Order Code RL34572
Phthalates in Plastics and
Possible Human Health Effects
July 14, 2008
Linda-Jo Schierow
Specialist in Environmental Policy
Resources, Science, and Industry Division
Margaret Mikyung Lee
Legislative Attorney
American Law Division

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Phthalates in Plastics and
Possible Human Health Effects
Summary
Roughly a dozen chemicals known as phthalates are used to make the plastics
found in thousands of consumer products, ranging from medical tubing to automotive
dashboards to bath toys. These phthalates are not tightly held by the plastics and are
released into the environment over time. Congress is concerned about possible
human health effects from exposure to six of these chemicals: di-(2-ethylhexyl)
phthalate (DEHP), dibutyl phthalate (DBP), benzyl butyl phthalate (BBP), diisononyl
phthalate (DINP), diisodecyl phthalate (DIDP), and di-n-octyl phthalate (DnOP).
DEHP, DBP, BBP, and (to less extent) DINP are known to be toxic to the
reproductive systems of rodents. Recent experiments demonstrate that pre-natal
exposure at a sufficient level to these same phthalates disrupts the normal action of
hormones and can cause malformations of the reproductive organs of offspring
(especially males).
Disruption of hormonal functions in humans is known to result in abnormal
reproductive development. Many scientists believe that the phthalates toxic to
rodents might be able to cause similar malformations in humans. However, human
health effects of phthalate exposure have not been conclusively demonstrated. Very
few studies have looked at possible effects in humans, but their results have been
consistent with the results of rodent experiments. More research would be needed
to test this hypothesis. Recent surveys have found almost universal exposure to
phthalates. Individuals may be exposed to high enough levels of phthalates to cause
reproductive abnormalities. Scientists at the National Toxicology Program have
expressed “serious concern” about human male infants undergoing intensive medical
procedures, and “concern” about development of human males less than a year old
who are exposed to DEHP. In light of these concerns, the National Academy of
Sciences is evaluating the risk of aggregate human exposure to multiple phthalates.
Federal agencies have taken several actions, some as early as the mid 1980s, to
evaluate and regulate phthalates, but no product to date has been banned outright.
The agency responsible for regulating toys and most other child-care products is the
Consumer Product Safety Commission (CPSC). In March 2008, the Senate approved
an amendment to H.R. 4040, the Consumer Product Safety Commission Reform
Act, that would restrict the use of six phthalates in toys and child-care products. The
House version has no phthalate amendment. Thus, conferees are to determine the fate
and form of the phthalate provisions.
The scientific basis for concerns about human health risks appears to be strong
in the case of some phthalates (such as DEHP), adequate with respect to others
(perhaps DINP), and weak for the remaining chemicals (for example, DIDP and
DnOP). The strongest evidence with respect to developmental effects has been
produced since about the year 2000. The Senate amendment would codify the
voluntary agreements reached by CPSC with product manufacturers and reduce
exposure to one particular phthalate. New formulations for toys and child-care
products may pose greater or fewer risks than current formulations.

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Contents
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Health Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Human Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
The Six Phthalates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Di-(2-ethylhexyl) phthalate (DEHP) . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Dibutyl phthalates (DBP) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Benzyl butyl phthalate (BBP or sometimes BzBP) . . . . . . . . . . . . . . . . 6
Diisononyl phthalate (DINP) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
Diisodecyl phthalate (DIDP) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
Di-n-octyl phthalate (DnOP) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
Federal Evaluation and Regulation of Phthalates . . . . . . . . . . . . . . . . . . . . 10
Food and Drug Administration (FDA) . . . . . . . . . . . . . . . . . . . . . . . . . 11
Consumer Product Safety Commission . . . . . . . . . . . . . . . . . . . . . . . . 13
Regulation in the European Union (EU) and the States . . . . . . . . . . . . . . . . 14
European Union . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14
States . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16
Proposed Legislation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18
Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19
Scientific Basis for Health Concerns . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19
Would the Amendment Reduce the Risks Without Generating
Greater Risks? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

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Phthalates in Plastics and
Possible Human Health Effects
Introduction
“Phthalates”1 refers to a group of chemical compounds that are heavily
produced and widely used to make the plastics found in thousands of consumer
products. The most common use of phthalates is to increase the flexibility of
polyvinyl chloride (PVC) and polyvinylidene chloride (PVDC) polymers. Phthalates
are released from those products over time, and are dispersed to the air, water, soil,
and living things. Some (but not all) of these phthalates are known to cause
reproductive damage in rodents. Recent interest by governmental bodies, including
Congress, in the potential adverse human health effects that might be related to
phthalate exposure has focused on six phthalates that are produced and used in very
large quantities.2 The six phthalates are di-(2-ethylhexyl) phthalate (DEHP), dibutyl
phthalate (DBP), benzyl butyl phthalate (BBP), diisononyl phthalate (DINP),
diisodecyl phthalate (DIDP), and di-n-octyl phthalate (DnOP). The Senate version
of H.R. 4040, the Consumer Product Safety Commission Reform Act, as amended,
would restrict the use of these chemical compounds in products made for children.
The bill is in conference.
Background
Health Effects
Compared to some other chemicals in commerce, phthalates are not extremely
toxic. That is, they do not cause acute illness after a short period of low-level
exposure. However, controlled experiments with rodents have demonstrated that
some phthalates3 at high doses damage reproduction and development.4 Moreover,
1 The ph is silent.
2 A high-production-volume chemical is defined by the U.S. Environmental Protection
Agency as a chemical produced in amounts exceeding 1 million pounds annually. Hundreds
of millions of pounds of phthalates are produced annually in the United States.
3 Di-(2-ethylhexyl) phthalate, dibutyl phthalate, and benzyl butyl phthalate.
4 A high dose is relative and varies depending on the chemical. For DEHP, for example, a
high dose might be considered to be roughly more than 100 milligrams of phthalate (mg) per
kilogram of the exposed animal’s body weight (kg) per day.

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if administered at sufficient levels5 and at the appropriate time to pregnant females,
some phthalates can cause malformations of the reproductive organs of offspring,
especially males.6 In rats, exposure during gestation to some phthalates can cause
testicular cancer in mature offspring.7 The higher the phthalate exposure, the more
frequent and severe are the effects on the reproductive system. Rat fetuses are most
susceptible, but older rats can also be affected at somewhat higher levels of
exposure.8
Disruption of hormonal functions in humans is known to result in abnormal
reproductive development. Many scientists believe that the phthalates toxic to rats
and mice might be able to cause similar malformations in humans, because the male
hormones affected by phthalates are important to the normal development of the male
reproductive tract in all species of mammals. However, human health effects of
phthalate exposure have not been conclusively demonstrated. Very few studies have
looked at possible effects in humans,9 but their results have been consistent with the
results of rodent experiments. A study published in 2005 provided the first evidence
5 For example, 14-23 milligrams of DEHP per kilogram of body weight per day.
6 Gray, Jr., L. Earl, Joseph Ostby, Johnathan Furr, et al. 2000. Perinatal exposure to the
phthalates DEHP, BBP, and DINP, but not DEP, DMP, or DOTP, alters sexual
differentiation of the male rat. Toxicological Sciences, v. 58, n. 2, p. 350-365.
Mylchreest, E., R.C. Cattley, and P. M. Foster. 1998. Male reproductive tract malformations
in rats following gestational and lactational exposure to Di(n-butyl) phthalate: an
antiandrogenic mechanism? Toxicological Sciences, v. 43, n. 1, p. 47-60.
Parks, Louise G., Joe S. Ostby, Christy R. Lambright, et al. 2000. The plasticizer
diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis
during sexual differentiation in the male rat. Toxicological Sciences, v. 58, p. 339-349.
Wilson, Vickie S., Christy Lambright, Johnathan Furr, et al. 2004. Phthalate ester-induced
gubernacular lesions are associated with reduced ins13 gene expression in the fetal rat testis.
Toxicology Letters, v. 146, p. 207-215.
7 Fisher, Jane S., S. Macpherson, N. Marchetti, et al. 2003. Human ‘testicular dysgenesis
syndrome’: a possible model using inutero exposure of the rat to dibutyl phthalate. Human
Reproduction, v. 18, n. 7, p. 1383-1394.
8 Ibid.
U.S. Congress. House of Representatives. Committee on Energy and Commerce,
Subcommittee on Commerce, trade, and consumer Protection. Hearing on Safety of
Phthalates and Bisphenol-A in Everyday Consumer Products. June 10, 2008. Written
testimony of Leon Earl Gray, Jr., Senior Reproductive Biologist and Toxicologist, U.S.
EPA.
9 Main, Katharina M., Gerda K. Mortensen, Marko M. Kaleva, et al. 2006. Human breast
milk contamination with phthalates and alterations of endogenous reproductive hormones
in infants three months of age. Environmental Health Perspectives, v. 114, p. 270-276.
Swan, Shanna H., Katharina M. Main, Fan Liu, et al. 2005. Decrease in anogenital distance
among male infants with prenatal phthalate exposure. Environmental Health Perspectives,
v. 113, n. 8, p. 1056-1061.

