DIBUTYL PHTHALATE
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~y29lA2:1
DIBUTYL PHTHALATE
CASRN: 84-74-2
For other data, click on the Table of Contents
Human Health Effects:
Toxicity Summary:
... The principal media of exposure to dibutyl
phthalate (DBP) for the general population, listed in order of their
relative importance based upon estimated intake, are as follows: food, indoor
air and drinking water. ... Intake of DHP in the diet can vary considerably,
depending upon the nature and extent of packaged food consumed and the nature of
use of food wrapping in food preparation. ... There is also potential for
exposure to DHP in cosmetics. ... In studies on rats, DBP is absorbed through
the skin, although in in vitro studies human skin has been found to be less
permeable than rat skin to this compound. Studies in laboratory animals indicate
that DBP is rapidly absorbed from the gastrointestinal tract, distributed
primarily to the liver and kidneys of rats and excreted in urine as metabolites
following oral or intravenous administration. Following inhalation, it was
consistently detected at low concentrations in the brain. Available data
indicate that in rats, following ingestion, DBP is metabolized by nonspecific
esterases mainly in the small intestine to yield mono-n-butyl
phthalate with limited subsequent biochemical oxidation of the alkyl side
chain. Mono-n-butyl phthalate is stable and resistant
to hydrolysis of the second ester group. Mono-n-butyl
phthalate and other metabolites are excreted in the urine mainly as
glucuronide conjugates. Species differences in the excretion of conjugates and
unconjugated metabolites of DHP in the urine of rats and hamsters have been
observed. ... Accumulation has not been observed in any organ. The profile of
effects following exposure to DBP is similar to that of other phthalate esters,
which, in susceptible species, can induce hepatomegaly, increased numbers of
hepatic peroxisomes, fetotoxicity, teratogenicity, and testicular damage. The
acute toxicity of DBP in rats and mice is low. ... Signs of acute toxicity in
laboratory animals include depression of activity, labored breathing, and lack
of coordination. ... In short-term repeated-dose toxicity studies, effects ...
in rats after oral administration ... included peroxisome proliferation and
hepatomegaly. ... In longer-term studies, the effects in rats ... included
reduced rate of weight gain .... Increase in relative liver weight ...
Peroxisomal proliferation with increased peroxisomal enzyme activity. ...
Necrotic hepatic changes in Wistar rats ... but not in F-344 or Sprague-Dawley
rats. ... Alteration in testicular enzymes and degeneration of testicular
germinal cells of rats. ... There are considerable species differences in
effects on the testes following exposure to DBP, minimal effects being observed
in mice and hamsters. ... DBP appears to have little potential to irritate skin
or eyes or to induce sensitization. In humans, a few cases of sensitization
after exposure to DBP have been reported. ... In a continuous breeding protocol
... results suggest that the adverse effects of DBP are more marked in animals
exposed during development and maturation than in animals exposed as adults
only. ... DBP generally induces fetotoxic effects in the absence of maternal
toxicity. Available data also indicate that DBP is teratogenic at high doses and
that susceptibility to teratogenesis varies with developmental state and period
of administration. ... The weight of the available evidence indicates that DBP
is not genotoxic. ... Since DBP causes peroxisomal proliferation, it is possible
that it might be a rodent liver carcinogen, although it is much weaker in
inducing hepatomegaly and peroxisome proliferation than diethylhexyl phthalate.
... Since DBP is not genotoxic and is expected to be a less potent carcinogen
than diethylhexyl phthalate ... It is unlikely that DBP presents any
significantly increased risk of cancer at concentrations generally present in
the environment. Ingestion is by far the principal route of exposure to DBP;
moreover, the toxicological data for other routes of administration are
insufficient for evaluation. ... The risk to aquatic organisms associated with
the present mean concentrations of DBP in surface water is low. However, in
highly polluted rivers the safety margin is much smaller. ...
Evidence for Carcinogenicity:
CLASSIFICATION: D; not classifiable as to
human carcinogenicity. BASIS FOR CLASSIFICATION: Pertinent data regarding
carcinogenicity was not located in the available literature. HUMAN
CARCINOGENICITY DATA: None. ANIMAL CARCINOGENICITY DATA: None.
Human Toxicity Excerpts:
CHEMICAL WORKER IS SAID TO HAVE SWALLOWED 10 G
BY MISTAKE WITH NO SYMPTOMS UNTIL SEVERAL HOURS LATER WHEN HE DEVELOPED A SEVERE
KERATITIS IN BOTH EYES WITH LOSS OF CORNEAL EPITHELIUM, ALSO TRANSITORY TOXIC
NEPHRITIS, CHARACTERIZED BY PRESENCE OF RED & WHITE BLOOD CELLS & MANY
OXALATE CRYSTALS IN URINE.
WOMEN WORKING IN SYNTHETIC LEATHER INDUSTRY
WHERE PHTHALATES ARE USED HAD HIGHER INCIDENCE OF MISCARRIAGES & MENSTRUAL
DISORDERS. /PHTHALATES/
IN WOMEN OCCUPATIONALLY DEALING WITH
PHTHALATES INCOMPLETE PREGNANCY, REDUCED GESTATION & DELIVERY RATES, INCR
ABORTIONS, & PRESENCE OF ANOVULATORY HYPOESTROGENOUS CYCLES WERE OBSERVED.
/PHTHALATES/
DIBUTYL PHTHALATE @ 0.25
MG/ML IN HUMAN LEUKOCYTE CULTURES /DOES NOT CAUSE/ CHROMATID ABERRATION.
... The toxicity to HeLa cells of 29
plasticizers was determined /in/ the metabolic inhibition test-24 system. The
7-day IC50 (median inhibitory concn) for HeLa cells /ranged/ from 260 to 1.5
g/l. Phthalates, adipates, sebacates, azelates, and phosphates with long carbon
chain alcohol were very non-toxic to the cells probably due to insolubility. ...
/Phthalates, sebacates, azelates, phosphates/
IN A PRELIMINARY STUDY OF 150-250 WORKERS
EXPOSED TO VAPORS IN AIR MIXTURES OF DIBUTYL PHTHALATE, DIETHYL
PHTHALATE, & DI-2-ETHYL HEXYL PHTHALATE, 19 PERSONAL AIR SAMPLES (COLLECTED
IN THE BREATHING ZONE OF EMPLOYEES), 4 HR DURATION EACH, WERE TAKEN OVER 8
DIFFERENT DAYS AT A NUMBER OF LOCATIONS IN THE VICINITY OF THE OPERATIONS. THE
RESULTS OF THE AIR ANALYSIS RANGED FROM 1-6 PPM, (8-15 MG/CU M). IN A
DIAGNOSTIC, MULTIPHASIC TESTING OPERATION, NO PHTHALATES IN BLOOD WERE FOUND
BEFORE AND AFTER THE PHTHALATE EXPOSURE, AND NO PERIPHERAL POLYNEURITIS WAS
OBSERVED IN THE POPULATION.
... BREATHING PLASTICIZER AS SPRAY CAN CAUSE
THROAT IRRITATION. ... /IT/ HAS IRRITATING ACTION ON MUCOUS MEMBRANES OF RESP
PASSAGES.
Contact may cause burns to skin and eyes.
In humans, an olfactory threshold value
ranging from 0.26 to 1.47 mg/cu m /was found/. Atmospheric concentraions of 0.12
and 0.15 mg/cu m resulted in abnormal encephalographic responses in the three
human subjects in the study. When the level was reduced to 0.093 mg/cu m no
conditioned reflex was noted. A PSC value of 0.1 mg/cu m is recommended.
Caution: Potential symptoms of overexposure
are irritation of upper respiratory tract and stomach.
Vapors from very hot material may irritate
eyes and produce headache, drowsiness, and convulsions.
Analysis of reports in the world's literature
suggests that average sperm densities for groups of unselected males were
relatively constant at about 108 million cells per ml prior to 1950. Subsequent
to that time mean sperm densities appear to have declined. Regression analysis
indicates the existence of significant negative correlations between mean sperm
densities and production of synthetic organic chemicals among other parameters.
Phthalate esters are one class of large volume organic chemicals that are known
to disturb testicular function in laboratory animals. These compounds are also
the most abundant man made chemicals in the environment. Plots of the
concentration of dibutyl phthalate in the cellular
fraction of ejaculates against either the sperm density or the total number of
sperm for the same ejaculates gave two clusters of points.
COMPARATIVE TOXICITY OF PHTHALATE ESTERS TO
HELA-S3 CELLS WAS STUDIED BY DETERMINING THEIR EFFECT ON DOUBLING TIME OF THE
CELLS. THE TOXICITY OF THE ESTERS DECREASING IN ORDER: DIETHYL PHTHALATE, BUTYL
PHTHALYL BUTYL GLYCOLATE, DI-ISO-BUTYL PHTHALATE, ETHYL
PHTHALYL ETHYL GLYCOLATE, BIS(2-ETHYLHEXYL) PHTHALATE, DIMETHYL ISOPHTHALATE, DIBUTYL
PHTHALATE, METHYL PHTHALYL ETHYL GLYCOLATE, DIMETHYL PHTHALATE, &
DIOCTYL PHTHALATE.
Skin, Eye and Respiratory Irritations:
Contact may cause burns to skin and eyes.
CONTACT WITH SURFACE OF ... EYES ... BY
ACCIDENTAL DROPLET SPLASH AS WELL AS BY EXPTL APPLICATION ... HAS CAUSED ...
SEVERE STINGING PAIN. PAIN STIMULATES PROFUSE TEARING ...
Caution: Potential symptoms of overexposure
are irritation of upper respiratory tract and stomach.
Medical Surveillance:
Routine medical examinations should be
provided to each employee who is exposed to dibutyl phthalate at
potentially hazardous levels.
Probable Routes of Human Exposure:
NIOSH (NOES Survey 1981-1983) has
statistically estimated that 370,025 workers (138,570 of these are female) are
potentially exposed to dibutyl phthalate in the US(1).
Occupational exposure may be through inhalation of dusts or vapors and dermal
contact with this compound at workplaces where dibutyl
phthalate is produced or used. The general population may be exposed to dibutyl
phthalate via inhalation of ambient air, ingestion of food and drinking
water, and dermal contact with products containing dibutyl
phthalate(SRC).
Body Burden:
Human adipose tissue 0.10-0.30 ppm(1),
0.57-0.79 ppm(2). Detected in human tissue and blood(3). Dibutyl
phthalate was detected, not quantified, in human adipose tissue(4).
Average Daily Intake:
AIR INTAKE: (assume 0-6 ng/cu m) 0-400 ng(1);
WATER INTAKE: (assume 0-2.5 ug/l(2)) 20 ng-10,000 ng; FOOD INTAKE: insufficient
data(SRC).
Animal Toxicity Studies:
Toxicity Summary:
... The principal media of exposure to dibutyl
phthalate (DBP) for the general population, listed in order of their
relative importance based upon estimated intake, are as follows: food, indoor
air and drinking water. ... Intake of DHP in the diet can vary considerably,
depending upon the nature and extent of packaged food consumed and the nature of
use of food wrapping in food preparation. ... There is also potential for
exposure to DHP in cosmetics. ... In studies on rats, DBP is absorbed through
the skin, although in in vitro studies human skin has been found to be less
permeable than rat skin to this compound. Studies in laboratory animals indicate
that DBP is rapidly absorbed from the gastrointestinal tract, distributed
primarily to the liver and kidneys of rats and excreted in urine as metabolites
following oral or intravenous administration. Following inhalation, it was
consistently detected at low concentrations in the brain. Available data
indicate that in rats, following ingestion, DBP is metabolized by nonspecific
esterases mainly in the small intestine to yield mono-n-butyl
phthalate with limited subsequent biochemical oxidation of the alkyl side
chain. Mono-n-butyl phthalate is stable and resistant
to hydrolysis of the second ester group. Mono-n-butyl
phthalate and other metabolites are excreted in the urine mainly as
glucuronide conjugates. Species differences in the excretion of conjugates and
unconjugated metabolites of DHP in the urine of rats and hamsters have been
observed. ... Accumulation has not been observed in any organ. The profile of
effects following exposure to DBP is similar to that of other phthalate esters,
which, in susceptible species, can induce hepatomegaly, increased numbers of
hepatic peroxisomes, fetotoxicity, teratogenicity, and testicular damage. The
acute toxicity of DBP in rats and mice is low. ... Signs of acute toxicity in
laboratory animals include depression of activity, labored breathing, and lack
of coordination. ... In short-term repeated-dose toxicity studies, effects ...
in rats after oral administration ... included peroxisome proliferation and
hepatomegaly. ... In longer-term studies, the effects in rats ... included
reduced rate of weight gain .... Increase in relative liver weight ...
Peroxisomal proliferation with increased peroxisomal enzyme activity. ...
Necrotic hepatic changes in Wistar rats ... but not in F-344 or Sprague-Dawley
rats. ... Alteration in testicular enzymes and degeneration of testicular
germinal cells of rats. ... There are considerable species differences in
effects on the testes following exposure to DBP, minimal effects being observed
in mice and hamsters. ... DBP appears to have little potential to irritate skin
or eyes or to induce sensitization. In humans, a few cases of sensitization
after exposure to DBP have been reported. ... In a continuous breeding protocol
... results suggest that the adverse effects of DBP are more marked in animals
exposed during development and maturation than in animals exposed as adults
only. ... DBP generally induces fetotoxic effects in the absence of maternal
toxicity. Available data also indicate that DBP is teratogenic at high doses and
that susceptibility to teratogenesis varies with developmental state and period
of administration. ... The weight of the available evidence indicates that DBP
is not genotoxic. ... Since DBP causes peroxisomal proliferation, it is possible
that it might be a rodent liver carcinogen, although it is much weaker in
inducing hepatomegaly and peroxisome proliferation than diethylhexyl phthalate.
... Since DBP is not genotoxic and is expected to be a less potent carcinogen
than diethylhexyl phthalate ... It is unlikely that DBP presents any
significantly increased risk of cancer at concentrations generally present in
the environment. Ingestion is by far the principal route of exposure to DBP;
moreover, the toxicological data for other routes of administration are
insufficient for evaluation. ... The risk to aquatic organisms associated with
the present mean concentrations of DBP in surface water is low. However, in
highly polluted rivers the safety margin is much smaller. ...
Evidence for Carcinogenicity:
CLASSIFICATION: D; not classifiable as to
human carcinogenicity. BASIS FOR CLASSIFICATION: Pertinent data regarding
carcinogenicity was not located in the available literature. HUMAN
CARCINOGENICITY DATA: None. ANIMAL CARCINOGENICITY DATA: None.
Non-Human Toxicity Excerpts:
FOUR DIFFERENT CONCN OF DIBUTYL
PHTHALATE 0.01%, 0.05%, & 1.25%) WERE USED IN DAILY FOODS OF 4 GROUPS
EACH OF 10 RATS WITH A SUPPLEMENTARY GROUP AS A CONTROL ONE. THE TESTS RAN FOR
TWELVE MO. THE FIRST CONCN (0.01% & 0.05%) DID NOT AFFECT RATS WHICH
TOLERATED THE DAILY DOSES WELL. AT A CONCN OF 1.25% HALF OF THE ANIMALS DIED IN
FIRST WK. HOWEVER, NO ORGANIC LESIONS WERE FOUND WHEN AUTOPSIES WERE PERFORMED.
/WHITE RATS, AGES 5 TO 6 WK & WEIGHING
60-75 G/ ACUTE TOXICITY: THE TWO MODES OF ADMIN CHOSEN WERE THE ORAL ONE AND IM
ONE. THE FIRST GAVE A RATHER HIGH LETHAL DOSE LD50, 8-10 G/KG BODY WEIGHT (@ 4
G/KG ALL THE ANIMALS REMAINED ALIVE, @ 8 G/KG 4 OUT OF 9 DIED, & @ 16 G/KG 6
OUT OF 6 DIED). THE FATAL IM DOSE WAS EVEN HIGHER, SINCE DOSES OF 8 G/KG BODY
WEIGHT DID NOT BRING ABOUT THE DEATH OF A SINGLE ANIMAL.
/WISTAR RATS/ WERE KEPT ON DIETS CONTAINING,
PER KILO, 100 MG, 300 MG & 500 MG DIBUTYL PHTHALATE ON
THE FIRST DIET (100 MG/KG) TESTS WERE CARRIED OUT FOR 5 GENERATIONS, AND WITH
THE OTHER DIETS (300 MG AND 500 MG) FOR 3 GENERATIONS. GROWTH CURVES OF MALE AND
FEMALE RATS SHOWED NO ANOMALIES COMPARED WITH CONTROL RATS OF THE SAME
GENERATION. LONG TERM TESTS ON THE SAME ANIMAL MADE IT POSSIBLE TO CONCLUDE THAT
DIBUTYL PHTHALATE IS HARMLESS, AND THAT IT IS WITHOUT
CARCINOGENIC PROPERTIES UNDER THE PARTICULAR EXPERIMENTAL CONDITIONS.
