Publication 100,’’ guidelines published
by NTIS and available at
bad on the Accredited Certification Body’s review or asssment conducted
no more than three years prior to the date of submission of the Person’s or Certified Person’s completed certification statement, and, if an audit of a Certified Person by an Accredited Certification Body is required by NTIS, no more than three years prior to the date upon which NTIS notifies the Certified Person of NTIS’s requirement for audit, but such review or asssment or audit need not have been conducted specifically or solely for the purpo of submission under this part.
公章使用登记表(c) Where review or asssment or
audit by an Accredited Certification Body was not conducted specifically or solely for the purpo of submission under this part, the written attestation or asssment report (if an audit) shall describe the nature of that review or asssment or audit, and the Accredited Certification Body shall attest that on the basis of such review or asssment or audit, the Person or Certified Person has systems,
facilities, and procedures in place as required under
§1110.102(a)(2). In so attesting, an Accredited Certification Body may reference ‘‘Limited Access Death Master File (LADMF) Certification Program Publication 100,’’ guidelines published by NTIS and available at
(d) Notwithstanding paragraphs (a) through (c) of this ction, NTIS may, in its sole discretion, require that review or asssment or audit by an Accredited Certification Body be conducted specifically or solely for the purpo of submission under this part.
§1110.503Acceptance of accredited certification bodies.
(a) NTIS will accept written
attestations and asssment reports from an Accredited Certification Body that attests, to the satisfaction of NTIS, as provided in §1110.502.
(b) NTIS may decline to accept
written attestations or asssment reports from an Accredited Certification Body, whether or not it has attested as provided in §1110.502, for any of the following reasons:
(1) When it is in the public interest under Section 203 of the Bipartisan Budget Act of 2013, and notwithstanding any other provision of this part;
(2) Submission of fal or misleading information concerning a material
fact(s) in an Accredited Certification Body’s attestation under §1110.502;
(3) Knowing submission of fal or
misleading information concerning a
material fact(s) in an attestation or
asssment report by an Accredited
Certification Body of a Person or
Certified Person;
(4) Failure of an Accredited
Certification Body to cooperate in
respon to a request from NTIS verify
the accuracy, veracity, and/or
completeness of information received in
connection with an attestation under
§1110.502 or an attestation or
asssment report by that Body of a
Person or Certified Person. An
Accredited Certification Body ‘‘fails to
cooperate’’ when it does not respond to
NTIS inquiries or requests, or it
responds in a manner that is
unresponsive, evasive, deceptive, or
substantially incomplete; or
(5) Where NTIS is unable for any
reason to verify the accuracy of the
Accredited Certification Body’s
attestation.
[FR Doc. 2014–30199 Filed 12–29–14; 8:45 am]
BILLING CODE 3510–04–P
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: Notice of Propod Rulemaking.
音乐的英文怎么写SUMMARY: Section 108 of the Consumer
Product Safety Improvement Act of
2008 (CPSIA), requires the United States
Consumer Product Safety Commission
(Commission or CPSC) to convene a
Chronic Hazard Advisory Panel (CHAP)
to study the effects on children’s health
of all phthalates and phthalate
alternatives as ud in children’s toys
and child care articles and to provide
recommendations to the Commission
regarding whether any phthalates or
phthalate alternatives other than tho
already permanently prohibited should
be prohibited. The CPSIA requires the
Commission to promulgate a final rule
after receiving the final CHAP report.
The Commission is proposing this rule
pursuant to ction 108(b) of the CPSIA.
DATES: Submit comments by March 16,
2015.
ADDRESSES: You may submit comments,
identified by Docket No. CPSC–2014–
0033, by any of the following methods:
Electronic Submissions: Submit
electronic comments to the Federal
eRulemaking Portal at:
instructions for submitting comments.
The Commission does not accept
comments submitted by electronic mail
(email), except through
encourages you to submit electronic
comments by using the Federal
eRulemaking Portal, as described above.