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of subtle developmental effects, similar to those seen in animal studies, in human
male infants exposed prenatally to breakdown products of phthalates.10 More
research would be needed to determine with certainty the effects of phthalates in
humans. Additional information about health effects is provided below in the section
“The Six Phthalates.”
Human Exposure
Results of the National Health and Nutrition Examination Survey (NHANES)
indicated almost universal American exposure to low levels of the most common
phthalates, usually multiple phthalates.11 Women tend to have greater exposure than
men, but children appear to be the group most exposed to DEHP, DBP, and BBP.
Children also are more exposed to DnOP, but these exposures appear to be lower
than those for DEHP, di-n-butyl phthalate, and BBP. Levels of a breakdown product
of DINP were not detectable in children surveyed (but see section below on DINP)
and DIDP was not measured in 2001-2002.12 Studies of amniotic fluid have also
documented exposure to multiple phthalates for human fetuses.13 More generally,
babies may be the most heavily exposed group.14
Phthalates are dispersed throughout the air, water, soil, and living things in the
developed world. According to the Department of Health and Human Services
(DHHS), food probably is the major source of exposure to some phthalates for the
general population.15,16 However, air also appears to be important.17 For the human
fetus, maternal exposure leads to prenatal exposure through the placenta. Personal
care items, including baby lotion and powder, may be significant sources of exposure
for infants.18 For some individuals, certain medications also may be important
10 Swan et al. 2005.
11 DHHS. 2005. Third National Report on Human Exposure to Environmental Chemicals.
p. 253. [http://www.cdc.gov/exposurereport/pdf/thirdreport.pdf].
12 Ibid., p. 282.
13 Silva, M.J., J.A. Reidy, A.R. Herbert, et al. 2004. Detection of phthalate metabolites in
human amniotic fluid. Bulletin of Environmental Contamination and Toxicology, v. 72, p.
1226-1231.
14 Wormuth, Matthias, Martin Scheringer, Meret Vollenweider, et al. 2006. What are the
sources of exposure to eight frequently used phthalic acid esters in Europeans? Risk
Analysis, v. 26, n. 3, p. 803-824.
15 DHHS, ibid., p. 253.
16 Fromme, H., L. Gruber, M. Schlummer, et al. 2007. Intake of phthalates and di-(2-
ethhylhexyl) adipate: results of the integrated exposure assessment survey based on
duplicate diet samples and biomonitoring data. Environment International, v. 33, n. 8, p.
1012-1020.
17 Adibi, Jennifer J., Robin M. Whyatt, Paige L. Williams, et al. 2008. Characterization of
phthalate exposure among pregnant women assessed by repeat air and urine samples.
Environmental Health Perspectives, v. 116, n. 4, p. 467-473.
18 Sathyanarayana, S. C.J. Karr, P. Lozano, et al. 2008. Baby care products: possible sources
(continued...)

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sources.19 Finally, medical devices may dominate exposure sources for critically ill
patients. Individuals, such as newborns in intensive care, may be exposed to levels
of DEHP much closer to, but still less than 1% of, levels that cause reproductive
harm in rats.20
Phthalates do not bioaccumulate in the body or the environment; rather they
break down rapidly. However, exposure to phthalates is continuous and substantial
in the modern world.21
The Six Phthalates
The Senate bill would require regulation of six phthalates, following the
example of the European Union and the state of California. They differ from one
another in structure, uses, and toxicities. The extent to which they have been studied
varies widely. Compared to the other commercially produced phthalates, these six,
arguably, are more studied, more toxic, or more prevalent in consumer products and
the environment. All six have been evaluated by the National Toxicology Program
(NTP), an interagency program administered through the National Institute of
Environmental Health Sciences/National Institutes of Health (NIEHS/NIH).22
Di-(2-ethylhexyl) phthalate (DEHP). DEHP is the most abundantly
produced and the most studied phthalate.23 It is used primarily to improve the
18 (...continued)
of infant phthalate exposure. Pediatrics, v. 121, n. 2, p. e260-268.
19 Hauser, Russ, Susan Duty, Linda Godfrey-Bailey, et al. 2004. Medications as a source
of human exposure to phthalates. Environmental Health Perspectives, v. 112, n. 6, p. 751-
753.
20 Weuve, Jennifer, Brisa N. Sanchez, Antonia M. Calafat, et al. 2006. Exposure to
phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and
oxidative metabolites. Environmental Health perspectives, v. 114, n. 9., p. 1424-1431.
Calafat, Antonia M., Larry L. Needham, Manori J. Silva, et al. 2004. Exposure to di-(2-
ethylhexyl) phthalate among premature neonates in a neonatal intensive care unit.
Pediatrics, v. 113, n. 5., p. e429-e434.
21 Silva, Manori J., E. Samandar, J.L. Preau, Jr., et al. 2007. Quantification of 22 phthalate
metabolites in human urine. Journal of Chromatography. B, Analytical Technologies in the
Biomedical and Life Sciences, v. 860, n. 1, p. 106-112.
22 Center for the Evaluation of Risks to Human Reproduction (CERHR), National
Toxicology Program, DHHS. “CERHR Chemicals.” [http://cerhr.niehs.nih.gov/chemicals/
index.html].
23 For example, some important scientific studies include Akingbemi, Benson T., Renshan
Ge, Gary R. Klinefelter, et al., 2004, Phthalate-induced Leydig cell hyperplasia is
associated with multiple endocrine disturbances, Proceedings of the National Academy of
Sciences, v. 101, n. 3, p. 775-780; Gray, Jr., L. Earl, Joseph Ostby, Johnathan Furr, et al.,
2000, Perinatal exposure to the phthalates DEHP, BBP, and DINP, but not DEP, DMP, or
DOTP, alters sexual differentiation of the male rat, Toxicological Sciences, v. 58, n. 2, p.
350-365; Lin, H., Renshan S. Ge, Gary R. Chen, et al., 2008, Involvement of testicular
(continued...)

