recent NHANES data, 

the MOEs for WORA exposed to DINP 

range from 2300 to 150,000 (median) 

and 220 to 14,000 (95th percentile) for 

all three cases. 

CPSC disagrees with the assertion that 

doubling the DINP exposure would not 

increase the risk substantially, and notes 

that currently, a certain proportion of 

actual WORA have a DINP HQ greater 

than one and a certain proportion of 

actual WORA have DINP HQs near one. 

Increasing exposure to DINP may 

increase the number of individuals with 

an HQ greater than one or may increase 

the HQs of individuals with an HQ 

greater than one. Furthermore, doubling 

DINP exposures would lower the MOE 

for DINP to 110 to 7000 (95th 

percentile). The CHAP noted that MOEs 

exceeding 100 to 1000 are typically 

‘‘considered adequate for protecting 

public health.’’ CHAP report at p. 4. 

Current analysis suggests, therefore, that 

DINP MOEs, in isolation, (e.g., the MOE 

is 220 for Case 2) are below the upper 

limit, and are nearing the lower limit 

considered adequate for protecting 

public health. 

Comment: Safety of DINP compared 

to alternatives. Numerous commenters 

expressed concern about prohibiting the 

use of DINP in children’s toys and child 

care articles when not much is known 

about the toxicity and safety of 

alternative chemicals. Some 

commenters stated that the safety of 

alternative plasticizers should be 

thoroughly tested before placing 

restrictions on DINP. Commenters stated 

that DINP is well studied, has been used 

for over 50 years, and has been found 

safe for its intended uses. Commenters 

were concerned that prohibiting the use 

of DINP in children’s toys and child 

care articles could potentially put 

people at greater risk as substitutes with 

uncertain safety are used instead. 

(Comment 10.5). 

Response: CPSC shares the 

commenters’ concerns about the shift of 

chemical use from phthalates with 

known toxicity to phthalate alternatives 

with less toxicity or exposure 

information. The CHAP identified 

several data gaps for phthalate 

alternatives. CPSC agrees with the 

CHAP’s recommendation that 

appropriate federal agencies should 

perform additional research and risk 

assessment activities on phthalates and 

phthalate alternatives to fill in data 

gaps. However, CPSC does not believe 

that the lack of data on alternative 

plasticizers means we should not take 

action regarding DINP. DINP has in fact 

been covered by the interim prohibition 

since February 2009. As explained in 

the NPR and throughout this document 

and the staff’s briefing package, based 

on the CHAP report and staff’s analysis, 

we conclude that DINP causes adverse 

effects on male reproductive 

development and contributes to the 

cumulative risk of these effects from 

other antiandrogenic phthalates. Thus, 

the Commission determines that 

prohibiting children’s toys and child 

care articles containing concentrations 

of more than 0.1 percent of DINP is 

necessary to ensure a reasonable 

certainty of no harm and to protect the 

health of children. 

(c) Scope of Prohibition Regarding DINP 

Comment: Support for expanding 

scope to all children’s toys rather than 

those that can be placed in a child’s 

mouth. Several commenters stated that 

the Commission lacked justification to 

expand the restriction on DINP from 

‘‘children’s toys that can be placed in a 

child’s mouth’’ to all children’s toys. 

One commenter noted that it is not clear 

the CHAP intended to recommend this 

expansion. Other commenters noted 

that because the MOEs for DINP show 

that it does not present a risk in 

isolation, there is no basis for expanding 

the interim prohibition to cover all 

children’s toys. Commenters asserted 

that the Commission had little 

justification for the change and that it 

would have little effect on the risk. They 

noted that any risk comes primarily 

from mouthing. However, other 

commenters, citing evidence that DINP 

is associated with MRDE and the 

CHAP’s CRA analysis, stated that the 

CRA clearly supported the proposed 

prohibition involving DINP and the 

proposed expansion of scope from toys 

that can be placed in a child’s mouth to 

all children’s toys. (Comments 6.1 and 

6.2). 

Response: As discussed previously, 

this rule is based on the cumulative risk 

analysis demonstrating that DINP (and 

other antiandrogenic phthalates) causes 

MRDE and, and the most recent 

NHANES data that shows that there 

were from two to nine individuals with 

a HI greater than one in a sample of 538 

WORA. Limiting the rule to children’s 

toys that can be placed in a child’s 

mouth would exclude toys that could 

also expose children to DINP through 

mouthing behaviors other than placing 

the toy in the mouth and through hand 

to mouth exposure (e.g., licking) as well 

as direct exposure through dermal 

contact. The 2013/2014 NHANES data 

indicate that exposure to DINP is 

increasing, even with the CPSIA’s 

interim prohibition in effect. Covering 

all children’s toys (rather than only 

those that can be placed in a child’s 

mouth) will decrease exposure to DINP 

and thus reduce the risk of MRDE. 

Comment: Reliance on low cost and 

low dermal exposure as rationale in 

NPR. Commenters asserted that the NPR 

had provided faulty rationales for the 

expansion. A commenter asserted that 

the Commission had inappropriately 

based the expansion to all children’s 

toys on consideration of testing costs 

rather than on risk. A commenter stated 

that the reasoning stated in the NPR in 

favor of expanding the rule to all 

children’s toys was inconsistent with 

the reasons CPSC had stated for not 

expanding the prohibition to all 

children’s products. The commenter 

understood that CPSC did not propose 

to cover all children’s products because 

of negligible exposure due to the 

infrequency of mouthing of children’s 

products (that are not children’s toys or 

child care articles). The commenter 

asserted that this same rationale 

indicates that the rule should not be 

expanded beyond children’s toys that 

can be placed in a child’s mouth. 

(Comment 6.3 and 6.6). 

Response: The NPR mentioned that 

the proposed expansion would have 

little impact on testing costs. 79 FR 

78335. However, the NPR merely noted 

this anticipated impact; the reason for 

the expansion is to reduce the risk of 

adverse health effects. Regarding any 

inconsistency between proposing to 

expand the interim prohibition to all 

children’s toys and proposing not to 

cover additional children’s products, we 

note that the proposal concerning all 

children’s products was based primarily 

on a lack of information to assess the 

impact on children’s health. 

Comment: Reliance on European 

assessment as rationale in NPR. 

Commenters objected to the NPR’s 

discussion of the Europe Union’s 

regulations on phthalates. Commenters 

noted that the NPR stated that the 

European Commission’s 2005 directive 

on phthalates had distinguished 

between all children’s toys and toys that 


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77 57 FR 46626 (Oct. 9, 1992). 

can be placed in the mouth due to 

uncertainties about DINP, DNOP and 

DIDP. The NPR suggested that, now that 

the CHAP had issued its report, these 

uncertainties no longer exist. 

Commenters objected to the NPR’s 

reliance on this reasoning to support the 

expansion of the regulation of DINP. In 

addition, the EU submitted a related 

comment noting that the European 

Chemicals Agency (ECHA) conducted 

an extensive review in 2010 on DINP, 

DIDP and DNOP, and concluded that 

exposure other than mouthing did not 

present further risk. (Comments 6.4 and 

6.5). 

Response: Regarding the ECHA’s reevaluation, that report did not 

specifically address the distinction 

between children’s toys and toys that 

can be placed in a child’s mouth. 

Additionally, the 2013 ECHA report 

used different health end points (liver 

toxicity) as the focus, rather than the 

MRDE focus used by the CHAP and 

CPSC. Moreover, the 2013 ECHA report 

did not consider cumulative health risks 

from multiple phthalates. 

b. Di-n-octyl phthalate (DNOP) 

The CHAP concluded that DNOP does 

not lead to male developmental 

reproductive toxicity in animals and, 

therefore, does not contribute to the 

cumulative risk. Although DNOP does 

cause other developmental 

(supernumerary ribs) and systemic 

effects (liver, thyroid, immune system, 

and kidney), the MOEs in humans are 

very high. Therefore, the CHAP 

recommended that the current 

prohibition involving DNOP be lifted. 

