Phthalates in Plastics and Possible Human Health Effects
Prepared for Members and Committees of Congress
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 rodent 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 appear consistent with the results of rodent experiments. More research would be
needed to test this hypothesis. Recent U.S. surveys have found almost universal human 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 consumer 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). The Consumer Product Safety Improvement Act of 2008 (P.L. 110-314,
enacted August 14, 2008) includes a provision intended to ensure protection of children from six
phthalates by restricting their use in toys and child-care products.
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 new law codifies
voluntary agreements previously reached by CPSC with product manufacturers, and should
reduce exposure to one particular phthalate. New formulations for toys and child-care products
may pose greater or fewer risks than current formulations.
Introduc tion ..................................................................................................................................... 1
Backgr ound ..................................................................................................................................... 1
The Six Phthalates.....................................................................................................................3
Di-(2-ethylhexyl) phthalate (DEHP)...................................................................................4
Dibutyl phthalates (DBP)....................................................................................................4
Benzyl butyl phthalate (BBP or sometimes BzBP).............................................................5
Diisononyl phthalate (DINP)..............................................................................................6
Diisodecyl phthalate (DIDP)...............................................................................................8
Di-n-octyl phthalate (DnOP)...............................................................................................8
Federal Evaluation and Regulation of Phthalates.....................................................................9
Food and Drug Administration (FDA)................................................................................9
Consumer Product Safety Commission.............................................................................11
Regulation in the European Union (EU) and the States..........................................................12
St ates ................................................................................................................................. 14
Federal Legislative Activity....................................................................................................16
Consumer Product Safety Improvement Act of 2008.......................................................16
Senate Version of H.R. 4040.............................................................................................16
Conclusion ..................................................................................................................................... 17
Scientific Basis for Health Concerns......................................................................................17
Reducing Risks Without Generating Greater Risks................................................................18
Author Contact Information..........................................................................................................19
“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 2
on six phthalates that are produced and used in very large quantities. 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). Newly enacted
P.L. 110-314, the Consumer Product Safety Improvement Act of 2008 (CPSIA), prohibits the sale
of children’s toys and child care articles that contain more than 0.1% of DEHP, DBP, or BBP. A
similar ban applies for DINP, DIDP, and DnOP, until the Consumer Product Safety Commission
issues a rule either establishing or eliminating the ban on a permanent basis.
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 3
experiments with rodents have demonstrated that some phthalates at high doses damage 45
reproduction and development. Moreover, if administered at sufficient levels and at the
appropriate time to pregnant females, some phthalates can cause malformations of the 6
reproductive organs of offspring, especially males. In rats, exposure during gestation to some 7
phthalates can cause testicular cancer in mature offspring. The higher the phthalate exposure, the
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 (mg) of phthalate per kilogram (kg) of the exposed animal’s body
weight per day.
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
more frequent and severe are the effects on the reproductive system. Rat fetuses are most 8
susceptible, but older rats can also be affected at somewhat higher levels of exposure.
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. 9
Very few studies have looked at possible effects in humans, but their results have been consistent
with the results of rodent experiments. A study published in 2005 provided the first evidence of
subtle developmental effects, similar to those seen in animal studies, in human male infants 10
exposed prenatally to breakdown products of phthalates. 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.”
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 11
phthalates. 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 12
DINP) and DIDP was not measured in 2001-2002. Studies of amniotic fluid have also 13
documented exposure to multiple phthalates for human fetuses. More generally, babies may be 14
the most heavily exposed group.
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 1516
source of exposure to some phthalates for the general population., However, air also appears to
using in utero 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.
10 Swan et al. 2005.
11 DHHS. 2005. Third National Report on Human Exposure to Environmental Chemicals. p. 253. http://www.cdc.gov/
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.
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 1819
exposure for infants. For some individuals, certain medications also may be important sources.
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 20
less than 1% of, levels that cause reproductive harm in rats.
Phthalates do not bioaccumulate in the body or the environment; rather they break down rapidly. 21
However, exposure to phthalates is continuous and substantial in the modern world.