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flexibility of “vinyl” (that is, polyvinyl chloride (PVC) plastic). DEHP is found in
medical devices, such as plastic tubing used for catheters and intravenous drug and
fluid delivery, and many home and garden products. The NTP has expressed
“serious concern24 that certain intensive medical treatments of male infants may
result in DEHP exposure levels that adversely affect development of the male
reproductive tract.”25 In addition, the NTP expressed “concern for effects of DEHP
exposure on development of the male reproductive tract for infants less than one year
old,” “some concern for effects of DEHP exposure on development of the
reproductive tract of male children older than one year,” and also some concern for
developmental effects for the offspring of pregnant women.26 After this DEHP
monograph was issued, several studies began to explore associations between DEHP
and other health effects, such as effects on thyroid hormone levels, asthma, and
obesity.27 Additional research is warranted in these areas and it is too soon to draw
any conclusions regarding the potential role of DEHP in causing such problems.
Dibutyl phthalates (DBP). There are two DBPs: di-n-butyl and di-isobutyl
phthalate. The former is more studied, especially in Europe. DBPs are used in latex
adhesives, nail polish, cosmetics, some inks and dyes, insecticides, and
pharmaceutical coatings. The most recent NTP monograph on DBP (di-n-butyl
23 (...continued)
growth factors in fetal Leydig cell aggregation after exposure to phthalate in utero,
Proceedings of the National Academy of Sciences of the United States of America, v. 105,
n. 290, p.7218-7222; Parks, Louise G., Joe S. Ostby, Christy R. Lambright, et al., 2000, The
plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone
synthesis during sexual differentiation in the male rat, Toxicological Sciences, v. 58, p. 339-
349; Swan, Shanna H., Katharina M. Main, Fan Liu, et al., 2005, Decrease in anogenital
distance among male infants with prenatal phthalate exposure, Environmental Health
Perspectives, v. 113, n. 8, p. 1056-1061; and Wilson, Vickie S., Christy Lambright,
Johnathan Furr, et al., 2004, Phthalate ester-induced gubernacular lesions are associated
with reduced ins13 gene expression in the fetal rat testis, Toxicology Letters, v. 146, p. 207-
215.
24 The expression of “serious concern” is the greatest level of concern on a qualitative scale
used by NTP. In order, from greatest to least, the levels of concern are: serious concern,
concern, some concern, minimal concern, and negligible concern.
25 Center for the Evaluation of Risks to Human Reproduction, National Toxicology Program,
U.S. Department of Health and Human Services. NTP-CERHR Monograph on the Potential
Human Reproductive and Developmental Effects of Di(2-Ethylhexyl) Phthalate (DEHP).
NIH Publication No. 06-4476. November 2006. p. vii-viii. [http://cerhr.niehs.nih.gov/
chemicals/dehp/DEHP-Monograph.pdf].
26 Ibid.
27 For example, see Meeker, John D., Antonia M. Calafat, and Russ Hauser, 2007, Di(2-
ethylhexyl) phthalate metabolites may alter thyroid hormone levels in men, Environmental
Health Perspectives, v. 115, n. 7, p. 1029-1034; Stahlhut, R.W., E. van Wijngaarden, T.D.
Dye, et al., 2007, Concentrations of urinary phthalate metabolites are associated with
increased waist circumference and insulin resistance in adult U.S. males, Environmental
Health Perspectives, v. 115, n. 6, p. 876-882; Jaakkola, Jouni J.K., and Trudy L. Knight,
2008, The role of exposure to phthalates from polyvinyl chloride products in the
development of asthma and allergies: a systematic review and meta-analysis, Environmental
Health Perspectives, v. 116, n. 7, p. 845-853.

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phthalate) found “clear evidence of adverse effects” on the developing male
reproductive tract in rodents.28 Furthermore, the NTP concluded, “Based on recent
data ... the NTP believes it is reasonable and prudent to conclude that the results
reported in laboratory animals indicate a potential for similar or other adverse effects
in humans.”29 As a result, NTP has “some concern for DBP causing adverse effects
to human development, particularly development of the male reproductive system.”30
In the seven years since this NTP monograph, numerous studies have bolstered these
findings.31 Of particular note is the study by Lehmann et al. (2004).32 It established
the relationship between exposure to DBP and effects on synthesis of testosterone in
fetal male rats. A 2006 study found that di-isobutyl phthalate had testicular and
developmental effects similar to di-n-butyl phthalate and DEHP.33
Benzyl butyl phthalate (BBP or sometimes BzBP). BBP is used in vinyl
flooring, automotive trim, food conveyor belts, and artificial leather. The latest NTP
monograph on BBP was released in 2003, but was based on papers published before
2001. NTP determined that the evidence from animal studies was clear that adverse
developmental effects could result from exposure to BBP.34 However, effects were
28 Ibid. p.2.
29 Center for the Evaluation of Risks to Human Reproduction, National Toxicology Program,
U.S. Department of Health and Human Services. NTP-CERHR Monograph on the Potential
Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). 2001. p.
4. [http://cerhr.niehs.nih.gov/chemicals/phthalates/dbp/DBP_Monograph_Final.pdf].
30 Ibid. p. 2.
31 For example, see Barlow, N.J., B.S. McIntyre, and P.M. Foster, 2004, Male reproductive
tract lesions at 6, 12, and 18 months of age following in utero exposure to di(n-butyl)
phthalate, Toxicologic Pathology, v. 32, n. 1, p. 79-90; Fisher, Jane S., S. Macpherson, N.
Marchetti, et al., 2003, Human ‘testicular dysgenesis syndrome’: a possible model using
in-utero exposure of the rat to dibutyl phthalate, Human Reproduction, v. 18, n. 7, p. 1383-
1394; Mahood, I. Kim, Nina Hallmark, Chris McKinnell, et al., 2005, Abnormal Leydig cell
aggregation in the fetal testis of rats exposed to di(n-butyl) phthalate and its possible role
in testicular dysgenesis, Endocrinology, v. 146, p. 613-623; Thompson, Christopher J.,
Susan M. Ross, and Kevin W. Gaido, 2004, Di(n-butyl) phthalate impairs cholesterol
transport and steroidogenesis in the fetal rat testis through a rapid and reversible mechanism,
Endocrinology, v. 145, p. 1227-1237; Wilson, Vickie S., Christy Lambright, Johnathan
Furr, et al., 2004, Phthalate ester-induced gubernacular lesions are associated with reduced
ins13 gene expression in the fetal rat testis, Toxicology Letters, v. 146, p. 207-215; and
Zhang,Y., X. Jiang, and B. Chen, 2004, Reproductive and developmental toxicity in F1
Sprague-Dawley male rats exposed to di-n-butyl phthalate in utero and during lactation and
determination of its NOAEL, Reproductive Toxicology, v. 18, n. 5, p. 669-676.
32 Lehmann, Kim P., Suzanne Phillips, Madhabananda Sar, et al. 2004. Dose-dependent
alterations in gene expression and testosterone synthesis in the fetal testes of male rats
exposed to di-(n-butyl) phthalate. Toxicological Sciences, v. 81, p. 60-68.
33 Borch, J., M. Axelstad, A.M. Vinggaard, et al. 2006. Diisobutyl phthalate has comparable
anti-androgenic effects to di-n-butyl phthalate in fetal rat testis. Toxicology letters, v. 163,
n. 3, p. 183-190.
34 Center for the Evaluation of Risks to Human Reproduction, National Toxicology Program,
U.S. Department of Health and Human Services. NTP-CERHR Monograph on the Potential
(continued...)