CHAP report at pp. 91–95. The NPR 

noted that DNOP levels in people are so 

low that they are not detectable in about 

90 percent of humans, and that DNOP 

is not antiandrogenic, and, therefore, 

does not contribute to the cumulative 

risk. 79 FR 78334. Based on the CHAP 

report and staff’s analysis, the 

Commission concludes that continuing 

the prohibition of children’s toys that 

can be placed in a child’s mouth and 

child care articles containing more than 

0.1 percent of DNOP is not necessary to 

ensure a reasonable certainty of no harm 

to children, pregnant women, or other 

susceptible individuals with an 

adequate margin of safety. 

c. Diisodecyl phthalate (DIDP) 

The CHAP concluded that DIDP does 

not lead to male developmental 

reproductive toxicity in animals and, 

therefore, does not contribute to the 

cumulative risk. The CHAP considered 

the risk of DIDP in isolation and found 

that DIDP does cause other 

developmental (supernumerary ribs) 

and systemic effects (liver, and kidney). 

However, because the MOEs in humans 

are sufficiently high (range from 2,500 

to 10,000 for median DIDP exposures 

and 586 to 3,300 for upper-bound 

exposures), the CHAP recommended 

that the interim prohibition involving 

DIDP be lifted. CHAP report at pp. 100– 

105. As noted in the NPR, DIDP 

exposure would need to increase by 

more than 250 times to exceed an 

acceptable level. 79 FR 78334. Based on 

the CHAP report and staff’s analysis, the 

Commission concludes that continuing 

the prohibition of children’s toys that 

can be placed in a child’s mouth and 

child care articles containing more than 

0.1 percent of DIDP is not necessary to 

ensure a reasonable certainty of no harm 

to children, pregnant women, or other 

susceptible individuals with an 

adequate margin of safety. 

d. Comments Concerning DNOP and 

DIDP 

Comment: Prohibition concerning 

DNOP and DIDP should be made 

permanent. Some commenters asked the 

Commission to make the interim 

prohibition regarding DNOP and DIDP 

permanent. Commenters reiterated the 

CHAP’s conclusions that DNOP is a 

potential developmental toxicant, 

causing supernumerary ribs, and a 

potential systemic toxicant, causing 

adverse effects on the liver, thyroid, 

immune system, and kidney. They 

noted that the CHAP stated that DIDP 

was a ‘probable toxicant’ based on 

reproductive and developmental effects, 

and adverse systemic effects on the liver 

and kidney. A commenter suggested 

that ‘‘there could be a cumulative 

impact from exposures to a mixture of 

DINP, DNOP and DIDP, which would 

enhance the concern about harm.’’ 

Commenters asserted that without 

enough data to conduct a robust risk 

assessment, lifting the prohibition 

involving DNOP and DIDP will lead to 

elevated exposure to these two 

phthalates when others are covered by 

prohibitions. (Comments 5.8 and 5.9). 

Response: The CHAP concluded that 

DIDP and DNOP do not appear to 

possess antiandrogenic potential and 

therefore the CHAP did not include 

them in the cumulative risk assessment. 

As discussed above, the CHAP’s 

analysis of DIDP and DNOP in isolation 

showed high MOEs (greater than 1,000 

for all populations) that are sufficient to 

protect human health. The CHAP found 

that DNOP exposure levels are so low 

that one of the metabolites, MNOP, was 

not detectable in about 90 percent of 

humans. CHAP report at Table 2.6. 

Exposures would have to increase by a 

large measure before the acceptable 

levels of exposure would be exceeded. 

Thus, the CHAP report and staff’s 

analysis do not support a conclusion 

that prohibiting the use of DNOP or 

DIDP in children’s toys that can be 

placed in a child’s mouth and child care 

articles is necessary to ensure a 

reasonable certainty of no harm to 

children, pregnant women, or other 

susceptible individuals with an 

adequate margin of safety. 

Comment: ‘‘Reasonable certainty of no 

harm’’ and DNOP and DIDP. Some 

commenters asserted that lifting the 

interim prohibition concerning DNOP 

and DIDP while banning other 

phthalates would raise questions about 

whether such action meets the 

‘‘reasonable certainty of no harm’’ 

standard. They noted that the CHAP 

report found exposure to these 

chemicals from toys and child care 

articles and that the CHAP reported 

developmental and systemic toxic 

effects caused by these chemicals in 

animal studies. (Comment 5.9). 

Response: The CHAP concluded that 

DIDP and DNOP do not appear to 

possess antiandrogenic potential and 

therefore the CHAP did not include 

these two phthalates in the cumulative 

risk assessment. Assessing these 

chemicals in isolation, the CHAP found 

that the margins of exposure were 

sufficiently high to protect human 

health. Therefore, staff concludes that 

there is no justification to continue the 

prohibition involving DNOP or DIDP. 

2. Phthalates Subject to the Rule But 

Not Currently Prohibited Under the 

CPSIA. In addition to determining what 

action to take regarding the interim 

prohibition, the CPSIA directed the 

Commission to ‘‘evaluate the findings 

and recommendations of the Chronic 

Hazard Advisory Panel and declare any 

children’s product containing any 

phthalates to be a banned hazardous 

product under section 8 of the 

Consumer Product Safety Act (15 U.S.C. 

2057), as the Commission determines 

necessary to protect the health of 

children.’’ 15 U.S.C. 2057c(b)(3)(B). 

In the absence of a definition or other 

guidance on the meaning of the phrase 

‘‘necessary to protect the health of 

children,’’ CPSC interprets the phrase in 

the context of the CHAP report and 

CPSC’s chronic hazard guidelines,77

which consider that an HI less than or 

equal to one is necessary to protect the 

health of children. As explained in the 

CHAP report, the four additional 

phthalates all cause male reproductive 

developmental effects and would 

contribute to the cumulative risk. 


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78Furr et al. (2014). 

79Furr et al. (2014); Hannas et al. (2011). 

80 Dreyfus and Babich (2011). 

81Patton, (2010). 

82Hannas et al. (2011a). 

83Silva et al. (2010). 

84Patton (2010). 

The CHAP reviewed the potential 

health risks associated with eight 

phthalates that were not prohibited by 

the CPSIA, and it recommended that 

four additional phthalates (DIBP, 

DPENP, DHEXP, and DCHP) be 

prohibited from use in children’s toys 

and child care articles. The CHAP found 

that these four phthalates are associated 

with adverse effects on male 

reproductive development and 

contribute to the cumulative risk from 

antiandrogenic phthalates. CPSC staff 

has reviewed the CHAP’s assessment 

and agrees with the recommendation. 

Based on the CHAP’s evaluation and the 

staff’s assessment, the Commission 

proposed to prohibit children’s toys and 

child care articles containing more than 

0.1 percent of DIBP, DPENP, DHEXP, 

and/or DCHP. 79 FR 78335–78337. The 

Commission determines that prohibiting 

children’s toys and child care articles 

that contain concentrations of more than 

0.1 percent of DIBP, DPENP, DHEXP, 

and/or DCHP is necessary to protect the 

health of children and issues this final 

rule to establish this prohibition. 

Although current exposures to these 

four phthalates are low, these phthalates 

could be used as substitutes for the 

phthalates subject to prohibition, thus 

increasing human exposures from 

MRDE phthalates. All of these four 

phthalates are capable of contributing to 

the cumulative risk. A 2014 study 

demonstrated that three of these four 

phthalates (DPENP, DHEXP, and DCHP) 

had much greater potency than DEHP 

which the CPSIA permanently prohibits 

from use in children’s toys and child 

care articles.78 The potency of the fourth 

(DIBP) was slightly less or similar to 

DEHP.79 In addition, these four 

phthalates may have a greater potential 

for exposure than DINP, because lower 

molecular weight plasticizers generally 

have higher migration rates.80

a. Diisobutyl Phthalate (DIBP) 

The CHAP recommended prohibiting 

the use of diisobutyl phthalate (DIBP) in 

children’s toys and child care articles. 

CHAP report at pp. 110–113. DIBP is 

associated with adverse effects on male 

reproductive development and 

contributes to the cumulative risk from 

antiandrogenic phthalates. Furthermore, 

as noted in the NPR, DIBP has been 

found in some toys and child care 

articles during compliance testing by 

CPSC. The CHAP estimated that DIBP 

contributes up to 5 percent of the 

cumulative risk in infants from all 

products and sources. CHAP report at 

Table 2.16. More recent biomonitoring 

data show that DIBP exposures and risks 

have increased by about 50%. TAB A of 

staff briefing package. 