The new law requires regulation of six phthalates, following the example of the European Union
and the state of California. These phthalates 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 22
of Environmental Health Sciences/National Institutes of Health (NIEHS/NIH).
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 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-
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.
DEHP is the most abundantly produced and the most studied phthalate.23 It is used primarily to
improve the 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, 24
and many home and garden products. The NTP has expressed “serious concern that certain
intensive medical treatments of male infants may result in DEHP exposure levels that adversely 25
affect development of the male reproductive tract.” 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 26
offspring of pregnant women. After this DEHP monograph was issued, several studies began to
explore associations between DEHP and other health effects, such as effects on thyroid hormone 27
levels, asthma, and obesity. Additional research is being conducted in these areas, and it is too
soon to draw any conclusions regarding the potential role of DEHP in causing such problems.
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
phthalate) found “clear evidence of adverse effects” on the developing male reproductive tract in
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 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,
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
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.
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.
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 29
potential for similar or other adverse effects in humans.” As a result, NTP has “some concern
for DBP causing adverse effects to human development, particularly development of the male 30
reproductive system.” In the seven years since this NTP monograph, numerous studies have 3132
bolstered these findings. Of particular note is the study by Lehmann et al. (2004). 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 33
effects similar to di-n-butyl phthalate and DEHP.
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
developmental effects could result from exposure to BBP. However, effects were 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 35
developmental effects due to estimated BBP exposure. Papers published after 2001 confirm the 36
developmental toxicity of BBP. However, the testimony of Leon Earl Gray, Jr., Senior
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/
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 Human Reproductive and Developmental
Effects of Butyl Benzyl Phthalate (BBP). NIH Publication No. 03-4487. March 2003. p. 2. http://cerhr.niehs.nih.gov/
35 Ibid. p. 4.
36 Wilson, Vickie S., Christy Lambright, Johnathan Furr, et al. 2004. Phthalate ester-induced gubernacular lesions are
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 37
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 38
manufacturers. 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 development of the human fetus if the levels of 39
exposure are sufficiently high,” according to NTP. 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 40
phthalates, DINP was found to be less potent than DEHP or DBP by an order of magnitude. 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 41
to DEHP, DBP (both forms), and BBP which he rated 1.0. A number of studies of the potential
effects on rodents of DINP exposure were published after 2001, but they appear consistent with
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/
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.
the earlier work with respect to developmental toxicity.42 In addition, there is some evidence of 43
enhanced allergic responses due to DINP exposure.
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 3-44
4 years, in light of further scientific developments.
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 45
analysis of DINP movement out of various toys. NTP used that data to conclude that its concern 46
was “minimal” for developmental effects in children. NTP also had minimal concern for DINP 47
causing adverse effects to human reproduction or fetal development. However, this conclusion 48
was controversial. A Japanese study also looked at DINP release from toys and and time spent 49
mouthing and found considerably higher exposures than the CPSC.
As mentioned above, it appeared from the NHANES that exposure to DINP was negligible in 50
children surveyed by the Centers for Disease Control and Prevention (CDC) in 2001-2002.
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)
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.
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.
48 Shea, K.M. 2003. Pediatric exposure and potential toxicity of phthalate plasticizers. Pediatrics, v. 111, n. 6, Pt 1, p.
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.
50 DHHS, ibid., p. 282.
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.
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 52
developmental effects.” NTP concluded that exposures to DIDP were probably not high enough
to cause concern, and that scientists had minimal concern for developmental effects in fetuses and 5354
children. NTP also found that DIDP would not adversely affect human reproduction. Studies
published since 2001 have not conflicted with the NTP conclusions. However, several recent 55
studies have found endocrine-disrupting effects following rodent exposure to DIDP.
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 5657
exposed rodents. No evidence of reproductive effects was found in the available studies. 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 58
have relevance for human exposure. An online search by CRS of publications using Medline
revealed no new studies after 2001 that might better inform a risk evaluation.