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seen only at high levels of BBP exposure and estimated human exposure was much
lower, although detailed exposure data were lacking. NTP concluded that it had
minimal concern for fetal and infant developmental effects due to estimated BBP
exposure.35 Papers published after 2001 confirm the developmental toxicity of
BBP.36 However, the testimony of Leon Earl Gray, Jr., Senior Reproductive biologist
and Toxicologist with the U.S. Environmental Protection Agency, indicated that
DEHP, DBP (both forms), and BBP were equivalent in toxicity, based on four
studies.37
Diisononyl phthalate (DINP). This phthalate is used primarily to improve
the flexibility of plastics in such products as gloves, drinking straws, garden hoses,
and toys. It has been used to replace DEHP in toys and other applications. DINP is
the most commonly used phthalate for toys, according to the Phthalate Esters Panel
of the American Chemistry Council, a trade group representing chemical
manufacturers.38 The NTP monograph on DINP was published in 2003, but like the
other monographs that have not been updated, it primarily considers research
published before 2001. The scientific evidence for developmental effects from DINP
exposure of rodents is adequate “to conclude that DINP might adversely affect
34 (...continued)
Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). NIH
Publication No. 03-4487. March 2003. p. 2. [http://cerhr.niehs.nih.gov/chemicals/phthalates/
bb-phthalate/BBP_Monograph_Final.pdf].
35 Ibid. p. 4.
36 Wilson, Vickie S., Christy Lambright, Johnathan Furr, et al. 2004. Phthalate ester-
induced gubernacular lesions are associated with reduced ins13 gene expression in the fetal
rat testis. Toxicology Letters, v. 146, p. 207-215.
Aso, S. H. Ehara, K. Miyata, et al. 2005. A two-generation reproductive toxicity study of
butyl benzyl phthalate in rats. Journal of Toxicological Sciences, Dec., v. 30, p. 39-58.
37 U.S. Congress. House of Representatives. Committee on Energy and Commerce,
Subcommittee on Commerce, trade, and consumer Protection. Hearing on Safety of
Phthalates and Bisphenol-A in Everyday Consumer Products. June 10, 2008. Written
testimony of Leon Earl Gray, Jr., Senior Reproductive Biologist and Toxicologist, U.S.
EPA.
The studies referenced by Dr. Gray were: Gray, Jr., L. Earl, Joseph Ostby, Johnathan Furr,
et al., 2000, Perinatal exposure to the phthalates DEHP, BBP, and DINP, but not DEP,
DMP, or DOTP, alters sexual differentiation of the male rat, Toxicological Sciences, v. 58,
n. 2, p. 350-365; Hotchkiss, A.K., L.G. Parks-Saldutti, J.S. Ostby, et al. 2004, A mixture of
the ‘antiandrogens’ linuron and butyl benzyl phthalate alters sexual differentiation of the
male rat in a cumulative fashion, Biology of Reproduction, v. 71, n. 6, p. 1852-1861;
Howdeshell, Kembra L., Vickie S. Wilson, Johnathan Furr, et al., 2008, A mixture of five
phthalate esters inhibits fetal testicular testosterone production in the Sprague Dawley rat
in a cumulative, dose additive manner, Toxicological Sciences Advance Access (reprint
received from the author); and Tyl,R.W., C.B, Myers, M.C. Marr, et al., 2004, Reproductive
toxicity evaluation of dietary butyl benzyl phthalate (BBP) in rats, Reproductive Toxicology,
v. 18, n. 2, p. 241-264.
38 American Chemistry Council, Phthalates Panel. Phthalates and children’s toys.
[http://www.phthalates.org/yourhealth/childrens_toys.asp].

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development of the human fetus if the levels of exposure are sufficiently high,”
according to NTP.39 But the evidence for effects was not as strong as for DEHP and
DBP, and in one study that compared the effects of exposure to various phthalates,
DINP was found to be less potent than DEHP or DBP by an order of magnitude.40
In his recent testimony before a House subcommittee, Dr. Leon Earl Gray rated the
relative potency for producing developmental harm of various phthalates. He gave
DINP a rating of 0.15 relative to DEHP, DBP (both forms), and BBP which he rated
1.0.41 A number of studies of the potential effects on rodents of DINP exposure were
published after 2001, but they appear consistent with the earlier work with respect
to developmental toxicity.42 In addition, there is some evidence of enhanced allergic
responses due to DINP exposure.43
A review by the European Commission (EC) in 2006 concluded:
“[i]n light of the divergent scientific views ... and the conclusions of the
assessment of the risk for consumers under this Regulation, and taking into
account the uncertainties in the evaluation of exposure to DINP from toys and
childcare articles, precautionary considerations support the consideration at
Community level of proportionate restrictions ... for the use of DINP in toys and
childcare articles. Such measures should be reviewed after 3-4 years, in light of
further scientific developments.44
39 CERHR, National Toxicology Program, U.S. Department of Health and Human Services.
NTP-CERHR Monograph on the Potential Human Reproductive and Developmental Effects
of Di-isononyl Phthalate (DINP). NIH Publication No. 03-4484. March 2003. p. 2.
40 “Less by an order of magnitude” is roughly equivalent to one-tenth. Gray, Jr., L. Earl,
Joseph Ostby, Johnathan Furr, et al. 2000. Perinatal exposure to the phthalates DEHP,
BBP, and DINP, but not DEP, DMP, or DOTP, alters sexual differentiation of the male rat.
Toxicological Sciences, v. 58, n. 2, p. 350-365.
41 U.S. Congress. House of Representatives. Committee on Energy and Commerce,
Subcommittee on Commerce, trade, and consumer Protection. Hearing on Safety of
Phthalates and Bisphenol-A in Everyday Consumer Products. June 10, 2008. Written
testimony of Leon Earl Gray, Jr., Senior Reproductive Biologist and Toxicologist, U.S.
EPA.
42 For example, Borch, J., O. Ladefoged, U. Hass, et al., 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, Reproductive Toxicology, v. 18, n. 1, p.
53-61; and Wenzel, A., C. Franz, E. Breous, et al., 2005, Modulation of iodide uptake by
dialkyl phthalate plasticisers in FRTL-5 rat thyroid follicular cells, Molecular and Cellular
Endocrinology, v. 244, n. 1-2, p.63-71.
43 Lee, M.H., J. Park, S.W. Chung, et al. 2004. Enhancement of interleukin-4 production
in activated CD4+ T cells by diphthalate plasticizers via increased NF-AT binding activity.
International Archives of Allergy and Immunology, v. 134, n. 3, p. 213-222.
44 European Commission. Commission Communication on the results of the risk evaluation
and the risk reduction strategies for the substances: Dibutylphthalate; e,4-Dichloroaniline;
Di-isodecyl phthalate; 1,2-Benzenedicarboxylic acid, di-c9-11-branched alkyl esters, c9-
rich; Ethylenediaminetetraacetate; Methyl acetate; Monochloroacetic acid; n-Pentane;
Tetrasodium ethylenediaminetetraacetate. Official Journal of the European Union. April
13, 2006. Available through Eur-Lex at [http://eur-lex.europa.eu/LexUriServ/LexUriServ.
do?uri=OJ:C:2006:090:0004:0028:EN:PDF].

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Several studies have been conducted to estimate the level of exposure of
children to DINP in toys due to mouthing. One study by the Consumer Product
Safety Commission (CPSC) estimated DINP exposure through measurement of the
time children spent in mouthing behavior and an analysis of DINP movement out of
various toys.45 NTP used that data to conclude that its concern was “minimal” for
developmental effects in children.46 NTP also had minimal concern for DINP
causing adverse effects to human reproduction or fetal development.47 However, this
conclusion was controversial.48 A Japanese study also looked at DINP release from
toys and and time spent mouthing and found considerably higher exposures than the
CPSC.49
As mentioned above, it appeared from the NHANES that exposure to DINP was
negligible in children surveyed by the Centers for Disease Control and Prevention
(CDC) in 2001-2002.50 However, this result was based on measurement of the
metabolite monoisononyl phthalate (MINP), the traditional measure of exposure to
DINP. A recent study of how the human body processes DINP found that MINP is
a minor metabolic product, while mono(carboxyisooctyl) phthalate (MCIOP),
mono(oxoisononyl) phthalate (MOINP), and mono(hydroxyisononyl) phthalate
(MHINP) are the major metabolites in DINP-dosed rats.51 The authors of this study
concluded that estimates of exposure to DINP might be underestimates if based on
MINP levels.
Diisodecyl phthalate (DIDP). DIDP is another plasticizer used primarily in
electrical cords, leather for car interiors, and PVC flooring. As for the other
phthalates addressed by the NTP, the expert panel found “no direct evidence that
exposure of people to DIDP adversely affects reproduction or development”
[emphasis added], but “studies with rats have shown that exposure to DIDP can cause
adverse developmental effects.”52 NTP concluded that exposures to DIDP were
45 Babich, M.A., S.B. Chen, M.A. Greene, et al. 2004. Risk assessment of oral exposure to
diisononyl phthalate from children’s products. Regulatory Toxicology and Pharmacology,
v. 40, n. 2, p. 151-167.
46 CERHR, p. 3.
47 Ibid.
48 Shea, K.M. 2003. Pediatric exposure and potential toxicity of phthalate plasticizers.
Pediatrics, v. 111, n. 6, Pt 1, p. 1467-1474.
49 Sugita, T., Y. Kawamura, M. Tanimura, et al. 2003. Estimation of daily oral exposure to
phthalates derived from soft polyvinyl chloride baby toys. Shokuhin eiseigaku zasshi.
Journal of the Food Hygienic Society of Japan, v. 44, n. 2, p. 96-102.
50 DHHS, ibid., p. 282.
51 Silva, M.J., J.A. Reidy, J.L. Preau, Jr., et al. 2006. Oxidative metabolites of diisononyl
phthalate as biomarkers for human exposure assessment. Environmental Health Perspectives
v. 114, n. 8, p. 1158-61.
52 Center for the Evaluation of Risks to Human Reproduction, National Toxicology Program,
U.S. Department of Health and Human Services. NTP-CERHR Monograph on the Potential
Human Reproductive and Developmental Effects of Di-isodecyl Phthalate (DIDP). NIH
(continued...)

