Phthalates
TEACH Chemical Summary
U.S. EPA, Toxicity and Exposure Assessment for Children's Health
This TEA CH Chemical Summary is a compilation of information derived primarily from U. S. EPA and A TSDR resources, and the
TEACH Database. The TEACH Database contains summaries of research studies pertaining to developmental exposure and/or
health effects for each chemical or chemical group. TEACH does not perform any evaluation of the validity or quality of these
research studies. Research studies that are specific for adults are not included in the TEACH Database, and typically are not
described in the TEACH Chemical Summary.
I. INTRODUCTION
Phthalates are a group of chemicals used as plasticizers, which provide flexibility and durability to
plastics such as polyvinyl chloride (PVC). Phthalates are dialkyl or alkyl aryl esters of 1,2-
benzenedicarboxylic acid. Phthalates in pure form are usually clear liquids, some with faint sweet odors
and some with faint yellow color (1-6). Plastics that contain phthalates are commonly used in
applications that include building materials, clothing, cosmetics, perfumes, food packaging, toys, and
vinyl products (e.g., flooring, shower curtains, and rain coats); and in medical applications that include
blood transfusion bags and tubing, intravenous fluid bags and tubing, and other medical devices.
Phthalates are also found in lubricating oils, solvents, and detergents (1-6).
With respect to health effects, phthalates are often classified as endocrine disrupters or hormonally-
active agents (HAAs) because of their ability to interfere with the endocrine system in the body (6, 7).
Exposure to phthalates has been reported to result in increased incidence of developmental
abnormalities such as cleft palate and skeletal malformations, and increased fetal death in experimental
animal studies (1-7). The most sensitive system is the immature male reproductive tract, with phthalate
exposure resulting in increased incidence of undescended testes, decreased testes weight, decreased
anogenital distance (distance between the anus and the base of the penis), and other effects (1-7).
The ubiquitousness of phthalates in items used daily by children is of concern for children's health
because it increases the likelihood of exposure. Exposure media of concern for children include breast
milk, retail cow's milk, and infant formulas (8-10); foods contained in plastic packaging (6, 11-13);
plastic toys and feeding items, such as cups and bowls (12-15); indoor air (16); and medical devices
such as plastic tubing used during intravenous treatments, transfusions, extracorporeal membrane
oxygenation (ECMO) treatments, or dialysis (17-26). The use of phthalates in bottle nipples and
pacifiers was voluntarily discontinued beginning in 1986 (1-6, 27).
Unless stated otherwise, most studies described in this Chemical Summary focused on diethylhexyl
phthalate (DEHP) exposure, one of the most commonly used and produced phthalates in the United
States. Other phthalates of concern include: diisononyl phthalate (DINP), butyl benzyl phthalate (BBP),
diethyl phthalate (DEP), di-n-butyl phthalate (DnBP), di-n-octyl phthalate (DnOP), dimethyl phthalate
(DMP), and dimethyl-terephthalate (DMT).
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
II. EXPOSURE MEDIA AND POTENTIAL FOR CHILDREN'S EXPOSURE1
Exposure
Media
Diet
Dermal
Indoor Air
Ambient Air
Sediment
Soil
Drinking Water
Relative
Potential for
Children's
Exposure2'3
Higher
Medium
Lower
Lower
Lower
Lower
Lower
Basis4
Phthalates can be found throughout the diet, including infant
formulas and baby food. Phthalates can leach into foods
heated in plastic containers. Mouthing of toys containing
phthalates can also result in phthalate exposure. Individuals
receiving multiple treatments, feedings, or transfusions
through medical tubing containing phthalates are likely to be
exposed to phthalates. Infants in Neonatal Intensive Care
Units (NICU) are one group of concern for phthalate
exposure.
Some cosmetics, fragrances, and lotions may contain
phthalates. Some insect repellants also contain phthalates.
Indoor air concentrations can be increased from offgassing of
building materials such as new vinyl flooring or newly
painted rooms. Phthalates have been measured in house dust.
Ambient air is generally not considered a significant
exposure media.
Sediment is generally not considered an environmental
medium of concern.
Phthalates are not generally found in soil.
Phthalates have been detected in drinking water, though
generally at low concentrations.
1 For more information about child-specific exposure factors, please refer to the Child-Specific Exposure Factors
Handbook (http ://cfpub. epa. gov/ncea/cfm/recordisplav .cfm?deid=5 5145).
2 The Relative Potential for Children's Exposure category reflects a judgment by the TEACH Workgroup, U.S. EPA, that
incorporates potential exposure pathways, frequency of exposure, level of exposure, and current state of knowledge. Site-
specific conditions may vary and influence the relative potential for exposure. For more information on how these
determinations were made, go to http://www.epa. gov/teach/teachprotocols_chemsumm.html.
3 Childhood represents a lifestage rather than a subpopulation, the distinction being that a subpopulation refers to a
portion of the population, whereas a lifestage is inclusive of the entire population.
4 Information described in this column was derived from several resources (e. g., 1-5) including studies listed in the
TEACH Database (http://www.epa.gov/teach').
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
III. TOXICITY SUMMARY5 6
Phthalates are a group of numerous chemicals, which share a common chemical structure (see Introduction). Some
phthalates are classified as "endocrine disrupters "for their ability to modify the endocrine, or hormonal, system. Only
certain phthalates have toxicity reference values listed through U.S. federal agencies. The phthalates listed in this section are
those for which toxicity reference values are available. Toxicity information for individual phthalates is listed separately for
each phthalate. An identified "critical data need" is for information on the effects of mixture of phthalates including
questions ofadditivity and interference (28).
Butyl benzyl phthalate (BBP)
One study reported that increased incidences of eczema and rhinitis in children were associated with
increased concentrations of BBP in house dust (29). Prenatal exposure of rats to BBP resulted in
teratogenic effects in offspring that included skeletal malformations, increased incidence of cleft palate,
and decreased number of live fetuses at birth (30-32). Defects in male rat reproductive organ
development following prenatal exposure included increased incidence of undescended testicles,
hypospadias (urethra on the underside of the penis), and other anatomical differences (33-35). A two-
generation study reported similar effects in offspring, and in addition, delayed puberty in both sexes
(36). Pregnant rats exposed to BBP had reductions in ovarian and uterine weights, progesterone levels,
and ovulatory follicles (37, 38). In adult female rats, BBP exposure resulted in increased incidence of
mononuclear cell leukemia and liver effects, including increased liver size (6).