DIBP is similar in toxicity to DBP, 

which is one of the phthalates subject to 

the CPSIA’s permanent prohibition. 

DIBP was shown to be antiandrogenic in 

numerous studies and it acts in concert 

with other antiandrogenic phthalates. 

The CHAP found that current exposures 

to DIBP are low. When considered in 

isolation, DIBP has a MOE of 3,600 or 

more. CHAP report at pp. 24, 110–111. 

DIBP contributes roughly 1 to 2 percent 

of the cumulative risk from phthalate 

exposure to pregnant women and 1 

percent to 5 percent in infants. 

However, the CHAP based its 

recommendation on cumulative risk. 

Based on evaluation of the CHAP 

report and staff’s review, the 

Commission concludes that there is 

sufficient evidence to conclude that 

DIBP is antiandrogenic and contributes 

to the cumulative risk. The Commission 

also concludes that, applying the CPSC 

chronic hazard guidelines, this 

phthalate is considered ‘‘probably 

toxic’’ to humans based on sufficient 

evidence in animal studies. As 

discussed previously, the Commission 

considers that a HI less than or equal to 

one is necessary ‘‘to protect the health 

of children.’’ Using the most recent 

biomonitoring data, some WORA in the 

sample have an HI that exceeds one. For 

PEAA Case 1, three WORA had an HI 

greater than one; for PEAA Case 2, nine 

WORA had an HI greater than one; and 

for PEAA Case 3, two WORA had an HI 

greater than one. In addition, CPSC staff 

has identified DIBP in a small portion 

of toys and child care articles during 

routine compliance testing. Therefore, 

the rule prohibits children’s toys and 

child care articles containing 

concentrations of more than 0.1 percent 

of DIBP. The Commission concludes 

that this action is necessary to protect 

the health of children because it would 

prevent current and future use of this 

antiandrogenic phthalate in children’s 

toys and child care articles. 

b. Di-n-pentyl Phthalate (DPENP) 

The CHAP recommended prohibiting 

the use of DPENP in children’s toys and 

child care articles. CHAP report at pp. 

112–113. DPENP is associated with 

adverse effects on male reproductive 

development and contributes to the 

cumulative risk from antiandrogenic 

phthalates. Furthermore, DPENP is the 

most potent of the antiandrogenic 

phthalates. Prohibiting the use of 

DPENP would prevent its use as a 

substitute for other banned phthalates. 

The Commission agrees with the 

CHAP’s recommendation for DPENP. 

Based on the CHAP report and previous 

toxicity reviews by CPSC staff and a 

contractor,81 the Commission concludes 

that there is sufficient evidence that 

DPENP is antiandrogenic and 

contributes to the cumulative risk. For 

example, the CHAP noted studies by 

Howdeshell et al. and Hannas et al., 

which found that exposure to DPENP 

reduced fetal testicular testosterone 

production. Id. at p. 112. The 

Commission also concludes that, 

applying the CPSC chronic hazard 

guidelines, this phthalate is considered 

‘‘probably toxic’’ to humans, based on 

sufficient evidence in animal studies. 

Furthermore, DPENP is roughly two- to 

three-fold more potent than DEHP.82

Although CPSC staff has not detected 

DPENP in children’s toys or child care 

articles, metabolites of DPENP have 

been detected in humans,83 indicating 

that some exposure to DPENP does 

occur. In the CHAP’s analysis, up to five 

percent of infants and up to 10 percent 

of pregnant women exceed the 

negligible risk level (HI greater than 

one). Using the most recent 

biomonitoring data, some WORA in the 

sample have an HI greater than one. 

Allowing the use of DPENP in 

children’s toys and child care articles 

would further increase the cumulative 

risk. As discussed previously, the 

Commission considers that a HI less 

than or equal to one is necessary ‘‘to 

protect the health of children.’’ 

Therefore, the rule prohibits children’s 

toys and child care articles containing 

concentrations of more than 0.1 percent 

of DPENP. The Commission concludes 

that this action is necessary to protect 

the health of children because it would 

prevent current and future use of this 

antiandrogenic phthalate in toys and 

child care articles. 

c. Di-n-hexyl Phthalate (DHEXP) 

The CHAP recommended prohibiting 

the use of DHEXP in children’s toys and 

child care articles. CHAP report at pp. 

114–116. DHEXP is associated with 

adverse effects on male reproductive 

development and may contribute to the 

cumulative risk from antiandrogenic 

phthalates. The Commission agrees with 

the CHAP’s recommendation for 

DHEXP. Based on the CHAP report and 

previous review by CPSC staff and a 

contractor,84 the Commission concludes 

that there is sufficient evidence that 

DHEXP is antiandrogenic and 

contributes to the cumulative risk. The 


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85 Versar/SRC (2010b). 

CHAP report noted a 1980 study by 

Foster et al. that found severe testicular 

atrophy in rats, among other effects. Id. 

at p. 114. The Commission also 

concludes that, by applying the CPSC 

chronic hazard guidelines, this 

phthalate may be considered ‘‘probably 

toxic’’ to humans based on sufficient 

evidence in animal studies. The CHAP 

found that up to five percent of infants 

and up to 10 percent of pregnant women 

exceed the negligible risk level (HI 

greater than one). Using the most recent 

biomonitoring data, some WORA in the 

sample have an HI that exceeds one. 

Allowing the use of DHEXP in 

children’s toys and child care articles 

would further increase the cumulative 

risk. As discussed previously, the 

Commission considers that a HI less 

than or equal to one is necessary ‘‘to 

protect the health of children.’’ 

Although CPSC staff has not detected 

DHEXP in toys and child care articles 

during routine compliance testing thus 

far, prohibiting children’s toys and child 

care articles containing DHEXP would 

prevent its use in these products as a 

substitute for other banned phthalates. 

Therefore, the rule prohibits children’s 

toys and child care articles containing 

concentrations of more than 0.1 percent 

of DHEXP. The Commission concludes 

that this action is necessary to protect 

the health of children because it would 

prevent future use of this 

antiandrogenic phthalate in toys and 

child care articles. 

d. Dicyclohexyl Phthalate (DCHP) 

The CHAP recommended prohibiting 

the use of DCHP in children’s toys and 

child care articles. CHAP report at pp. 

116–118. DCHP is associated with 

adverse effects on male development 

and contributes to the cumulative risk 

from antiandrogenic phthalates. 

The Commission agrees with the 

CHAP’s recommendation for DCHP. 

Based on the CHAP report and previous 

reviews by CPSC staff and a 

contractor,85 the Commission concludes 

that there is sufficient evidence that 

DCHP is antiandrogenic and contributes 

to the cumulative risk. For example, the 

CHAP noted two studies that found 

such effects as reduced AGD and nipple 

retention in rats exposed to DCHP. Id. 

at p. 116. The Commission also 

concludes that, by applying the CPSC 

chronic hazard guidelines, this 

phthalate is considered ‘‘probably 

toxic’’ to humans based on sufficient 

evidence in animal studies. 57 FR 46626 

(Oct. 9, 1992). The CHAP found that up 

to five percent of infants and up to 10 

percent of pregnant women exceed the 

negligible risk level (HI greater than 

one). Using the most recent 

biomonitoring data, some WORA in the 

sample have an HI that exceeds one. 

Allowing the use of DCHP in children’s 

toys and child care articles would 

further increase the cumulative risk. As 

discussed previously, the Commission 

considers that a HI less than or equal to 

one is necessary ‘‘to protect the health 

of children.’’ Although the CPSC staff 

has not detected DCHP in toys and child 

care articles during routine compliance 

testing thus far, prohibiting the use of 

DCHP would prevent its use as a 

substitute for other banned phthalates. 

Therefore, the rule prohibits children’s 

toys and child care articles containing 

concentrations of more than 0.1 percent 

of DCHP. The Commission concludes 

that this action is necessary to protect 

the health of children because it would 

prevent future use of this 

antiandrogenic phthalate in toys and 

child care articles. 

e. Comments Concerning Phthalates 

Subject to the Rule But Not Currently 

Prohibited Under the CPSIA 

Comment: Regulating DIBP, DPENP, 

DHEXP, DCHP. One commenter stated 

that DIBP, DPENP, DHEXP and DCHP 

are not widely used in children’s toys 

and child care articles and are not 

prohibited in the European Union. The 

commenter stated that the proposed rule 

‘‘inevitably will extend inspection 

range, add cost to manufacturers and 

exporters and result in an unnecessary 

trade barrier.’’ (Comment 5.7). 

