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Dibutyl Phthalate 1

Dibutyl Phthalate

David R Wallace

by the rat liver esterases. Monobutyl phthalate

(MBP) was a common metabolite in different spe-

cies. The glucuronide conjugate was also detected in

rat, hamster, and guinea pig together as well as a

small amount of phthalic acid and unchanged com-

pound. Omega or omega-1 oxidation products of

MBP were also detected in the urine.

This article is a revision of the previous print edition article

by Sushmita M Chanda, volume 1, pp. 459–460, & 1998,

Elsevier Inc.

* C HEMICAL A BSTRACTS S ERVICE R EGISTRY N UMBER :

CAS 84-74-2

* S YNONYMS : Dibutyl-1,2-benzenedicarboxylate;

o -Benzenedicarboxylic acid; Dibutyl ester; DBP

* C HEMICAL /P HARMACEUTICAL /O THER C LASS : Plasti-

cizer and softener; Aromatic dicarboxylic acid

ester

* C HEMICAL F ORMULA :C 16 H 22 O 4

* C HEMICAL S TRUCTURE :

Mechanism of Toxicity

Dibutyl phthalate acts as an uncoupler of oxidative

phosphorylation in rats.

Acute and Short-Term Toxicity

(or Exposure)

The majority of the studies focusing on dibutyl

phthalate exposure has centered on acute exposure

via inhalation, ingestion, and dermatological contact.

CH 3

Animal

Exposures to dibutyl phthalate have caused photo-

phobia, conjunctivitis, edema, and keratitis. Increase

in mean liver weight and testicular atrophy have been

observed in rats exposed to dibutyl phthalate. The

LD 50 in rats is 8–10 g kg 1 (oral) and 4 g kg 1 (in-

traperitoneal). Aerosol (2 h) exposure of dibutyl

phthalate at a concentration of 250mgm 3 in mice

produced symptoms of irritation to the upper respi-

ratory tract and eyes. Increased concentrations result-

ed in bronchospasms causing difﬁculty in breathing,

ataxia, weakness, convulsions, and eventually death.

The LC 50 in mice was determined to be 25 gm 3 .

Dibutyl phthalate has weak estrogenic activity in a

number of assays and may act as an anti-androgen.

Uses

Dibutyl phthalate has multiple uses in a variety of

materials. Primary uses for dibutyl phthalate are to

soften and increase plastic ﬂexibility, for example, in

shower curtains, raincoats, food wraps, and car

interiors to name a few. It has been used in insect

repellents and as a solvent for perfume oil and resins.

Dibutyl phthalate can be used as a plasticizer in ni-

trocellulose lacquers, elastomers, explosives, nail

polish, and solid rocket propellants. Other uses in-

clude perfume ﬁxative, textile lubricating agent, safe-

ty glass additive, printing inks, and adhesives.

Human

Exposure Routes and Pathways

Exposure to dibutyl phthalate is usually by inhala-

tion. It is known to leech out from ﬁnished plastics

into blood, milk, and other food materials and,

therefore, can be ingested orally. Dermal and ocular

exposures are also possible.

Dibutyl phthalate has low acute toxicity based on

animal studies. It can cause an immediate stinging

and burning sensation upon contact by splashing.

Following ingestion, it can also cause dizziness and

nausea. Contact with the skin has been reported to

result in contact dermatitis.

Toxicokinetics

In rats, greater than 90% of dibutyl phthalate was

excreted in the urine within 48 h following i.v. or oral

dosing, but elimination in the feces was low. No

accumulation was observed in tissues 24 h after

exposure. Dibutyl phthalate was hydrolyzed rapidly

Chronic Toxicity (or Exposure)

Information regarding the long-term, chronic, expo-

sure to dibutyl phthalate is lacking. There is no

information on human carcinogenicity and only limi-

ted effects in animals. No information is available on

human teratogenicity, but animal studies have shown

a reduced body weight. No information on dibutyl

2 Dicamba

phthalate effects on the human reproductive system

is available.

for at least 15min. Treatment is supportive and

symptomatic and no specific antidote is available.