Metabolites: A metabolite of BBP, mono-n-butyl phthalate (MBP), has been shown to be teratogenic in
rats following maternal exposure during pregnancy, leading to increased fetal death and increased fetal
skeletal malformations (31, 39-45). Increased incidence of undescended testes, decreased testes weight,
and decreased anogenital distance were also observed following MBP exposure during development
(46-48).
Carcinogenicity weight-of-evidence classification : The US EPA classified BBP as class C, a
possible human carcinogen (under the 1986 U.S. EPA guidelines), based on increased mononuclear cell
leukemia in female rats (www.epa.gov/iris/subst/0293.htm, II.A.I). The World Health Organization
(WHO) International Agency for Research on Cancer (IARC) classified BBP in 1999 as "Not
Classifiable" as to carcinogenicity (http://monographs.iarc.fr/ENG/Monographs/vol73/volume73.pdf).
Note: BBP is currently undergoing reassessment in IRIS (49).
Continued on next page
5 Please refer to research article summaries listed in the TEACH Database for details about study design considerations
(e.g., dose, sample size, exposure measurements).
6 This toxicity summary is likely to include information from workplace or other studies of mature (adult) humans or
experimental animals if child-specific information is lacking for the chemical of interest. Summaries of articles focusing
solely on adults are not listed in the TEACH Database because the TEACH Database contains summaries of articles
pertaining to developing organisms.
7 For recent information pertaining to carcinogen risk assessment during development, consult "Guidelines for
Carcinogen Risk Assessment and Supplemental Guidance on Risks from Early Life Exposure" at
http://www.epa.sov/cancersuidelines.
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
Dibutyl phthalate (DBP)
Prenatal exposure of rats to DBP resulted in teratogenic effects in offspring that included skeletal
malformations, increased incidence of cleft palate, and decreased number of live fetuses at birth (30, 50-
52). Defects in male reproductive organ development following prenatal exposure to DBP included
increased incidence of undescended testicles, hypospadias, and other anatomical differences (34, 53-66).
Decreased testosterone (60), decreased pituitary hormones (67), and delayed puberty (56) were
associated with prenatal DBP exposure. Exposure to DBP during adulthood resulted in increased
mortality in rats (4).
Metabolites: Mono-N-butyl phthalate (MBP) is a metabolite of DBP (see Toxicity Summary for
metabolites of BBP on the previous page).
Carcinogenicity weight-of-evidence classification: The U.S. EPA classified DBP as class D, "Not
Classifiable," stating that "pertinent data regarding carcinogenicity was not located in the available
literature" (http://www.epa.gov/iris/subst/003 8.htm), and the WHO IARC has not evaluated DBP
(http://monographs.iarc.fr/ENG/Classification/index.php).
Note: DBP is currently undergoing reassessment in IRIS (49).
Di(2-ethylhxyl)phthalate (DEHP)
Increased incidence of asthma in children was associated with increased DEHP concentrations in house
dust (29). Exposure of some infants and children to DEHP from medical devices was associated with
cholestasis (reduced bile flow) (19) and unusual lung disorders (21). Another study of adolescents who
were exposed to DEHP during ECMO treatments as infants reported no adverse effects on several
hormone levels tested (68).
Prenatal exposure of rats to DEHP resulted in teratogenic effects in offspring that included skeletal
malformations, increased incidence of cleft palate, and decreased number of live fetuses at birth (69,
70). Defects in male reproductive organ development following prenatal exposure of rats to DEHP
included increased incidence of undescended testicles, hypospadias, and other anatomical differences
(34, 35, 71-73). Decreased sperm production (71) and decreased testosterone levels (72) were also
reported. Prenatal exposure of rats to DEHP led to adverse effects on lung tissue development (74).
Exposure of neonatal, suckling, and adult rats to DEHP resulted in reduced hepatic enzyme activities
(75-77). DEHP exposure resulted in anovulation (lack of release of eggs from the ovaries) in adult
female rats (1, 6).
Metabolites: Metabolites of DEHP, MEHP and 2-ethylhexanoic acid, have been shown to be
teratogenic in rats and mice, with effects including skeletal abnormalities and exencephaly (brain growth
outside of the skull) in offspring (78-81).
Continued on next page
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
Di(2-ethylhxyl)phthalate (DEHP) continued
Carcinogenicity weight-of-evidence classification: The U.S. EPA classified DEHP as class B2,
probable human carcinogen (under the 1986 U.S. EPA guidelines), based on increased liver tumors in
adult male and female rats (www.epa.gov/iris/subst/0014.htm, II.A.I). The WHO IARC classified
DEHP in 2000 as "Not Classifiable" (Group 3) as to carcinogenicity, based on inadequate evidence in
humans, and sufficient evidence in experimental animals
http://monographs.iarc.fr/ENG/Monographs/vol77/volume77.pdf).
Note: DEHP is currently undergoing reassessment in IRIS (49).
Diethyl phthalate (DEP)
Prenatal exposure of rats to DEP resulted in skeletal variations and delayed ossification (hardening) of
bones in offspring (82). Prenatal and lactational exposure to DEP resulted in abnormal sperm and
decreased testosterone in male offspring during adulthood (83). In adult rats, DEP exposure resulted in
increased liver weights (3). The U.S. EPA recently reassessed available DEP toxicity information and
concluded that DEP is minimally or mildly toxic via the oral or dermal route; upon review the U.S. EPA
noted that increased incidence of extra ribs in offspring was observed at maternally toxic doses, and
concluded that "there was no evidence of increased susceptibility in a rat reproductive study" (84).
Carcinogenicity weight-of-evidence classification: The U.S. EPA has classified diethyl phthalate as
class D, not classifiable as to carcinogenicity (under the 1986 U.S. EPA Cancer Guidelines), because
pertinent data regarding carcinogenicity was not located in the available literature (85). The U.S. EPA
OPPTS recently concluded that DEP is neither mutagenic nor carcinogenic (84). The WHO IARC has
not evaluated DEP (http://monographs.iarc.fr/ENG/Classification/index.php).
Dimethyl terephthalate (DMT)
Exposure of adult rats to DMT was associated with chronic kidney inflammation (6).
Carcinogenicity weight-of-evidence classification: US EPA IRIS has not completed evaluation
pertaining to carcinogenicity of DMT (http://www.epa.gov/iris/subst/0046.htm). The WHO IARC has
not evaluated DMT (http://monographs.iarc.fr/ENG/Classification/index.php).