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probably not high enough to cause concern, and that scientists had minimal concern
for developmental effects in fetuses and children.53 NTP also found that DIDP would
not adversely affect human reproduction.54 Studies published since 2001 have not
conflicted with the NTP conclusions. However, several recent studies have found
endocrine-disrupting effects following rodent exposure to DIDP.55
Di-n-octyl phthalate (DnOP). DnOP is used primarily to improve the
flexibility of plastics. DnOP is found in mixtures of phthalates that are used to make
flooring, tarps, pool liners, bottle cap liners, conveyor belts, and garden hoses. There
are few studies on which to evaluate the potential toxicity or exposure to DnOP.
NTP found limited evidence that DnOP might cause developmental effects in highly
exposed rodents.56 No evidence of reproductive effects was found in the available
studies.57 NTP concluded that it had negligible concern for effects on adult
reproductive systems, but it was unable to form an opinion on an appropriate level
of concern with respect to developmental risks, due to the lack of available exposure
data and lack of toxicity data for exposure levels that might have relevance for
human exposure.58 An online search by CRS of publications using Medline revealed
no new studies after 2001 that might better inform a risk evaluation.
Federal Evaluation and Regulation of Phthalates59
Depending on use, phthalates are potentially regulated by various regulatory
agencies, including the Environmental Protection Agency (EPA), the Occupational
Safety and Health Administration (OSHA), the Food and Drug Administration
52 (...continued)
Publication No. 03-4485. April 2003. p. 1.
53 Ibid. p. 3.
54 Ibid.
55 Wenzel, A., C. Franz, E. Breous, et al. 2005. Modulation of iodide uptake by dialkyl
phthalate plasticisers in FRTL-5 rat thyroid follicular cells. Molecular and Cellular
Endocrinology, v. 244, n. 1-2, p.63-71.
Turan, N., R.H. Waring, and D.B. Ramsden. 2005. The effect of plasticisers on “sulphate
supply” enzymes. Molecular and Cellular Endocrinology, v. 244, n. 1-2, p. 15-19.
Harris, R., N. Turan, C. Kirk, et al. 2007. Effects of endocrine disruptors on
dehydroepiandrosterone sulfotransferase and enzymes involved in PAPS synthesis: genomic
and nongenomic pathways. Environmental Health Perspectives, v. 115, Supp. 1, p. 51-54.
56 Center for the Evaluation of Risks to Human Reproduction, National Toxicology Program,
U.S. Department of Health and Human Services. NTP-CERHR Monograph on the Potential
Human Reproductive and Developmental Effects of Di-n-octyl Phthalate (DnOP). NIH
Publication No. 03-4488. May 2003. p. 1.
57 Ibid.
58 Ibid. p. 3.
59 This section was written by Sarah A. Lister, Specialist in Public Health and Epidemiology,
Domestic Social Policy Division.

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(FDA), and the Consumer Product Safety Commission (CPSC). EPA regulates
various phthalates released to the environment under most of its statutes. For
example, DEHP is regulated as a hazardous air pollutant, a drinking water
contaminant, a water pollutant, and a hazardous waste. OSHA regulates worker
exposure to phthalates.
The current focus of congressional concern, however, is federal regulation of
consumer products from which phthalates might be released. Federal agencies have
taken several actions, some as early as the mid 1980s, to evaluate and regulate
phthalates. For example, EPA has required manufacturers of phthalates to conduct
certain tests to better inform federal regulators. These test orders were withdrawn in
1996, when EPA determined that it had received the necessary information (which
focused at the time on carcinogenic potential). To date, however, no phthalate-
containing product has been banned outright.
Food and Drug Administration (FDA). FDA-regulated products that may
contain phthalates include (1) medical devices; (2) food contact substances, such as
plastic wrap;60 and (3) cosmetics. FDA reported in June 2008 that, in tandem with
its review of the safety of bisphenol A (BPA) in the products it regulates,61 it is also
conducting a comprehensive inventory of regulated products that contain phthalates.62
FDA regulates a wide variety of medical devices in commerce. Many of these
products are made of, or contain PVC. These include intravenous fluid bags and
lines, tubing used for procedures such as cardiac bypass and dialysis, and indwelling
medical devices, such as peripherally inserted central catheters, or “PICC lines.”
According to reports, phthalates in tubing can leach into the fluids they contain and
pass into the body, and can leach directly from indwelling devices. In 2001, FDA
completed a safety assessment of DEHP, which was the softener most commonly
used in PVC-containing medical devices.63 The assessment underpinned a public
health notification in 2002 in which FDA identified a number of medical procedures
that posed the highest risk of exposure to DEHP, and recommended the use of
alternatives to DEHP-containing medical devices if these procedures were to be
performed on high-risk individuals.64 Depending on the procedure, these individuals
include infants, boys, pregnant or nursing women, and, for some procedures, healthy
60 Manufacturers maintain that phthalates are not used in food wrap in the United States. See
the trade group website [http://www.phthalates.org/pdfs/Phthalates_mvf.pdf].
61 See CRS Report RS22869, Bisphenol A (BPA) in Plastics and Possible Human Health
Effects, by Linda-Jo Schierow and Sarah A. Lister.
62 Statement of Norris Alderson, Ph.D., FDA Associate Commissioner for Science, before
the Subcommittee on Commerce, Trade and Consumer Protection, House Committee on
Energy and Commerce, hearing on “Safety of Phthalates and Bisphenol A in Everyday
Consumer Products,” June 10 , 2008, 110th Cong., 2nd sess., Washington, DC, hereafter
referred to as FDA testimony.
63 FDA, “Safety Assessment of Di(2-ethylhexyl)phthalate (DEHP) Released from PVC
Medical Devices,” undated, at [http://www.fda.gov/cdrh/ost/dehp-pvc.pdf].
64 FDA, “FDA Public Health Notification: PVC Devices Containing the Plasticizer DEHP,”
July 12, 2002, at [http://www.fda.gov/cdrh/safety/dehp.html].