Written Submissions: Submit written
衬衫怎么读
submissions in the following way: Mail/
Hand delivery/Courier, preferably in
five copies, to: Office of the Secretary,
Consumer Product Safety Commission,
Room 820, 4330 East West Highway,
Bethesda, MD 20814; telephone (301)
504–7923.
Instructions: All submissions received
must include the agency name and
docket number for this propod
rulemaking. All comments received may
be posted without change, including在前进
any personal identifiers, contact
information, or other personal
information provided, to:
confidential business information, trade
cret information, or other nsitive or
protected information that you do not
want to be available to the public. If
强国有我手抄报
furnished at all, such information
should be submitted in writing.
Docket: For access to the docket to
read background documents or
comments received, go to:
docket number, CPSC–2014–0033, into
the ‘‘Search’’ box, and follow the
prompts.
FOR FURTHER INFORMATION CONTACT: Kent
R. Carlson, Ph.D., Toxicologist, Division
of Toxicology & Risk Asssment,
Directorate for Health Sciences, U.S.
Consumer Product Safety Commission,
5 Rearch Place, Rockville, MD 20850–
3213; email: v.
SUPPLEMENTARY INFORMATION:
I. Background
A. Consumer Product Safety
Improvement Act
1. Statutory Prohibitions
Section 108 of the CPSIA establishes
requirements concerning phthalates.
The term ‘‘phthalates’’ generally refers
to ortho-phthalate diesters (phthalate
esters, phthalates), which are a class of
organic compounds ud primarily as
plasticizers for polyvinyl chloride
(PVC). Phthalates also are ud as
solvents and stabilizers for fragrances.
Phthalates have been ud in teethers,
plastic toys, home furnishings, air
fresheners, automobile interiors,
cosmetics, medications, medical
devices, and many other products.
1The CHAP met in one clod meeting as part of
the peer review process, January 28–29, 2014.
Phthalates are also found in food,
indoor air, outdoor air, houhold dust, soil, and other environmental media. 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). Section 108(b)(1) of the CPSIA 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 plac
ed 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). The CPSIA defines a ‘‘children’s toy’’ as ‘‘a consumer product designed or
intended by the manufacturer for a child 12 years of age or younger for u by the child when the child plays.’’ Id. Section 108(g)(1)(B). A ‘‘child care article’’ is defined as ‘‘a consumer product designed or intended by the
太空大战manufacturer to facilitate sleep or the feeding of children age 3 and younger, or to help such children with sucking or teething.’’ Id. Section 108(g)(1)(C). 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.’’ Id. Section 108(g)(2)(B). The 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. Section 108(b)(1). 2. Chronic Hazard Advisory Panel
Section 108(b)(2) of the CPSIA directs the CPSC to convene a CHAP ‘‘to study the effects on children’s health of all phthalates and phthalate alternatives as ud in children’s toys and child care articles.’’ Section 108(g) of the CPSIA defines a ‘‘phthalate alternative’’ as ‘‘any common substitute to a phthalate, alternative material to a phthalate, or alternative plasticizer.’’
Section 28 of the Consumer Product Safety Act (CPSA), requires a CHAP to consist of ven independent scientists appointed by the Commission from a
list of nominees nominated by the president of the National Academy of Sciences (NAS). CHAP members must ‘‘have demonstrated the ability to critically asss chronic hazards and risks to human health prented by the exposure of humans to toxic substances or as demonstrated by the exposure of animals to such substances.’’ 15 U.S.C. 2077(b)(2). Additionally, CHAP members must not receive
compensation from, or have any substantial financial interest in, any manufacturer, distributor, or retailer of a consumer product. Id. at 15 U.S.C. 2077(b)(1). Members of the CHAP may not be employed by the federal government, except the National Institutes of Health, the National Toxicology Program, or the National Center for Toxicological Rearch. Id. Section 108(b)(2) directs t
he CHAP to recommend to the Commission whether any phthalates or phthalate alternatives other than tho permanently prohibited should be declared banned hazardous substances. Specifically, ction 108(b)(2) directs the CHAP to:
Complete an examination of the full range of phthalates that are ud 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 the 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, bad on a reasonable estimation of normal and foreeable u and abu 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, peer- reviewed, scientific studies of the 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-to- mouth, 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 ud in children’s toys and child care articles. CPSIA ction 108(b)(2)(B). The CHAP’s examinations must be
conducted de novo, and the findings and conclusions of any previous CHAP on this issue and other studies
conducted by the Commission must be reviewed by the CHAP but are not to be considered determinative. Id.