Supporting references and summaries are provided in the TEACH Database at http://epo.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
IV. EXPOSURE AND TOXICITY STUDIES FROM THE TEACH DATABASE
This section provides a brief description of human and animal studies listed in the TEACH Database. These descriptions generally include
the overall conclusion in each study -without evaluation or assessment of scientific merit by TEACH. For more details about doses and
exposure levels, query the TEACH Database. Any consideration of adverse events should include an understanding of the relative
exposure on a body -weight basis. In many cases, exposure levels in animal studies are greater than exposure levels normally encountered
by humans.
A. HUMAN EXPOSURE AND EFFECTS
> One recent study of adult males in Sweden found significantly fewer motile sperm for men with
higher urine concentrations of the phthalate metabolite MEP (86). Reduced sperm motility (motion)
was significantly associated with blood concentrations of some polychlorinated biphenyls (PCBs)
and urine concentrations of some phthalate metabolites (e.g., MBeP and PCB 153) (87).
*• Infants and children can be exposed to phthalates through several dietary sources (8, 9, 11, 88, 89).
Phthalates were found in every sample analyzed of baby food and infant formula in a Danish study
(8). DEHP and other phthalates were found in almost all of the analyzed milk, cream, butter, and
cheese samples tested in a study that included the United Kingdom, Norway, and Spain (9).
Furthermore, phthalates were found in food samples packaged in plastics, and the presence of
phthalates was attributed to plastic residues from the packaging (11) or from plastic gloves used in
packaging the food (88).
> Infants and children can be exposed to phthalates through mouthing of plastic toys, and use of
plastic eating containers. Phthalates, mainly DEHP and diisononyl phthalate (DINP), are found in
some plastic products that children use, such as toys and plastic food containers (1, 6, 15); phthalates
can be extracted from these products into a solution that mimics saliva (12, 14). The quantity of
phthalate exposure to children from toys remains equivocal, and difficult to quantitate. One study in
Holland estimated the amount of DEHP and DINP ingested by children under 3 years of age from
toys by measuring leaching of these phthalates into solution (14). Another study in the U.S. by the
Consumer Product Safety Commission concluded that levels of DINP leached from a different panel
of toys did not pose a significant risk to children (13).
> Phthalate concentrations in particulate dust collected in homes suggested that inhalation of
phthalates may be an important route of exposure for some children (27, 29, 90-92). Both BBP (29,
91) and DEHP (27, 29) have been detected in house dust. One study in Sweden detected phthalates
in dust in 38 out of 372 homes tested (29). However, a study looking at house dust found no
significant association between metabolites in children's urine and DEHP levels in house dust (90).
*• As evidence of exposure, phthalates and their metabolites have been measured in blood and urine of
pregnant women (93), infants and children (24, 29, 90, 94-102), and also in breast milk (95).
Metabolites of DEHP include mono-ethylhexyl phthalate (MEHP) and 2-ethylhexanoic acid (2-
EHA); metabolites of DnBP include mono-n-butyl phthalate (MBP); and metabolites of BBP include
MBP and mono-n-benzyl phthalate (MBeP).
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
> Newborn infants may be exposed to phthalates from some medical procedures. Neonates are
exposed to DEHP when receiving medical intervention with PVC-containing devices (i.e.,
intravenous [I.V.] tubing which may contain 20-40% DEHP by weight) (1). DEHP and its toxic
metabolite monoethylhexyl phthalate (MEHP) have been measured in the serum of neonates
following blood transfusions and intravenous fluid administration (17, 18, 95, 97), extracorporeal
membrane oxygenation (ECMO) (19, 20, 68), mechanical ventilation (21), and intravenous
parenteral feeding with nutrients (22, 23).
*• Infants and children exposed to phthalates from specific medical interventions have been reported to
have some health effects that correlated with the exposure. In infants who underwent ECMO, a
significant association was found between the degree of cholestasis (reduced bile formation or flow)
and increasing DEHP serum levels (19). Another study reported an unusual lung disorder in three
pre-term infants who were artificially ventilated with tubing containing DEHP (22). In contrast,
another study found no acute effects in pre-term infants who had increased serum levels of DEHP
(25). Also, adolescents who had been exposed to DEHP during ECMO as infants were reported to
have normal levels of testosterone and pituitary hormones during adolescence (68).
> Recent evidence in humans provides evidence that maternal exposure to phthalates during pregnancy
can adversely affect male reproductive tract development. Specifically, decreased anogenital
distance (the distance between the anus and the base of the penis) in boys ages 2-36 months was
significantly associated with increased maternal urine concentrations of four phthalate metabolites
(MEP, MBP, monobenzyl phthalate, and monoisobutyl phthalate (MiBP) (103).
*• A Swedish study on persistent allergic symptoms in children found significant positive associations
between incidence of rhinitis or incidence of eczema and BBP concentrations; and between
incidence of asthma and DEHP concentrations in household dust (29).
*• Premature thelarche (breast development) was significantly associated with plasma concentrations of
DEHP, DBF, DEP, DMP, and the DEHP metabolite MEHP in a case control study of young girls in
Puerto Rico (94).
B. EXPERIMENTAL ANIMAL EXPOSURE AND EFFECTS
There are numerous experimental animal studies that have examined health effects of phthalates during development. The
studies summarized here represent some of the more recent studies available in the literature through 2005. Comprehensive
and detailed summaries of animal studies are available for individual phthalates elsewhere (see Considerations for Decision
Makers in this Chemical Summary) (1-6).
> The tissue distribution and metabolism of phthalates have been studied in experimental animals.
Young mice injected with DEHP retained a minimal amount in the brain (104). In rats, phthalates
and their metabolites have been shown to cross the placenta, and to pass into offspring through
breast milk when pregnant or lactating rats were exposed by injection (75, 105, 106) or ingestion
(76, 107-109).
> Maternal exposure to phthalates during pregnancy has been shown to be teratogenic (cause birth
defects) in offspring. The specific phthalates shown to have effects on fetuses following maternal
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
ingestion include DnBP (50-52); DEHP and its metabolites, MEHP and 2-EHA (41, 69, 70, 78);
BBP and its metabolites, MBP and MBeP (30-32, 39); as well as DEP and DMP (82). Two studies
of prenatal exposure to phthalates demonstrated no effects on fetuses, with one study using
inhalation exposure of pregnant rats to DEHP (110), and another study using injection of pregnant
rabbits with the DEHP metabolite, MEHP (111). The U.S. EPA reported toxicology studies
demonstrating minimal or no developmental toxicity in offspring exposed in utero (84).