... 1 ML/KG & 0.5 ML/KG OF 50% DIBUTYL
PHTHALATE ... REGULARLY ADMIN /ORALLY/ TO 2 GROUPS OF RATS TWICE WK FOR
FIFTY-TWO WK. @ END OF PERIOD ANIMALS ... OBSERVED FOR 3 MO. ... 2 FEMALES &
1 MALE HAD SARCOMAS. ... AUTHORS DO NOT THINK THAT IT IS POSSIBLE TO CONCLUDE
FROM THIS THAT DIBUTYL PHTHALATE CAN CAUSE SARCOMAS.
...
IRRITATIVE RESPONSE IN RABBITS TO INTRADERMAL
INJECTIONS OF DIBUTYL PHTHALATE: DEGREE OF
EXTRAVASATION @ 10 MIN MILD; @ 15 MIN MILD, @ 20 MIN MODERATE. /FROM TABLE/
1 MG/L /AEROSOL/ INHALED FOR 5.5 HR CAUSED
NASAL IRRITATION IN CATS. /FROM TABLE/
DIBUTYL PHTHALATE (1.25
UL/EGG) INJECTED INTO AIR SPACE OF FERTILIZED EGG GAVE 50% ABNORMAL EMBRYO
DEVELOPMENT; 15 UL/EGG GAVE 30% HATCHABILITY.
DIBUTYL PHTHALATE 0.5%
ORALLY TO MICE FROM DAY 0-18TH OF GESTATION: NO EFFECT ON MOTHER BUT INCR
EMBRYONIC MORTALITY. TERATOGENESIS AFTER 0.1% & 0.5%, BUT NO ABNORMALITY IN
ORGANS.
WHEN RATS WERE /ORALLY/ DOSED TWICE WEEKLY ...
(1 ML/KG OF BODY WEIGHT OF A SOLN IN OIL) FOR A PERIOD OF 6 WK, NO ADVERSE
EFFECTS WERE REPORTED. ... IN A CHRONIC GAVAGE STUDY, RATS WERE MAINTAINED ON
DBP (1 ML/KG OF BODY WEIGHT OF A SOLUTION IN OIL) FOR 1.5 YR WITHOUT ANY ADVERSE
EFFECTS ON THE PARAMETERS STUDIED WHICH INCLUDED HEMATOLOGY, PATHOLOGY OF ORGAN
TISSUE, & ORGAN WEIGHTS.
... 2 HR EXPOSURE OF MICE TO AN AEROSOL CONCN
APPROX 250 MG/CU M OF DIBUTYL PHTHALATE RESULTED IN
SEVERE IRRITATION OF EYES AND UPPER RESPIRATORY TRACT, LABORED BREATHING,
INCOORDINATION, PARTIAL PARALYSIS, CONVULSIONS, /CNS DEPRESSION/, AND IN SOME
ANIMALS, DEATH FROM PARALYSIS OF THE RESPIRATORY SYSTEM.
DIBUTYL PHTHALATE WAS
NOT TOXIC TO FEMALE HOUSE FLIES, MUSCA DOMESTICA, WHEN APPLIED AT HIGH DOSAGES
TOPICALLY OR BY INJECTION.
SINGLE IP ADMIN OF 3.05 ML/KG DIBUTYL
PHTHALATE IN RATS INHIBITED THE ACTIVITY OF HEPATIC AMINOPYRINE N-DEMETHYLASE
& ANILINE HYDROXYLASE; HOWEVER, NO DECREASE IN ENZYME ACTIVITY WAS OBSERVED
AFTER DAILY IP ADMIN FOR 7 DAYS.
IN SPRAGUE-DAWLEY RATS, HEPATIC CONCN OF
CYTOCHROME P450 & CYTOCHROME-C-REDUCTASE INCR AFTER INTRAGASTRIC DOSES OF
0.01 MMOL/KG BODY WT FOR 5 DAYS. LUNG ENZYME ACTIVITIES WERE NOT AFFECTED BUT IP
ADMIN CAUSED DECR IN CYTOCHROME P450 & B5.
DIBUTYL PHTHALATE WAS
MIXED WITH FOOD & GIVEN TO PREGNANT MICE THROUGHOUT GESTATION. 1.0% LEVEL
RESULTED IN DECR MATERNAL WEIGHT GAIN, & INCR RESORPTION & MALFORMATION
RATES WITH NEURAL TUBE DEFECTS (EXENCEPHALY & SPINA BIFIDA), GROWTH
RETARDATION, & DELAYED OSSIFICATION NOTED.
ZINC CONCENTRATIONS IN THE TESTES OF MICE FED
A DIET CONTAINING 2% DIBUTYL PHTHALATE WERE LESS THAN
THOSE OF CONTROL ANIMALS. THE RELATIVE WEIGHT OF TESTES INCREASED IN DIBUTYL
PHTHALATE TREATED MICE.
CULTURES OF THE DIATOM SKELETONEMA COSTATUM
GROWN @ 5 DIFFERENT SALINITIES WERE EXPOSED TO VARIOUS CONCN OF DIBUTYL
PHTHALATE (DBP). RESULTS SHOW THAT DBP WAS MORE TOXIC IN MEDIA OF LOWER
SALINITY; INCREASING SALINITY HAD A GREATER EFFECT ON THE GROWTH RATE THAN DBP.
RATS EXPOSED TO DIBUTYL
PHTHALATE MIST @ 0.5 MG/CU M & 50 MG/CU M 6 HR/DAY FOR 6 MO SHOWED
SMALLER BODY WEIGHT GAINS, GREATER BRAIN & LUNG WEIGHTS, ABNORMAL SERUM
FINDINGS (HIGH UREA NITROGEN & LOW CHOLESTEROL LEVELS), & HIGH
TRANSAMINASE ACTIVITY WHEN COMPARED TO CONTROLS.
... Dibutyl phthalate (10-100
ul/ml) was not mutagenic in Saccharomyces with or without metabolic activation
... /the compound/ was cytotoxic at these concn if treatment continued beyond 24
hr.
... 6/10 mice died within 7 hr of oral
administration of 200 mg/day/animal dibutyl phthalate, whereas
3/10 animals died within 2 days after administration of 100 mg/day/animal.
/Toxic signs/ ... shortness of breath, lung edema, lung congestion, and
testicular atrophy. ...
Dibutyl phthalate (DBP)
was administered to pregnant female rats (ip) at 1/10, 1/5, and 1/3 the acute
LD50. (0.305 ml/kg of dibutyl phthalate)... control
groups included: untreated rats, rats treated with 10 ml/kg of distilled water,
... 10 ml/kg of normal saline ... 5 ml/kg cottonseed oil. ... Treatments took
place on day 5, 10, and 15 of gestation ... 20th day ... rats were sacrificed
... DBP esters produced gross or skeletal abnormalities which were dose related
... absence of tail, anophthalmia, twisted ... legs, hematomas ... elongated and
fused ribs ... absence of tail bones ... abnormal or incomplete skull bones ...
incomplete or missing leg bones ... /and/ reduced weight of fetuses compared to
controls.
Oral administration of dibutyl
phthalate ... produced severe seminiferous tubular atrophy in rats and
guinea pigs but caused only focal atrophy in mice. Hamsters showed no testicular
changes. ...
... Chronic administration of 20 mg di-butyl
phthalate/kg for 80 days ... caused leukocytosis in rats. ...
Mallard ducks ... /fed a/ duck mash diet
containing 10 mg/kg phthalate ester, showed no significant accumulation of dibutyl
phthalate ... after 5 months of continuous dietary exposure.
When flexible plastic glazing strips
containing dibutyl phthalate were in an enclosed
volume, such as a greenhouse, the vapors of /this compound/ reached toxic
concentrations and killed cabbage seedlings. The phenomenon varied in severity
between varieties. Concentrations of /dibutyl phthalate/ less
than or equal to 2010 pg/l were recorded in such glasshouses. The problem was
resolved by replacing the glazing strip with a strip plasticized with
di-iso-decyl phthalate. A residual dibutyl phthalate concentration
of 120 pg/l was traced to contaminants in the strip. Other plastic items used in
glasshouses such as hosepipes and flexible pots may also be toxic.
Male rats exposed to dibutyl
phthalate by inhalation with concentrations of 0.5, 2.5, and 7.0 ppm in
the air for 5 days. The concentrations were considered relevant to human
exposure. No quatitative changes were observed in the liver microsomal
cytochrome p450 /content/, but significant incr was observed in the liver
microsomal metabolism of benzo(a)pyrene and n-hexane, in the 2.5 ppm and 0.5 ppm
groups, respectively. Inhaled dibutyl phthalate decreased
in a dose-dependent way the lung microsomal concentration of cytochrome p450 by
as much as 63%, which was reflected in a significant reduction of the microsomal
metabolism of n-hexane and benzo(a)pyrene in the 7.0 ppm group. Thus, dibutyl
phthalate in doses relevant to human air exposure influences the
cytochrome p450 enzyme system in both liver and lung, with lung as the main
target organ. The observed effects in lung microsomes were similar to those
earlier reported after ip administration of dibutyl phthalate.
Monoethylhexyl phthalate at concentrations
that can occur in blood stored in plastic bags (0.1-0.5 mg/ml), reduced
contractions of rat isolated gastric fundus to PGE2 and acetylcholine; the
diethyl compound was less effective. In contrast, dibutyl
phthalate (1 and 10 ug/ml) and, to a lesser extent, di-isobutyl phthalate
increased the muscle tone. These results are discussed in relation to blood
transfusion, and structural similarities between phthalates and prostaglandins.
The toxicities of di-n-butyl
phthalate (DBP) and di-n-octyl phthalate was assessed by measuring the
effect of exposure to these compounds on the fecundity of Daphnia magna and on
the hatching and survival of the early life stages of the fathead minnow
Pimephales promelas. For Daphnia magna, exposure to 1.8 mg/l DBP or 1.0 mg/l
di-n-octyl phthalate caused a significant reduction in reproduction. Doses of
0.56 mg/l DBP or 0.32 mg/l di-n-octyl phthalate had no significant effect in
decreasing reproduction. Survival of fathead minnow embryos was decreased by
exposure to 1.8 mg/l DBP; none of the embryos exposed to this dose hatched
successfully. Hatching and larval survival were affected by exposure to 1.0 mg/l
DBP, but not to 0.56 mg/l. Exposure to di-n-octyl phthalate did not affect
survival of either early embryos or larvae of the fathead minnow at doses up to
10 mg/l (the highest dose tested). Hatching of the embryos was significantly
decreased at 10 mg/l, but not at 3.2 mg/l di-n-octyl phthalate.
Male rats were fed 1% dibutyl
phthalate in their diet for 26 days and sleeping time with pentobarbital
(30 mg/kg ip) was determined. Sleeping time of rats fed only the basal diet was
101.0 minutes and that of rats fed dibutyl phthalate was
60.7 minutes. When rats were fed tryptophan sufficient diet or 1% dibutyl
phthalate plus a tryptophan sufficient diet for 33 days, dibutyl
phthalate did not cause an increase in growth rate; the levels of
quinolinic acid, nicotinic acid, N1-methylnicotinamide and ascorbic acid in
urine were higher in the dibutyl phthalate fed group
than in the basal diet group. Thus, the conversion of anthranilic acid to
3-hydroxyanthranilic acid was considered to be increased by the administration
of dibutyl phthalate, presumably by induction of the
cytochrome p450 system.
Dibutyl phthalate may
induce testicular atrophy in rats. In this study, the ester was dissolved in
corn oil and administered orally (by intubation) for a period of time. The dose
administered was was 2 g/kg while control animals received corn oil in a volume
of 5 ml/kg. The initial effect was a progressive reduction in weight of the
testes. In 14 days, the reduction amounted to 60 to 70 percent of the original
weight. A decrease in body and testicular weight /was observed/.
Histopathological examination of testes tissue demonstrated morphological
damage. Further investigations revealed that the ester adversely affects zinc
metabolism and increases urinary zinc excretion. /It was/ suggested that after
oral administration, dibutyl phthalate is metabolized
by nonspecific esterases in the gastrointestinal tract to the monobutyl
phthalate prior to absorption into the bloodstream. The monoester or another
metabolite of dibutyl phthalate may act as a chelating
agent by removing zinc from the testes. Testicular zinc deficiency /may be a/
causative factor leading to testicular atrophy.
Dibutyl phthalate (DBP),
a plasticizer, is a teratogen in mice and rabbits but produces fetal loss in the
rat. Long term dosing studies indicating reduced fertility in rat suggested a
maternal effect of the compound. The decidual cell response and pregnant rats
were used to examine whether DBP affects maternal physiological parameters
independent of the compound's fetotoxic effect. DBP has no effect on the
decidual cell response, pregnant uterine weight, number of implantation sites,
ovarian weight, or serum progesterone concentration during early pregnancy or
pseudopregnancy.
This study /examines/ responses in fecundity,
viability of embryos, and skeletal anomalies during and after exposure of
cyprinodontiform fish, Rivulus marmoratus, to the plasticizer,
di-n-butylphthalate (DBP). Skeletal anomalies among offspring were classified as
mild, moderate, or severe compared with non-deformed normal offspring. The
frequency of skeletal anomalies increased from 4% (all categories combined) in
controls, to 10% and 19% of the offspring from adults exposed to 1 and 2 mg 1/1
DBP, respectively. DBP treatment was conducted over a 21 week interval, followed
by a 9 week post treatment observation interval. During post treatment,
frequency of skeletal anomalies decreased to less than 5% in all groups.
The toxicity caused by a volatile constituent
from certain samples of flexible polyvinyl chloride was due to dibutyl or
diisobutyl phthalate plasticisers. Radish (Raphanus sativus) seedlings, exposed
to an air stream containing 160-180 ng dm/3 of butyl phthalates developed
chlorotic leaves within 3-4 days. Within 12 days neither dioctyl nor diisodecyl
phthalate produced damage in the test plants. Measurements of photosynthetic and
respiratory gas exchange in intact shoots of affected radishes showed that
photosynthesis was severely inhibited while respiration was virtually
unaffected. Electron micrographs of sections from young leaves showed disruption
of thylakoid formation and granal stacking. In mature leaves, thylakoids and
grana were well formed but chloroplasts were swollen and the thylakoids were
pushed towards the vacuolar side of the chloroplasts. Sensitivity to toxic
phthalates varies between species; all members of the Cruciferae tested were
susceptible, tomato less so, and lettuce and ryegrass were resistant.
These studies compared the reproductive
toxicity of four phthalates by a continuous breeding protocol. Mice were given
diets with di-n-butyl phthalate (DBP) (0.00, 0.03, 0.3,
or 1.0%). Both male and female CD-1 mice were dosed for 7 days prior to and
during a 98 day cohabitation period. Reproductive function was evaluated during
the cohabitation period by measuring the numbers of litters per pair and of live
pups per litter, pup weight, and offspring survival. DBP exposure resulted in a
reduction in the numbers of litters per pair and of live pups per litter and in
the proportion of pups born alive at the 1.0% amount, but not at lower dose
levels. A crossover mating trial demonstrated that female mice, but not males,
were affected by DBP, as shown by significant decreases in the percentage of
fertile pairs, the number of live pups per litter, the proportion of pups born
alive, and live pup weight.
Seven phthalate esters of different chain
lengths and degrees of branching were evaluated for their ability to induce
peroxisomes in the livers of Fischer-344 rats. The esters included
di(2-ethylhexyl)phthalate, butyl(benzyl)phthalate di(n-butyl)phthalate,
di(isodecyl)phthalate, di(isononyl)phthalate, di(undecyl)phthalate,
di(n-hexyl,n-octyl,undecyl) phthalate, and di(heptyl,nonyl,undecyl)phthalate.
Each of the compounds was fed to groups of five male and five female rats in the
diet at concentrations of 2.5, 1.2, and either 0.6 or 0.3 percent for a period
of 21 days. Cyanide insensitive palmitoyl-CoA oxidation,
lauric-acid-11-hydroxylase, and lauric-acid-12-hydroxylase were assayed in the
liver microsomes. Cholesterol and triglyceride concentrations were measured in
the serum. The results indicated that none of the esters was more potent than
di(2-ethylhexyl) phthalate. The most sensitive parameters were relative liver
weight and cyanide insensitive palmitoyl-CoA oxidation. The latter parameter was
assumed to be an indicator of peroxisome proliferation and thereby predictive of
liver tumorigenesis.