Section 108(b)(2)(C) of the CPSIA requires the CHAP to complete its examination and final report within 2 years of the CHAP’s appointment. In the final report, the CHAP is required to recommend to the Commission whether any ‘‘phthalates (or combinations of phthalates)’’ in addition to tho
permanently prohibited, including the phthalates covered by the interim prohibition or phthalate alternatives, should be declared banned hazardous substances. 3. Rulemaking
Section 108(b)(3) of the CPSIA
requires the Commission to promulgate a final rule, pursuant to ction 553 of the Administrative Procedure Act
(APA), not later than 180 days after the Commission receives the final CHAP report. The Commission must ‘‘determine, bad 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 ...’’ CPSIA ction 108(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 ction 8 of the Consumer Product Safety Act (15 U.S.C. 2057), as the Commission determines necessary to protect the health of children.’’ Id. Section 108(b)(3)(B). B. CHAP Process
The CHAP held its first meeting on April 14–15, 2010. The CHAP met in public ssion ven times and met via teleconference (also open to the public) six times.1The meetings were held at the CPSC offices in Bethesda, MD, and also aired via webcast. A record of the CHAP’s public meetings, including video recordings and information
submitted to the CHAP, in addition to
v/chap .
3Nipple retention does not normally occur in
rodents, as it does in humans. 4That is, the effect occurring at the lowest do. 5A malformation of the penis.
6Distance between the anus and genitals, which
is greater in males than in females.
the final CHAP report, are available on the CPSC Web site.2
At a July 26–28, 2010 meeting, the CHAP heard testimony from the public, including from federal agency
reprentatives who discusd federal activities on phthalates. The CHAP also invited experts to prent their latest rearch findings at the July 2010 and subquent meetings. Members of the public who prented testimony to the CHAP at the July 2010 meeting included manufacturers of phthalates and phthalate alternatives, as well as reprentatives 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/or 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 lecting the peer reviewers as is required for the CHAP members. Peer 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 Rearch. The CHAP report was due to the
Commission on April 13, 2012 bad on the requirement in ction 108(b)(2)(C) of the CPSIA. The CHAP submitted the final report to the Commission on July 18, 2014.
C. The Propod Rule The Commission propos this rule in accordance with the CPSIA’s direction to follow ction 553 of the APA. CPSC staff reviewed the CHAP report and provided the Commissio
n with a briefing package that assd the CHAP report and made recommendations for a notice of propod rulemaking (NPR). The staff’s briefing package is available on CPSC’s Web site at v/Global/Newsroom/FOIA/CommissionBriefingPackages/2015/PropodRule-Phthalates-112514.pdf . As discusd in this preamble, the Commission agrees with the staff’s recommendations. II. CHAP Report
A. Summary of the CHAP Report
1. Health Effects in Animals As staff explained in their briefing
package, the CHAP reviewed all of the
potential health effects of phthalates.
Although phthalates are associated with a number of adver health effects, the
CHAP considered effects on male
reproductive development to be the
most relevant for human risk
asssment. This is, in part, becau
the effects constitute the ‘‘most
nsitive and most extensively studied
endpoint’’ for phthalates. (CHAP 2014;
pp. 1–2, 12–13). In support of this
decision, the CHAP noted that a 2008
National Rearch Council (NRC) report
also recommended using male
reproductive development effects as the
basis for a cumulative risk asssment of
phthalates. (CHAP, 2014; NRC, 2008).