Observed teratogenic effects (birth defects) following prenatal phthalate or phthalate metabolite
exposure included skeletal variations in ribs and sterna, and delayed ossification (hardening) of
bones (30-32, 42, 50, 78, 82, 112-114); increased pre- and post-implantation loss (fetal death) and
decreased number of live fetuses (37-40, 52, 63, 70, 114); increased incidence of malformations of
the forebrain, optic system, and mandibular and maxillary processes (50); decreased fetal body
weight (70); increased incidence of cleft palate (30-32, 39, 51, 52); and increased dilation of the
renal pelvis (30-32, 39).
Teratogenic effects following prenatal exposure to phthalates were dependent on the stage of
pregnancy when exposed (31, 42, 112), on the water solubility of the phthalate (113), and on the
stereochemical form of the phthalate (78). Teratogenic effects on fetuses (skeletal malformations and
testicular dysgenesis) were noted when pregnant dams were exposed by ingestion (31, 42, 112) or by
injection (78, 113).
In support of the classification of phthalates as endocrine disrupters, sexual development of males
has been affected by exposure to phthalates and their metabolites. Ingestion exposure of pregnant
rats to DEHP (35, 71-73, 115), BBP (33, 35), or DBF (53-67, 115) resulted in male offspring with an
increased incidence of hypospadias; decreased testicular and plasma testosterone levels; abnormal
Sertoli and Leydig cells in testicles; shortened anogenital distances; and female-like nipples. Similar
effects were seen in male rabbits exposed to DBF in utero and during adolescence, but not exposed
as adults (116). The DBF-induced effects in rats were similar to those seen in human testicular
dysgenesis syndrome (TDS) (55). Some other studies of neonatal ingestion exposure found no
significant effects on male reproductive system development for DEHP (117), DBF (62), or BBP
(118).
Metabolites of phthalates are thought to be the biologically active compounds that exert
developmental effects following phthalate exposure. Exposure to the metabolites MBP (31, 39-42)
or MEHP (78, 108, 111) resulted in skeletal malformations and testicular development
abnormalities, as seen with exposure to the phthalates BBP or DEHP.
Major adverse changes in neonatal lung tissue were noted following prenatal exposure to DEHP via
maternal ingestion, such that changes in lung tissue resulted in an estimated 50% decrease in the
ability of lung cells to exchange gas (74).
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
Exposure to DEHP (76, 77) or DBF (119) via ingestion has been shown to affect several hepatic
enzyme activities in fetal, neonatal, suckling, and adult rats. Suckling rats exposed to DEHP through
maternal milk had significant increases in hepatic peroxisomal enzyme activities (palmitoyl CoA
oxidase and carnitine acetyltransferase) (76); these effects were also observed in neonatal and adult
male rats following oral exposure to DEHP (77). Furthermore, suckling rats exposed to DEHP
through maternal milk had significant decreases in several other hepatic enzyme activities (aniline
hydroxylase, ethylmorphine N-demethylase, and arylhydrocarbon hydroxylase) and in cytochrome
P450 content (75).
Behavioral effects in young rats exposed to DEHP via intracisternal injection (inside the brain) have
been reported (120, 121). Exposed mice experienced significant, dose-dependent increases in motor
activity, and this model is being explored as a model for attention-deficit hyperactivity disorder
(ADHD) in children (120, 121).
V. CONSIDERATIONS FOR DECISION-MAKERS
This section contains information that may be useful to risk assessors, parents, caregivers, physicians, and other decision-
makers who are interested in reducing the exposure and adverse health effects in children for this particular chemical.
Information in this section focuses on ways to reduce exposure, assess possible exposure, and, for some chemicals,
administer treatment.
Information about Reducing or Preventing Exposure
> The daily levels of exposure to DEHP for the general public may approach or exceed the U.S. EPA
RfD, 0.02 mg/kg/day (equivalent to 1.4 mg/day for an average 70-kg person); see Toxicity
Reference Values section of this Chemical Summary. Compiling estimates from several studies, the
average total daily individual exposure to DEHP in the U.S. was estimated to be 0.003-0.03
mg/kg/day in one report (1), and 0.006-0.02 mg/kg/day in another report (16).
*• The likelihood of exposure of children to phthalates is quite high, given that phthalates are
plasticizers that can leach out of polyvinyl chloride and other plastic products widely used in the
U.S. (2-6, 8-12, 14, 15, 88). Children ages 3-12 months are at highest risk for exposure to phthalates
from leaching from plastic toys by mouthing (1, 6).
> Quantifying exposures of children from mouthing of toys has been difficult for numerous reasons,
but exposures are likely to be low (1, 5, 6, 122, 123). Many manufacturers have voluntarily stopped
the use of phthalates in nipples, teethers, and rattles; and many retailers voluntarily refuse to sell
such products if they contain phthalates (1, 122).
Supporting references and summaries are provided in the TEACH Database at http://epo.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
Premature infants and other children who require dialysis, prolonged feeding, or mechanical
ventilation via plastic tubing are at risk for significant exposure to phthalates in medical devices (1,
6, 9, 11, 15). Neonatal exposure to DEHP and MEHP, via exchange transfusion, can be up to 3,300
jig/kg and 360 |ig/kg, respectively, per transfusion (17, 18). Recently the U.S. EPA National
Toxicology Program (NTP) issued a report that included a concern for critically-ill male infants who
may be exposed to DEHP in medical tubing (124). The U.S. FDA also recommended reducing use
of DEHP-containing tubing in some medical procedures, including exchange transfusions and
ECMO treatments of infants (125).
The U.S. Food and Drug Administration (FDA) urges careful use of plastic containers to reheat food
in the microwave (126, 127). Recommendations include: 1) microwave-safe plastic wrap should be
placed loosely over food so that steam can escape, and should not directly touch your food; 2)
carry out containers from restaurants and margarine tubs should not be used in the microwave; and 3)
containers that hold prepared microwavable meals after you use them because they are meant for
one-time use.
Other Exposure Information
*• Concentrations of phthalate metabolites in urine of children six years of age and older were
measured for the National Health and Nutrition Examination Survey (NHANES) (128). This
ongoing comprehensive national survey is administered by the U.S. Centers for Disease Control and
Prevention National Center for Health Statistics (129). A total of 12 phthalate metabolites were
measured as part of this study.