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 Publication No. 03-4485. April 2003. p. 1.
53 Ibid. p. 3.
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.
58 Ibid. p. 3.
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 (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
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 consumer product has been banned outright.
FDA-regulated products that may contain phthalates include (1) medical devices; (2) food contact 60
substances, such as plastic wrap; and (3) cosmetics. FDA reported in June 2008 that, in tandem 61
with its review of the safety of bisphenol A (BPA) in the products it regulates, it is also 62
conducting a comprehensive inventory of regulated products that contain phthalates.
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
in PVC-containing medical devices. 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 64
devices if these procedures were to be performed on high-risk individuals. Depending on the
59 This section was written by Sarah A. Lister, Specialist in Public Health and Epidemiology, Domestic Social Policy
60 Manufacturers maintain that phthalates are not used in food wrap in the United States. See the trade group website
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 thnd
Phthalates and Bisphenol A in Everyday Consumer Products,” June 10 , 2008, 110 Cong., 2 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
64 FDA, “FDA Public Health Notification: PVC Devices Containing the Plasticizer DEHP,” July 12, 2002, at
procedure, these individuals include infants, boys, pregnant or nursing women, and, for some
procedures, healthy 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 65
beverages. FDA permits the use of a variety of phthalates for these purposes. 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 66
regulatory action to remove these materials from the marketplace.
Under the authority of the Federal Food, Drug, and Cosmetic Act (FFDCA), FDA regulates the 67
safety of cosmetics and personal care products, such as nail polish, shampoo and lotions, 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 68
injurious to users” under labeled or customary conditions of use. 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 accurately assess infant 69
exposure. Under the authority of the Fair Packaging and Labeling Act (P.L. 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 70
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
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.
69 FDA, “Phthalates and Cosmetic Products,” February 7, 2008, at http://www.cfsan.fda.gov/~dms/cos-phth.html.
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 that it administers and enforces. Consumer products
as defined in the CPSA do 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 and car seats, and other children’s consumer products, including pacifiers,
teething rings, and apparel. P.L. 110-314, the Consumer Product Safety Improvement Act
(CPSIA), signed by the President on August 14, 2008, strengthened regulatory and enforcement 71
The CPSC may regulate phthalates under either the CPSA or the FHSA. The CPSA and the FHSA
differ with regard to the rulemaking procedures; the precise nature of the acts prohibited with
regard to products or substances that fail to comply with safety standards; and other issues.
Therefore, there are advantages and disadvantages to promulgating standards under the CPSA
versus the FHSA. One disadvantage of the CPSA rulemaking procedure was eliminated by the
CPSIA. The CPSA formerly did not expressly provide injunctive enforcement authority for state
attorneys general, unlike the FHSA, which did. CPSIA amends the CPSA to provide state
attorneys general authority to enjoin violations of the federal standard.
Additionally, the recent reform legislation addressed other concerns. Critics alleged problems
with the ability of the CPSC to establish safety standards in a timely fashion. For example, some
asserted that the rulemaking procedures under the CPSA and other acts under the CPSC’s
jurisdiction, such as the FHSA, were unnecessarily onerous, requiring protections beyond those 72
required by the Administrative Procedure Act. The CPSIA streamlined the rulemaking
procedures of the CPSA by eliminating the required extra step of an advance notice of proposed
rulemaking. The CPSIA did not amend the CPSA provisions that encourage the CPSC to rely
heavily 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 that
can be taken by the CPSC for violations. However, the CPSIA legislated mandatory safety
standards or rulemaking for certain children’s products, including toys, durable infant or toddler
products, and standards for lead content and phthalates in certain children’s products. The CPSIA
revised and expanded the scope of acts prohibited under the CPSA to include manufacture, sale or
importation of products that are the subject of a voluntary recall. Under both the CPSA and the
FHSA, the CPSC may order a recall and/or other remedies for products that violate a safety
standard under the pertinent act and may inspect factories where products are made. Products
violating a safety standard may be denied importation.