The CHAP explained that exposing
pregnant female rodents to certain
phthalates caus a suite of effects on
the male reproductive tract in male pups, known as the ‘‘phthalate syndrome in rats.’’ The syndrome includes: malformations of the testes, prostate, and penis (hypospadias); undescended testes; reduced anogenital distance (AGD); and retention of nipples.3Male pups also have reduced fertility as adults. The incidence and verity of the effects increas with do. In addition, the male fetus is the most nsitive, followed by juveniles and adults. The phthalate syndrome effects are due largely to the suppression of testosterone production (Foster 2006), as well as reduced expression of the insulin-like hormone 3 gene (CHAP 2014; Wilson et al. 2004; p. 16). Thus, the CHAP refers to the effects as ‘‘antiandrogenic’’ to reflect their effect on testosterone production. Not all phthalates cau antiandrogenic effects; only phthalates meeting certain structural criteria, termed ‘‘active’’ phthalates, are associated with the
phthalate syndrome. (CHAP 2014; p. 16; Foster et al. 1980; Gray et al. 2000).
The CHAP, citing published reports, noted (CHAP 2014, p.2) an additional reason for focusing on effects on male
reproductive development: is empirical evidence demonstrates that the effects of active phthalates on male reproductive
development are additive (Hannas et al. 2011b; 2012; Howdeshell et al. 2007;
2008). That is, exposures to multiple phthalates at lower dos act in concert to produce the same effect as a higher do of a single phthalate. The additive effects of different phthalates are
significant becau humans are expod
to multiple phthalates simultaneously.
(CHAP 2014; p. 2). The CHAP also
noted that, in addition to phthalates, other chemicals, including certain pesticides and prervatives, add to the male reproductive effects of phthalates.
(CHAP 2014; pp. 26–27, p. D–26; Rider et al. 2010). The CHAP also reviewed available
toxicity data on six phthalate
alternatives. (CHAP 2014; p. 22). The
CHAP found none of the alternatives to
be antiandrogenic, that is, causing
effects consistent with the phthalate
syndrome. Therefore, becau the
phthalate alternatives did not contribute
to the cumulative antiandrogenic effect,
the CHAP assd the potential risks of
phthalate alternatives, as well as non-
antiandrogenic phthalates, in isolation.
The asssments were bad on the
most nsitive health endpoint 4for
each chemical, such as liver toxicity, for
asssing risk. (CHAP 2014, pp. 121–
142).
2. Health Effects in Humans The CHAP noted that the phthalate syndrome in rats rembles the ‘‘testicular dysgenesis syndrome’’ (TDS) in humans. (CHAP 2014, pp. 2, 28). TDS includes poor men quality, reduced fertility, testicular cancer, undescended testes, and hypospadias.5After reviewing all of the available studies on associations between phthalate exposure and human health (CHAP 2014, pp. 27–33; Appendix C), the CHAP noted that two of three studies found an association between prenatal or neonatal phthalate exposure and reduced anogenital distance 6in male infants. Several studies also found associations between prenatal or neonatal exposure and neurobehavioral effects in children. The effects included reductions in mental and
psychomotor development and
increas in attention deficits and behavioral symptoms. The CHAP cited veral studies that found associations
between phthalate exposure in adult males and reduced sperm quality and infertility. (Reviewed in CHAP 2014, p. C–8).
Bad on this information, the CHAP concluded that there is a growing body
of studies reporting associations between phthalate exposure and human
health. (CHAP 2014, p. 27). Many of the reported health effects are consistent with testicular dysgenesis syndrome in
humans. (CHAP 2014, p. 28). However, the CHAP acknowledged the limitations of the studies, noting that the epidemiological studies were not designed specifically to provide information on sources of exposure or the relative contributions of different phthalates. Furthermore, the studies were limited by simultaneous human exposure to multiple phthalates and other environmental chemicals and by the study design. (CHAP 2014, pp. 2–3).