> Some jurisdictions have set regulations that limit or ban phthalate use in children's toys.
—The use of six phthalates in children's toys and childcare articles have been banned in Europe
by the European Parliament: use of BBP, DBF, DEHP in toys and childcare articles; use of
DINP, DIDP, and DNDP in toys and childcare articles that are put in children's mouths (130).
—The San Francisco government has banned the manufacture, sale, and distribution within the
metropolitan area of toy or child care article or child feeding product intended for use by a child
that is made with or contains more than 0.1% of these phthalates: DEHP; DBF; BBP; DINP;
DnOP; and diisononyl phthalate (131, 132).
* Detailed toxicological summaries of the phthalates BBP, DEHP, DINP, DBF, DnOP, diisodecyl
phthalate, and di-n-hexylphthalate are provided in a series of monographs (issued in 2003) and
expert panel reports (issued in 2000) provided by the U.S. National Toxicology Program; a recent
2006 draft report is available for DEHP (6). Detailed Toxicological Profiles are also available from
the U.S. ATSDR for DEHP (1), DEP (3), DBF (4), and DnOP (5). Hazard Summaries are available
from the U.S. EPA for DBF (133), DMP (134), and DEHP (135). A recent evaluation of DEP by the
U.S. EPA OPPTS is available (84).
Supporting references and summaries are provided in the TEACH Database at http://epo.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
Some phthalates are listed by the U.S. EPA as inert (or "other") ingredients in pesticides, indicating
the ingredient is not an "active" ingredient for the product, but may require evaluation or has been
evaluated as to its potential toxicity to humans. Many inert ingredients are categorized by the U.S.
EPA according to level of concern for toxicity to humans. There are 10 phthalates included on the
EPA inert pesticide ingredient list, with the phthalate of highest concern being phthalic acid, bis(2-
ethylhexyl) ester C1980 on List 1, Inert Ingredients of Toxicological Concern (136). DEP was
recently reevaluated as an inert, and the U.S. EPA concluded that DEP is minimally toxic via the
oral and dermal routes (84).
Other Information Resources
> Three phthalates (BBP, DBF, and DEHP) are listed on the 2005 Priority List of Hazardous
Substances for the Comprehensive Environmental Response, Compensation, and Liability Act
(CERCLA) section 104 (i), as amended by the Superfund Amendments and Reauthorization Act
(SARA). This is a list, in the order of priority of concern, of substances most commonly found at
sites listed on the National Priorities List (NPL); there are currently 275 substances on this list. The
phthalate DBF is listed as number 52, DEHP is listed as number 76, and BBP is listed as number 195
on the NPL (137). DEHP has been identified in at least 737 of 1,613 hazardous waste sites proposed
for inclusion on the NPL (1).
> Consult the U.S. EPA "Child-Specific Exposure Factors Handbook" (EPA-600-P-00-002B) for
factors to assess children's ingestion and inhalation rates (138). An updated External Draft of the
2006 version of this handbook is available (139).
VI. TOXICITY REFERENCE VALUES
Phthalates consist ofnumerous chemicals, only some of which have toxicity reference values listed through U.S. federal agencies.
The phthalates listed in this section are those for which toxicity reference values are available.
Butyl benzyl phthalate (BBP)
A. Oral/Ingestion
U.S. EPA Reference Dose (RfD) for Chronic Oral Exposure: 2E-1 (or 0.2) mg/kg/day, based on
significantly increased liver-to-body weight and liver-to-brain weight ratios in adults
(www.epa.gov/iris/subst/0293.htm, I.A.I) (140). Last Workgroup Verification Date 6/15/89.
B. Inhalation
Not available.
Continued on next page
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
Dibutyl phthalate (DBP)
A. Oral/Ingestion
U.S. EPA Reference Dose (RfD) for Chronic Oral Exposure: 1E-1 (or 0.1) mg/kg/day, based on
increased mortality in adult animals (www.epa.gov/iris/subst/0038.htm, I.A.I) (141). Last
Workgroup Verification Date 1/22/86.
U.S ATSDR Minimal Risk Level (MRL): Oral acute exposure, 0.5 mg/kg/day, based on
developmental effects (www.atsdr.cdc.gov/mrls.html) (142). Last revised 9/01.
B. Inhalation
U.S ATSDR Minimal Risk Level (MRL): Oral acute exposure, 0.5 mg/kg/day, based on
developmental effects (www.atsdr.cdc.gov/mrls.html) (142). Last revised 9/01.
Di(2-ethylhexyl)phthalate (DEHP)
A. Oral/Ingestion
U.S. EPA Reference Dose (RfD) for Chronic Oral Exposure: 2E-2 (or 0.02) mg/kg/day, based on
increased relative liver weight in adult animals (www.epa.gov/iris/subst/0014.htm, LA. 1) (143).
Last Workgroup Verification Date 1/22/86.
U.S. EPA Cancer Oral Slope Factor: 1.4E-2 (or 0.014) per mg/kg/day, based on hepatocellular
carcinoma and adenoma, using the linearized multistage procedure, extra risk
(www.epa.gov/iris/subst/0014.htm, II.B.l) (143). Last Workgroup Verification Date 10/7/87.
U.S. EPA Cancer Drinking Water Unit Risk: 4.0E-7 (or 0.0000004) per (ng/L)
(www.epa.gov/iris/subst/0014.htm, II.B.l) (143). Last Workgroup Verification Date 10/7/87.
U.S. EPA Drinking Water Concentrations at Specified Risk Levels for Cancer: E-4 (or 1 in
10,000), 3E+2 (or 300) ng/L; E-5 (or 1 in 100,000), 3E+1 (or 30) ng/L; E-6 (or 1 in 1,000,000),
3E+0 (or 3.0) ng/L (www.epa.gov/iris/subst/0014.htm, II.B.l) (143). Last Workgroup
Verification Date 10/7/87.
U.S. EPA Maximum Contaminant Level (MCL) for Drinking Water: 0 006 mg/L, based on
reproductive difficulties, liver problems, and increased risk of cancer in adult animals
(www.epa.gov/safewater/mcl.html#mcls) (144). Last revised 7/02.
U.S. EPA Maximum Contaminant Level Goal (MCLG): 0 mg/L Last revised 7/02
U.S. ATSDR Minimal Risk Level (MRL): Oral intermediate exposure, 0.1 mg/kg/day, based on
reproductive effects in adult animals. Oral chronic exposure, 0.06 mg/kg/day, based on
reproductive effects in adult animals (www.atsdr.cdc.gov/mrls.html) (142). Last revised 9/02.