71 For a general discussion of the statutes administered and enforced by the CPSC, see CRS Report RL34684,
Consumer Product Safety Improvement Act of 2008: P.L. 110-314, by Margaret Mikyung Lee.
72 The Administrative Procedure Act (Title 5, Subchapter II of the U.S. Code, §551-559) directs federal administrative
agencies to promulgate regulations according to a standard procedure, which includes such required actions as
provision of public notice, receiving public comments, allowing for administrative hearings, and so on, unless
otherwise specified by the law that authorizes a particular rulemaking.
Although the European Union and some states have enacted safety standards regarding phthalates
in children’s products, as discussed below, the CPSC had not promulgated such standards prior to
the CPSIA. In 1983, the CPSC determined that DEHP in children’s products might result in 73
substantial exposure of children to an animal carcinogen. 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, 74
and teethers. 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 75
products intended for children five years of age and younger.
The new federal legislation and several state statutes concerning phthalates apparently were 76
modeled on EU laws. Under Council Directive 76/769/EEC, as amended by Council Directive 77
2005/84/EC, 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.”
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).
76 1976 Official Journal (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.
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 79
Committee on Toxicity, Ecotoxicity and the Environment. 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 80
of Council Directive 2005/84/EC and the Regulation (EC) No. 1907/2006, 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
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.
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 81
of harm, these phthalates were banned under the precautionary principle of the European Union 82
given the potential risk posed to children.
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).
81 The European Union has adopted a “precautionary principle” to guide its decisions when faced with potentially
hazard to human or animal health, but scientific uncertainty concerning the nature or extent of the risk (Commission of
the European Communities, Communication from the Commission on the precautionary principles, February 2, 2000,
available at http://ec.europa.eu/dgs/health_consumer/library/pub/pub07_en.pdf). In simple terms, the “precautionary
principle”might be described as a risk management approach that chooses to err on the side of caution so as to provide
a high degree of protection for human health and the environment.
82 Information received via email communications with the Delegation of the European Commission in Washington,
D.C., July 11, 2008.
California, Vermont, and Washington have recently enacted legislation establishing safety
standards for phthalate content in children’s articles. The permanent and interim federal
phthalates safety standards of the CPSIA are considered safety standards under the CPSA, and as
such they preempt any non-identical standards in these statutes, except as the CPSA otherwise
provides for exemptions. Any permanent standard resulting from the consideration of the interim
standard for DINP, DIDP, or DnOP would also similarly preempt non-identical state laws. The
CPSIA clarifies that neither it nor the CPSA shall be construed as preempting any state
requirements concerning phthalate alternatives that are not specifically regulated in a consumer
product safety standard under the CPSA. Under the CPSA, upon application by a state or locality,
the CPSC may, by rule, exempt from preemption a state or local standard that provides a
significantly higher degree of protection from injury than the federal standard, and that does not
unduly burden interstate commerce.
The three state phthalate 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.” In
addition to these state standards, 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 83
legislation before the 2009 legislative session. Oregon’s legislature has adopted a joint memorial
urging Congress to regulate phthalates at the federal level as a substance in cosmetics, personal 84
care products, and children’s toys. Additionally, several other states have introduced legislation
Beginning January 1, 2009, the California statute85 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 that 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
83 S.Res. 68, 24th Leg. (Haw. 2008).
84 S. Jt. Memorial 8, 74th Leg. (Or. 2007).
85 Cal. Health & Safety Code §§108935-108939 (current on LexisNexis).
age limit regarding 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 statute86 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 statute87
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 it to include
children’s clothing, and also includes toys, children’s cosmetics (for children under the age of 12),
children’s jewelry (for children under the age of 12), and car seats (it also includes a list of items
not considered “children’s products”).