3. Human Phthalate Exposure
The CHAP assd human exposure to phthalates by two different, but complementary, methods: human biomonitoring (HBM) and exposure scenario analysis. HBM relies on measurements of phthalate metabolites in human urine to estimate phthalate exposure. (CHAP 2014, pp. 34–48; Appendix D). The HBM method provides good estimates of total exposure bad on empirical measurements (CHAP 2014, p. 6, 75,
E1–38; Clark et al. 2011), but the method does not provide information on sources of exposure. The CHAP ud two data sources for HBM—each will be described in turn. The National Human Health and Nutrition Survey (NHANES), which is conducted by the U.S. Department of Health and Human Services, periodically measures phthalates and other chemicals in human urine and blood in a statistically reprentative sample of thousands of U.S. residents. The CHAP ud data from NHANES to estimate daily exposures to various phthalates in pregnant women and women of reproductive age. (CDC 2012). NHANES does not measure phthalate metabolites in children younger than 6 years old. Therefore, the CHAP ud measurements from an NIH- and EPA- funded study of mother-child pairs, the Study for Future Families (SFF), to obtain exposure estimates for infants. (Sathyanarayana et al. 2008a; 2008b). The SFF study also provided additional data for the mothers, both before and after they gave birth.
The CHAP also found, bad on the HBM studies, that ‘‘exposure to phthalates in the United States (as worldwide) is omniprent.’’ (CHAP 2014, p. 37). Virtually all Americans are expod simultaneously to multiple phthalates. (CHAP 2014, p. 37). Bad on NHANES data, pregnant women have median exposures that are roughly similar to tho of women of reproductive age. (CHAP 2014, Table 2.7, page 45). Bad on the SFF data, infants have threefold to fourfold greater median exposures than their mothers. (CHAP 2014, Table 2.7, p. 45).
The cond method that the CHAP
ud to asss human exposure was
through analyzing numerous exposure
scenarios. The CHAP ud the scenario-
bad method becau that method
provides information on sources of
exposure. (CHAP 2014, pp. 49–60,
Appendix E1). Thus, the scenario-bad
method complements the information
obtained from the HBM method, which
provides estimates of total exposure.
The CHAP estimated exposure from
individual sources using data on
phthalate levels in products and
environmental media, migration rates,
and product u information. (CHAP
2014, pp. 49–60; Appendices, E1, E3).
For most phthalates, the CHAP found
that food, rather than children’s toys or
child care articles, provides the primary
source of exposure to both women and
children. (CHAP 2014, pp. 52–53, Table
2.1). For example, DINP exposure to
infants and children is primarily from
diet, although mouthing of DINP-
containing toys or contact with DINP-
containing toys and child care articles
may contribute to the overall exposure.
(CHAP 2014, Figure 2.1, page 59; Table
E1–23, page E1–32; and Table E1–24,
page E1–36). The CHAP also found that
personal care products (cosmetics) are a
major source of exposure to diethyl
phthalate (DEP) and dibutyl phthalate
(DBP) (id.). Indoor air and houhold
dust are also major sources of diethyl
phthalate (DEP), dibutyl phthalate
(DBP), and butyl benzyl phthalate (BBP)
(id.).
4. Risk
a. Cumulative Risk Asssment
Generally
Section 108(b)(2)(B)(iv) of the CPSIA
directed the CHAP specifically to
‘‘consider the cumulative effect of total
exposure to phthalates, both from
children’s products and from other
sources.’’
Cumulative risk asssment (CRA)
generally refers to the combined effects
of multiple environmental stressors.
(Sexton and Hattis, 2007). CRA may
combine different types of hazards, such自然生态环境
as air pollution combined with
psychological stress. More commonly,
CRA includes mixtures of different
chemicals. Chemical mixtures may be
complex mixtures, such as air pollution
or combustion emissions. Mixtures may
include unrelated chemicals or, in the
ca of phthalates, a family of cloly
related chemicals. Human exposure to
phthalates is a ‘‘coincidental’’ exposure,
meaning that different individuals are
expod to phthalates in different
proportions.