The effects of feeding dibutyl
phthalate to groups of rats. At concentrations of 0.01, 0.05, and 0.25
percent of dibutyl phthalate in food, no adverse
effects were noted after one year. When the dose level was increased to 1.25
percent, approximately half of the animals died in the first week but the
remaining animals grew normally as compared to the untreated controls.
Rats were exposed continuously for 93 days at
chamber concentrations of 0.098, 0.256 and 0.98 mg/cu m. No behavioral changes
were noted nor any weight loss discerned. The important finding was that gamma
globulin was increased and appeared to be dose related.
Dimethyl phthalate, dibutyl
phthalate (DBP), and di(2-ethylhexyl)phthalate were given ip (3.8 mM/kg)
to Sprague Dawley rats for 5 days. DBP increased significantly the liver concn
of cytochrome p450, but decreased the lung concn by about 40%. DBP decreased the
lung concn of cytochrome b5 and reduced nicotinamide adenine
dinucleotide-cytochrome-c-reductase activity by about 30%. Only minor effects
were observed after treatment with dimethyl phthalate and di(2-ethylhexyl)
phthalate. The direction of benzo(a)pyrene metabolism was changed and the
formation of 2- and 3- hexanol metabolites were increased in liver microsomes
after DBP treatment. All phthalate esters decreased the lung metabolism of
benzo(a)pyrene. The cytochrome p450 enzyme system in the lung was ten times more
effective than that in the liver as far as metabolism of n-hexane was concerned.
Only minor effects were observed in the serum enzyme activities, but a
significant decr in the serum level of albumin was observed after treatment with
DBP. No relationship was found between the carbon chain length of the
investigated chemicals and effects on microsomal enzymatic activities.
VAPOR OF DIBUTYL PHTHALATE IN
LIGHT PRODUCES DISTURBANCES IN CAROTENOID SYNTHESIS OF GREEN PLANTS (BROWALLIA
SPECIOSA & RAPHANUS SATIVUS) RESULTING IN CHLOROPHYLL DEFICIENCY & IN
EXTREME CASES COMPLETELY CHLOROPHYLL-FREE LEAVES HAVING A WHITE COLOR.
Phthalate esters such as di-n-butyl,
di-n-pentyl and di-n-hexyl and their major metabolites, the corresponding
monoesters, also cause a decrease in testes weights, damage the seminiferous
tubules, and deplete gonadal zinc in the rat. In the mouse, dibutyl and di-isobutyl
phthalate also cause decreases in testicular weights and zinc content.
Features of the testicular effects of
phthalate esters in rats were described, emphasizing the Sertoli cell as a
primary target and effects of phthalate monoesters on cultures of testicular
cells. ... Rats treated with di-n-butyl-phthlate, 2000 mg/kg per day for 5 days,
showed a marked decreased in testis and seminal vesicle weight and severe
testicular atrophy; administration of serum gonadotrophin increased seminal
vesicle weights in phthalate treated and control animals. Development of
testicular lesions was not due to lack of availability of pituitary hormones or
testosterone, suggesting an action site in the seminiferous tubules.
Isolated rat liver mitochondria were exposed
to mono- and di-n-butyl phthalate (DBP) and mono- and
di(2-ethylhexyl) phthalate. DBP and mono(2-ethylhexyl) phthalate stimulated
succinate state 4 respiration, impaired K+-valinomycin induced swelling with
succinate, ascorbate, or ATP as the energy source, and inhibited succinate state
3 respiration and succinate cytochrome c reductase activity. At concentrations
which uncouple energy linked reactions, mono(2-ethylhexyl) phthalate and DBP
produced only slight energy independent swelling and release of soluble proteins
from isolated mitochondria. Uncoupling by mono-butyl phthalate
may involve disruption of mitochondrial membrane integrity, while
uncoupling by DBP and mono(2-ethylhexyl) phthalate is probably due to an
increase in membrane permeability to H+ and other small ions.
FIVE PHTHALATE ESTERS, DIMETHYL PHTHALATE,
DIETHYL PHTHALATE, DIBUTYL PHTHALATE, DIHEXYL
PHTHALATE, & DIOCTYL PHTHALATE, WERE TESTED FOR THE HATCHING OF BRINE SHRIMP
(ARTEMIA SALINA) EGGS. DIBUTYL PHTHLATE ESTER WAS THE MOST TOXIC OF THE
PHTHALATES TESTED. THE TOXIC ORDER OF 3 OF THE ESTERS WAS DIBUTYL
PHTHALATE GREATER THAN DIETHYL PHTHALATE GREATER THAN DIMETHYL PHTHALATE.
CONCN WERE 10, 20, & 50 PPM.
In a continuous breeding protocol COBS-Crl:CD-outbred-albino-mice
were fed diets containing diethyl phthalate (DEP), di-n-butyl-phthalate
(DBP), di-n-hexyl-phthalate (DHP), or di(2-ethylhexyl)phthalate (DEHP) to
determine the reproductive effects of these compounds. The following levels of
the phthalic acid esters were used: diethyl phthalate, 0.25, 1.25, or 2.5%; di-n-butyl-phthalate,
0.03, 0.3, or 1.0%; di-n-hexyl-phthalate, 0.3, 0.6, or 1.2%;
di(2-ethylhexyl)phthalate , 0.01, 0.1, 0.3%. The number of fertile matings was
adversely affected by the highest dose levels of di-n-butyl-phthalate,
di-n-hexyl-phthalate and di(2-ethylhexyl)phthalate. Some decrease in body
weight gain was noted for the top dose levels of di-n-butyl-phthalate
and di-n-hexyl phthalate, but not di(2-ethylhexyl)phthalate. At dose
levels where fertile matings occurred, a decrease was noted either in the number
of live pups per litter or in the proportion of pups born alive. Diethyl
phthalate caused decreased body weight gain, but did not affect reproduction.
While diethyl phthalate did not affect fertility in the first generation, it was
associated with decreased litter size in the second generation.
Di-n-hexyl-phthalate and di(2-ethylhexyl)phthalate decreased epididymal sperm
concentration, increased the percentage of abnormal sperm, and decreased
percentages of motile sperm. The failure of di-n-butyl-phthalate
to produce significant adverse effects in male mice fertility seems to be
a species/specific response.
... Oral administration of
di(2-ethylhexyl)-phthalate led to decreased testicular weight and associated
histological changes within the seminiferous tubules, and depletion of germinal
epithelium to only Sertoli cells, spermatogonia and a small number of
spermatocytes. ... Similar pathobiologic effects were associated with
administration of d-n-pentyl-phthalate, di-n-hexyl-phthalate, and particularly
di-n-butyl-phthalate. These phthalates were found to be
metabolized in vivo to their corresponding monoesters by nonspecific esterases
in the intestinal mucosa and other tissues. Such monoesters also were effective
in producing testicular damage in exposed rats. Phthalates induced increased
urinary zinc excertion and a reduced level of this element within testicular
tissue. ...
The mutagenic activities of several phthalate
esters have been evaluated in an 8-azaguanine resistance assay in Salmonella
typhimurium. Three phthalate esters were found to be mutagenic: dimethyl
phthalate, diethyl phthalate and di-n-butyl phthalate. A
number of other phthalate esters were not found to be mutagenic, including
di(2-ethylhexyl)phthalate, di-n-octyl phthalate, diallyl phthalate, diisobutyl
phthalate and diisodecyl phthalate. A metabolite of di(2-ethylhexyl) phthalate,
2-ethylhexanol, was also noted to be mutagenic. The mutagenic activity of this
agent and others in this series was dose dependent but weak. No dose response
curve exceeded more than 3.5 times background at maximally testable
concentrations. A liquid suspension histidine reversion assay of dimethyl
phthalate showed levels of mutagenic activity similar to that observed in the
azaguanine resistance assay. ...
The effects of phthalic acid esters on
concentrations of testosterone and zinc in testicular tissues were studied.
Young male Wistar rats were fed diets containing 2% dimethyl, diethyl, di-n-butyl,
di-iso-butyl (DIBP), di-n-octyl (DOP), di-2-ethylhexyl phthalate, or o-phthalic
acid for one week. The animals were then killed, samples of blood were
collected, and the fresh weights of the testes, liver, and kidneys were
obtained. ... Testicular weights were decreased in rats fed di-n-butyl,
di-iso-butyl and di-2-ethylhexyl phthalates. Rats treated with di-n-butyl,
di-iso-butyl or di-2-ethylhexyl phthalate had decreased zinc concentrations in
the testes and liver, while di-n-octyl-treated rats had decreased zinc
concentrations ... were found in the serum and tested of dimethyl, and diethyl,
treated rats, while testosterone levels were significantly increased in the
testes of rats fed di-n-butyl, di-iso-butyl and di-2-ethlyhexyl phthalate.
Eight phthalic acid esters were studied in a
rat teratogenicity study. The esters included dimethyl, dimethoxyethyl, diethyl,
dibutyl, diisobutyl, butyl carbobutoxymethyl, dioctyl and di-(2-ethylhexyl)
phthalates. For all the esters, except two, the dose administered
intraperitoneally to pregnant female rats was 1/10, 1/5, or 1/3 the acute LD50.
For these esters, the doses /administered undiluted/ ranged from a low of 0.305
ml/kg for dibutyl phthalate to a high of 2.296 ml/kg
for butyl carbobutoxymethyl phthalate. Di-(2-ethylhexyl) phthalate and dioctyl
phthalate were given at doses of 5 and 10 ml/kg because of their very low acute
toxicity. Control groups included: untreated rats, treated with 10 mg/kg of
distilled water, rats treated with 10 ml/kg of normal saline and rats treated
with 10 ml/kg and 5 ml/kg of cottonseed oil. All treatments took place on days
5, 10, and 15 of gestation. On the 20th day, all rats were sacrificed and the
uterine horns and ovaries were surgically exposed to permit counting and
recording of the number of corpora lutea, resorption sites, and viable and dead
fetuses. Additionally, both viable and nonviable fetuses were excised, weighed,
and examined for gross malformation. Thirty to fifty percent of the fetuses
(using those which showed no gross malformation when possible) were prepared as
transparent specimens to permit visualization of skeletal deformities. All of
the esters produced gross or skeletal abnormalities which were dose related. The
most common gross abnormalities in the treated animals were absence of tail,
anophthalmia, twisted hands and legs, and hematomas. Skeletal abnormalities
included elongated and fused ribs (bilateral and unilateral), absence of tail
bones, abnormal or incomplete skull bones, and incomplete or missing leg bones.
Dead fetuses were found in the groups treated with dimethyl, dimethoxyethyl, and
diisobutyl phthalates. The most embryotoxic agent in the series was
dimethoxyethyl phthalate. Each of the esters also reduced the weight of the
fetuses when compared to the controls. Even at the high dose levels (5 and 10
ml/kg), di-2-ethylhexyl and dioctyl phthalates had the least adverse effects on
embryo/fetus development.
Eight phthalic acid esters were included in a
rat teratogenicity study. The esters included dimethyl, dimethoxyethyl, diethyl,
dibutyl, diisobutyl, butyl carbobutoxymethyl, dioctyl and di-(2-ethylhexyl)
phthalates. For all the esters, except two, the dose administered
intraperitoneally to pregnant female rats was 1/10, 1/5, or 1/3 the acute LD50.
For these esters, the doses ranged from a low of 0.305 ml/kg for dibutyl
phthlate to a high of 2.296 ml/kg for butyl carbobutoxymethyl phthalate. Di-(2-ethylhexyl)
phthalate and dioctyl phthalate were given at doses of 5 and 10 ml/kg because of
their very low acute toxicity. Control groups included: untreated rats, rats
treated with 10 ml/kg of distilled water, rats treated with 10 ml/kg of normal
saline, and rats treated with 10 ml/kg and 5 ml/kg of cottonseed oil. All
treatments took place on days 5, 10, and 15 of gestation. On the 20th day, all
rats were sacrificed and the uterine horns and ovaries were surgically exposed
to permit counting and recording of the number of corpora lutea, resorption
sites, and viable and dead fetuses. Additionally, both viable and nonviable
fetuses were excised, weighed, and examined for gross malformation. 30-50% of
the fetuses (using those which showed no gross malformation when possible) were
prepared as transparent specimens to permit visualization of skeletal
deformities. All of the esters produced gross of skeletal abnormalities which
were dose related. The most common gross abnormalities in the treated animals
were absence of tail, anophthalmia, twisted hands and legs, and hematomas.
Skeletal abnormalities included elongated and fused ribs (bilateral and
unilateral), absence of tail bones, abnormal or incomplete skull bones, and
incomplete or missing leg bones.
... At high doses when injected ip, the esters
can act as teratogenic agents and possibly as mutagenic agents in rats. These
esters also have an effect upon gonads in rats. /Also/ the esters may bring
about biochemical and pathological changes in the liver of rats when repeatedly
administered orally or by ip. /Phthalic acid esters/
National Toxicology Program Studies:
Di(n-butyl) phthalate (DBP)
was evaluated using the "Reproductive Assessment by Continuous
Breeding" protocol & Swiss CD-1 mice. In the present study ... dietary
levels of 0.0, 0.03, 0.3 & 1.0% DBP (> or =99% pure) were employed in
Task 2. Continuous exposure of CD-l mice (11 wks of age at outset) to the 1.0%
dietary level of DBP significantly diminished (p< 0.01) the number of
breeding pairs able to produce at least one litter as compared to the control
pairs. In contrast, the 0.03 & 0.3% dietary levels of DBP had no effect on
the fertility of breeding pairs. DBP at the highest dietary level (1.0%) also
significantly decreased the number of litters delivered/pair, the average litter
size, & the proportion of pups born alive as compared to the control &
two lower dose groups. In addition, the proportion of live males/litter
(males/total) was significantly greater in the 1.0% DBP group versus the
control, & the 0.03 & 0.3% DBP groups, implying that male fetuses may be
slightly more resistant to the toxic effects of DBP than female fetuses.
Further, live pup weight adjusted for the total number of pups/litter tended to
be lower for the pairs receiving the 1.0% DBP diet as compared to the pairs fed
the control, 0.03% DBP, or 0.3% DBP diets. Since DBP exerted significant
deleterious effects on fertility & reproductive performance in the F0
breeding pairs (Task 2), it was decided to conduct a crossover mating trial with
the control & high dose F0 mice in order to determine whether one or both
sexes were adversely affected (Task 3). Three combinations of breeding pairs
were utilized in the crossover mating trial immediately following the 18-wk
exposure period in Task 2. These were: Control male x Control female, 1.0% DBP
male x Control female, & Control male x 1.0% DBP female. Although the
proportion of detected matings did not differ significantly across the 3
combinations of breeding pairs, the proportion fertile was significantly reduced
in the Control male x 1.0% DBP female pairing vs the Control male x Control
female & 1.0% DBP male x Control female pairings. In addition, the number of
live pups/litter, the proportion of pups born alive, & the absolute &
relative live pup weights were significantly decreased for the Control male x
1.0% DBP female pairs as compared to the other two combinations of breeding
pairs. As observed initially for the F0 pairs fed the 1.0% DBP diet, the
proportion of live males/litter (males/total) in Task 3 tended to be higher for
the Control male x 1.0% DBP female pairs relative to the other 2 pairings. Taken
together, these data clearly show that the female parent & her offspring in
utero were selectively affected by exposure to 1.0% DBP in the diet. The control
& 1.0% DBP-exposed F0 mice were necropsied 26 days after the completion of
the 7-day crossover mating trial. Sperm assessment indicated no significant
difference in the % motile sperm, sperm concn, or % abnormal sperm in the cauda
epididymis between male mice exposed to 0.0 or 1.0% DBP in the diet. On the
other hand, body weight was significantly decreased & the relative liver
weight was significantly increased in the male mice fed the 1.0% DBP- containing
diet versus male mice given the control diet. In the F0 females, absolute &
relative liver weight was significantly increased & absolute & relative
uterine weight was significantly decreased in the 1.0% DBP-exposed group vs the
combined control group. No treatment related gross or histopathologic lesions
were noted for the testis, epididymis, prostate or seminal vesicles in male
mice, or for the ovary, oviduct, uterus, or vagina in the female mice.