Response: CPSC agrees that DIBP, 

DPENP, DHEXP and DCHP are not 

widely used in children’s toys and child 

care articles. However, as explained 

above, studies demonstrate that these 

four phthalates all cause MRDE and 

they are as, or more, potent than DEHP. 

Regarding the commenter’s assertion 

that the prohibition of children’s toys 

and child care articles containing these 

four phthalates would add costs and 

result in a trade barrier, because these 

phthalates are not widely used in 

children’s toys and child care articles, 

the cost to manufacturers to reformulate 

the few products that might contain 

these phthalates should be small. 

Moreover, third party testing is already 

required for children’s toys and child 

care articles containing prohibited 

phthalates and the incremental cost of 

adding the additional phthalates to the 

analysis is expected to be very small. 

Staff estimates that the additional 

materials needed would cost $0.35 per 

test or about 0.1 percent of a typical 

$300 phthalates test for a component 

part or material. The data analysis 

procedure would need to be modified to 

include the new phthalates, but staff 

does not expect this would additional 

burdens to qualified laboratories. 

f. Children’s Products 

The scope of this rule covers 

children’s toys and child care articles. 

The CPSIA authorizes the Commission 

to ‘‘declare any children’s product 

containing any phthalates to be a 

banned hazardous product’’ if such 

action is necessary to protect the health 

of children. 15 U.S.C. 2057c(b)(3)(B). As 

explained in the NPR, the Commission 

is not expanding the rule to cover other 

children’s products. 79 FR 78337– 

78338. Only limited data on exposure to 

phthalates from other children’s 

products exist. The general information 

available does not support a 

determination that prohibiting any 

products other than children’s toys and 

child care articles is necessary. Toys are 

more likely than many other children’s 

products to be made of materials that 

could be plasticized with phthalates. 

Toys and child care articles are more 

likely than other children’s products to 

provide a pathway of exposure to 

phthalates both through oral exposure 

(from direct contact with the mouth and 

indirect contact when children place 

their hands in their mouths) and dermal 

exposure. We received few comments in 

response to the NPR that addressed 

expansion of the scope of the regulation 

to all children’s products. 

Comment: Expanding the scope to all 

children’s products. One commenter 

expressed disappointment that CPSC is 

not expanding the scope of the 

provisions involving phthalates to 

include other children’s items such as 

raincoats, footwear, backpacks, school 

supplies, and clothes. The commenter 

asserted that a lack of data does not 

mean CPSC should assume there is no 

problem. (Comment 6.6). 

Response: Staff has not found new 

information that would change the basis 

underlying the Commission’s decision 

not to propose expanding the scope of 

the rule to all children’s products. There 

is not enough information to adequately 

assess the health impact of children’s 

products other than children’s toys and 

child care articles. In contrast to 

children’s products in general, a wealth 

of information regarding use exists for 

children’s toys and child care articles 

from other agencies, such as EPA, and 

in scientific publications. The general 

information available indicates that 

exposure from children’s products is 

comparatively less than that from 

children’s toys and childcare articles. 


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g. Other Phthalates Not Included in the 

Rule 

The CHAP examined 14 phthalates: 

The three subject to the CPSIA’s 

permanent prohibition, the three subject 

to the CPSIA’s interim prohibition, and 

eight additional phthalates. Of the eight 

additional phthalates, the CHAP 

recommended that four be prohibited 

from use in children’s toys and child 

care articles, that three (Dimethyl 

Phthalate (DMP), Diethyl Phthalate 

(DEP), Di(2-propylheptyl) Phthalate 

DPHP) be free of any restriction, and the 

one (Diisooctyl Phthalate (DIOP)) be 

subject to an interim prohibition. CHAP 

report at pp. 1118–119. As discussed in 

the NPR, DIOP has a chemical structure 

consistent with other antiandrogenic 

phthalates. However, the CHAP 

concluded that there is not sufficient 

evidence to support a permanent 

prohibition. 79 FR 78337. The CPSIA 

did not provide for an interim 

prohibition as an option for the 

Commission’s rule under section 108, 

and as the CHAP explained, insufficient 

data exists to determine that a 

permanent prohibition of DIOP is 

necessary to protect the health of 

children. We received a few comments 

concerning phthalates that the CHAP 

assessed but are not covered by CPSC’s 

rule. 

Comment: DIOP. Some commenters 

suggested that the CPSC permanently 

prohibit children’s toys and child care 

articles containing DIOP. They stated 

that the CHAP had noted DIOP’s 

structural similarity to antiandrogenic 

phthalates and they concluded that 

CPSC should not assume that it would 

meet the CPSIA criteria when hazard 

and exposure data are lacking. 

(Comment 5.10). 

Response: Although the CHAP 

recognized that the structure of DIOP 

suggests that it may be associated with 

antiandrogenic effects, no experimental 

data exist that would support a 

conclusion that DIOP causes MRDE. 

Additionally, potency and exposure 

data are lacking. Thus, there is no basis 

for regulatory action on DIOP at this 

time. 

Comment: Prohibitions involving 

other phthalates. Some commenters 

asserted that ‘‘The CHAP’s lack of 

recommendations for additional 

regulatory action on phthalates like 

DIOP, DMP, DEP, DPHP or many of the 

alternatives evaluated is not an 

endorsement of their safety’’ because of 

the lack of sufficient hazard and 

exposure data on these chemicals. The 

commenters suggested that CPSC 

continue to review and monitor these 

phthalates and to recommend that other 

federal agencies take appropriate 

actions. (Comment 10.4). 

Response: CPSC staff participates in 

several interagency collaborations to 

discuss issues of mutual interest, 

including phthalates. CPSC will 

continue these cooperative activities. 

E. The Concentration Limit 

For both the permanent and interim 

prohibitions, the CPSIA established a 

concentration limit of 0.1 percent. The 

CHAP stated: 

When used as plasticizers for polyvinyl 

chloride (PVC), phthalates are typically used 

at levels greater than 10%. Thus, the 0.1% 

limit prohibits the intentional use of 

phthalates as plasticizers in children’s toys 

and child care articles but allows trace 

amounts of phthalates that might be present 

unintentionally. There is no compelling 

reason to apply a different limit to other 

phthalates that might be added to the current 

list of phthalates permanently prohibited 

from use in children’s toys and child care 

articles. 

CHAP report at p. 79. As discussed in 

the NPR, this concentration limit is not 

based on risk, and the Commission 

found no risk-based justification to 

change the limit from the 0.1 percent 

specified in the CPSIA. Thus, the 

Commission proposed to maintain this 

concentration limit. 79 FR 78338. We 

did not receive any comments 

concerning the concentration limit. The 

final rule retains the 0.1 percent 

concentration limit. 

F. International and Other Countries’ 

Requirements for Children’s Toys and 

Child Care Articles Containing 

Phthalates 

1. Summary of Requirements 

Other countries have restrictions 

concerning the use of various phthalates 

in children’s toys and child care 

articles. The requirements vary, but the 

following countries have some 

regulatory restrictions on phthalates that 

can be used in children’s toys and child 

care articles: The European Union (EU), 

Denmark, Canada, Japan, Australia, 

Brazil, Argentina, Taiwan, and Hong 

Kong. The requirements differ on the 

phthalates restricted and products 

covered. Unlike CPSC’s rule, these 

restrictions are based on evaluations of 

phthalate exposures in isolation, not in 

combination with other phthalates. 

There is no international standard that 

establishes substantive requirements for 

phthalates in children’s toys and child 

care articles. International Organization 

for Standardization (ISO) 8124–6:2014 

specifies a method for testing toys and 

children’s products to determine if they 

contain phthalates; it does not establish 

any content limits. We provide a 

summary of other countries’ 

requirements concerning phthalates in 

children’s toys and child care articles: 

DINP: 

• Denmark: Prohibits all phthalates at 

concentrations above 0.05 percent in 

toys and child care articles intended for 

children under 3 years old. 

• EU: Limits the use of DINP (as well 

as DIDP and DNOP) individually or as 

mixtures in toys and child care articles 

which can be placed in the mouth by 

children to no greater than 0.1 percent 

by weight of the plasticized material. 