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adults. FDA recommended, however, that needed medical procedures not be
deferred solely because of concerns about DEHP exposure.
Phthalates are not added to foods directly, but are regulated by FDA as food
contact substances or indirect food additives, where they are components of
packaging that may leach into foods or beverages. FDA permits the use of a variety
of phthalates for these purposes.65 In recent congressional testimony, FDA reported
that:
[FDA] has recently established a Phthalate Task Group (PTG) to review all
available use and toxicology information associated with phthalate exposure
from food contact use and to better characterize any potential risk from these
uses. The primary focus of the PTG will be to determine the most realistic
exposure estimation and risk associated with phthalate use in food packaging.
The PTG will review and address past studies on phthalates and any new
information available. If our review indicates that existing data no longer
supports the continued safe use of these materials in food contact material, FDA
will take appropriate regulatory action to remove these materials from the
marketplace.66
Under the authority of the Federal Food, Drug, and Cosmetic Act (FFDCA),
FDA regulates the safety of cosmetics and personal care products, such as nail polish,
shampoo and lotions,67 many of which contain phthalates. Cosmetic products and
ingredients are not subject to FDA premarket approval, but FDA can prohibit the
marketing of a cosmetic product if it is adulterated, meaning, among other things,
that it contains “any poisonous or deleterious substance which may render it injurious
to users” under labeled or customary conditions of use.68 According to FDA, the
principal phthalates used in cosmetic products are DBP, dimethylphthalate (DMP),
and diethylphthalate (DEP). FDA reports that at the present time, it “does not have
compelling evidence that phthalates, as used in cosmetics, pose a safety risk. ...,” but
that it is conducting a survey of phthalate levels in certain cosmetic products to more
65 For example, a search for “phthalate” in FDA’s regulations at [http://www.accessdata.fda.
gov/scripts/cdrh/cfdocs/cfcfr/cfrsearch.cfm] yields almost two dozen approved phthalates,
including DEHP, in adhesives used for food packaging.
66 FDA testimony. FDA’s definition of safety with respect to food additives and food
contact substances is that “there is a reasonable certainty in the minds of competent
scientists that the substance is not harmful under the intended conditions of use.” 21 CFR
§ 170.3(i).
67 “Cosmetic” is defined as “ (1) articles intended to be rubbed, poured, sprinkled, or sprayed
on, introduced into, or otherwise applied to the human body or any part thereof for
cleansing, beautifying, promoting attractiveness, or altering the appearance, and (2) articles
intended for use as a component of any such articles; except that such term shall not include
soap.” Federal Food, Drug, and Cosmetic Act (FFDCA) section 201(i); [21 U.S.C. 321(i)].
For more information, see FDA, “Cosmetics: FDA Authority and Policy,” at [http://www.
cfsan.fda.gov/~dms/cos-pol.html].
68 FFDCA section 601; 21 U.S.C. 361.

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accurately assess infant exposure.69 Under the authority of the Fair Packaging and
Labeling Act (Public Law 89-755), FDA requires that retail cosmetic products carry
ingredient labels, which would include phthalates. However, the listing of individual
fragrance ingredients, which may contain phthalates, is not required.70
Consumer Product Safety Commission. The Consumer Product Safety
Commission (CPSC) may regulate phthalates in consumer products, including toys
and other children’s products, under either the Federal Hazardous Substances Act
(FHSA, 15 U.S.C. §§1261 et seq.) or the Consumer Product Safety Act (CPSA, 15
U.S.C. §§2051 et seq.), two of the statutes which it administers and enforces.
Consumer products as defined in the CPSA does not include food, drugs, medical
devices, and cosmetics, which fall under the jurisdiction of the FDA. The FDA has
jurisdiction over food containers with regard to substances that may leach into food
from the container. CPSC has jurisdiction with regard to other defects, such as
shattering or choking hazards. It also has jurisdiction over toys, children’s furniture
such as cribs, car seats, pacifiers and teething rings, and other children’s consumer
products.
Although the CPSC may regulate phthalates under either the CPSA or the
FHSA, if it chooses to promulgate safety standards pursuant to the CPSA for a
product that may be regulated under the FHSA, it must promulgate a rule finding that
it is in the public interest to regulate the risk of injury under the CPSA.71 Since the
CPSA and the FHSA differ with regard to the rule-making procedures, the precise
nature of the acts prohibited with regard to products or substances that fail to comply
with safety standards, and other issues, there are advantages and disadvantages to
promulgating standards under the CPSA versus the FHSA. For example, injunctive
enforcement authority for States attorneys general is expressly provided by the
FHSA, but not by the CPSA; the apparent ambiguity of the CPSA on this point has
led to clarifying provisions in both the Senate and House versions of H.R. 4040, the
CPSC reform legislation now in conference. Therefore, if a phthalates standard were
to be promulgated under the FHSA, States attorneys general would have the authority
to enjoin violations of the federal standard, whereas arguably they would not have
similar authority to enforce a similar standard under the CPSA.
Additionally, critics allege problems with the ability of the CPSC to establish
safety standards in a timely fashion. For example, some assert that the rulemaking
procedures under the CPSA and other acts under the CPSC’s jurisdiction, such as the
FHSA, are unnecessarily onerous, requiring protections beyond those required by the
Administrative Procedures Act. Also, the CPSA requires the CPSC to rely on
voluntary standards where an adequate standard exists with which the industry widely
and substantially complies. The voluntary nature of some safety standards limits the
action which can be taken by the CPSC for violations. Under both the CPSA and the
FHSA, the CPSC may order a recall and/or other remedies for products that violate
69 FDA, “Phthalates and Cosmetic Products,” February 7, 2008, at [http://www.cfsan.fda.
gov/~dms/cos-phth.html].
70 Ibid.
71 CPSA §30(d) (15 U.S.C. §2079).

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a safety standard under the pertinent act and may inspect factories where products
are made.72 Products violating a safety standard may be denied importation.
Although the European Union and some states have enacted safety standards
regarding phthalates in children’s products, as discussed below, the CPSC has not
promulgated such standards. In 1983, the CPSC determined that DEHP in children’s
products might result in substantial exposure of children to an animal carcinogen.73
The CPSC is not permitted to initiate rule-making relating to risks of cancer, birth
defects or gene mutations unless it first establishes a Chronic Hazard Advisory Panel
to study the issue and make recommendations. The panel appointed to study the risks
of DEHP concluded that it could put children at risk of cancer from mouthing of
products containing DEHP. Accordingly, the CPSC worked with the children’s
products industry to reach a voluntary agreement banning the use of DEHP from
pacifiers, rattles, and teethers.74 Although other children’s products were not
included in the agreement between CPSC and the industry, most manufacturers
substituted other phthalates for DEHP in other children’s products. DINP was the
substitute. Despite studies conducted by the industry in the late 1990s linking DINP
to liver toxicity and cancer in rodents, the CPSC concluded that the risk to children
from mouthing children’s products was minimal. However, the CPSC achieved a
voluntary agreement with the industry banning DINP and dioctyl phthalate from
pacifiers and bottle nipples. The CPSC appointed a Chronic Hazard Advisory Panel
on DINP and conducted other studies in response to a petition to initiate rule-making
regarding phthalates in children’s products. The panel concluded in 2001 that DINP
posed a minimal or nonexistent risk of cancer to humans. After further consideration
of the panel report and other studies, in 2003 the CPSC denied the petition to
establish a safety standard for PVC containing phthalates in children’s products
intended for children five years of age and younger.75
Regulation in the European Union (EU) and the States
European Union. Proposed federal legislation and several state statutes
concerning phthalates apparently were modeled on EU laws. Under Council
72 For a general discussion of the statutes administered and enforced by the CPSC, see CRS
Report RL34399, Consumer Product Safety Commission Reform: Senate and House
Versions of H.R. 4040, by Margaret Mikyung Lee.
73 See the discussion of scientific studies for various phthalates above and the discussion of
CPSC actions in Young Children and Plastic Toys and Phthalates in Plastic Toys, 8
Consumer Product Safety Review 3-5 (2003).
74 Although the CPSC has promulgated safety standards for pacifiers and rattles at 15 C.F.R.
parts 1510 and 1511, these primarily concern choking/mechanical hazards, not hazards from
phthalates or other chemical constituents.
75 Denial letter from the CPSC to the National Environmental Trust, dated February 26,
2003, available at [http://www.cpsc.gov/LIBRARY/FOIA/FOIA03/petition/Ageunder.pdf]
(last visited July 11, 2008).