Histological evaluation of the cell types in the vaginal mucosa indicated that
there were no treatment-related effects on the estrous cycle. Under the
conditions of this study, 1.0% DBP in the diet was a reproductive toxicant in
female CD-l mice as evidenced by decreased fertility, decreased number of
litters, decreased number of live pups/litter, decreased proportion of pups born
alive, decreased live pup weights, & an increased proportion of live
males/litter (males/total). Uterine weight also was significantly lower in 1.0%
DBP exposed females vs controls, perhaps reflecting the production of fewer
& smaller litters in the DBP-treated group. Finally, liver weights were
greater in 1.0% DBP-exposed males & females & body weight was
significantly decreased in 1.0% DBP-fed males as compared to these same
endpoints in control male & female mice.Thus, DBP is a reproductive toxicant
in the presence of systemic toxicity.
Di(n-butyl)phthalate (DBP)
... in feed was tested for its effects on fertility & reproduction in CD
Sprague-Dawley rats according to the Continuous Breeding Protocol. Based on
results of a dose-finding study & the information available in the
literature, 0.1, 0.5, & 1.0% were chosen to investigate effect on fertility
& reproduction. This yielded average doses of approx 66, 320 & 651 mg
DBP/kg/day. Male & female rats (F0) were continuously exposed for a 7-day
precohabitation & a 112-day cohabitation period (Task 2). Treated male &
female body weights in Task 2 were within 10% of control body weights. Feed
consumption values for 1.0% treated females were 18 & 8% lower compared to
the control value for wk 1 & 6 respectively, & body weights of the F0
dams were decreased at all time points. Reproductive endpoints adversely
affected by DBP in the F0 generation were the total number of live pups/litter
(all groups) & live pup weights (middle & high dose groups). In Task 3,
designed to determine the affected sex, the weights of pups from treated females
were significantly decreased. At necropsy, F0 females showed decreased body
weights & increased kidney- & liver- to-body weight ratios compared to
controls. F0 males had increased absolute liver weights & increased liver-,
kidney-, right cauda-, & epididymis-to-body weight ratios. Sperm parameters
were not affected. The F1 pups from the final litter in the control & all
three groups were weaned for second generation studies. Mating, pregnancy &
fertility indices for F1 rats in the 1.0% dose group were all significantly
decreased in the presence of a significant decr in F1 female dam body weights.
Live F2 pup weights were significantly lower in all treated groups. At F1 female
necropsy, body & organ weights were significantly lower in the 1.0% group
For F1 males, body weight & all reproductive organ-to-body weight ratios
were lower while kidney & liver ratios were higher. Epididymal sperm count
& testicular spermatid head count were significantly decreased in the 1.0%
treated group. In the 1.0% group, histopathologic evaluation showed degenerated
seminiferous tubules in the testis in 8 of 10 animals & underdeveloped
epididymis in 5 of 19 animals examined. The present study showed that DBP is a
reproductive toxicant in the presence of systemic toxicity in Sprague-Dawley
rats exposed both as adults & during development. Overall, the data indicate
that effects on the second generation were greater than on the first generation.
Non-Human Toxicity Values:
LD50 Rat ip 3.05 ml/kg.
LD50 Rat im 8.0 g/kg
LD50 Rabbit dermal 20 ml/kg.
LD50 Mouse oral 9 g/kg.
LD50 Mouse intraperitoneal 4.0 g/kg.
LD50 rat oral 8,000 mg/kg
... Cytotoxicity of dibutyl
phthalate ... in terms of 50% survival rate during cultivation for two
days ... mouse neuroblastoma (n-18) cells 0.019 mM; hamster lung cells (HmLV
strain) 0.02 mM; rabbit kidney cells (RK13 strain) 0.047 mM.
Ecotoxicity Values:
EC50 Gymnodinium breve (alga) 200 ug/l/96 hr,
toxic effect: chlorophyll. /Conditions of bioassay not specified/
EC50 Gymnodinium breve (alga) 3.4 ug/l/96 hr,
toxic effect: chlorophyll a. /Conditions of bioassay not specified/
EC50 Gymnodinium breve (alga) 600 ug/l/96 hr,
toxic effect: cell number. /Conditions of bioassay not specified/
Artemia salina (brine shrimp) 10 mg/l toxic
effect: 20% reduction in number of larvae hatched over 24 hr. /Conditions of
bioassay not specified/
Artemia salina (brine shrimp) 50 mg/l toxic
effect: 40% reduction in number of larvae hatched over 24 hr. /Conditions of
bioassay not specified/
LC50 Gammarus fasciatus (scud) 0.21 mg/l/1500
hr. /Conditions of bioassay not specified/
DIBUTYL PHTHALATE IS
TOXIC TO SYNCHRONOUSLY DEVELOPING LARVAE OF THE BRINE SHRIMP, ARTEMIA. THE LD50
FOR 24 HR EXPOSURE WAS 30 UMOL (8 PPM). /CONDITIONS OF BIOASSAY NOT SPECIFIED/
ACUTE TOXICITY (48 HR LC50 & EC50 (MEDIAN
EFFECTIVE CONC) CHIRONOMOUS PLUMOSUS (MIDGE LARVAE) 0.76 MG/L 48 HR. /CONDITIONS
OF BIOASSAY NOT SPECIFIED/
LC50 Red-tide dinoflagellate (Gymnodinium
breve) 0.3 mg/L/96 hr /Conditions of bioassay not specified/
LC50 Brine shrimp (Palaemonetes pugio) 30
mg/L/96 hr /Conditions of bioassay not specified/
LC50 Crayfish (Orconectes nais) >10 mg/L/96
hr /Conditions of bioassay not specified/
LC50 Scud (Gammarus pseudolimnaeus) 2.1
mg/L/96 hr /Conditions of bioassay not specified/
LC50 Bluegill (Lepomis macrochirus) 0.7; 1.2
mg/L/96 hr /Conditions of bioassay(s) not specified/
LC50 Fathead minnows (pimephales promelas) 1.3
mg/L/96 hr /Conditions of bioassay not specified/
LC50 Rainbow trout (Salmo gairdneri) 6.5
mg/L/96 hr /Conditions of bioassay not specified/
LC50 Red-tide dinoflagellate (Gymnodinium
breve) 0.02-0.6 ppm /Conditions of bioassay not specified/
LC50 Brine shrimp (Palaemonetes pugio) Holt
larvae 10-50 ppm/24 hr /Conditions of bioassay not specified/
LC50 Brine shrimp (Palaemonetes pugio) Holt
larvae 0.1-1 ppm/17 d /Conditions of bioassay not specified/
TSCA Test Submissions:
Effects on the liver and liver lipids were
evaluated in groups of male and female Fischer 344 rats (5/sex/dose level) fed
nominal levels of 0, 0.6, 1.2 or 2.5% di-n-butyl phthalate in
the diet for 21 days. Toxicity was evident by statistical differences between
dosed groups and controls for: mean body weights (2.5% and 1.2% group males
& 2.5% group females), food consumption (2.5% group males & females),
absolute and relative liver weights (all treated animals), relative kidney
weights (1.2 and 2.5% group males & 2.5% group females) and absolute and
relative testis weights (2.5% group males). There was a statistically
significant decrease in serum cholesterol (all treated animals) and a
significant decrease in serum triglycerides (all treated males), although these
effects were not considered dose-related. Also observed was an significant
increase in serum triglycerides for 2.5% group females. There was a moderate
increase in peroxisome proliferation for the high dose animals. Liver
biochemistry revealed statistically significant differences between treated and
controls as indicated by cyanide-insensitive palmitoyl-CoA oxidation levels (1.2
and 2.5% group males & 2.5% group females), lauric acid 11- and 12-
hydroxylase activities (all treated males & 2.5% group females) and total
hepatic protein levels (0.6 and 1.2% group males, 1.2 and 2.5% group females).
There was no consistent dose response relationship among treatment groups for
lipid content in the liver. Histological changes attributable to di-n-butyl
phthalate were reduction in cytoplasmic basophilia in the livers of the
high dose rats and some of the 1.2% group males. Severe testicular atrophy was
observed at the 2.5% dietary level.
The toxicity of di-n-butyl
phthalate was evaluated in the mouse lymphoma L5178Y cell line in the
presence and absence of rat liver S9 metabolic activation. All cultures were
treated in duplicate with concentrations of 9.77, 19.50, 39.10, 78.10, 156.00,
313.00, 625.00, 1250.00, 2500.00 or 5000.00nl/ml, and growth was determined at
24 and 48 hours after initiation of the treatment. Under nonactivated
conditions, di-n-butyl phthalate was soluble up to
5000nl/ml, and treatments at 78.10nl/ml were highly toxic (5.4% of average
solvent (acetone) control suspension growth). Treatments at 156nl/ml were lethal
to nonactivated cultures. Assays with metabolic activation appeared to be
soluble at 5000nl/ml, but after 24 hours a precipitate was observed. Activated
treatments at 1250nl/ml were lethal, and at 625nl/ml and 313nl/ml were highly
toxic (less than 9% relative suspension growth).
The ability of di-n-butyl
phthalate to induce morphological transformation was evaluated in the
Balb/c-3T3 A-31 mouse cell line (Cell Transformation Assay). Based on
preliminary toxicity determinations (exposure time = 72hrs), di-n-butyl
phthalate was tested at concentrations of 3.4, 13.7, 27.5, 55.0 or
82.3nl/ml, resulting in a range of 80% to 10% relative survival. None of the
treatments produced significantly greater transformation frequencies (95%
confidence level) relative to the negative control (culture medium).
The ability of di-n-butyl
phthalate to induce specific locus mutations at the TK locus in cultured
L5178Y mouse lymphoma cells (Mouse Lymphoma Mutagenicity Assay) was evaluated in
the presence and absence of Aroclor-induced rat liver S-9 metabolic activation.
Based on preliminary toxicity tests, 10 nonactivated cultures treated in
duplicate with 15, 30, 40, 50 and 60nl/ml were cloned, producing a range of 85.4
- 18.5% relative growth. Ten S-9 activated cultures treated in duplicate with
12.5, 50, 75, 100 and 150nl/ml were cloned, producing a range of 120.6 - 7.0%
relative growth. None of the nonactivated cultures produced mutant frequencies
significantly greater than the solvent control (acetone). Activated cultures
treated above 12.5nl/ml produced mutant frequencies significantly greater than
the solvent control.
Subchronic toxicity was evaluated in 3 Macacus
rhesus monkeys (sex not reported) receiving oral gavage doses of 400, 800 or
1200 mg/kg dibutyl phthalate 2 to 3 times a week for
periods of 9 to 13 weeks, and in 4 dogs (mixed breeds, sex not reported)
receiving oral doses of 400, 800 or 1200 mg/kg dibutyl
phthalate 2 to 3 times a week for periods of 8 to 11 weeks. Mortality was
not observed in any animal at any dose level, and all animals exhibited normal
behavior during the dosing period. One dog (dose group not specified) had
reduced weight gain compared to control. The monkey receiving 1200 mg/kg test
article had a reduced red blood cell count and decreased hemoglobin values when
compared to control; while total white cell counts, and differential white cell
counts were normal in all monkeys and dogs. The monkey treated at 1200 mg/kg had
levels of dextrose in urine higher than control values in one blood test out of
seven. Albumin was detected in 50% of the urine samples taken from the above
animal and a second monkey that received 800 mg/kg test article; while urine
values were normal for dogs at all treatment levels. Micropathological
examination of liver, kidney and spleen sections revealed no abnormal cell
structures in any animal at any dose level. Exact dosing schemes and statistical
analyses were not reported.
Subchronic toxicity was evaluated in groups of
10 albino rats (5 males and 5 females) ingesting di-n-butyl
phthalate via the diet at concentrations of 0.1, 1.0 or 5% for 4 months.
During treatment deaths were reported for male animals (2 at 1.0% and 1 at 0.1%)
and female animals (1 each at 5, 1.0 and 0%). A decrease in body weight was
observed in male and female rats at the 1% and 5% levels. Hematological
observations at the 5% level included a slight decrease in the red blood cell
count and a decrease in hemoglobin values in male rats; high white cell counts
observed in males at all levels were suggested to be a result of a low grade
respiratory infection. No effects on hematological parameters were observed in
females. Substantial decreases in testes weight in male rats, and an increase in
liver weights in male and female rats were observed in the 5% dose group;
however, the decrease in testes weight was not attributed to the effect of di-isobutyl
phthalate. Pathological effects were not evident in sections of liver and
kidneys taken from animals exposed at any dose level. Statistical analyses were
not performed.
Subchronic toxicity was evaluated in 1 male
and 1 female dog ingesting di-n-butyl phthalate via the
diet at dose levels of 0.1 cc/kg (male) and 2.0 cc/kg (female) for 2 months. The
percentages of sugar and protein in urine samples collected at the end of the
treatment period were reported to be within normal values when compared to urine
samples collected prior to treatment in both animals. A slight decrease in red
blood cell counts, and an increase in hemoglobin values were observed in blood
samples taken from the male dog during and after treatment when compared to
samples taken before treatment; a similar effect was observed in the female dog,
except that hemoglobin values were decreased. On necropsy, the weight of the
liver, kidneys, lungs, brain, heart and spleen were reported to be within normal
values in the male dog, however, the female dog exhibited increased liver
weight. Chronic prostatitis was observed on histopathological examination of the
male dog, while chronic pyelonephritis of the kidney, and a papillary cyst in
the ovary was observed in the female animal. Control experiments and statistical
analyses were not performed.
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
In vitro studies with pancreatic lipase
indicated that DBP is metabolized along the same or parallel pathways for
unsaturated fats. However, rats given DBP orally excreted the monobutyl ester as
the principal metabolite in the urine with phthalic acid as the secondary
metabolite.
/DIBUTYL PHTHALATE METAB
IN RATS NOTED/ ... ONLY TRACES OF PARENT CMPD WERE FOUND IN THE EXCRETA, &
MONOBUTYL PHTHALATE WAS THE MAJOR METABOLITE (70-80%). THE LATTER WAS MAINLY IN
URINE, AS WERE TWO PRODUCTS OF OMEGA-OXIDATION ... (2-3%), & TWO OF
(OMEGA-1)-OXIDATION ... (3-6%).
THE MAJOR METABOLITES FOUND WERE THE
MONOESTERS, PHTHALIC ACID, & A GROUP OF UNIDENTIFIED POLAR METABOLITES,
PROBABLY CONJUGATES.
Main urinary metabolite of (14)C-dibutyl
phthalate in the rat, guinea pig and hamster ... the monoester, MBP and
its glucuronide. ... small amount of phthalic acid, unchanged DBP and omega and
omega-1 oxidation products of MBP.
Metabolites found in rat urine after a single
oral dose of (14)C-dibutyl phthalate included: phthalic
acid, mono-butyl phthalate, mono-(3-hydroxy-butyl)
phthalate, and mono-(4-hydroxy butyl) phthalate.
Absorption, Distribution & Excretion:
DIBUTYL ... /PHTHALATE/, AFTER
ORAL ADMIN TO RATS ... EXCRETED IN URINE PRIMARILY AS ... RESPECTIVE ...
/MONOESTER/. SOME FREE ACID ... ALSO FOUND. ... /MONOESTER/ EXHIBITED GREATER
TOXICITY THAN THE INITIAL COMPOUNDS, THE DIESTERS.
DIBUTYL PHTHALATE ADMIN
ORALLY TO RATS & MICE RAPIDLY ABSORBED & EXCRETED IN URINE & FECES
WITHIN 48 HR. MAX CONCN IN BLOOD /SRP: NOT DBP ITSELF BUT A METABOLITE/ PLASMA
& VARIOUS ORGANS @ 20-30 MIN; GREATER IN LIVER THAN FAT THAN SPLEEN.
DIBUTYL PHTHALATE GIVEN
ORALLY TO RATS WAS EXCRETED IN URINE 30.6-43.5% & IN FECES 20.0-22.0% IN 24
HR. AMT ABSORBED BY FETUSES WAS APPROX SAME AS BY FAT TISSUES.
Dibutyl phthalate was
detected in the bile of rats after oral administration. ... A small part of the
dose was absorbed intact through the intestine.
The presence of phthalate esters in the blood
of individuals /who had/ ingested food /that/ had been in contact with flexible
plastics ... dibutyl phthalate levels detected in the
blood were much higher than prior to eating the food in the plastic packaging
system ... dibutyl phthalate levels in blood /were/
0.35 ppm ... compared to an average value of 0.02 ppm prior to the meals.
No specific organ affinity /was observed/ in
rats after a single /iv/ dose of (14)C-dibutyl phthalate. No
apparent differences in the distribution pattern between dibutyl
phthalate and diethylhexyl phthalate, although dibutyl
phthalate had a lesser affinity for the liver. The (14)C distribution in
the liver at one hr following intravenous injection of dibutyl
phthalate was 6%, whereas, it was 76% for diethylhexyl phthalate. Dibutyl
phthalate had a shorter retention than diethylhexyl phthalate in the
heart, lung, and spleen. (14)C-diethylhexyl phthalate affinity for adipose
appeared to be a little higher than that of dibutyl phthalate.