• Canada: Limits use in the vinyl in 

any part of a toy or child care article 

that can be placed in the mouth of a 

child under four years of age to no 

greater than 0.1 percent of DINP, DIDP 

or DNOP. 

• Japan: For toys that are intended to 

come in contact with the mouth 

(excluding pacifiers and teething rings), 

parts made from plasticized materials 

that are intended to come in contact 

with the mouth must not contain more 

than 0.1 percent DINP (or DIDP or 

DNOP); PVC parts not intended to come 

in contact with mouth must not use 

DINP as a raw material. 

• Brazil: Limits use of DINP in plastic 

materials in all kinds of toys for 

children under three to no greater than 

0.1 percent. 

• Argentina: Limits use of DINP in 

toys and child care articles made of 

plastic material that can be placed in the 

mouth to no greater than 0.1 percent. 

• Taiwan: Limits DINP use in toys 

and child care articles to no greater than 

0.1 percent individually or in 

combination with DEHP, DBP, BBP, 

DIDP, or DNOP. 

• Hong Kong: Limits the combination 

of DINP, DIDP and DNOP to no greater 

than 0.1 percent of the total weight of 

the plasticized materials in toys or 

children’s products any part of which 

can be placed in the mouth of a child 

under four years of age. 

• Australia: Considered but rejected 

limiting DINP in children’s toys and 

child care articles. 

Other Phthalates Covered by CPSC’s 

Rule (DIBP, DPENP, DHEXP, DCHP) 

• Denmark: In 2009 instituted a 

national prohibition on all phthalates at 

concentrations above 0.05 percent in 

toys and child care articles intended for 

children under 3 years old. This covers 

all four phthalates: DIBP, DPENP, 

DHEXP, DCHP. 

• No restrictions concerning DIBP, 

DPENP, DHEXP, DCHP in children’s 

toys and child care articles in other 

countries. 

As this summary demonstrates, 

requirements concerning DINP in 


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86Section 108(g)(2)(B) of the CPSIA states that ‘‘a 

toy can be placed in a child’s mouth if any part of 

the toy can actually be brought to the mouth and 

kept in the mouth by a child so that it can be sucked 

and chewed. If the children’s product can only be 

licked, it is not regarded as able to be placed in the 

mouth. If a toy or part of a toy in one dimension 

is smaller than 5 centimeters, it can be placed in 

the mouth.’’ 

children’s toys and child care articles 

vary across different countries. 

However, even if the precise 

requirements differ, numerous countries 

have some limitation on the use of DINP 

in children’s toys and child care 

articles, and one other country restricts 

the use of DIBP, DPENP, DHEXP, and 

DCHP in children’s toys and child care 

articles. 

2. Comments Concerning Other 

Countries’ and International 

Requirements 

Comment: Differences between 

CPSC’s proposed rule and other 

countries’ requirements. Some 

commenters observed that CPSC’s NPR 

differed from restrictions in other 

countries. These comments focused on 

CPSC’s expansion of the interim 

prohibition regarding DINP to cover all 

children’s toys. Commenters noted the 

inconsistency between the EU’s 

requirements concerning DINP and the 

CPSC’s proposed rule. Two commenters 

stated that the CPSC’s rule is consistent 

with the EU. A commenter expressed 

concerns that the rule might be a barrier 

to international trade under the World 

Trade Organization (WTO) Agreement 

on Technical Barriers to Trade (TBT) 

due to the differences between CPSC’s 

rule and other countries’ approaches. 

(Comment 5.6). 

Response: As discussed above, CPSC’s 

rule concerning DINP differs from other 

countries’ restrictions. However, there is 

variation among these countries; no 

uniform consensus on regulation of 

DINP in children’s toys and child care 

articles exists. Regarding the TBT, we 

note that there is no international 

standard establishing restrictions on 

phthalates in toys. ISO 8124–6:2014 

only specifies a test method to 

determine if toys and children’s 

products contain phthalates. Rather, 

countries have established their own 

technical regulations. The TBT states 

that technical regulations shall not be 

more trade-restrictive than necessary to 

fulfill a legitimate objective. CPSC’s rule 

would not be a barrier to trade because 

it will apply equally to both domestic 

manufacturers and importers. We also 

note that the TBT recognizes that 

protection of human health or safety is 

a legitimate objective. 

G. Description of the Final Rule 

The text of the final rule is the same 

as the proposed rule with one 

exception. For clarity, we have added 

language from section 108(c) of the 

CPSIA (as amended by Pub. L. 112–28) 

regarding the application of the rule. 

This addition does not change the 

substance of the rule because the 

statutory provision applies regardless of 

whether it is stated in the rule. Section 

108(c) of the CPSIA states that the 

permanent and interim phthalate 

prohibitions, and any phthalates rule 

the Commission issues under section 

108(b)(3) of the CPSIA, ‘‘shall apply to 

any plasticized component part of a 

children’s toy or child care article or 

any other component part of a 

children’s toy or child care article that 

is made of other materials that may 

contain phthalates.’’ 15 U.S.C. 2057c(c). 

The Commission received comments 

on various aspects of the substance of 

the proposed rule. These comments and 

responses to them are summarized 

throughout this document. More 

detailed comment summaries and 

responses are at Tab B of staff’s briefing 

package. 

Section 1307.1—Scope and Application 

Section 1307.1 describes the actions 

that the rule prohibits. This provision 

tracks the language in section 108(a) of 

the CPSIA regarding the permanent 

prohibition and prohibits the same 

activities: Manufacture for sale, offer for 

sale, distribution in commerce, or 

importation into the United States of a 

children’s toy or child care article that 

contains any of the prohibited 

phthalates. 

Section 1307.2—Definitions 

Section 1307.2 provides the same 

definitions of ‘‘children’s toy’’ and 

‘‘child care article’’ found in section 

108(g) of the CPSIA. ‘‘Children’s toy’’ 

means a consumer product designed or 

intended by the manufacturer for a child 

12 years of age or younger for use by the 

child when the child plays. ‘‘Child care 

article’’ means a consumer product 

designed or intended by the 

manufacturer to facilitate sleep or the 

feeding of children age 3 and younger, 

or to help such children with sucking or 

teething. Although these definitions are 

stated in the CPSIA, the rule text 

restates them for convenience. We did 

not receive comments on these 

definitions, which re-state statutory 

definitions. 

Section 1307.3—Prohibition on 

Children’s Toys and Child Care Articles 

Containing Specified Phthalates 

Section 1307.3(a) states the products 

the rule prohibits. For convenience, this 

section provides both the items that are 

subject to the CPSIA’s existing 

permanent prohibition and the items 

that are subject to prohibition under the 

rule. Stating all prohibitions in this 

section will allow a reader of the CFR 

to be aware of all the CPSC’s restrictions 

concerning phthalates, both statutory 

and regulatory. 

Paragraph (a) sets out the CPSIA’s 

existing permanent prohibition which 

makes it unlawful to manufacture for 

sale, offer for sale, distribute in 

commerce, or import into the United 

States any children’s toy or child care 

article that contains concentrations of 

more than 0.1 percent of DEHP, DBP, or 

BBP. The restriction on these products 

was established by section 108(a) of the 

CPSIA. This statutory prohibition is not 

affected by the rule, but is merely 

restated in the regulatory text. 

Paragraph (b) prohibits the 

manufacture for sale, offer for sale, 

distribution in commerce, or 

importation into the United States of 

any children’s toy or child care article 

that contains concentrations of more 

than 0.1 percent of DINP, DIBP, DPENP, 

DHEXP, and DCHP. As explained above, 

in accordance with section 108(b)(2) of 

the CPSIA, the Commission appointed a 

CHAP that considered the effects on 

children’s health of phthalates and 

phthalate alternatives as used in 

children’s toys and child care articles 

and presented the Commission with a 

report of its findings and 

recommendations. After reviewing the 

CHAP’s report, the most recent exposure 

data, and public comments, the 

Commission is finalizing this rule in 

accordance with section 108(b)(3) of the 

CPSIA. 

For the reasons explained in this 

preamble, the Commission concludes 

that prohibiting children’s toys and 

child care articles that contain 

concentrations of more than 0.1 percent 

of DINP would ensure a reasonable 

certainty of no harm to children, 

pregnant women, or other susceptible 

individuals with an adequate margin of 

safety. DINP is currently subject to the 

CPSIA’s interim prohibition. 15 U.S.C. 