Continued on next page
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
B. Inhalation
Not available.
Diethyl phthalate (DEP)
A. Oral/Ingestion
U.S. EPA Reference Dose (RfD) for Chronic Oral Exposure: 8E-1 (or 08) mg/kg/day, based on
Decreased growth rate, food consumption and altered organ weights in adult rats
(http://www.epa.gov/iris/subst/0226.htm. I.A.I) (85). Last Workgroup Verification Date 7/16/87.
B. Inhalation
Not available.
Dimethyl phthalate (DMP)
A. Oral/Ingestion
U.S. EPA Reference Dose (RfD) for Chronic Oral Exposure: not available at this time
(http://www.epa.gov/iris/subst/0353.htm, I.A.I) (145). Last Workgroup Verification Date
8/26/87.
B. Inhalation
U.S. EPA Reference Concentration (RfC) for Chronic Inhalation Exposure: available health effects
data were insufficient to derive an RfC (http://www.epa.gov/iris/subst/0353.htm, IB.) (145).
Last Workgroup Verification Date 7/26/90.
Dimethyl terephthalate (DMT)
A. Oral/Ingestion
U.S. EPA Reference Dose (RfD) for Chronic Oral Exposure: 1E-1 (or 0.1) mg/kg/day, based on
chronic kidney inflammation in adult rats (http://www.epa.gov/iris/subst/0046.htm, I.A.I) (146).
Last Workgroup Verification Date 10/9/85.
U.S. ATSDR Minimal Risk Level (MRL): Oral acute exposure, 7 mg/kg/day, based on reproductive
effects. Oral intermediate exposure, 6 mg/kg/day, based on hepatic effects
(www.atsdr.cdc.gov/mrls.html) (142). Last revised 6/95.
B. Inhalation
Not available.
Continued on next page
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
Di-N-octyl phthalate (DnOP)
A. Oral/Ingestion
U.S. ATSDR Minimal Risk Level (MRL): Oral acute exposure, 3 mg/kg/day, based on hepatic effects.
Oral intermediate exposure, 0.4 mg/kg/day, based on hepatic effects
(www.atsdr.cdc.gov/mrls.html) (142). Last revised 9/97.
B. Inhalation
Not available.
VII. U.S. FEDERAL REGULATORY INFORMATION
•> The U.S. EPA IRIS is currently reviewing toxicity reference values for BBP, DBF, and DEHP (49).
*• There are no U.S. regulations on the use of phthalates in children's toys, although many
manufacturers voluntarily stopped using phthalates in teethers and rattles in 1999, and the use of
phthalates in nipples was voluntarily discontinued beginning in 1986 (1, 6, 122).
*• DBF, DEHP, and DMP are included on the list of 188 hazardous air pollutants (HAPs) listed under
section 112(b) of the 1990 Clean Air Act Amendments and are regulated from more than 170
industrial source categories (147).
> There are 10 phthalates are listed by the U.S. EPA as inert ingredients in pesticides, each listed on
one of four lists ranked by level of toxicological concern and amount of toxicological information
available (136). DEP was recently moved from List 2 (Potentially Toxic Other Ingredients/High
Priority for Testing Inerts) to List 4B (Other ingredients for which EPA has sufficient information to
reasonably conclude that the current use pattern in pesticide products will not adversely affect public
health or the environment) (136).
*• The U. S. EPA requires reporting of quantities of certain chemicals that exceed a defined reportable
quantity, and that quantity varies for different chemicals (148). Under the Emergency Planning and
Community Right-to-Know Act (EPCRA) Section 313 "Toxic Chemicals," reporting of quantities of
DBF, DEHP, or DMP greater than 10,000 pounds manufactured or processed, or otherwise used, is
required (148). Under the Comprehensive Environmental Response, Compensation, and Liability
Act (CERCLA), quantities of releases for required reporting vary depending on the phthalate: DBF,
10 pounds; BBP and DEHP, 100 pounds; DEP, 1,000 pounds; and DMP, 5,000 pounds (148).
Supporting references and summaries are provided in the TEACH Database at http://epo.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
Page 14
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Chemical Summary, Phthalates (continued)
VIM. BACKGROUND ON CHEMICAL
A. CAS Numbers: Butyl benzyl phthalate, 85-68-7; Diethyl phthalate, 84-66-2; Dibutyl phthalate,
84-74-2; Di(2-ethylhexyl) phthalate, 117-81-7; Dimethyl terephthalate 120-61-6
B. Physicochemical Properties: Phthalates in pure form are clear-to-yellowish liquids, some with mild
odors; go to http://chem.sis.nlm.nih.gov/chemidplus/ and search for each phthalate by name or by CAS
number.
C. Production: Phthalates are widely used industrial and commercial chemicals, mainly as plasticizers
in polyvinyl chloride (95% of DEHP industrial use) and other polymers such as rubber, cellulose, and
styrene (149). Production of DEHP was estimated to be 258 million pounds in 1994 (150), and
production of all dioctyl phthalates was estimated to be 285 million pounds in 1998 (1). More recent
numbers are not available because the information is considered proprietary by the chemical
manufacturing companies (1).
D. Uses: Phthalates or phthalic esters are a group of compounds used as plasticizers in polyvinyl
chloride and other polymers, as well as for other polymers (1-6). Many packaging materials contain
phthalates, including food and beverage items and some medical products. They are widely used
compounds found in a diverse range of products, including: cosmetics, pesticides (as carriers), soaps and
detergents, inks, lacquers, lubricating oils, adhesives, photographic film, wire and cable, toys,
toothbrushes, and defoaming agents. For phthalates listed in TRI, total reported releases and disposals in
2004 were: DEHP over 840,000 pounds; DBF over 177,000 pounds; and DMP over 414,000 pounds.
Note these reported releases and disposals should be considered a minimum estimate because only
certain types of facilities are required to report (150).
E. Environmental Fate: Phthalates can leach from plastic packaging into the food and beverage items
they surround (1-6). In the environment, phthalates are found largely as a result of industrial releases.
DEHP and the other phthalates can strongly adsorb to soils and sediments and rarely leaches into
groundwater or evaporates (1-6). In the air, phthalates are fairly stable and can be carried long distances.
When released into water, phthalates can degrade somewhat quickly; for example, DEHP has a half-life
of two to three weeks in water. DEHP can bioconcentrate in aquatic systems, although not all phthalates
bioconcentrate.