Of a single oral dose of dibutyl
phthalate /administered to rats/, 80-90% is metabolized and excreted in
the urine within 48 hr. Phthalic acid, monobutyl phthalate, mono(3-hydroxybutyl)
phthalate and mono(4-hydroxybutyl) phthalate were identified as metabolites in
the urine. Rats fed for 12 weeks on a diet containing dibutyl
phthalate at 1 g/kg feed did not accumulate either dibutyl
phthalate or monobutyl phthalate in tissues or organs.
The phthalic acid esters and/or their
metabolites are readily absorbed from the intestinal tract, the intraperitoneal
cavity, and the lung. There is also evidence indicating that these esters can be
absorbed through the skin. /Phthalate esters/.
The percutaneous absorption of a series of
typical phthalate esters, dimethylphthalate, diethylphthalate, dibutyl
phthalate, and di-(2-ethylhexyl) phthalate, was measured through human
and rat epidermal membranes mounted in glass diffusion cells. The esters were
applied directly to the epidermal membranes. Following application to the
membranes, a lag phase followed by a linear phase of absorption was detected for
each phthalate diester. Human skin was less permeable than rat skin for all four
diesters. There appeared to be a trend to an increasing lag time with increasing
molecular weight, but this relationship did not always hold true. The phthalate
diesters were determined to have a 300 fold range of aqueous solubility and a
wide range of lipophilicity. Once the diesters had contacted the human epidermal
membrane, a slight increase in the permeability of the skin was detected.
Relatively large changes in permeability were detected in the membrane following
exposure.
Frequency of detection = 44% and max observed
concn = 1700 ng/g /Broad scan analysis of composite specimens of human adipose
tissue for the U.S. National Adipose Tissue Registry, Fiscal Year 1982; From
table/
This study examined the extent of dermal
absorption of a series of phthalate diesters in the rat. Those tested were
dimethyl, diethyl, dibutyl, diisobutyl, dihexyl, di(2-ethylhexyl), diisodecyl,
and benzyl butyl phthalate. Hair from a skin area (1.3
cm in diameter) on the back of male F344 rats was clipped, the 14(C)phthalate
diester was applied in a dose of 157 mumol/kg, and the area of application was
covered with a perforated cap. The rat was restrained and housed for 7 days in a
metabolic cage that allowed separate collection of urine and feces. Urine and
feces were collected every 24 hr, and the amount of (14)C excreted was taken as
an index of the percutaneous absorption. At 24 hr, diethyl phthalate showed the
greatest excretion (26%). As the length of the alkyl side chain increased, the
amount of (14)C excreted in the first 24 hr decreased signficantly. The
cumulative percentage dose excreted in 7 days was greatest for diethyl, dibutyl,
and diisobutyl phthalate, about 50-60% of the applied (14)C; and intermediate
(20-40%) for dimethyl, benzyl butyl, and dihexyl phthalate. Urine was the major
route of excretion of all phthalate diesters except for diisodecyl phthalate.
This compound was poorly absorbed and showed almost no urinary excretion. After
7 days, the percentage dose for each phthalate that remained in the body was
minimal showed no specific tissue distribution. Most of the unexcreted dose
remained in the area of application. These data show that the structure of the
phthalate diester determines the degree of dermal absorption. Absorption
maximized with diethyl phthalate and then decreased significantly as the alkyl
side chain length increased.
Interactions:
AN ANTAGONISTIC INTERACTION WAS OBSERVED IN
HOUSEFLIES UPON SIMULTANEOUS APPLICATION OF DI-2-ETHYLHEXYL PHTHALATE OR DIBUTYL
PHTHALATE WITH 21 ORGANOPHOSPHATES.
... Adsorption of dimethyl, di-n-butyl, and
di(2-ethylhexyl) phthalates using everted gut sac preparation from rat small
intestine /was studied/. Monoesters were absorbed more rapidly than
corresponding diesters. Esterases of the mucosal epithelium hydrolyzed the
diesters to mono esters during absorption. When esterase ... inhibited by an
organo-phosphate, absorption of di-n-butyl phthalate was
significantly reduced.
Pharmacology:
Therapeutic Uses:
/FORMER USE:/ MITICIDAL AGENT FOR /CONTROL/ OF
RICKETTSIAL INFECTIONS
Interactions:
AN ANTAGONISTIC INTERACTION WAS OBSERVED IN
HOUSEFLIES UPON SIMULTANEOUS APPLICATION OF DI-2-ETHYLHEXYL PHTHALATE OR DIBUTYL
PHTHALATE WITH 21 ORGANOPHOSPHATES.
... Adsorption of dimethyl, di-n-butyl, and
di(2-ethylhexyl) phthalates using everted gut sac preparation from rat small
intestine /was studied/. Monoesters were absorbed more rapidly than
corresponding diesters. Esterases of the mucosal epithelium hydrolyzed the
diesters to mono esters during absorption. When esterase ... inhibited by an
organo-phosphate, absorption of di-n-butyl phthalate was
significantly reduced.
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Dibutyl phthalate's production
and use as a plasticizer, solvent for resins, fuel propellant and insect
repellent has lead to its release to the environment through various waste
streams. Based on a measured vapor pressure of 2.01X10-5 mm Hg at 25 deg C, dibutyl
phthalate is expected to exist in both the vapor and particulate-phase in
the ambient atmosphere. Vapor-phase dibutyl phthalate is
degraded in the atmosphere by reaction with photochemically-produced hydroxyl
radicals with an atmospheric half-life of about 42 hours. Particulate-phase dibutyl
phthalate is removed from the atmosphere by wet and dry deposition. Dibutyl
phthalate is expected to have low mobility in soil based upon a measured
log Koc value of 3.14. Volatilization from dry soil surfaces is not expected
based upon the vapor pressure of this compound. Volatilization from moist soil
surfaces is expected based upon the measured Henry's Law constant of 4.5X10-6
atm-cu m/mole. Biodegradation of dibutyl phthalate is
expected to occur under both aerobic and anaerobic conditions based upon
numerous screening and river die-away tests. In water, dibutyl
phthalate is expected to adsorb to sediment or particulate matter given
its measured Koc value. This compound is expected to volatilize from water
surfaces given its experimental Henry's Law constant. Estimated half-lives for a
model river and model lake are 14 and 105 days respectively. Hydrolysis may be
an important environmental fate for this compound based upon an estimated
hydrolysis half-life of 125 days at pH 8. The potential for bioconcentration in
aquatic organisms is considered low to moderate based upon experimental BCF
values in the range of 12 to 117 measured in oysters, shrimp and fish.
Occupational exposure may be through inhalation of dusts and dermal contact with
this compound at workplaces where dibutyl phthalate is
produced or used. The general population will be exposed to dibutyl
phthalate via inhalation of ambient air, ingestion of food and drinking
water, and dermal contact with products containing dibutyl
phthalate. (SRC)
Probable Routes of Human Exposure:
NIOSH (NOES Survey 1981-1983) has
statistically estimated that 370,025 workers (138,570 of these are female) are
potentially exposed to dibutyl phthalate in the US(1).
Occupational exposure may be through inhalation of dusts or vapors and dermal
contact with this compound at workplaces where dibutyl
phthalate is produced or used. The general population may be exposed to dibutyl
phthalate via inhalation of ambient air, ingestion of food and drinking
water, and dermal contact with products containing dibutyl
phthalate(SRC).
Body Burden:
Human adipose tissue 0.10-0.30 ppm(1),
0.57-0.79 ppm(2). Detected in human tissue and blood(3). Dibutyl
phthalate was detected, not quantified, in human adipose tissue(4).
Average Daily Intake:
AIR INTAKE: (assume 0-6 ng/cu m) 0-400 ng(1);
WATER INTAKE: (assume 0-2.5 ug/l(2)) 20 ng-10,000 ng; FOOD INTAKE: insufficient
data(SRC).
Artificial Pollution Sources:
Dibutyl phthalate's production
and use as a plasticizer(1), solvent for resins(1), fuel propellant(1) and
insect repellent(2) may lead to its release to the environment through various
waste streams(SRC).
Environmental Fate:
TERRESTRIAL FATE: Based on a recommended
classification scheme(1) and a log Koc value of 3.14 determined from
measurements on soil samples from Broome County, NY(2,3), dibutyl
phthalate is expected to have low mobility in soil(SRC). Volatilization
from dry soil surfaces is not expected based on the experimental vapor pressure
of 2.01X10-5 mm Hg at 25 deg C(4). Volatilization from moist soil surfaces is
expected based on the measured Henry's Law constant of 4.5X10-6 atm-cu
m/mole(5). Biodegradation is expected to occur under both aerobic and anaerobic
conditions as indicated by several screening studies(6-9).
AQUATIC FATE: Based on a recommended
classification scheme(1) and a log Koc value of 3.14 determined from
measurements on soil samples from Broome County, NY(2,3), dibutyl
phthalate is expected to adsorb to suspended solids and sediment in
water(SRC). Dibutyl phthalate is expected to volatilize
from water surfaces(4,SRC) based on an experimental Henry's Law constant of
4.5X10-6 atm-cu m/mole(5). Estimated half-lives for a model river and model lake
are 14 and 125 days respectively(4,SRC). Biodegradation is expected to occur
based upon aerobic and anaerobic river die-away studies(6-8). This compound is
expected to hydrolyze in the environment with an estimated half-life of 125 days
at pH 8(9,SRC). According to a classification scheme(10), the potential for
bioconcentration in aquatic organisms is considered low to moderate based upon
experimental BCF values of 12 for minnows(11) and 117 measured in fish(12).
ATMOSPHERIC FATE: According to a model of
gas/particle partitioning of semivolatile organic compounds in the
atmosphere(1), dibutyl phthalate, which has a measured
vapor pressure of 2.01X10-5 mm Hg at 25 deg C(2), is expected to exist in both
the vapor and particulate phases in the ambient atmosphere. Vapor-phase dibutyl
phthalate is degraded in the atmosphere by reaction with photochemically-produced
hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to
be about 42 hours(3,SRC). Particulate-phase dibutyl phthalate may
be physically removed from the air by wet and dry deposition(SRC).
Environmental Biodegradation:
Dibutyl phthalate is
biodegraded in biodegradation tests utilizing sewage(3,4) and activated
sludge(2,4) inoculum, as well as inoculum composed of sewage, soil, and natural
waters(1). In a shake flask biodegradation test, after 28 days 68->99% of the
dibutyl phthalate had disappeared and 80.6->99% was
converted to CO2(4). The lag period averaged 4.5 days(4). 60-70% removal were
reported in three treatment plants using activated sludge(5).
In Davidson clay loam and Lakeland sand, 98
and 66% loss occurred in 26 weeks, respectively as a result of
biodegradation(1). While 86% removal of dibutyl phthalate in
secondary sewage occurred in a well acclimated 2.5 m loamy sand soil column(2),
no removal occurred in another laboratory study of a rapid infiltration site
employing 1 m columns(3). The feed rate was greater in the first case and the
acclimation may have been longer(SRC).
100% degradation of dibutyl
phthalate occurred in 4 days in water from an urban river in Japan and
utilizing water from the Rhine, Meuse, and Ijssel Rivers(1) in the Netherlands,
90% degradation occurred in three days(3). In an aerobic pond water-sediment
mixture, 97% degradation was noted in 5 days(2). The intermediate products of
degradation were the mono-n-butyl ester and phthalic acid(2).
Biodegradation under anaerobic conditions was
slower with 41% and 98% degradation occurring after 7 and 30 days respectively
in a sediment-pond water mixture(1). Dibutyl phthalate is
completely mineralized in digester sludge in 2 weeks under anaerobic
conditions(2) and 28% was lost after 7 days in a composting mixture(3).
A synthetic waste feedstock degraded 94
percent of an initial concn of dibutyl phthalate in 12
days(1). Microbial cultures isolated from an industrial wastewater facility
completely degraded dibutyl phthalate within 40 to 220
days depending upon the strain of the microorganisms used and concn of the dibutyl
phthalate sample(2). Batch experiments using enriched microbial cultures
completely degraded dibutyl phthalate in 15 hours(3).
Enriched microbial cultures isolated from a wastewater treatment facility
resulted in 85 percent degradation of a 200 mg/l sample of dibutyl
phthalate in 90 days(4). Dibutyl phthalate was
completely mineralized in digester sludge in 2 weeks under anaerobic
conditions(5) and 28% was degraded after 7 days in a composting mixture(6). Dibutyl
phthalate was completely degraded by Rhine River water within 10 days(7).
A die-away test using river and seawater degraded 75-80 percent dibutyl
phthalate in 3 days(8). In natural waters, the biodegradation half-life
of dibutyl phthalate is estimated as 1-2 days(9). An
aquifer slurry resulted in 9.2 percent mineralization of dibutyl
phthalate in 27.5 hours(10).
Factors affecting the decomposition of
carboxyl-labeled (14)C phthalic acid, monobutyl phthalate and dibutyl
phthalate (DBP) were studied in soil incubation experiments conducted
under laboratory conditions. A lag phase of 10-20 days occurred before soil
microbes initiated metabolism of mono-butyl phthalate and
DBP while phthalic acid was rapidly decomposed. Approximately 90% of DBP added
to soils at rates of 0.1-0.4% was decomposed within 80 days under aerobic and
anerobic conditions. Decomposition of DBP was enhanced in soils by increasing
soil pH from 5.2 to 7.0, by adding organic matter and by elevating the
temperature from 23 deg C to 30 deg C. Varying soil characteristics and the
simultaneous addition of ammonium, CaCO3, or sewage sludge had little effect on
the rate or extent of DBP degradation. The addition of DBP in sewage sludge or
other waste materials to soils should not pose a long term persistence
problem(1).
Environmental Abiotic Degradation:
The rate constant for the vapor-phase reaction
of dibutyl phthalate with photochemically-produced
hydroxyl radicals has been estimated as 8.71X10-12 cu cm/molecule-sec at 25 deg
C(SRC) using a structure estimation method(1,SRC). This corresponds to an
atmospheric half-life of about 42 hours at an atmospheric concn of 5X10+5
hydroxyl radicals per cu cm(1,SRC). A base-catalyzed second order hydrolysis
rate constant of 6.41X10-2 L/mol-sec (SRC) was estimated using a structure
estimation method(2); this corresponds to half-lives of 1,241 and 125 days at pH
values of 7 and 8, respectively(2,SRC).
Environmental Bioconcentration:
The log BCF of oysters exposed to 100 ug/l of dibutyl
phthalate for 1 day was measured as 1.32(1). Experimental BCF values of
1,500, 31 and 3 were reported in shrimp(2). Experimental BCF values of 22 and 42
were reported for oysters(2). Experimental BCF values of 12(2) and 117(3) were
reported for fathead minnows and bluegill fish respectively. According to a
classification scheme(4), the BCF data suggest that bioconcentration in aquatic
organisms is low to moderate(SRC).
Soil Adsorption/Mobility:
A log Koc value of 3.14 was determined from
measurements on soil samples from Broome County, NY(1,2). An experimental log
Koc of 3.05 was determined from unsaturated soil columns(3). According to a
recommended classification scheme(4), these reported Koc values suggest that dibutyl
phthalate has low mobility in soil(SRC).
Volatilization from Water/Soil:
The Henry's Law constant for dibutyl
phthalate has been measured as 4.5X10-6 atm-cu m/mole(1). This value
indicates that dibutyl phthalate is expected to
volatilize from water surfaces(2,SRC). Based on this Henry's Law constant, the
volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind
velocity of 3 m/sec) is estimated as approximately 14 days(2,SRC). The
volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind
velocity of 0.5 m/sec) is estimated as approximately 114 days(2,SRC). This
Henry's Law constant(1,SRC) indicates that volatilization from moist soil
surfaces may occur(SRC). Dibutyl phthalate is not
expected to volatilize(SRC) from dry soil surfaces based on the measured vapor
pressure of 2.01X10-5 mm Hg(3).
Environmental Water Concentrations:
DRINKING WATER: Dibutyl
phthalate was detected in 3 drinking water supplies in New Orleans, LA at
concns of 0.1-0.36 ppb(1) and in a drinking water supply in NY at a concn of 470
ppb(2). Dibutyl phthalate was identified, not
quantified, in 8 drinking water works in Japan(3) and at concns of 190-240 ppb
in tap water from Japan(4). Dibutyl phthalate was
identified, not quantified, in 12 of 14 drinking water supplies in England(5). Dibutyl
phthalate was detected in the drinking water supply of Toronto, Canada at
a mean concn of 2.547 ug/l(6). Dibutyl phthalate was
reported in the drinking water of Tokyo, Japan at a concn of 2.3 ug/l(7).