2057c(b)(1). Section 1307.3(b) changes 

the scope of regulation of DINP from the 

current interim scope of ‘‘any children’s 

toy that can be placed in a child’s 

mouth’’ 86 (and child care articles) to 

include all children’s toys. Based on the 

recommendations in the CHAP report, 

the Commission is not continuing the 

interim prohibitions on DIDP and 

DNOP. 

Additionally, § 1307.3(b) prohibits 

children’s toys and child care articles 


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containing four phthalates that are not 

currently subject to restrictions under 

the CPSIA: DIBP, DPENP, DEXP, and 

DCHP. For the reasons explained 

previously, the Commission concludes 

that prohibiting children’s toys and 

child care articles containing 

concentrations of more than 0.1 percent 

of DIBP, DPENP, DEXP, or DCHP is 

necessary to protect the health of 

children. 

The final rule adds paragraph (c) to 

§ 1307.3 to clarify the application of the 

rule. Section 108(c), as amended by 

Public Law 112–28 (August 12, 2011), 

addresses the application of the 

Commission’s phthalates rule. For 

convenience and clarity, we are 

restating that statutory provision in 

§ 1307.3 (c). 

H. Effective Date 

The APA generally requires that the 

effective date of a rule be at least 30 

days after publication of the final rule. 

5 U.S.C. 553(d). The Commission 

proposed an effective date of 180 days 

after publication of the final rule in the 

Federal Register. The final rule 

provides a 180-day effective date. As 

discussed in the NPR and in section V. 

of this preamble, the Commission 

expects that this rule will have a 

minimal impact on manufacturers, and 

that changes to testing procedures to 

include children’s toys and child care 

articles containing the four additional 

prohibited phthalates would require 

minimal effort by testing laboratories. 79 

FR 78339. In accordance with the 

CPSIA, restrictions on the use of certain 

phthalates in children’s toys and child 

care articles are currently in effect. This 

rule does not affect the permanent 

prohibition on children’s toys and child 

care articles containing more than 0.1 

percent of DEHP, BBP, and DBP. The 

CPSIA’s interim prohibition currently 

applies to children’s toys that can be 

placed in a child’s mouth and child care 

articles containing DINP. Thus, with 

regard to DINP, the impact from the rule 

would be only on children’s toys that 

cannot be placed in a child’s mouth. 

CPSC expects that a relatively small 

percentage of children’s toys that cannot 

be placed in a child’s mouth would 

need to be reformulated to remove 

DINP. Because the four additional 

phthalates (DIBP, DPENP, DHEXP, and 

DCHP) are not widely used in children’s 

toys and child care articles, few 

manufacturers will need to reformulate 

products to comply with this aspect of 

the rule. Regarding third party testing, 

testing laboratories are already testing 

children’s toys and child care articles 

for the permanently prohibited 

phthalates and are testing children’s 

toys that can be placed in a child’s 

mouth and child care articles for DINP. 

Testing laboratories can expand their 

procedures to include the four 

additional phthalates with minimal 

effort. CPSC received a few comments, 

summarized below, concerning the 

effective date. 

Comment: Effective date. Two 

commenters stated that the Commission 

should set an effective date of at least 1 

year from finalizing the rule. They 

asserted that DIDP and DINP are 

difficult to differentiate through testing, 

and that if the interim prohibition 

concerning DIDP was lifted while DINP 

continues to be restricted, laboratories 

would need additional time to address 

the technical testing difficulties. 

Another commenter urged the 

Commission to shorten the proposed 

180-day effective date based on the 

minimal impact CPSC anticipates to 

‘‘ensure that there is no gap in the 

protections from DINP.’’ Another 

commenter asked for clarification that 

the rule would not be retroactive (back 

to 2011). (Comment 5.11). 

Response: CPSC acknowledges that 

differentiating DINP and DIDP may be 

difficult. However, laboratories can 

differentiate DINP and DIDP using 

currently available equipment and 

methods. Manufacturers can maintain 

current formulations while they address 

any perceived challenges differentiating 

DINP and DIDP. As explained above, 

CPSC expects that the rule will require 

minimal changes for manufacturers and 

testing laboratories. Therefore 180 days 

from publication in the Federal Register 

should be sufficient time for the rule to 

take effect. We see no need to shorten 

the effective date. The interim 

prohibition established by section 

108(b)(1) remains in effect until this rule 

becomes effective. We confirm that the 

rule is prospective and will apply to 

products manufactured and imported on 

or after the effective date. As mentioned, 

however, the interim prohibition 

remains in place until the final rule 

takes effect. 

V. Regulatory Flexibility Act 

A. Certification 

The Regulatory Flexibility Act (RFA) 

requires an agency to prepare a 

regulatory flexibility analysis for any 

rule subject to notice and comment 

rulemaking requirements under the 

Administrative Procedure Act or any 

other statute unless the agency certifies 

that the rulemaking will not have a 

significant economic impact on a 

substantial number of small entities. 5 

U.S.C. 603 and 605. Small entities 

include small businesses, small 

organizations, and small governmental 

jurisdictions. The Commission certified 

in the NPR that this rule will not have 

a significant impact on a substantial 

number of small entities pursuant to 

section 605(b) of the RFA, 5 U.S.C. 

605(b) in the NPR. 79 FR 78324, 78339– 

41. Some comments expressed general 

concerns about the economic impact of 

the proposed rule, but none provided 

information or evidence that the rule 

would have a significant impact on a 

substantial number of small entities. 

Summaries of these comments and 

CPSC’s responses are provided below. 

More detailed summaries and responses 

are in Tab B of the staff’s briefing 

package. None of the comments 

received by the Commission changes the 

basis for the certification, nor has 

Commission staff received any other 

information that would require a change 

or revision the Commission’s previous 

analysis of the impact of the rule on 

small entities. Therefore, the 

certification of no significant impact on 

a substantial number of small entities is 

still appropriate. 

As explained in greater detail in the 

NPR, the certification is based on 

CPSC’s determination that: 

(1) Few, if any, manufacturers would 

need to alter their formulations to 

comply with the rule because: 

• Children’s toys that can be placed 

in a child’s mouth and child care 

articles containing DINP have been 

prohibited since 2009. Thus, no 

manufacturer would have to reformulate 

any products in these categories. 

• Only children’s toys that cannot be 

placed in a child’s mouth (no dimension 

of the toy is less than 5 cm) containing 

DINP would have to be reformulated. 

Thus, only a small subset of children’s 

toys that cannot be placed in a child’s 

mouth would be affected by the rule. 

• DIBP, DPENP, DHEXP, and DCHP 

are not widely used in children’s toys 

and child care articles. Therefore, 

relatively few manufacturers would 

have to reformulate products to 

eliminate these phthalates due to the 

rule. 

(2) The rule would have a small 

marginal impact on the cost of third 

party testing because: 

• All children’s toys and child care 

articles are already subject to third party 

testing for DEHP, DBP, and BBP. 

• Currently, children’s toys that can 

be placed in a child’s mouth and child 

care articles must also be tested for the 

presence of DINP. 

• Laboratory equipment and methods 

are already in place for testing the 

prohibited phthalates, therefore the 

additional cost of testing for DIBP, 


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DPENP, DHEXP, and DCHP would be 

very low. 

• Identification and quantification 

protocols for prohibited phthalates 

would need minimal modification to 

include DIBP, DPENP, DHEXP, and 

DCHP because each of these phthalates 

can be isolated at unique elution times 

by gas chromatography. Thus, the 

additional cost of analysis would be 

very low. 

• The additional cost of laboratory 

materials would be very low. Chemical 

standards for testing would be required 

for the four additional phthalates, but 

the standards for DNOP and DIDP 

would no longer be required. Therefore, 

the number of chemical standards 

needed would increase by two which 

CPSC expects would increase the cost of 

third party testing for phthalates by less 

than 35 cents per test, which is 

relatively small compared to current 

cost of phthalate testing (approximately 

$300 per product or component part). 