F. Synonyms and Trade Names: (for a more complete list, go to
http://chem.sis.nlm.nih.gov/chemidplus/and search for each phthalate by name or by CAS number)
Butylbenzyl phthalate: Benzyl butyl phthalate; benzyl butylphthalate; benzyl n-butyl phthalate;
butyl phenylmethyl 1,2-benzenedicarboxylate; CCRIS 104; Caswell No. 125G; EINECS 201-622-7;
HSDB 2107; NCI-C54375; NSC 71001; Palatinol BB; Phthalic acid, benzyl butyl ester; Santicizer
160; Sicol; Sicol 160; Unimoll BB; n-Butyl benzyl phthalate, and others.
Continued on next page
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
Di(2-ethylhexyl)phalate: DEHP; OOP; bis(2-Ethylhexyl) phthalate; Dioctyl Phthalate; 1,2-
Benzenedicarboxylic acid bis(2-ethylhexyl) ester; Octoil; Ethyl hexyl phthalate; 2-Ethylhexyl
phthalate; bis-(2-ethylhexyl) 1,2-benzenedicarboxylate; octyl phthalate; phthalic acid dioctyl ester;
BEHP; bisoflex 81; bisoflex dop; compound 889; DAF 68; ergoplast fdo; eviplast 80; eviplast 81;
fleximel; flexol dop; flexol plasticizer dop; good-rite gp 264; hatcol dop; hercoflex 260; kodaflex
dop; mollan o; nuoplaz dop; palatinol ah; Pittsburgh px-138; platinol ah; platinol dop; re plasticizer
dop; reomol dop; reomol d 79p; sicol 150; staflex dop; truflex dop; vestinol ah; vinicizer 80; witcizer
312; Benzenedicarboxylic acid, bis(2-ethylhexyl) ester; Union carbide flexol 380; bis (2-Etheylexyl)
Phthalate; Bis(2-Ethylhexyl)Phthalate (DEHP); Bis (2-Ethylhexyl) Phthalate (Dioctyl phthalate),
and others.
Diethyl phthalate: Ethyl phthalate; DEP; 1,2-benzenedicarboxylic acid diethyl ester; diethyl o-
phthalate; anozol; estol 1550; neantine; palatinol a; phthalol; placidol e; solvanol;
Benzenedicarboxylic acid, diethyl ester; and others.
Di-n-butyl phthalate: DBF; Di-n-Butyl Phthalate; n-Butyl phthalate; 1,2-Benzenedicarboxylic acid
dibutyl ester; Phthalic acid dibutyl ester; o-benzenedicarboxylic acid, dibutyl ester; benzene-o-
dicarboxylic acid di-n-butyl ester; dibutyl 1,2-benzenedicarboxylate; celluflex dpb; Elaol; hexaplas
m/b; palatinol c; polycizer dbp; PX 104; staflex dbp; witcizer 300; Araldite 502;
benzenedicarboxylic acid, dibutyl ester; dibutyl o-Phthalate; and others.
Dimethyl phthalate: DMP; 1,2-benzenedicarboxylic acid; dimethyl ester; dimethyl 1,2-
benzenedicarboxylate; dimethyl benzene-o-dicarboxylate; dimethyl phthalate; methyl phthalate;
phthalic acid; dimethyl ester; and others.
Additional information on phthalates is available in the TEACH Database for Phthalates, and at the
following Web sites:
www.epa.gov/ost/drmkmg/standards/dwstandards.pdf
www.epa.gov/safewater/dwh/c-soc.html
http://ntp-server. niehs. nih. gov/ntp/roc/eleventh/profiles/s08 7dehp.pdf
http://cerhr.mehs.mh.gov/chemicals/dehp/DEHP-Monograph.pdf
http://cerhr. niehs. nih. gov/chemicals/
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
Page 16
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Chemical Summary, Phthalates (continued)
REFERENCES
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Di(2-Ethylhexyl)phthalate (DEHP)." http://www.atsdr.cdc.gov/toxprofiles/tp9.html.
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Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
Page 17
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Chemical Summary, Phthalates (continued)
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38. Ema, M., et al. 1998. "Reproductive effects of butyl benzyl phthalate in pregnant and
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Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
Page 18
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Chemical Summary, Phthalates (continued)
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51. Ema, M., et al. 1993. "Teratogenic evaluation of di-n-butyl phthalate in rats." Toxicol.Lett.
69(2): 197-203.
52. Ema, M., et al. 1994. "Characterization of the developmental toxicity of di-n-butyl phthalate in rats."
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53. Foster, P.M., et al. 2000. "Effects of di-n-butyl phthalate (DBF) on male reproductive development
in the rat: implications for human risk assessment." Food Chem.Toxicol. 38(1 Suppl):S97-S99.
54. Ema, M., et al. 2000. "Critical period for adverse effects on development of reproductive system in
male offspring of rats given di-n-butyl phthalate during late pregnancy." Toxicol.Lett. 111(3):271-
278.
55. Fisher, J.S., et al. 2003. "Human 'testicular dysgenesis syndrome': a possible model using in-utero
exposure of the rat to dibutyl phthalate." Hum.Reprod. 18(7): 1383-1394.
56. Salazar, V., et al. 2004. "Effect of oral intake of dibutyl phthalate on reproductive parameters of
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57. Barlow, N.J., et al. 2004. "Male reproductive tract lesions at 6, 12, and 18 months of age following
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58. Bowman, C.J., et al. 2005. "Altered gene expression during rat Wolffian duct development following
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Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
59. Carruthers, C.M., and P.M. Foster. 2005. "Critical window of male reproductive tract development
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62. Zhang, Y., et al. 2004. "Reproductive and developmental toxicity in Fl Sprague-Dawley male rats
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63. Mylchreest, E., et al. 1998. "Male reproductive tract malformations in rats following gestational and
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64. Mylchreest, E., et al. 1999. "Disruption of androgen-regulated male reproductive development by
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65. Mylchreest, E., et al. 2000. "Dose-dependent alterations in androgen-regulated male reproductive
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66. Mylchreest, E., et al. 2002. "Fetal testosterone insufficiency and abnormal proliferation of Leydig
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67. Lee, K.Y., et al. 2004. "Diverse developmental toxicity of di-n-butyl phthalate in both sexes of rat
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68. Rais-Bahrami, K., et al. 2004. "Follow-up study of adolescents exposed to di(2-ethylhexyl) phthalate
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69. Pennanen, S., et al. 1992. "The developmental toxicity of 2-ethylhexanoic acid in Wistar rats."