GROUNDWATER: Groundwater underlying 2 rapid
infiltration sites was contaminated with dibutyl phthalate at
concns of 0.73-2.38 ppb(1). Dibutyl phthalate was
identified, not quantified, in the groundwater of a landfill in Norman, OK(2). Dibutyl
phthalate was detected in groundwater in Cape Cod, MA at concns of 0-450
ng/l(3).
SURFACE WATER: dibutyl
phthalate was detected in the Delaware River (0.1-0.6 ppb)(1) the
Tennessee River (42 ppb)(2), the St. Clair River (1-2 ppb)(3), Missouri River
(0.09 ppb)(4) and the Monatiquote River (1-30 ppb)(5). Dibutyl
phthalate was detected in Lake Erie (2 sites) 1 ppb(3), Lake Michigan (9
sites) 1-4 ppb(3) and Lake Huron (2 sites) 0.04-2 ppb(3,4). Dibutyl
phthalate was detected in the Rhine and Meuse Rivers in the Netherlands
at concns of 0-2.8 ppb(6). Dibutyl phthalate was
detected in the Tama River (0.71-3.14 ppb)(7) and Shizuoka River in Japan (1.39
ppb average)(8). Dibutyl phthalate was detected in the
Irwell and Etherow Rivers in England at concns of 6-33.5 ug/l(9). Dibutyl
phthalate was detected in the Yssel River (2.5 ug/l) and the Rhine River
(0.1-1.2 ug/l) in the Netherlands(10). Dibutyl phthalate was
detected in the Klang River in Malaysia at concns of 0.8-4.8 ug/l(11). Dibutyl
phthalate was identified, not quantified, in the Fox River in
Wisconsin(12) and the Po and Lambro Rivers in Italy(13). Dibutyl
phthalate was detected at concns of 114-2,116 ng/l in the Mersey Estuary
in the UK(14).
SEAWATER: dibutyl phthalate was
detected in the Gulf of Mexico, Mississippi Delta 9.5 ppb average; Gulf Coast
3.4-265 parts per trillion (74 parts per trillion average); open Gulf 3.0-133
parts per trillion (93 parts per trillion average)(1). Dibutyl
phthalate was identified, not quantified, in the Dokai Bay, Japan(2).
RAIN/SNOW: Ewewetak Atoll (North Pacific)
2.6-72.5 parts per trillion, 31 parts per trillion avg(1). Dibutyl
phthalate was detected in the precipitation over the Great Lakes at
concns of 4-10 parts per trillion(1). Dibutyl phthalate was
identified, not quantified, in water and particulate fractions of rain and snow
in Norway(2) and Los Angeles(3). Dibutyl phthalate was
detected in Antarctic snow at concns of 15-280 ng/l (surface snow) and 13-136 ng/l
(deep snow)(4). Dibutyl phthalate was detected in the
rainfall of College Station, TX at a concn of 52.5 ng/l(5).
Effluent Concentrations:
An average concn of 428 ug/l of dibutyl
phthalate was detected in the leachate of a wastewater treatment
plant(1). The concn of dibutyl phthalate in the
leachate of an industrial landfill was 0.035 mg/l and in a municipal landfill
was 0.011 mg/l(2). Dibutyl phthalate is commonly found
in landfill leachate at concns of 5-15 ug/l(3). Hazardous waste incinerators
released 54 tons of dibutyl phthalate in the US in
1990(4). Dibutyl phthalate was identified, not
quantified in the leachate of a Florida landfill(5). Dibutyl
phthalate was detected in the effluent of a waste incinerator in Germany
at a concn of 7.66 ug/cu m(6). Dibutyl phthalate was
detected in the effluent of pulp mills at concns of 3 grams per ton of pulp(7). Dibutyl
phthalate was detected at a concn of 0.25 ppb in the effluent of sewage
in Phoenix, AZ(8). Dibutyl phthalate was detected in
the emissions of cigarette smoke (45 ppm) and wood smoke (8 ppm)(9). Dibutyl
phthalate was detected in New York City wastewater at concns of 3-4 ug/l(10)
and in the effluent of 3 publicly owned treatment works in NJ at concns of 5-103
ppb(11).
Sediment/Soil Concentrations:
Dibutyl phthalate was
detected in the soil of an abandoned strip-mine in Pennsylvania at a concn of
10,600 ppm(1). Dibutyl phthalate was detected in the
sediment of the Klang River in Malaysia at concns of 67-637 ng/g(2). Dibutyl
phthalate was detected at concns of 20-698 ng/g (3) and 0.092-260 ng/g(4)
in the sediment of the Mersey Estuary in the UK. Dibutyl
phthalate was detected in the sediment of the Usk River, England (8,000
ng/g), Rhine River, Netherlands (2,100 ng/g), Meuse River, Netherlands (500 ng/g),
Ijssel River, Netherlands (1,100 ug/g), Lake Superior, Canada (100 ng/g), Lake
Constance, Switzerland (200 ug/g) and the Chesapeake Bay (42 ug/g)(5).
Atmospheric Concentrations:
URBAN AIR: Dibutyl phthalate
was detected in Atwerp, Belgium (55-79 ng/cu m), College Station, TX (3.8
ng/cu m), Houston, TX (6.2 ng/cu m), La Paz Bolivia (19-36 ng/cu m), New York
city (4 ng/cu m) and Osaka, Japan (25-192 ng/cu m)(1). Dibutyl
phthalate was detected in New York city at concns of 3.3-5.7 ng/cu m and
College Station, TX at concns of 0.48-3.60 ng/cu m(2). Dibutyl
phthalate was detected in 3 locations in the US at concns of 0.5-6 ng/cu
m(3) and in Portland, OR at a concn of 0.37 ng/cu m(4).
RURAL/REMOTE: Dibutyl
phthalate was detected in the atmosphere over the Great Lakes at concns
of 0.5-5.0 ng/cu m(1). Dibutyl phthalate was detected
in the Sterling Forest,NY and Barrow,AK at concns of 1 ng/cu m(2). Dibutyl
phthalate was detected in the air of the Pacific Ocean (0.87 ng/cu m)(3),
Atlantic Ocean (1 ng/cu m)(2) and the Gulf of Mexico (0.3-1.3 ng/cu m)(2). Dibutyl
phthalate was detected in rural locations in Texas at concns of less than
0.2 ng/cu m to 2.1 ng/cu m(4).
INDOOR AIR: Dibutyl
phthalate particulates were detected at office buildings in the US at an
average concn of 1 ng/cu m(1). Dibutyl phthalate was
detected at 3 locations in a building in the US exhibiting sick building
syndrome at concns of 1.2, 5.9 and 4 ug/cu m(2).
Food Survey Values:
Canned tuna (Canada) 0-78 ppb, canned salmon
(Canada) <37 ppb(1). Egg white (Japan-retail stores) <150 ppb(2). Fresh
and processed food in Japan: meat 100 ppb average, fish 180 ppb average, eggs 80
ppb average with 70% of samples positive(3). Dibutyl phthalate
is used as a plasticizer in food wrappings and food containers and it can
migrate from the plastic packaging into foods(4). It has been estimated that 150
mg of dibutyl phthalate will migrate into 1 kg cheese
with 15% fat content(4). Cereal, gelatin, corn starch and casein components of
commercial fish food 20-30 ppb(5).
Dibutyl phthalate was
identified, not quantified in bacon(1). Dibutyl phthalate was
detected in vodka (28-204 ppb)(2) and in 1 of 234 ready to eat food products at
a concn of 2.5 ug/g(3). Dibutyl phthalate was
identified, not quantified, in the volatiles of beef, mutton and chicken(4). In
Japan, dibutyl phthalate was detected in fresh and
processed meat (100 ppb average), fish (180 ppb average) and eggs (80 ppb
average) with 70 percent of samples positive(5).
Fish/Seafood Concentrations:
Clams - 2 sites Portland, Me 40 and 100 ppb;
Neanthes virens - 2 sites Portland, Me 70 and 180 ppb(1). Not detected (<0.1
ppb) in 18 species of marine organisms from 14 locations in Mississippi Delta
and coastal areas in NW part of the Gulf of Mexico(2). Detected, not quantified
in White sucker, longnose sucker and yellow perch from Nepugin Bay, Lake
Superior(3), in burbot from 2 sites in Lake Huron(4). Lake Superior (adjacent to
Isle Royale, MI): fat siscowet trout trace, lean lake trout 200 ppb, white fish
70 ppb(5). Selected areas of North America: channel catfish 0-200 ppb, dragonfly
niads 200 ppb, tadpoles 500 ppb(6).
Dibutyl phthalate was
detected in edible fish from Wisconsin lakes and rivers at concns of less than
0.02 mg/kg to 35.0 mg/kg(1). Dibutyl phthalate was
detected in fish at concns of 0.598 ppm(2). Dibutyl phthalate was
detected in canned tuna at concns of 0-78 ppb and canned salmon at concns of
less than 37 ppb in Canada(3). Dibutyl phthalate was
detected, not quantified in white sucker, longnose sucker and yellow perch from
Nepugin Bay, Lake Superior(4), and in burbot from 2 sites in Lake Huron(5).
Animal Concentrations:
Dibutyl phthalate was
detected in double crested cormorants and herring gulls at concns of 11-19 ug
per g lipid(1).
Milk Concentrations:
Not detected in milk in Japan(1).
Environmental Standards & Regulations:
FIFRA Requirements:
As the federal pesticide law FIFRA directs,
EPA is conducting a comprehensive review of older pesticides to consider their
health and environmental effects and make decisions about their future use.
Under this pesticide reregistration program, EPA examines health and safety data
for pesticide active ingredients initially registered before November 1, 1984,
and determines whether they are eligible for reregistration. In addition, all
pesticides must meet the new safety standard of the Food Quality Protection Act
of 1996. Pesticides for which EPA had not issued Registration Standards prior to
the effective date of FIFRA, as amended in 1988, were divided into three lists
based upon their potential for human exposure and other factors, with List B
containing pesticides of greater concern and List D pesticides of less concern. Dibutyl
phthalate is found on List C. Case No: 3112; Case Status: OPP is
reviewing data from the pesticide's producers regarding its human health and/or
environmental effects, or OPP is determining the pesticide's eligibility for
reregistration and developing the Reregistration Eligibility Decision (RED)
document.; Active ingredient (AI): Dibutyl phthalate; AI
Status: The active ingredient is no longer contained in any registered pesticide
products ... "cancelled.
TSCA Requirements:
A testing consent order is in effect for di-n-butyl
phthalate for environmental effects testing. FR citation: 1/9/89.
Pursuant to section 8(d) of TSCA, EPA
promulgated a model Health and Safety Data Reporting Rule. The section 8(d)
model rule requires manufacturers, importers, and processors of listed chemical
substances and mixtures to submit to EPA copies and lists of unpublished health
and safety studies. 1,2-Benzenedicarboxylic acid, dibutyl ester is included on
this list.
CERCLA Reportable Quantities:
Persons in charge of vessels or facilities are
required to notify the National Response Center (NRC) immediately, when there is
a release of this designated hazardous substance, in an amount equal to or
greater than its reportable quantity of 10 lb or 4.54 kg. The toll free number
of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202)
426-2675. The rule for determining when notification is required is stated in 40
CFR 302.4 (section IV. D.3.b).
RCRA Requirements:
U069; As stipulated in 40 CFR 261.33, when
1,2-benzenedicarboxylic acid, dibutyl ester, as a commercial chemical product or
manufacturing chemical intermediate or an off-specification commercial chemical
product or a manufacturing chemical intermediate, becomes a waste, it must be
managed according to Federal and/or State hazardous waste regulations. Also
defined as a hazardous waste is any residue, contaminated soil, water, or other
debris resulting from the cleanup of a spill, into water or on dry land, of this
waste. Generators of small quantities of this waste may qualify for partial
exclusion from hazardous waste regulations (40 CFR 261.5).
Atmospheric Standards:
Listed as a hazardous air pollutant (HAP)
generally known or suspected to cause serious health problems. The Clean Air
Act, as amended in 1990, directs EPA to set standards requiring major sources to
sharply reduce routine emissions of toxic pollutants. EPA is required to
establish and phase in specific performance based standards for all air emission
sources that emit one or more of the listed pollutants. Dibutyl
phthalate is included on this list.
Clean Water Act Requirements:
Protection of human health from the toxic
properties of dibutyl phthalate ingested through water
and contaminated organisms, the ambient water criterion is calculated at 34
mg/l.
For the protection of human health from the
toxic properties of dibutyl phthalate ingested through
contaminated aquatic organisms alone, the ambient water criterion is determined
to be 154 mg/l.
State Drinking Water Guidelines:
(ME) MAINE 220 ug/l
(FL) FLORIDA 700 ug/l
(MN) MINNESOTA 700 ug/l
(NH) NEW HAMPSHIRE 800 ug/l
(WI) WISCONSIN 100 ug/l
FDA Requirements:
Dibutyl phthalate is
an indirect food additive for use only as a component of adhesives.
Chemical/Physical Properties:
Molecular Formula:
C16-H22-O4
Molecular Weight:
278.35
Color/Form:
COLORLESS TO FAINT YELLOW VISCOUS LIQUID
Colorless to faint yellow, oily liquid.
Odor:
SLIGHT CHARACTERISTIC ESTER ODOR
Slight, aromatic odor.
Taste:
TASTE STRONG & BITTER
Boiling Point:
340 deg C
Melting Point:
-35 DEG C
Critical Temperature & Pressure:
CRITICAL TEMP: 932 DEG F= 500 DEG C= 773 DEG
K; CRITICAL PRESSURE: 250 PSIA= 17 ATM= 1.7 MN/SQ M
Density/Specific Gravity:
1.0465 @ 20 DEG C
Heat of Combustion:
-13,300 BTU/LB= -7400 CAL/G= -310X10+5
JOULES/KG
Heat of Vaporization:
17,747.0 cal/mole
Octanol/Water Partition Coefficient:
log Kow= 4.9
Solubilities:
VERY SOL IN ACETONE, BENZENE, ALCOHOL, ETHER
SOL IN MOST ORG SOLVENTS & OILS
0.001% IN WATER @ 30 DEG C
13 mg/l at 25 deg C in water
In water, 11.2 + or - 0.003 mg/l at 20 deg C.
Spectral Properties:
INDEX OF REFRACTION: 1.4900 @ 20 DEG C/D
MAX ABSORPTION (ALCOHOL): 226 NM (LOG E=
3.98); 272 NM (LOG E= 3.18)
SADTLER REFERENCE NUMBER: 285 (IR, GRATING)
225 nm max methanol.
274 max methanol.
IR: 1902 (Sadtler Research Laboratories Prism
Collection)
UV: 529 (Sadtler Research Laboratories
Spectral Collection)
NMR: 721 (Sadtler Research Laboratories
Spectral Collection)
MASS: 1851 (Atlas of Mass Spectral Data, John
Wiley & Sons, New York)
Intense mass spectral peaks: 149 m/z (100%),
86 m/z (18%), 57 m/z (18%), 223 m/z (17%)
Intense mass spectral peaks: 205 m/z, 222 m/z,
278 m/z
Surface Tension:
LIQUID SURFACE TENSION: 34 DYNES/CM= 0.034 N/M
@ 20 DEG C
Vapor Density:
9.58 (air= 1)
Vapor Pressure:
2.01X10-5 mm Hg at 25 deg C
Viscosity:
0.203 poise at 20 deg C
Other Chemical/Physical Properties:
DISTILLATION RANGE: 227-235 DEG C @ 37 MM HG;
WT/GAL: 8.72 LB @ 68 DEG F
MORE SOL IN /PERSPIRATION/ THAN IN WATER &
INCR SOL WITH PH RISE
Alkaline hydrolysis rate of
di-n-butylphthalate in a solvent water-toluene binary mixture at 25 deg C was
<3.0 x 10-8 sec -1 (NaOH concn 0.186 M).