B. Comments Concerning Impact on 

Small Business 

Comment: Testing costs. Two 

commenters agreed with CPSC that the 

rule will have a small impact on testing 

costs. One commenter asked for CPSC to 

clarify how testing of technical mixtures 

of DINP and DIDP would be performed, 

noting that when DINP is detected in a 

sample, additional analytical steps are 

needed (at additional cost) to determine 

if the DINP is present as a ‘pure’ 

chemical or if the DINP is part of a 

technical mixture. Some commenters 

asked the Commission to take action to 

reduce testing costs. (Comment 9.1). 

Response: For the reasons explained 

above, CPSC expects that the additional 

burden associated with the rule is small, 

with no significant impact on a 

substantial number of small entities. 

Regarding testing of mixtures of DINP 

and DIDP, the restriction on DINP 

applies whether DINP is in the product 

intentionally or unintentionally. Thus, 

laboratories will not need to undertake 

any additional effort to determine the 

source of DINP found in a children’s toy 

or child care article. Regarding steps to 

reduce testing burdens, the Commission 

has recently issued determinations that 

will lower testing costs for some 

children’s toys and child care article 

manufacturers. 82 FR 41163 (August 30, 

2017). The determinations rule went 

into effect on September 29, 2017. 

Comment: Costs and benefits of NPR. 

Regarding the NPR’s determination that 

the proposed rule’s economic impact 

would be minimal, one commenter 

stated CPSC had not considered the 

effect on consumers or the possibility 

that smaller manufacturers would be 

burdened by the rule in the future, 

‘‘which offers no demonstrated public 

health benefits in exchange for even 

‘minimal’ costs.’’ The commenter 

asserted that the rule would take a ‘‘safe 

and useful chemical’’ away from 

consumers. (Comment 9.4). 

Response: Because CPSC followed the 

rulemaking requirements stated in 

section 108 of the CPSIA, which differ 

from rulemaking requirements under 

the CPSA and the FHSA, CPSC did not 

prepare a regulatory analysis of the costs 

and benefits of the rule. However, as 

discussed above, CPSC did conduct an 

analysis of the impact of the proposed 

rule on small entities. The commenter 

did not explain how future small 

manufacturers would be burdened. For 

the reasons explained above and in the 

NPR, CPSC expects the costs for small 

businesses subject to this rule would be 

small. 

VI. Notice of Requirements 

The CPSA establishes certain 

requirements for product certification 

and testing. Children’s products subject 

to a children’s product safety rule under 

the CPSA must be certified as 

complying with all applicable CPSCenforced requirements. 15 U.S.C. 

2063(a). Certification of children’s 

products subject to a children’s product 

safety rule must be based on testing 

conducted by a CPSC-accepted third 

party conformity assessment body. Id. 

2063(a)(2). The Commission must 

publish a notice of requirements (NOR) 

for the accreditation of third party 

conformity assessment bodies (or 

laboratories) to assess conformity with a 

children’s product safety rule to which 

a children’s product is subject. Id. 

2063(a)(3). The final rule for 16 CFR 

part 1307, ‘‘Prohibition of Children’s 

Toys and Child Care Articles Containing 

Specified Phthalates,’’ is a children’s 

product safety rule that requires the 

issuance of an NOR. The Commission 

previously published in the Federal 

Register an NOR for the phthalatecontaining products prohibited by the 

permanent and interim prohibitions 

state in section 108 on August 10, 2011. 

(76 FR 49286). The codified listing for 

the NOR can be found at 16 CFR 

1112.15(b)(31). In this same issue of the 

Federal Register the Commission is 

publishing a notice of proposed 

rulemaking that would update the 

existing NOR for the phthalatecontaining products prohibited by this 

final rule. 

VII. Paperwork Reduction Act 

The final rule does not include any 

information collection requirements. 

Accordingly, this rule is not subject to 

the Paperwork Reduction Act, 44 U.S.C. 

3501–3520. 

VIII. Preemption 

Section 26(a) of the CPSA, 15 U.S.C. 

2075(a), provides that where a 

‘‘consumer product safety standard 

under [the Consumer Product Safety Act 

(CPSA)]’’ is in effect and applies to a 

product, no state or political 

subdivision of a state may either 

establish or continue in effect a 

requirement dealing with the same risk 

of injury unless the state requirement is 

identical to the federal standard. 

(Section 26(c) of the CPSA also provides 

that states or political subdivisions of 

states may apply to the Commission for 

an exemption from this preemption 

under certain circumstances.) Section 

108(f) of the CPSIA is entitled 

‘‘Treatment as Consumer Product Safety 

Standards; Effect on State Laws.’’ That 

provision states that the permanent and 

interim prohibitions and any rule 

promulgated under section 108(b)(3) 

‘‘shall be considered consumer product 

safety standards under the Consumer 

Product Safety Act.’’ That section 

further states: ‘‘Nothing in this section 

of the Consumer Product Safety Act (15 

U.S.C. 2051 et seq.) shall be construed 

to preempt or otherwise affect any State 

requirement with respect to any 

phthalate alternative not specifically 

regulated in a consumer product safety 

standard under the Consumer Product 

Safety Act.’’ 15 U.S.C. 2057c(f). This 

provision indicates that the preemptive 

effect of section 26(a) of the CPSA will 

apply to the final rule. 

IX. Environmental Considerations 

The Commission’s regulations 

provide a categorical exclusion for the 

Commission’s rules from any 

requirement to prepare an 

environmental assessment or an 

environmental impact statement 

because they ‘‘have little or no potential 

for affecting the human environment.’’ 

16 CFR 1021.5(c)(2). Because this rule 

falls within the categorical exclusion, no 

environmental assessment or 

environmental impact statement is 

required. 

X. List of References 

This section provides a list of the 

documents referenced in this preamble 

and in the staff’s briefing package. 

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J. (2009) Effects of maternal exposure to 

di-isononylphthalate (DINP) and 1,1- 

dichloro-2,2-bis(p-chlorophenyl)ethylene 

(p,p′-DDE) on steroidogenesis in the fetal 

rat testis and adrenal gland. Reprod 

Toxicol 28(1):66–74. 


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Human Chorionic Gonadotropin 

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Correlation between carcinogenic 

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Andrade AJ, Grande SW, Talsness CE, et al. 

(2006) A dose response study following 

in utero and lactational exposure to di- 

(2-ethylhexyl) phthalate (DEHP): 

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offspring rats. Toxicology 228(1):85–97. 

Arbuckle, TE, Davis, K, Marro, L, Fisher, M, 

Legrand, M, LeBlanc, A, Gaudreau, E, 

Foster, WG, Choeurng, V, Fraser, WD, 

and the MIREC Study Group. 2014. 

Phthalate and bisphenol A exposure 

among pregnant women in Canada— 

Results from the MIREC study. 

Environment International. 68. 55–65. 

Ashworth M, Cressey P. (2014) Health risk 

assessment of selected phthalates in 

children’s toys. New Zealand Ministry of 

Health. Client Report FW 14054. October 

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HEALTH-CONTENT/MoH-reports/ 

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Chemical Mixtures. May 2004. In: U.S. 

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Department of Health and Human 

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(2014) Mixtures of endocrine-disrupting 

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Aylward LL, Lorber M, Hays SM (2011) 

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21:615–624. 

Banks K, Tuazon E, Berhane K, et al. (2012) 

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science 109(8):1480–1486. 

Bellinger DC (2013) Prenatal Exposures to 

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Benson R (2009a) Hazard to the developing 

male reproductive system from 

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phthalate, dipentyl phthalate, and 

diisononyl phthalate. Regul Toxicol 

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Benson R (2009b) Hazard to the developing 

male reproductive system from 

cumulative exposure to phthalate 

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diethylhexyl phthalate, dipentyl 

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Biedermann-Brem S, Biedermann M, 

Pfenninger S, et al. (2008) Plasticizers in 

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Boberg J, Christiansen S, Axelstad M, et al. 

(2011) Reproductive and behavioral 

effects of diisononyl phthalate (DINP) in 

perinatally exposed rats. Reprod Toxicol 

31(2):200–9. 

Borch J, Ladefoged O, Hass U, Vinggaard AM 

(2004) Steroidogenesis in fetal male rats 

is reduced by DEHP and DINP, but 

endocrine effects of DEHP are not 

modulated by DEHA in fetal, prepubertal 

and adult male rats. Reprod Toxicol 

18(1):53–61. 