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Directive 76/769/EEC,76 as amended by Council Directive 2005/84/EC,77 the EU
currently prohibits the use (at concentrations greater than 0.1% by mass of the
plasticized material) of DEHP, DBP, and BBP in toys and child-care articles and of
DINP, DIDP, and DnOP in toys and child-care articles that can be mouthed by
children. It also prohibits the sale of toys and child-care articles containing
phthalates at a concentration exceeding the permitted level. It defines “childcare
article” as meaning “any product intended to facilitate sleep relaxation, hygiene, the
feeding of children or sucking on the part of children.”
Council Directive 2005/84/EC notes the existence of Commission Decision
1999/815/EC78 that banned phthalates in toys and child-care articles as a renewable
emergency measure in response to phthalate studies conducted by various Member
States and assessed by the Scientific Committee on Toxicity, Ecotoxicity and the
Environment.79 The language of the Decision differs from that of the Directive in
that it limits the ban on the six phthalates to products that can be mouthed by children
under three years of age, while the Directive does not contain the age limit. This
Decision apparently was last extended in 2004 until September 20, 2005, but Council
Directive 2005/84/EC refers to the Decision as being renewed regularly. Regardless
of whether the Decision continues to be renewed, EU Member States were required
to take necessary measures to comply with the standards described in the Decision,
therefore, those measures would continue in effect. It appears that the Decision may
not have been renewed in anticipation of Council Directive 2005/84/EC and the
Regulation (EC) No. 1907/2006,80 which was recently enacted and will repeal
Council Directive 76/769/EEC effective June 1, 2009, while retaining the same
phthalate in children’s product standard, effective June 1, 2009. The new Regulation
also retains the Directive’s requirement that the European Commission re-evaluate
this standard by January 16, 2010, in light of new scientific information and amend
the standard accordingly, if justified.
While the Directive is binding law on the Member States of the EU, requiring
them to take necessary measures to bring their respective national laws into
compliance with the Directive standards, the new Regulation is directly binding on
the Member States. This means they are obligated to comply with the standard and
enforce it without any implementing legislation or rule at the national level.
76 1976 O.J. (L 262) 201 (originally enacted July 27, 1976).
77 2005 O.J. (L 344) 40 (enacted December 14, 2005). This Directive amended the 1976
Directive to add the restrictions on phthalates in children’s products.
78 O.J. (L 315) 46 (issued December 7, 1999). This Decision in turn was preceded by
Commission Recommendation 98/485/EC of July 1, 1998, O.J. (L 217) 35, inviting Member
States to take measures to ensure a high level of child health protection with regard to child-
care articles and toys intended to be placed in the mouth by children less than three years
of age and made of PVC containing any of the six phthalates.
79 Information received via email communications with the Delegation of the European
Commission in Washington, D.C., July 11, 2008.
80 Arts. 139, 141, Annex XVII.51 & 52, 2006 O.J. (L 396) 1 (enacted December 18, 2006)
(popularly referred to as REACH, the acronym for Registration, Evaluation, Authorisation,
and Restriction of Chemicals).

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One group of phthalates, DEHP, DBP, and BBP, is banned without limitation
because they are classified as reproductive toxicants that present an unacceptable risk
given the general safety requirements of the European Union. The other group,
DINP, DIDP and DnOP, are banned only for products that can be placed in the mouth
by children. Despite inconclusive scientific evidence of harm, these phthalates were
banned under the precautionary principle of the European Union given the potential
risk posed to children.81
States. California, Vermont and Washington have recently enacted legislation
establishing safety standards for phthalate content in children’s articles. These
standards all appear to have been at least partly modeled on current or earlier versions
of the EU regulations. Aside from the age limit specified for the phthalate standard
or for subcategories of children’s products, if any, the existing state statutes do not
define children’s products generally in terms of an age ceiling for “child” or
“children.” Hawaii’s Senate has adopted a resolution requesting the Hawaii
Department of Health to monitor research being conducted regarding the risks posed
by phthalates and bisphenol-A in consumer products and to report recommendations
and proposed legislation before the 2009 legislative session.82 Oregon’s legislature
has adopted a joint memorial urging Congress to regulate phthalates at the federal
level as a substance in cosmetics, personal care products, and children’s toys.83
Additionally, several other states have introduced legislation concerning phthalates.
Beginning January 1, 2009, the California statute84 will prohibit the
manufacture, sale, or distribution in commerce of any toy or child-care article that
contains DEHP, DBP, or BBP in concentrations exceeding 0.1% and of any toy or
child-care article, intended for use by children under three years of age which can be
mouthed, that contains DINP, DIDP or DnOP in concentrations exceeding 0.1%.
The statute requires manufacturers to use the least toxic alternative when replacing
phthalates in such products and also prohibits them from replacing phthalates with
certain carcinogens (including substances known, likely to be, or suggestive of being
human carcinogens) or reproductive toxicants identified in accordance with federal
or California laws. “Toys” are defined as “all products designed or intended by the
manufacturer to be used by children when they play” and “child care article” is
defined as “all products designed or intended by the manufacturer to facilitate sleep,
relaxation, or the feeding of children, or to help children with sucking or teething.”
This statute appears to be partly modeled on an earlier version of the EU
Council Directive 76/769/EEC with regard to the threshold concentration level for
the ban and the definition of child-care articles and toys. It does not include the
amendment made by EU Directive 2005/84/EC (December 14, 2005) adding
“hygiene” to the scope of child-care articles, which effectively included items such
as lotion, powder, baby oil, etc. It also includes the three-year-old age limit regarding
81 Information received via email communications with the Delegation of the European
Commission in Washington, D.C., July 11, 2008.
82 S.Res. 68, 24th Leg. (Haw. 2008).
83 S. Jt. Memorial 8, 74th Leg. (Or. 2007).
84 Cal. Health & Safety Code §§108935-108939 (current on LexisNexis).

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products that can be placed in the mouth from the EU Commission Decision
1999/815/EC (December 7, 1999). It added “teething” to the scope of child-care
articles, for which the EU includes “sucking” but not teething.
The Vermont statute85 appears to be modeled on the California statute, but with
some differences. Beginning July 1, 2009, it will prohibit the manufacture, sale, or
distribution in commerce of any toy or child-care article intended for use by a child
under three years of age that contains DEHP, DBP, or BBP in concentrations
exceeding 0.1% and of any toy or child-care article intended for use by a child under
three years of age that can be placed in the mouth and that contains DINP, DIDP, or
DnOP in concentrations exceeding 0.1%. The Vermont statute provides for an
under- three-years-old age limit for the first group of phthalates, unlike the California
statute. The Vermont law adopts the California statutory definition of “child care
article” and “toy” and additionally defines “phthalate” as “any one of a group of
chemicals used as plasticizers to provide flexibility and durability to plastics such as
polyvinyl chloride (PVC).” Like the California statute, it requires manufacturers to
use the least toxic alternative to phthalates and prohibits them from substituting
carcinogens (including substances known, likely to be, or suggestive of being human
carcinogens) or reproductive toxicants identified by the EPA under federal law, but
not under state laws, apparently because Vermont does not have such environmental
laws identifying carcinogens or reproductive toxicants.
The Vermont law provides that a violation of the phthalates law shall be deemed
a violation of the Vermont Consumer Fraud Act and that the provisions of that act
concerning the enforcement authority of the Vermont Attorney General and the rights
of private parties shall apply to violations of the phthalates law. It further clarifies
that nothing in the phthalates law regulates firearms, ammunition, shooting ranges,
or hunting/fishing equipment.
The Washington provision banning phthalates in children’s products is part of
a broader statute86 concerning chemicals in children’s products generally. It covers
lead and cadmium content and also provides, among other things, for the
identification of chemicals of “high concern” to children and children’s products by
the Washington Department of Ecology, for notification to the Department by a
manufacturer that its children’s product contains a chemical of high concern, and for
a product safety education campaign to promote awareness of unsafe children’s
products. With regard to phthalates, beginning July 1, 2009, it prohibits a
manufacturer, wholesaler, or retailer from manufacturing, knowingly selling, offering
for sale, or distributing for sale or for use in the state a children’s product or product
component containing phthalates, individually or in combination, at a concentration
exceeding 0.1% by weight (a thousand parts per million). It defines phthalates as
meaning the six phthalates discussed in this report. It adopts the California definition
of “toy,” but does not refer to “child-care articles.” Instead, it defines “children’s
product,” which includes the California definition of a child-care article, expanding
85 Act of May 24, 2008, Act 171, 2008 Vt. Adv. Legis. Serv. 171 (LexisNexis) (relating to
phthalates in products for young children).
86 Act of June 12, 2008, ch. 288, 2008 Wash. Adv. Legis. Serv. 288 (LexisNexis) (relating
to the children’s safe products act).