LIQUID-WATER INTERFACIAL TENSION: 27 DYNES/CM=
0.027 N/M @ 22.7 DEG C
CONVERSION FACTORS: 11.36 MG/CU M= APPROX 1
PPM
Vapor pressure= 14 mm Hg at 200 deg C
Vapor pressure= 1.1 mm Hg at 150 deg C
Vapor pressure= .14 x 10(E-4)torr at 25 deg C
/Butyl/ phthalate esters
have low volatility at room temperatures. /Butyl phthalate esters/
Henry's Law constant = 4.5X10-6 atm-cu m/mole
Chemical Safety & Handling:
Hazards Summary:
The major hazards encountered in the use and
handling of dibutyl phthalate stem from its toxicologic
properties. Toxic by all routes (ie, inhalation, ingestion, dermal contact),
exposure to this colorless-to-yellow, oily liquid may occur from its use as a
plasticizer or solvent in lacquers, elastomers, chlorinated rubbers, polyvinyl
acetate, explosives, nail polish, perfumes, resins, printing inks, paper
coatings, and adhesives. Effects from exposure may include contact burns to the
skin and eyes, dermatitis, nausea, and dizziness. Both the OSHA PEL and the
ACGIH TLV have been set at 5 mg/cu m. Odor thresholds have been found as low as
0.26 mg/cu m. Ventilation should be used to maintain acceptable levels. In
activities where over-exposure may occur, wear a self-contained breathing
apparatus and protective clothing. If contact should occur, immediately flush
affected skin and eyes with running water for at least 15 minutes. While dibutyl
phthalate does not ignite easily, it may burn with the production of
irritating or poisonous gases. Fires involving dibutyl
phthalate may be extinguished with dry chemical, CO2, or Halon. Standard
foam or water fog, if used, should be applied with caution, as each may cause
violent frothing. Dibutyl phthalate may be shipped via
air, rail, road, and water. If small amounts of dibutyl
phthalate should spill, take up with sand or other noncombustible
absorbent and place into containers for later disposal. For large spills, first
dike far ahead of the area with soil, sand bags, foamed polyurethane, or foamed
concrete, then absorb bulk material with fly ash or cement powder. For large
spills in bodies of water, first use natural barriers or oil spill control booms
to limit spill motion, then apply detergent, soap, or alcohols to thicken
material. Apply "universal" gelling agent and remove trapped material
with suction hoses. If dissolved, apply activated charcoal, and use mechanical
dredges or lifts to remove immobilized masses. Before implementing land disposal
of waste dibutyl phthalate, consult with environmental
regulatory agencies for guidance. Also, dibutyl phthalate is
a good candidate for liquid injection, rotary kiln, and fluidized bed forms of
incineration.
DOT Emergency Guidelines:
Fire or explosion: Some may burn but none
ignite readily. Those substance designated with a "P" may polymerize
explosively when heated or involved in a fire. Containers may explode when
heated. Some may be transported hot.
Health: Inhalation of material may be harmful.
Contact may cause burns to skin and eyes. Inhalation of asbestos dust may have a
damaging effect on the lungs. Fire may produce irritating, corrosive and/or
toxic gases. Runoff from fire control may cause pollution.
Public safety: CALL Emergency Response
Telephone Number. ... Isolate spill or leak area immediately for at least 10 to
25 meters (30 to 80 feet) in all directions. Keep unauthorized personnel away.
Stay upwind.
Protective clothing: Wear positive pressure
self-contained breathing apparatus (SCBA). Structural firefighters' protective
clothing will only provide limited protection.
Evacuation: Fire: If tank, rail car or tank
truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all
directions; also, consider initial evacuation for 800 meters (1/2 mile) in all
directions.
Fire: Small fires: Dry chemical, CO2, water
spray or regular foam. Large fires: Water spray, fog or regular foam. Move
containers from fire area if you can do it without risk. Do not scatter spilled
material with high pressure water streams. Dike fire-control water for later
disposal. Fire involving tanks: Cool containers with flooding quantities of
water until well after fire is out. Withdraw immediately in case of rising sound
from venting safety devices or discoloration of tank. ALWAYS stay away from
engulfed in fire tanks.
Spill or leak: Do not touch or walk through
spilled material. Stop leak if you can do it without risk. Prevent dust cloud.
Avoid inhalation of asbestos dust. Small dry spills: With clean shovel place
material into clean, dry container and cover loosely; move containers from spill
area. Small spills: Take up with sand or other noncombustible absorbent material
and place into containers for later disposal. Large spills: Dike far ahead of
liquid spill for later disposal. Cover powder spill with plastic sheet or tarp
to minimize spreading. Prevent entry into waterways, sewers, basements or
confined areas.
First aid: Move victim to fresh air. Call 911
or emergency medical service. Apply artificial respiration if victim is not
breathing. Administer oxygen if breathing is difficult. Remove and isolate
contaminated clothing and shoes. In case of contact with substance, immediately
flush skin or eyes with running water for at least 20 minutes. Ensure that
medical personnel are aware of the material(s) involved, and take precautions to
protect themselves.
Odor Threshold:
In humans, an olfactory threshold value
ranging from 0.26 to 1.47 mg/cu m /was found/.
Skin, Eye and Respiratory Irritations:
Contact may cause burns to skin and eyes.
CONTACT WITH SURFACE OF ... EYES ... BY
ACCIDENTAL DROPLET SPLASH AS WELL AS BY EXPTL APPLICATION ... HAS CAUSED ...
SEVERE STINGING PAIN. PAIN STIMULATES PROFUSE TEARING ...
Caution: Potential symptoms of overexposure
are irritation of upper respiratory tract and stomach.
NFPA Hazard Classification:
Health: 0. 0= Materials that, on exposure
under fire conditions, offer no hazard beyond that of ordinary combustible
material.
Flammability: 1. 1= This degree includes
materials that must be preheated before ignition will occur, such as Class IIIB
combustible liquids and solids and semi-solids whose flash point exceeds 200 deg
F (93.4 deg C), as well as most ordinary combustible materials. Water may cause
frothing if it sinks below the surface of the burning liquid and turns to steam.
However, a water fog that is gently applied to the surface of the liquid will
cause frothing that will extinguish the fire.
Reactivity: 0. 0= This degree includes
materials that are normally stable, even under fire exposure conditions, and
that do not react with water. Normal fire fighting procedures may be used.
Flammable Limits:
LOWER: 0.5% BY VOL @ 456 DEG F (235 DEG C)
Flash Point:
315 DEG F (157 DEG C) CLOSED CUP
Autoignition Temperature:
757 DEG F (402 DEG C)
Fire Fighting Procedures:
EXTINGUISH WITH DRY CHEMICALS ... OR CARBON
DIOXIDE.
/Wear/ self-contained breathing apparatus with
a full facepiece operated in pressure-demand or other positive pressure mode.
If material on fire or involved in fire: Do
not extinguish fire unless flow can be stopped. Use water in flooding quantities
as fog. Solid streams of water may spread fire. Cool all affected containers
with flooding quantities of water. Apply water from as far a distance as
possible. Use foam, dry chemical, or carbon dioxide.
Toxic Combustion Products:
THE THERMAL DECOMPOSITION OF DIBUTYL
PHTHALATE WAS CARRIED OUT IN A FLOW SYSTEM @ 250-500 DEG C. THE MAJOR
PRODUCTS WERE 1-BUTENE, BUTANOL & PHTHALIC ANHYDRIDE. SRP: PHTHALIC
ANHYDRIDE IS VERY IRRITATING AND ALLERGENIC.
Hazardous Reactivities & Incompatibilities:
LIQUID CHLORINE REACTS EXPLOSIVELY WITH DIBUTYL
PHTHALATE.
Nitrates; strong oxidizers, alkalis &
acids; liquid chlorine.
A mixture of the ester /dibutyl
phthalate/ and liquid chlorine confined in a stainless steel bomb reacted
explosively at 118 deg C.
Hazardous Decomposition:
When heated to decomp it emits acrid smoke and
fumes.
Immediately Dangerous to Life or Health:
4000 mg/cu m
Protective Equipment & Clothing:
USE WITH /ADEQUATE/ VENTILATION ... SAFETY
GLASSES SHOULD BE WORN IN ANY TYPE OF INDUSTRIAL OPERATION.
Respiratory protection for dibutyl
phthalate includes the following conditions: particulate concentration at
250 mg/cu m or less: a high efficiency particulate filter respirator with a full
facepiece or any supplied-air respirator with a full facepiece, helmet, or hood
or any self-contained breathing apparatus with a full facepiece; 9300 mg/cu m or
less: Type-C supplied-air respirator with a full facepiece operated in
pressure-demand or other positive pressure mode or with a full facepiece,
helmet, or hood operated in continuous-flow mode; greater than 9,300 cu m or
entry and escape from unknown concentrations: self-contained breathing apparatus
with a full facepiece operated in pressure-demand or other positive pressure
mode or a combination respirator which includes a type-C supplied-air respirator
with a full facepiece operated in pressure-demand or other positive pressure or
continuous-flow mode and an auxiliary self-contained breathing apparatus
operated in pressure-demand or other positive pressure mode; firefighting:
self-contained breathing apparatus with a full facepiece operated in
pressure-demand or other positive pressure mode.
For di-n-butyl phthalate, breakthrough
times greater than one hour reported by (normally) two or more testers for butyl
rubber. For di-n-butyl phthalate, breakthrough times
greater than one hour reported by (normally) two or more testers for neoprene.
For di-n-butyl phthalate, breakthrough times greater
than one hour reported by (normally) two or more testers for nitrile rubber. For
di-n-butyl phthalate, breakthrough times greater than
one hour reported by (normally) two or more testers for viton. There is some
data for di-n-butyl phthalate suggesting breakthrough
of approximately an hour or more for polyvinyl alcohol.
Wear appropriate eye protection to prevent eye
contact.
Recommendations for respirator selection. Max
concn for use: 50 mg/cu m. Respirator Class(es): Any dust and mist respirator
with a full facepiece.
Recommendations for respirator selection. Max
concn for use: 125 mg/cu m. Respirator Class(es): Any supplied-air respirator
operated in a continuous flow mode. Eye protection needed. Any powered,
air-purifying respirator with a dust and mist filter. Eye protection needed.
Recommendations for respirator selection. Max
concn for use: 250 mg/cu m. Respirator Class(es): Any air-purifying, full-facepiece
respirator with a high-efficiency particulate filter. Any self-contained
breathing apparatus with a full facepiece. Any supplied-air respirator with a
full facepiece.
Recommendations for respirator selection. Max
concn for use: 4000 mg/cu m. Respirator Class(es): Any supplied-air respirator
that has a full facepiece and is operated in a pressure-demand or other
positive-pressure mode.
Recommendations for respirator selection.
Condition: Emergency or planned entry into unknown concn or IDLH conditions:
Respirator Class(es): Any self-contained breathing apparatus that has a full
facepiece and is operated in a pressure-demand or other positive-pressure mode.
Any supplied-air respirator that has a full facepiece and is operated in a
pressure-demand or other positive-pressure mode in combination with an auxiliary
self-contained breathing apparatus operated in pressure-demand or other
positive-pressure mode.
Recommendations for respirator selection.
Condition: Escape from suddenly occurring respiratory hazards: Respirator
Class(es): Any air-purifying, full-facepiece respirator with a high-efficiency
particulate filter. Any appropriate escape-type, self-contained breathing
apparatus.
Preventive Measures:
VENTILATION CONTROL: THE SYNTHESIS OF
PHTHALATES REQUIRE GOOD VENTILATION IN ORDER TO PREVENT CONTAMINATION OF AIR
WITH PHTHALIC ANHYDRIDE OR ALCOHOLS. /PHTHALATES/
Contact lenses should not be worn when working
with this chemical.
SRP: The scientific literature for the use of
contact lenses in industry is conflicting. The benefit or detrimental effects of
wearing contact lenses depend not only upon the substance, but also on factors
including the form of the substance, characteristics and duration of the
exposure, the uses of other eye protection equipment, and the hygiene of the
lenses. However, there may be individual substances whose irritating or
corrosive properties are such that the wearing of contact lenses would be
harmful to the eye. In those specific cases, contact lenses should not be worn.
In any event, the usual eye protection equipment should be worn even when
contact lenses are in place.
If material not on fire and not involved in
fire: Keep sparks, flames, and other sources of ignition away. Keep material out
of water sources and sewers. Build dikes to contain flow as necessary.
Personnel protection: Personnel protection:
Avoid breathing vapors or dusts. ... Do not handle broken packages unless
wearing appropriate personal protective equipment. Wash away any material which
may have contacted the body with copious amounts of water or soap and water.
Stability/Shelf Life:
EXCELLENT STABILITY TO LIGHT
Cleanup Methods:
1) REMOVE ALL IGNITION SOURCES. 2) VENTILATE
AREA ... 3) FOR SMALL QUANT, ABSORB ON PAPER TOWELS. EVAPORATE IN A SAFE PLACE
(SUCH AS FUME HOOD). ALLOW SUFFICIENT TIME FOR EVAPORATING VAPORS TO COMPLETELY
CLEAR HOOD DUCTWORK. BURN PAPER IN A SUITABLE LOCATION ... LARGE QUANT ...
ATOMIZED IN ... COMBUSTION CHAMBER.
Environmental considerations-land spill: Dig a
pit, pond, lagoon, or holding area to contain liquid or solid material. /SRP: If
time permits, pits, ponds, lagoons, soak holes, or holding areas should be
sealed with an impermeable flexible membrane liner./ Dike surface flow using
soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid
with fly ash or cement powder.
Environmental considerations - air spill:
Apply water spray or mist to knock down vapors.
Environmental considerations-water spill: Use
natural barriers or oil spill control booms to limit spill motion. Use surface
active agent (eg detergent, soaps, alcohols) to compress and thicken spilled
material. Inject "universal" gelling agent to solidify encircled spill
and increase effectiveness of booms. Remove trapped material with suction hoses
if dissolved, apply activated carbon at ten times the spilled amount in region
of 10 ppm or greater concentration. Use mechanical dredges or lifts to remove
immobilized masses of pollutants and precipitates.
Disposal Methods:
Generators of waste (equal to or greater than
100 kg/mo) containing this contaminant, EPA hazardous waste number U069, must
conform with USEPA regulations in storage, transportation, treatment and
disposal of waste.
Good candidate for incineration by liquid
injection with a temperature of 650-1600 deg C with a residence time of 0.1-2
seconds; rotary kiln with a temperature of 820-1,600 deg C with a residence time
for liquids and gases: seconds, solids: hours; fluidized bed with a temperature
of 450-980 deg C with a residence time for liquids and gases: seconds, solids:
longer.
Chemical Treatability of Dibutyl
Phthalate; Concentration Process: Activated Carbon; Chemical
Classification: Phthalates; Scale of Study: Batch flow, Laboratory scale; Type
of Wastewater Used: Pure compound (one solute in a solvent); Results of Study:
100% reduction; 38% desorbed from carbon by elutriation with solvent; (Calgon
FS-300 used. Solvents included pentane-acetone, diethyl ether, methylene
chloride-acetone, chloroform-acetone, and acetone.)
Chemical Treatability of Dibutyl
Phthalate; Concentration Process: Resin Adsorption; Chemical
Classification: Phthalates; Scale of Study: Batch flow, Laboratory Scale; Type
of Wastewater Used: Pure compound (one solute in a solvent; Results of Study:
100% reduction; 108% desorbed from resin by elutriation with solvent. (Amberlite
XAD-2 used. Solvents included pentane- acetone, diethyl ether, methylene
chloride-acetone, chloroform-acetone, and acetone.)
Dibutylphthalate may be disposed of: 1) By
adsorbing it in vermiculite, dry sand, earth or a similar material and disposing
in a secured sanitary landfill. 2) By atomizing in a suitable combustion
chamber. Combustion may be improved by mixing with a more flammable solvent.
Recommendable methods: Adsorption, landfill & incineration.
After material has been contained, use an
absorbent on the material. Collect material, sorbent, and contaminated soil,
place in lined metal drums, and ship back to the supplier. Material may be
incinerated in a chemical incinerator or buried in a specially designated
chemical landfill.
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-1 8-hr
Time Weighted Avg: 5 mg/cu m.
Threshold Limit Values:
8 hr Time Weighted Avg (TWA): 5 mg/cu m.
Excursion Limit Recommendation: Excursions in
worker exposure levels may exceed three times the TLV-TWA for no more than a
total of 30 min during a work day, and under no circumstances should they exceed
five times the TLV-TWA, provided that the TLV-TWA is not exceeded.
NIOSH Recommendations:
Recommended Expousre Limit: 10 Hr
Time-Weighted Avg: 5 mg/cu m.
Immediately Dangerous to Life or Health:
4000 mg/cu m
Other Occupational Permissible Levels:
MAC USSR 0.5 mg/cu m
Manufacturing/Use Information:
Major Uses:
The active ingredient is no longer contained
in any registered pesticide products ... "cancelled."