Section 108(b)(2)(B)(ii) of the CPSIA
also directed the CHAP to ‘‘consider the
potential health effects of each of [the
specified] phthalates both in isolation
and in combination with other
phthalates.’’ Components of a mixture
may interact in different ways regarding
health risks. For example, suppo two
chemicals produce the same health
effect in animals. Furthermore, assume
that 1 mg of A affects 10 percent of
animals tested, and 1 mg of B affects 15
percent of animals. If the effects of the
mixture are ‘‘do additive,’’ then 25
percent of animals would be affected. In
the ca of phthalates, there is evidence
in animal studies that the effects are
‘‘do additive.’’ (Howdeshell et al.,
2007; Howdeshell et al., 2008; Hannas
et al., 2011b; Hannas et al., 2012). In
other words, the whole equals the sum
of its parts. Do additivity does not
necessarily apply in all cas. With
other mixtures, the effects could be less
than, or more than, do additive. The
process of performing a CRA differs in
veral respects from that of single-
chemical risk asssment. One key
difference is the choice of health
endpoint. Risk asssments for
chemicals in isolation are usually bad
on the most nsitive health effect. The
most nsitive endpoint is the one that
is obrved at the lowest do or has the
greatest risk at a given do. CRAs are
generally bad on a health effect that is
common to the components of the
mixture. The common health endpoint
is not necessarily the most nsitive
health endpoint for each of the mixture
components.
b. Cumulative Risk and Risk in
Isolation—Hazard Index
As required by ction 108(b)(2)(B)(ii)
of the CPSIA, the CHAP assd the
potential risks from phthalates in
一路芳香
isolation and in combination with other
phthalates, that is, cumulative risk. The
CHAP cho antiandrogenic effects on
male reproductive development as the
focus of the CHAP’s cumulative risk
asssment. Only antiandrogenic (i.e.,
active) phthalates cau male
reproductive developmental effects and,
therefore, only active phthalates
contribute to the cumulative risk of
male developmental reproductive
effects. (CHAP 2014, pp. 61–70). The
CHAP applied the hazard index (HI)
approach to asss the cumulative risk
for antiandrogenic effects in males. The
HI approach is widely ud for chemical
mixtures and other cumulative risk
asssments. (Kortenkamp and Faust
2010; NRC 2008; Teuschler and
Hertzberg 1995). Calculating the HI is a
two-step process:
7The PEAA is esntially similar to a ‘‘reference
do’’ (RfD) or ‘‘acceptable daily intake’’ (ADI), which are commonly ud terms, except that the PEAA applies only to antiandrogenic effects. The RfD and ADI generally apply to the most nsitive
health effect of a given chemical. RfD and ADI are estimates of a do at which one could be expod to for up a lifetime with a negligible risk of adver effects.
8Having a HI greater than one does not
necessarily mean that adver effects will occur; however, this possibility cannot be ruled out.
1. Calculate the ‘‘hazard quotient’’ (HQ) for each phthalate. The HQ is the exposure divided by the ‘‘potency estimate for antiandrogenicity’’
(PEAA).7The PEAA is an estimate of the level of exposure at which the risk of antiandrogenic effects is considered negligible. If the HQ is greater than one
for a given phthalate, there may be a concern for antiandrogenic effects in the expod population due to the effect of
an individual phthalate.
2. The hazard index (HI) is the sum of the hazard quotients (HQs) for the phthalates of interest. If the HI is greater
than one, there may be a concern for antiandrogenic effects in the expod population due to the cumulative effects of phthalates.8
The CHAP calculated the HI for each individual in two populations of interest: (1) Pregnant women, and (2) children up to 36 months old. Pregnant women reprent exposure to the fetus, which is considered more nsitive than newborns, children, and adults.