Borgert CJ, Baker SP, Matthews JC (2013) 

Potency matters: Thresholds govern 

endocrine acivity. Regulatory Toxicology 

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Borgert CJ, Sargent EV, Casella G, Dietrich 

DR, McCarty LS, Golden RJ (2012) The 

human relevant potency threshold: 

Reducing uncertainty by human 

calibration of cumulative risk 

assessments. Regulatory Toxicology and 

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Bornehag CG, Carlstedt F, Jo ̈nsson BA, et al. 

(2015) Prenatal phthalate exposures and 

anogenital distance in Swedish boys. 

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123:101–107. 

Braun JM, Sathyanarayana S, Hauser R (2013) 

Phthalate exposure and children’s 

health. Current opinion in pediatrics 

25(2):247–54. 

Calafat AM, Needham LL, Silva MJ, Lambert 

G (2004) Exposure to di-(2-ethylhexyl) 

phthalate among premature neonates in 

a neonatal intensive care unit. Pediatrics 

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Calafat AM, Wong LY, Silva MJ, et al. (2011) 

Selecting adequate exposure biomarkers 

of diisononyl and diisodecyl phthalates: 

Data from the 2005–2006 National 

Health and Nutrition Examination 

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119(1):50–5. 

Carlson KR, Patton LE, Versar (2010) Toxicity 

review of dicyclohexyl phthalate 

(DCHP). U.S. Consumer product Safety 

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October 24, 2010. https://www.cpsc.gov/ 

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Carruthers CM, Foster PMD (2005) Critical 

window of male reproductive tract 

development in rats following 

gestational exposure to din-n-butyl 

phthalate. Birth Defects Res B Dev 

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CDC (2012) National Health and Nutrition 

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Department of Health and Human 

Services. Hyattsville, MD. 

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Chakraborty TR, Alicea E, Chakraborty S 

(2012) Relationships between urinary 

biomarkers of phytoestrogens, 

phthalates, phenols, and pubertal stages 

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nhsr067.pdf. 

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Product Safety Commission by the 

Chronic Hazard Advisory Panel on 

Diisononyl Phthalate (DINP). U.S. 

Consumer Product Safety Commission, 

Bethesda, MD. June 2001. https://

www.cpsc.gov/s3fs-public/pdfs/dinp.pdf. 

CHAP (2014) Report to the U.S. Consumer 

Product Safety Commission by the 

Chronic Hazard Advisory Panel on 

Phthalates and Phthalate Alternatives. 

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Commission, Bethesda, MD. July 2014. 

http://www.cpsc.gov/chap. 

Chevrier C, Petit C, Philippat C, et al. (2012) 

Maternal urinary phthalates and phenols 

and male genital anomalies. 

Epidemiology 23(2):353–6. 

Chou K, Wright RO (2006) Phthalates in food 

and medical devices. Journal of medical 

toxicology: Official journal of the 

American College of Medical Toxicology 

2(3):126–35. 

Christensen KL, Makris SL, Lorber M (2014) 

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cumulative exposure to phthalates for 

use in cumulative risk assessment. Regul 

Toxicol Pharmacol 69(3):380–9. 

Christiansen S, Boberg J, Axelstad M, et al. 

(2010) Low-dose perinatal exposure to 

di(2-ethylhexyl) phthalate induces antiandrogenic effects in male rats. Reprod 

Toxicol 30(2):313–21. 

Christiansen S, Scholze M, Dalgaard M, et al. 

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Clark K (2009) Phthalate ester concentration 

database. Prepared for the Phthalate 

Esters Panel, American Chemistry 

Council, Washington, DC. Transmitted 

by Steve Risotto, ACC May 28, 2010. 

https://www.cpsc.gov/s3fs-public/ 

Risotto%20052810.pdf. (Data base files 

are at: https://www.cpsc.gov/s3fs-public/ 

phthalateMono2009.pdf; https://

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phthalateRef2009.pdf; https://

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Clewell RA, Edwards K, Campbell J, Clewell 

H, Andersen M (2011) Determining 

structural determinants of phthalate 

antiandrogenic potency in vitro using rat 

and mouse Leydig tumor cells. The 

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Clewell RA, Sochaski M, Edwards K, Creasy 

DM, Willson G, Andersen ME (2013a) 

Disposition of diiosononyl phthalate and 

its effects on sexual development of the 

male fetus following repeated dosing in 

pregnant rats. Reproductive Toxicology 

35:56–69. 

Clewell RA, Thomas A, Willson G, Creasy 

DM, Andersen ME (2013b) A dose 

response study to assess effects after 

dietary administration of diisononyl 

phthalate (DINP) in gestation and 

lactation on male rat sexual 

development. Reproductive Toxicology 

35:70–80. 

Cohen SM, Meek MEB, Klaunig JE, Patton 

DE, Fenner-Crisp PA (2003) The human 

relevance of information on carcinogenic 

modes of action: Overview. Critical 

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Colon I, Caro D, Bourdony CJ, Rosario O 

(2000) Identification of phthalate esters 

in the serum of young Puerto Rican girls 

with premature breast development. 

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Conley JM, Lambright CR, Evans N, Cardon 

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List of Subjects in 16 CFR Part 1307 

Consumer protection, Imports, Infants 

and children, Law enforcement, Toys. 

■ For the reasons discussed in the 

preamble, the Commission amends title 

16 of the Code of Federal Regulations by 

adding part 1307 to read as follows: 

PART 1307—PROHIBITION OF 

CHILDREN’S TOYS AND CHILD CARE 

ARTICLES CONTAINING SPECIFIED 

PHTHALATES 

Sec. 

1307.1 Scope and application. 

1307.2 Definitions. 

1307.3 Prohibition on children’s toys and 

child care articles containing specified 

phthalates. 

Authority: Sec. 108, Pub. L. 110–314, 122 

Stat. 3016 (August 14, 2008); Pub. L. 112–28, 

125 Stat. 273 (August 12, 2011). 

§ 1307.1 Scope and application. 

This part prohibits the manufacture 

for sale, offer for sale, distribution in 

commerce or importation into the 

United States of any children’s toy or 

child care article containing any of the 

phthalates specified in § 1307.3. 

§ 1307.2 Definitions. 

The definitions of the Consumer 

Product Safety Act (CPSA) (15 U.S.C. 

2052(a)) and the Consumer Product 

Safety Improvement Act of 2008 

(CPSIA) (Pub. L. 110–314, sec. 108(g)) 

apply to this part. Specifically, as 

defined in the CPSIA: 

(a) Children’s toy means a consumer 

product designed or intended by the 

manufacturer for a child 12 years of age 

or younger for use by the child when the 

child plays. 

(b) Child care article means a 

consumer product designed or intended 

by the manufacturer to facilitate sleep or 

the feeding of children age 3 and 

younger, or to help such children with 

sucking or teething. 

§ 1307.3 Prohibition of children’s toys and 

child care articles containing specified 

phthalates. 

(a) As provided in section 108(a) of 

the CPSIA, the manufacture for sale, 

offer for sale, distribution in commerce, 

or importation into the United States of 

any children’s toy or child care article 

that contains concentrations of more 

than 0.1 percent of di-(2-ethyhexyl) 

phthalate (DEHP), dibutyl phthalate 

(DBP), or benzyl butyl phthalate (BBP) 

is prohibited. 

(b) In accordance with section 

108(b)(3) of the CPSIA, the manufacture 

for sale, offer for sale, distribution in 

commerce, or importation into the 

United States of any children’s toy or 

child care article that contains 

concentrations of more than 0.1 percent 

of diisononyl phthalate (DINP), 

diisobutyl phthalate (DIBP), di-n-pentyl 

phthalate (DPENP), di-n-hexyl phthalate 

(DHEXP), and dicyclohexly phthalate 

(DCHP) is prohibited. 

(c) In accordance with section 108(c) 

of the CPSIA, the restrictions stated in 

paragraphs (a) and (b) of this section 

apply to any plasticized component part 

of a children’s toy or child care article 

or any other component part of a 

children’s toy or child care article that 

is made of other materials that may 

contain phthalates. 

Alberta E. Mills, 

Acting Secretary, U.S. Consumer Product 

Safety Commission. 

[FR Doc. 2017–23267 Filed 10–26–17; 8:45 am] 

BILLING CODE 6355–01–P 


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