86 Act of May 24, 2008, Act 171, 2008 Vt. Adv. Legis. Serv. 171 (LexisNexis) (relating to phthalates in products for
87 Act of June 12, 2008, ch. 288, 2008 Wash. Adv. Legis. Serv. 288 (LexisNexis) (relating to the children’s safe
On July 28, 2008, the House and Senate conferees for H.R. 4040, the Consumer Product Safety
Improvement Act of 2008, announced that an agreement on a final text had been reached
resolving the differences between the Senate and House versions of the bill. The bill was
approved in both chambers before the August recess and signed into law by the President on
August 14, 2008 (P.L. 110-314).
Beginning 180 days after enactment, the CPSIA §108 permanently bans the three phthalates
whose toxicity is not disputed and temporarily bans three other phthalates pending a review by a
Chronic Hazard Advisory Panel (CHAP). It prohibits children’s toys or child care articles that
contain more than 0.1 percent DEHP, DBP, or BBP. The sale of children’s toys that can be placed
in the mouth or child care articles containing concentrations of more than 0.1 percent of DINP,
DIDP, or DnOP, is prohibited on an interim basis until a review by a CHAP. After the CPSC
receives the report from the CHAP, it would determine, by rule, whether to continue the interim
ban. The provision does not restrict phthalate alternatives. It defines “children’s toy” as “a
consumer product designed or intended by the manufacturer for “a child 12 years of age or
younger, for use by the child when the child plays.” “Child care article” is defined as “a consumer
product designed or intended by the manufacturer to facilitate sleep or the feeding of children age
3 and younger or to help such children with sucking or teething.” The statute includes guidelines
for determining whether a product was intended or designed for use by children of the specified
ages and whether a toy can be placed in a child’s mouth.
As discussed above, this provision also clarified any preemptive effect these standards would
have on state laws. Non-identical provisions would be preempted, unless a state applied for and
the CPSC granted an exemption for stronger protections under state laws, and the federal law
would not preempt restrictions on phthalate alternatives. The CPSIA standard differs somewhat
from each of the existing state laws described above. For example, the federal law differs from
the state laws with regard to the definition of toys, children’s products, or children’s articles, and
the age group for which these consumer products are intended. It appears that the new federal
phthalates safety standard preempts the recent state laws that were enacted in the absence of
federal standards, to the extent that they do not provide identical protection for the same risk of
The final phthalates provision resolved differences between the Senate and House treatment of a
phthalates ban and between proponents and opponents of a permanent ban on all six phthalates
named in the legislation, including restrictions on certain alternatives.
The final phthalates provision evolved from a Senate-approved amendment to H.R. 4040. The
House-passed version of H.R. 4040 had no phthalate amendment; the House Committee on
Energy and Commerce noted in its report that it became aware of the potential dangers posed by 88
phthalates in toys late in the legislative process and intended to take up the issue later.
88 H.Rept. 110-501, at 47 (2007).
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,
was modeled on the California statute, with some changes, but would have placed the provisions
in the context of the Federal Hazardous Substances Act (FHSA) framework. It adopted the
California statutory definition of “child care article” and did not adopt its definition of “toy,” but
instead defined “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 included the same
products as the California statute.
The provision would have treated 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 have
applied 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 have prohibited 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 have required manufacturers to use the least toxic alternative as a
substitute for phthalates.
Section 40 would have provided 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. As discussed above, generally under the
CPSC as amended by the CPSIA, non-identical State or local regulations are preempted unless an
exemption is granted by the CPSC upon request by the State or locality.
There were two issues of particular concern during development of the final phthalate provisions
of the CSPIA. First, what is the scientific basis for health concerns about exposure to these
chemicals? Second, would the provision reduce the risks without generating greater risks? These
issues are discussed briefly here, based on the scientific and legal information presented above.
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, 89
DBP, and DBB. 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 new law 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 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 90
well as to phthalates in combination with certain pesticides.
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.
By restricting the use of six phthalates in child-care items and toys, the new law codifies 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
should 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 prohibits their use as substitutes for DINP in toys,
toys should be eliminated as a source of exposure.
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.
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.
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.
Linda-Jo Schierow Margaret Mikyung Lee
Specialist in Environmental Policy Legislative Attorney
firstname.lastname@example.org, 7-7279 email@example.com, 7-2579