INSECT REPELLANT FOR IMPREGNATION OF CLOTHING
AS MANOMETER FLUID
SOLVENT FOR CHLORINATED RUBBER
PLASTICIZER IN NITROCELLULOSE LACQUERS,
ELASTOMERS, EXPLOSIVES, NAIL POLISH & SOLID ROCKET PROPELLANTS; SOLVENT FOR
PERFUME OILS; PERFUME FIXATIVE; IN TEXTILE LUBRICATING AGENT; IN SAFETY GLASS;
IN PRINTING INKS; RESIN SOLVENT; PAPER COATINGS; IN ADHESIVES
/AN/ ... INSECT REPELLANT, IN GENERAL NOT AS
EFFECTIVE AS DIMETHYL PHTHALATE EXCEPT TO TROMBICULID MITES.
IT ENTERS INTO COMPOSITION OF LEATHER
VARNISHES & MIXED LACQUERS ... DIBUTYL PHTHALATE IS
COMPATIBLE WITH MOST PIGMENTS & IS OFTEN USED WITH CASTOR OIL FOR GRINDING
COLORING MATTERS INTENDED FOR INCORPORATION IN FILMS OR PLASTIC MASSES.
Component used in fuel matrix of double base
rocket propellant.
Used in the measurement of void volume (a
method of structure analysis) for carbon blacks.
As a desensitizing agent for nitroglycerin
(makes it stable for transport).
PLASTICIZER FOR POLYVINYL ACETATE EMULSIONS
COMPONENT OF PVC PLASTISOL FOR CARPET
BACKCOATING
PLASTICIZER FOR OTHER SPECIALIZED VINYL
COMPOUNDS
... Used as a reaction media for chemical
reactions.
Component in elastic impression materials used
by dentists.
USED AS A CHIGGER REPELLANT BY IMPREGNATION OF
CLOTHING, BEING SOMEWHAT LESS VOLATILE THAN DIMETHYL PHTHALATE & MORE
RESISTANT TO LAUNDERING, ITS MAIN USE IS FOR IMPREGNATION OF CLOTHING ...
Manufacturers:
Aristech Chemical Corp, Hq, 600 Grant St,
Pittsburgh, PA 15219, (412) 433-2747; Production site: Neville Island, PA 15225
Eastman Chemical Co, Tennessee Eastman
Division, PO Box 511, Kingsport, TN 37662, (423) 229-2000. Production site:
Kingsport, TN 37662
Unitex Chemical Co., 520 Broome Rd.,
Greensboro, NC 27406, (910) 378-0965. Production site: Greensboro, NC 2740
Methods of Manufacturing:
/PREPN:/ ... FROM PHTHALIC ACID & BUTYL
HALIDE IN PRESENCE OF TERTIARY ALIPHATIC AMINE. MFR FROM PHTHALIC ACID &
BUTYL ALCOHOL IN PRESENCE OF H2SO4.
The (butyl, octyl, etc) alcohol is esterified
with phthalic anhydride in the presence of a catalyst (sulfuric acid or p-toluenesulfonic
acid) or non-catalytically at high temp. The esterification is carried out at
ordinary pressure or in a vacuum, the water formed during the reaction being
eliminated as it is formed by entrainment by a third component (hydrocarbon or
usually the alcohol used in the esterification). The hydrocarbon may be benzene,
toluene, or cyclohexane. The reaction can be carried out discontinuously or by a
continuous method. /Phthalic esters/
General Manufacturing Information:
... WIDELY USED AS PLASTICIZER, SINCE IT IS
COMPATIBLE WITH ... NUMBER OF RESINS. ... IT IS ONE OF MOST COMMON PLASTICIZERS
FOR NITROCELLULOSE, ETHYLCELLULOSE, & BENZYLCELLULOSE. ... /GIVES/ LONG LIFE
TO OUTSIDE VARNISHES EXPOSED TO SUN & WEATHER. ... PLASTICIZER ... FOR
POLYVINYL ACETATE & POLYMETHYLMETHACRYLATE.
Formulations/Preparations:
INSECT REPELLANT COMPOSITION, GER OFFEN PATENT
NO 2925589 01/08/81 (FICHTEL UND SACHS A-G), COMPOSITIONS CONTAINING DIBUTYL
PHTHALATE, DIETHYL-M-TOLUAMIDE & 2-PHENYLCYCLOHEXANOL ARE SYNERGISTIC
INSECT REPELLANTS. ...
Grade: Technical, 99-100% dibutyl
phthalate
Consumption Patterns:
PRIMARY USE IS AS A PLASTICIZER IN POLYVINYL
ACETATE EMULSIONS
U. S. Production:
(1993) 6,662,000 lbs (includes diisobutyl
phthalate)
(1977) 7.72X10+9 G
(1982) 7.72X10+9 G
U. S. Imports:
(1977) 7.47X10+8 G (PRINCPL CUSTMS DISTS)
(1981) 3.03X10+8 G (PRINCPL CUSTMS DISTS)
Laboratory Methods:
Analytic Laboratory Methods:
GAS CHROMATOGRAPHY-MASS SPECTROMETRY &
HIGH RESOLUTION MASS SPECTROMETRY. DI-N-BUTYL PHTHALATE WAS
AMONG CMPD FOUND @ 1-30 PPB.
Gas chromatographic separation ... on a 1% QFI
column using FID.
Normal and reverse-phase high performance
liquid chromatography.
EPA Method 8060: Phthalate Esters This method
provides gas chromatographic conditions for the detection of ppb levels. A 2 to
5 ug aliquot of the extract is injected into a gas chromatograph using the
solvent flush technique, and compounds in the gas chromatograph effluent are
detected by an electron capture detector or a flame ionization detector. Ground
water samples should be determined by electron capture detector. For dibutyl
phthalate, the method detection limit for electron capture detector is
0.36 ug/l and for flame ionization detector is 14 ug/l, the average recovery
range for four measurements is 10.3-29.6 ug/l, and the limit for the standard
deviation is 8.9 ug/l.
EPA Method 8250: Gas Chromatography/Mass
Spectrometry for Semivolatile Organics, Packed Column Technique. Under the
prescribed conditions, dibutyl phthalate has a
detection limit of 2.5 ug/l, a range for the average recovery of four
measurements of 8.4-111.0 ug/l, and a limit for the standard deviation of 16.7
ug/l.
EPA Method 8270: Gas Chromatography/Mass
Spectrometry for Semivolatile Organics, Capillary Column Technique. Under the
prescribed conditions, dibutyl phthalate has a
retention time of 21.78 min, a range for the average recovery of four
measurements of 8.4-110.0 ug/l, and a limit for the standard deviation of 16.7
ug/l.
EPA Method 606 A gas chromatography method for
the analysis of dibutyl phthalate in municipal and
industrial discharges, consists of a glass column. This method has a detection
limit of 0.36 ug/l and an overall precision of 0.29 times the average recovery +
0.06, over a working range of 0.7 to 106 ug/l.
EPA Method 625. A gas chromatography/mass
spectrometry method for the analysis of dibutyl phthalate in
municipal and industrial discharges, consists of a glass column. This method has
a detection limit of 2.5 ug/l and an overall precision of 0.39 times the average
recovery + 0.60, over a working range of 5 to 1300 ug/l.
EPA Method 1625: An isotope dilution gas
chromatography/ mass spectrometry method for the determination of semivolatile
organic compounds in municipal and industrial discharges, this method is
designed to meet the survey requirements of Effluent Guidelines Division (EGD)
and the National Pollution Discharge Elimination System (NPDES). Under the
prescribed conditions, unlabeled dibutyl phthalate has
a minimum level of 10 ug/l and a mean retention time of 1723 sec. This method
has an initial precision of 74-188 ug/l and an accuracy of 67-207 ug/l for the
unlabeled compound.
Sampling Procedures:
MONITORING METHOD: ANALYTE: DIBUTYL
PHTHALATE; MATRIX: AIR; PROCEDURE: FILTER COLLECTION EXTRACTION WITH
CARBON DISULFIDE, GAS CHROMATOGRAPHY.
Care is taken to avoid sample contact with any
plastic. Under the prescribed conditions, dibutyl phthalate has
a detection limit of 2.5 ug/l, a range for the average recovery of four
measurements of 8.4-111.0 ug/l, and a limit for the standard deviation of 16.7
ug/l.
Special References:
Special Reports:
PIERCE ET AL; PHTHALATE ESTERS IN THE AQUATIC
ENVIRONMENT; NATL RES COUNC CAN ASSOC COMM SCI CRITER ENVIRON QUAL PUBL 0
(17583): 1 (1980). THE PHYSICAL-CHEMICAL PROPERTIES, ANALYTICAL DETERMINATION
& ENVIRONMENTAL DYNAMICS OF PHTHALATE ESTERS (INDUSTRIAL PLASTICIZERS) ARE
REVIEWED.
AUTAIN J; ENVIRON HEALTH PERSPECT 4:3 (1973).
TOXICITY AND HEALTH THREATS OF PHTHALATE ESTERS: REVIEW OF THE LITERATURE.
DHHS/ATSDR; Toxicological Profile for
Di-n-butylphthalate (1990) ATSDR/TP-90/10
USEPA/ECAO; Phthalate Atlas Report (1980)
Nat'l Research Council Canada; Phthalate
Esters (1980) NRCC No.17583
Cosmetic, Toiletry and Fragrance Association;
Final Report on the Safety Assessment of Dibutyl Phthalate, Dimethyl
Phthalate, and Diethyl Phthalate (in Cosmetic Products). J Am Coll Toxicol 4
(3): 267-303 (1985)
Thomas JA, Thomas MJ; Crit Rev Tox 13 (4):
283-318 (1984)
Woodward KN et al; Review of the Toxicity of
the Esters of o-Phthalic Acid (Phthalate Esters) p.183 (1986). This review
covers: identities; absorption, biotransformation, distribution, and excretion;
animal toxicity (acute toxicity, irritation, and sensitization, subacute
toxicity, hypolipemic and related effects, hepatic effects, effects on
reproductive organs, mutagenicity, chronic toxicity and carcinogenicity);
metabolism and effects in humans.
Synonyms and Identifiers:
Synonyms:
AI-3-00283
**PEER REVIEWED**
O-BENZENEDICARBOXYLIC ACID, DIBUTYL ESTER
**PEER REVIEWED**
BENZENE-O-DICARBOXYLIC ACID DI-N-BUTYL ESTER
**PEER REVIEWED**
1,2-BENZENEDICARBOXYLIC ACID, DIBUTYL ESTER
**PEER REVIEWED**
BUTYL PHTHALATE
**PEER REVIEWED**
N-BUTYL PHTHALATE
**PEER REVIEWED**
Caswell no 292
**PEER REVIEWED**
CELLUFLEX DPB
**PEER REVIEWED**
DBP
**PEER REVIEWED**
DBP (ester)
**PEER REVIEWED**
DIBUTYL 1,2-BENZENEDICARBOXYLATE
**PEER REVIEWED**
DI-N-BUTYL PHTHALATE
**PEER REVIEWED**
DIBUTYL-O-PHTHALATE
**QC REVIEWED**
ELAOL
**PEER REVIEWED**
EPA Pesticide Chemical Code 028001
**PEER REVIEWED**
ERGOPLAST FDB
**PEER REVIEWED**
Ersoplast FDA.
**PEER REVIEWED**
GENOPLAST B
**PEER REVIEWED**
HEXAPLAS M/B
**PEER REVIEWED**
PALATINOL C
**PEER REVIEWED**
PHTHALIC ACID, DIBUTYL ESTER
**PEER REVIEWED**
POLYCIZER DBP
**PEER REVIEWED**
PX 104
**PEER REVIEWED**
RC PLASTICIZER DBP
**PEER REVIEWED**
STAFLEX DBP
**PEER REVIEWED**
Uniflex DBP
**PEER REVIEWED**
UNIMOLL DB
**PEER REVIEWED**
WITCIZER 300
**PEER REVIEWED**
Formulations/Preparations:
INSECT REPELLANT COMPOSITION, GER OFFEN PATENT
NO 2925589 01/08/81 (FICHTEL UND SACHS A-G), COMPOSITIONS CONTAINING DIBUTYL
PHTHALATE, DIETHYL-M-TOLUAMIDE & 2-PHENYLCYCLOHEXANOL ARE SYNERGISTIC
INSECT REPELLANTS. ...
Grade: Technical, 99-100% dibutyl
phthalate
Shipping Name/ Number DOT/UN/NA/IMO:
NA 9095; n-Butyl phthalate
EPA Hazardous Waste Number:
U069; A toxic waste when a discarded
commercial chemical product or a manufacturing chemical intermediate or an
off-specification commercial chemical product.
Administrative Information:
Hazardous Substances Databank Number: 922
Last Revision Date: 20021016
Last Review Date: Reviewed by SRP on 1/31/1998
Update History:
Complete Update on 10/16/2002, 2 fields
added/edited/deleted.
Complete Update on 07/22/2002, 1 field added/edited/deleted.
Complete Update on 01/18/2002, 8 fields added/edited/deleted.
Field Update on 01/14/2002, 1 field added/edited/deleted.
Complete Update on 10/10/2001, 1 field added/edited/deleted.
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 11/08/2000, 1 field added/edited/deleted.
Complete Update on 06/12/2000, 1 field added/edited/deleted.
Complete Update on 03/22/2000, 1 field added/edited/deleted.
Complete Update on 03/13/2000, 2 fields added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 08/26/1999, 1 field added/edited/deleted.
Complete Update on 07/27/1999, 5 fields added/edited/deleted.
Complete Update on 03/29/1999, 2 fields added/edited/deleted.
Field Update on 03/17/1999, 1 field added/edited/deleted.
Complete Update on 03/01/1999, 1 field added/edited/deleted.
Complete Update on 02/01/1999, 1 field added/edited/deleted.
Complete Update on 01/27/1999, 1 field added/edited/deleted.
Complete Update on 11/12/1998, 2 fields added/edited/deleted.
Complete Update on 09/02/1998, 1 field added/edited/deleted.
Complete Update on 06/18/1998, 77 fields added/edited/deleted.
Field Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 04/07/1997, 2 fields added/edited/deleted.
Complete Update on 03/17/1997, 1 field added/edited/deleted.
Complete Update on 02/27/1997, 1 field added/edited/deleted.
Complete Update on 02/24/1997, 1 field added/edited/deleted.
Complete Update on 10/13/1996, 1 field added/edited/deleted.
Complete Update on 05/09/1996, 1 field added/edited/deleted.
Complete Update on 03/19/1996, 7 fields added/edited/deleted.
Complete Update on 01/19/1996, 1 field added/edited/deleted.
Complete Update on 10/19/1995, 2 fields added/edited/deleted.
Complete Update on 01/18/1995, 1 field added/edited/deleted.
Complete Update on 12/22/1994, 1 field added/edited/deleted.
Complete Update on 11/09/1994, 1 field added/edited/deleted.
Complete Update on 08/11/1994, 1 field added/edited/deleted.
Complete Update on 07/22/1994, 1 field added/edited/deleted.
Complete Update on 05/05/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 02/24/1994, 2 fields added/edited/deleted.
Complete Update on 08/20/1993, 1 field added/edited/deleted.
Complete Update on 08/07/1993, 1 field added/edited/deleted.
Field update on 12/16/1992, 1 field added/edited/deleted.
Complete Update on 12/03/1992, 1 field added/edited/deleted.
Complete Update on 09/03/1992, 1 field added/edited/deleted.
Complete Update on 04/27/1992, 1 field added/edited/deleted.
Complete Update on 01/23/1992, 1 field added/edited/deleted.
Complete Update on 09/26/1991, 1 field added/edited/deleted.
Complete Update on 07/09/1991, 2 fields added/edited/deleted.
Complete Update on 05/08/1991, 2 fields added/edited/deleted.
Complete Update on 01/07/1991, 5 fields added/edited/deleted.
Field Update on 05/14/1990, 1 field added/edited/deleted.
Field Update on 03/06/1990, 1 field added/edited/deleted.
Field Update on 01/15/1990, 1 field added/edited/deleted.
Complete Update on 01/11/1990, 3 fields added/edited/deleted.
Complete Update on 07/12/1989, 107 fields added/edited/deleted.
Field Update on 07/06/1988, 1 fields added/edited/deleted.
Field Update on 07/06/1988, 1 fields added/edited/deleted.
Complete Update on 06/03/1985
GLCC RELATED TOXIC SUBSTANCES
FOUND IN THE CAMP POND
AND CAMP WATER WELL
2003 AND 2004
GREAT LAKES CHEMICAL CORPORATION AND THE PATHFINDERS CAMP