The CHAP ud three ts of PEAAs that were derived by different
approaches. (CHAP 2014, p. 62, 64;
Table 2.15). This was done to asss the effect of using different PEAAs on the overall conclusions. The CHAP report refers to the as cas 1, 2, and 3:
•Ca 1: Published values ud from a cumulative risk asssment for phthalates (Kortenkamp and Faust 2010);
•Ca 2: Values derived by the CHAP bad on relative potency comparisons across chemicals from the same study (Hannas et al. 2011b); and
•Ca 3: Values from the CHAP’s de novo literature review of reproductive and developmental endpoints bad on the no obrved adver effect levels (NOAEL) in Table 2.1 of the CHAP report. Results for the three ts of PEAAs were roughly similar; HIs were within 2- fold, although HIs were
slightly lower for Ca 3. (CHAP 2014, p. 65).
Using 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 t of PEAAs was ud.
Roughly 10 percent of pregnant women had HIs greater than one. (CHAP 2014, Table 2.16).
Using SFF data, the CHAP found that the mothers had median HIs about 0.1 (0.06 to 0.11), while the 95th percentiles were less than one (0.33 to 0.73). (CHAP 2014, Table 2.16). There was little
difference between pre- and post-natal exposures. The CHAP report shows that up to 5 percent of women had HIs greater than one. For infants, HIs were about twofold greater than their
mothers. Infants had median HIs about 0.2, while the 95th percentiles were between 0.5 and 1.0. About 5 percent of infants had HIs greater than one. Bad on the results, the CHAP concluded that there may be a concern for adver effects from the cumulative effects of phthalates in individuals with a hazard index greater than one, reprenting up to 10 percent of
pregnant women and up to 5 percent of infants. (CHAP 2014, p. 65).
Looking at the HQs for individual phthalates, the CHAP concluded:
‘‘Clearly, the hazard quotient for DEHP dominates the calculation of the HI, as expected, with high exposure levels and one of the lowest PEAAs.’’ (CHAP 2014, p. 65). Thus, DEHP (which the CPSIA permanently prohibits from u in children’s toys and child care articles) contributes the most to the cumulative risk. (CHAP 2014, Table 2.16). This is due to a combination of exposure and potency. (CHAP 2014, p. 65). The CHAP found that the median HQs for DEHP range from 0.1 to 0.2, with 95th
percentiles up to 12. DEHP contributed between 50 (ca 2) and 90 percent (ca 1) of the median HI in pregnant women (summarized in Table 1). For
comparison, DBP, BBP, and DINP each contributed up to 8 percent of the HI in pregnant women (Table 1).
T ABLE 1—P ERCENT C ONTRIBUTION OF I NDIVIDUAL P HTHALATES TO THE C UMULATIVE R ISK a
Ca 1
Ca 2 Ca 3
NHANES Pregnant Women:
Diisobutyl phthalate, DIBP ................................................................................................................0.7 2.3 <1.1 Dibutyl phthalate, DBP .....................................................................................................................7.1 7.7 1.1 Butyl benzyl phthalate, BBP .............................................................................................................0.7 7.7 1.1 Di(2-ethylhexyl) phthalate, DEHP .....................................................................................................85.7 53.8 77.8 Diisononyl phthalate, DINP ..............................................................................................................0.7 7.7 2.2 SFF Infants:
Diisobutyl phthalate, DIBP ................................................................................................................0.9 5.0 <0.8 Dibutyl phthalate, DBP .....................................................................................................................9.1 15.0 2.5 Butyl benzyl phthalate, BBP .............................................................................................................18.2 10.0 2.5 Di(2-ethylhexyl) phthalate, DEHP .....................................................................................................81.8 55.0 91.7 Diisononyl phthalate, DINP ..............................................................................................................
0.9 15.0 8.3
a Calculated from data in CHAP, 2014, Table 2.16. Bad on median exposures.