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it to include children’s clothing, and also includes toys, children’s cosmetics (for
children under the age of twelve), children’s jewelry (for children under the age of
twelve), and car seats (it also includes a list of items not considered “children’s
products”).
Proposed Legislation
In March 2008, the Senate approved an amendment to H.R. 4040, the Consumer
Product Safety Commission Reform Act, which would restrict the use of six
phthalates in certain toys and child-care products. The House-passed version of H.R.
4040 has no phthalate amendment; the House Committee on Energy and Commerce
noted in its report that it became aware of the potential dangers posed by phthalates
in toys late in the legislative process and intended to take up the issue later.87 At a
public meeting of the conference to reconcile the House and Senate versions of H.R.
4040, the conferees indicated that the regulation of phthalates was one of the
remaining issues that had yet to be resolved.88 Thus, conferees are to determine the
fate and form of the phthalate provisions.
Section 40 of the Senate version of H.R. 4040, also referred to as the Feinstein-
Boxer Amendment for the two California senators who introduced this specific
amendment to the bill, is modeled on the California statute, with some changes, but
places the provisions in the context of the Federal Hazardous Substances Act (FHSA)
framework. It adopts the California statutory definition of “child care article” and
does not adopt its definition of “toy,” but instead defines “children’s product” as “a
toy or any other product designed or intended by the manufacturer for use by a child
when the child plays” which effectively includes the same products as the California
statute.
The provision would treat as a banned hazardous substance under the FHSA
any children’s product or child-care article which (1) contains in any part any
combination of DEHP, DBP or BBP in concentrations exceeding 0.1% or (2) is
intended for use by a child that can be placed in a child’s mouth and either contains
any combination of DINP, DIDP or DnOP in concentrations exceeding 0.1% or
contains any combination of any of the six phthalates in concentrations exceeding
0.1%. Any prohibitions under FHSA §4 (15 U.S.C. §1263) would apply to such
products, including the introduction, receipt or delivery into interstate commerce of
such products; failure to permit inspections of any factory, warehouse, or other
establishment where such products are manufactured, processed, packed, or held; etc.
Like the California statute, the provision would prohibit a manufacturer from
replacing phthalates with certain carcinogens (including substances known, likely to
be, or suggestive of being human carcinogens) or reproductive toxicants identified
by the EPA. However, unlike the California statute, the provision would not require
manufacturers to use the least toxic alternative as a substitute for phthalates.
87 H.Rept. 110-501, at 47 (2007).
88 Conferees Agree on Certain Provisions, Differ on Phthalates, AGs, Other Issues, 36
Product Safety & Liability Rep. (BNA) No. 25, at 630 (June 30, 2008).

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CRS-19
Section 40 would provide that neither it nor FHSA §18(b)(1)(B) (15 U.S.C.
§1261 note), concerning preemption of non-identical State or local regulations of
banned hazardous substances, would preempt State or local laws applying to a
phthalate other than the six described in the bill; applying to a phthalate described in
the bill that is not otherwise regulated by the bill; requiring a warning of risk, illness,
or injury regarding any phthalate; or prohibiting the use of alternatives to phthalates
not prohibited under this bill. Generally, non-identical State or local regulations are
preempted unless an exemption is granted by the CPSC upon request by the State or
locality.
Conclusion
As the conferees consider the amendment to H.R. 4040, they may consider two
central questions about phthalates and the proposed amendment. First, what is the
scientific basis for health concerns about exposure to these chemicals? Second,
would the amendment reduce the risks without generating greater risks? These issues
are discussed briefly here, based on the scientific and legal information presented
above.
Scientific Basis for Health Concerns
The scientific basis for concerns about risks to human health appears to be
strong in the case of some phthalates, adequate with respect to others, and weak for
the remaining chemicals. The strongest evidence with respect to developmental
effects has been produced since about the year 2000. Many of these studies were not
available to the NTP or to CPSC when they reviewed the phthalate literature in 2000
or 2001. At that time, regulators focused on carcinogenic effects, rather than effects
on fetal development. This more recent animal evidence strongly supports a claim
that DEHP, DBP, and DBB can harm reproduction and damage fetal and juvenile
development in rats.
The structure-activity relationship (between the molecular structure of the
phthalates and developmental damage) is well understood, such that scientific
concern focuses now on DEHP, DBP, and DBB.89 DINP also is a developmental
toxicant, but is only about 15% as potent as the most potent phthalates. To the extent
that it is still studied, it is generally studied together with other more potent toxic
phthalates to evaluate additivity of effects. Scientific evidence regarding the other
phthalates mentioned in the amendment to H.R. 4040 is lacking. Limited evidence
indicates that DIDP, DINP, and DnOP might have effects on the immune system, but
these phthalates appear to be much less toxic to developing rodents.
Data indicate that people are exposed to many phthalates, especially DEHP,
DBP (di-n-butyl), and DBB. Children appear to be most heavily exposed. Data are
89 According to Dr. Paul Foster, Acting Toxicology Branch Chief of the National
Toxicology Program (personal communication, July 9, 2008), the structure that is known
to produce toxic effects is a benzene ring of 6 atoms with two linear side chains in the ortho
position of between 4 and 6 carbon atoms each. Longer or shorter side chains are not
developmentally toxic or are much less toxic.

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CRS-20
insufficient to judge exposure for DINP, DIDP, and DnOP. Individuals such as
newborn babies in the intensive care units of hospitals face multiple and continuous
phthalate exposures.
Scientists are just beginning to explore the additive effects of exposure to
multiple phthalates, as well as to phthalates in combination with certain pesticides.90
To date, studies suggest there may be additive effects of multiple phthalate
exposures.91 The National Academy of Sciences is evaluating the risk of aggregate
human exposure to multiple phthalates, and is expected to report before the end of
2008.
Would the Amendment Reduce the Risks
Without Generating Greater Risks?
By eliminating the use of six phthalates in child-care items and toys, the
proposed amendment would codify the voluntary agreements reached by CPSC with
product manufacturers (to keep DEHP and DINP out of nipples, pacifiers, and
teething toys, and DEHP out of toys that might be mouthed) and reduce exposure to
DINP, the only phthalate currently used in the United States to produce toys. The
effect of banning use of the other phthalates is less clear, because their child-related
uses are not known. However, because the law would prohibit their use as substitutes
for DINP in toys, toys would be eliminated as a source of exposure.
For each use, different chemicals might be used in lieu of the six phthalates.
Acetates might be used in some applications, phthalates other than the six specified
might be used in others. The risks of such chemicals may be known or unknown.
Given the lack of legal authority to require testing for a chemical proposed for most
uses, and the cost of testing, new formulations of products might pose either more or
less risk than the current formulations.
90 Rider, C.V., J. Furr, V.S. Wilson, et al. 2008. A mixture of seven antiandrogens induces
reproductive malformations in rats. International Journal of Andrology v. 31, n. 2, p.
249-262.
Fowler, Paul A., David R. Abramovich, Neva E. Haites, et al. 2007. Human fetal testis
Leydig cell disruption by exposure to the pesticide dieldrin at low concentrations. Human
Reproduction, v. 22, n. 11, p. 2919-2928.
91 Hotchkiss, A.K., L.G. Parks-Saldutti, J.S. Ostby, et al. 2004. A mixture of the
“antiandrogens” linuron and butyl benzyl phthalate alters sexual differentiation of the male
rat in a cumulative fashion. Biology of Reproduction, v. 71, p. 1852-1861.
Howdeshell, Kembra L., Vickie S. Wilson, Johnathan Furr, et al. April 14, 2008. A mixture
of five phthalate esters inhibits fetal testicular testosterone production in the Sprague
Dawley rat in a cumulative, dose additive manner. Toxicological Sciences Advance Access.
Reprint received from the author.
Rider, Cynthia V., Johnathan Furr, Vickie S. Wilson, et al. 2008, A mixture of seven
antiandrogens induces reproductive malformations in rats. International Journal of
Andrology, v. 31, p. 249-262.

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