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73. Parks, L.G., et al. 2000. "The plasticizer diethylhexyl phthalate induces malformations by decreasing
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Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
75. Parmar, D., et al. 1985. "Hepatic mixed function oxidases and cytochrome P-450 contents in rat pups
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78. Hauck, R.S., et al. 1990. "Asymmetric synthesis and teratogenic activity of (R)- and (S)-2-
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79. Ritter, E.J., et al. 1987. "Teratogenicity of di(2-ethylhexyl) phthalate, 2-ethylhexanol, 2-
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80. Tomita, I, et al. 1986. "Fetotoxic effects of mono-2-ethylhexyl phthalate (MEHP) in mice."
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81. Yagi, Y., et al. 1980. "Teratogenic potential of di- and mono-(2-ethylhexyl)phthalate in mice."
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83. Fujii, S., et al. 2005. "A two-generation reproductive toxicity study of diethyl phthalate (DEP) in
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84. U.S. Environmental Protection Agency. 2006. "Reassessment of the One Exemption from the
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85. U.S. Environmental Protection Agency. 1993. "Integrated Risk Information System (IRIS): Diethyl
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86. Jonsson, B.A., et al. 2005. "Urinary phthalate metabolites and biomarkers of reproductive function
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87. Hauser, R., et al. 2005. "Evidence of interaction between polychlorinated biphenyls and phthalates
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88. Tsumura, Y., et al. 2003. "Estimated daily intake of plasticizers in 1-week duplicate diet samples
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90. Becker, K., et al. 2004. "DEHP metabolites in urine of children and DEHP in house dust."
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92. Rudel, R.A., et al. 2003. "Phthalates, Alkylphenols, Pesticides,Polybrominated Diphenyl Ethers, and
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Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
94. Colon, I, et al. 2000. "Identification of phthalate esters in the serum of young Puerto Rican girls
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95. Calafat, A.M., et al. 2004. "Exposure to di-(2-ethylhexyl) phthalate among premature neonates in a
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96. Koch, H.M., et al. 2004. "Internal exposure of nursery-school children and their parents and teachers
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99. Koch, H.M., et al. 2005. "Di(2-ethylhexyl)phthalate (DEHP) exposure of voluntary plasma and
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101. Koch, H.M., et al. 2003. "An estimation of the daily intake of di(2-ethylhexyl)phthalate (DEHP)
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104. Eriksson, P., and P.O. Darnerud. 1985. "Distribution and retention of some chlorinated
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105. Singh, A.R., et al. 1975. "Maternal -fetal transfer of 14C-di-2-ethylhexyl phthalate and 14C-di ethyl
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106. Kremer, J.J., et al. 2005. "Pharmacokinetics of monobutylphthalate, the active metabolite of di-n-
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108. Kessler, W., et al. 2004. "Blood burden of di(2-ethylhexyl) phthalate and its primary metabolite
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110. Merkle, J., et al. 1988. "Developmental toxicity in rats after inhalation exposure of di-2-
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111. Thomas, J.A., et al. 1979. "Failure of monoethylhexyl phthalate to cause teratogenic effects in
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Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
113. Singh, A.R., et al. 1972. "Teratogenicity of phthalate esters in rats." J.Pharm.Sci. 61(l):51-55.
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116. Higuchi, T.T., et al. 2003. "Effects of dibutyl phthalate in male rabbits following in utero,
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117. Tanaka, T. 2002. "Reproductive and neurobehavioural toxicity study of bis(2-ethylhexyl) phthalate
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120. Masuo, Y., et al. 2004. "Effects of neonatal treatment with 6-hydroxydopamine and endocrine
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122. U.S. Consumer Product Safety Commission. 1998. "The Risk of Chronic Toxicity Associated with
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123. U.S. Consumer Products Safety Commission. 1998. "Study on Phthalates in Teethers, Rattles and
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125. U.S. Food and Drug Administration. 2002. "Public Health Notification: PVC Devices Containing
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126. U.S. Food and Drug Administration. 2002. "Plastics and the Microwave."
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127. USDA Food Safety and Inspection Service. 2000. "Food Safety Facts."
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128. U.S. Centers for Disease Control. 2005. "National Center for Health Statistics."
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Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
131. City and County of San Francisco Board of Supervisors. 2006. "Legislative Analyst Report:
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133. U.S. Environmental Protection Agency. 2003. "Dibutyl Phthalate: Hazard Summary."
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134. U.S. Environmental Protection Agency. 2003. "Dimethyl Phthalate: Hazard Summary."
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135. U.S. Environmental Protection Agency. 2000. "Technology Transfer Network Air Toxics Website:
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136. U.S. Environmental Protection Agency. 1989. "Inert (other) Pesticide Ingredients in Pesticide
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138. U.S. Environmental Protection Agency. 2002. "Child-Specific Exposure Factors Handbook
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139. U.S. Environmental Protection Agency. 2006. "Child-Specific Exposure Factors Handbook 2006
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140. U.S. Environmental Protection Agency. 1993. "Integrated Risk Information System (IRIS): Butyl
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141. U.S. Environmental Protection Agency. 1990. "Integrated Risk Information System (IRIS): Dibutyl
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142. U.S. Centers for Disease Control (ATSDR). 2006. "Minimal Risk Levels (MRLs) for Hazardous
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143. U.S. Environmental Protection Agency. 1991. "Integrated Risk Information System (IRIS): Di(2-
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145. U.S. Environmental Protection Agency. 1987. "Integrated Risk Information System (IRIS):
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146. U.S. Environmental Protection Agency. 1995. "Integrated Risk Information System (IRIS):
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147. U.S. Environmental Protection Agency. 2006. "Technology Transfer Network Air Toxics Website:
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148. U.S. Environmental Protection Agency. 2001. "Lists of Lists: Consolidated List of Chemicals
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Air Act." http://www.epa.gov/ceppo/pubs/title3.pdf
Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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Chemical Summary, Phthalates (continued)
149. Doull, J., et al. 1999. "A cancer risk assessment of di(2-ethylhexyl)phthalate: application of the
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150. U.S. Environmental Protection Agency. 2006. "TRI Explorer: Providing Access to EPA's Toxic
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Supporting references and summaries are provided in the TEACH Database at http://epa.sov/teach/.
Last revised 10/10/2007: includes research articles through 2005, and other information through 2006.
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