Animal

Rats exposed to 0.5mgm 3 for 6 h day 1 for 6 days

exhibited signiﬁcantly higher brain and lung weights,

smaller overall body weights compared to control

groups. The Environmental Protection Agency (EPA)

has classiﬁed dibutyl phthalate as ‘group D’ car-

cinogen, in that no deﬁnitive carcinogenic character-

istics have been reported.

Environmental Fate

Dibutyl phthalate is considered nonhazardous for air,

sea, and road freight. No other reports on dibutyl

phthalate are available.

Exposure Standards and Guidelines

Occupational Safety and Health Administration per-

missible exposure level, the National Institute for

Occupational Safety and Health recommended

exposure limit, and the ACGIH threshold limit value

has been set at 5.0mgm 3 for an 8–10 h day per

40 h week. Although dibutyl phthalate is not subject

to EPA emergency planning requirements, if dibutyl

phthalate is released in a quantity exceeding 10

pounds over 24 h, the appropriate local, state, and

federal authorities must be notiﬁed.

Human

Generalized symptoms of chronic exposure dibutyl

phthalate include pain, numbness, spasms, weakness,

and ﬁnally, polyneuritis. In an American Conference

of Governmental Industrial Hygienists (ACGIH)

study of 147 Russian workers exposed to several

dibutyl esters for a period of 0.5–19 years and an air

concentration of 1.7–66mgm 3 reported signiﬁcant

adverse effects. By the seventh year of work, reports

of pain, numbness, and muscle spasms were repor-

ted. These symptoms were followed by weakness in

the extremities and a 32% rate of polyneuritis.

See also: Fragrances and Perfumes; Nitrocellulose; Toxi-

city Testing, Dermal.

In Vitro Toxicity Data

Short-term studies with human cells have yielded

negative results. Long-term mutagenicity tests have

provided inconclusive results.

Further Reading

ACGIH (1991) Documentation of the Threshold Limit

Values and Biological Exposure Indices , 6th edn.

Cincinnati, OH: American Conference of Government

Industrial Hygienists.

Sittig M (1991) Handbook of Toxic and Hazardous Chem-

icals , 3rd edn. Park Ridge NJ: Noyes Publications.

Clinical Management

Induced emesis is not recommended if the victim has

any signs of esophageal or gastrointestinal tract

irritation or burns, or decreased sensory response,

depressed gag reﬂex, or impending shock. Activated

charcoal slurry with or without saline cathartic or

sorbitol can be given in cases of oral exposures. Skin

decontamination should be done with repeated

washing with soap. Exposed eyes should be irrigated

with copious amounts of room-temperature water

Relevant Websites

http://www.intox.org – Canadian Centre for Occupational

Health and Safety. Cheminfo: Dibutyl phthalate.

http://www.osha.gov – Occupational Safety and Health Ad-

ministration, US Department of Labor Health Guidelines.

http://www.epa.gov – US Environmental Protection Agency

Technology Transfer Network Air Toxics Website: Di-

butyl phthalate.

Dicamba

Xun Song

This article is a revision of the previous print edition by

Sushmita M Chanda, volume 1, p. 460, & 1998, Elsevier Inc.

* S YNONYMS : Banlen; Banvel 480; Brush buster;

Compound B dicamba; Velsicol compound ‘r’;

Velsicol 58-CS-11; Banvel herbicide; Banvel 4WS;

Banfel s ; Banvel s ; Banvel CST s ; Banvel D s ;

Banvel XG s ; Mediben s

* C HEMICAL /P HARMACEUTICAL /O THER C LASS : Benzoic

acid, 3,6-dichloro-2-methoxy-

* C HEMICAL A BSTRACTS S ERVICE R EGISTRY N UMBER :

CAS 1918-00-9

Dicamba 3

* C HEMICAL S TRUCTURE :

system effects (excitation or depression), inconti-

nence, and cyanosis. Inhalation can cause irritation

of the nasal passages and lungs and loss of voice.

Recovery from severe overdose is generally complete

within 2–3 days. Dicamba can cause severe, perma-

nent corrosive damage to the eyes. Dicamba may

cause skin burns.

COOH

O CH 3

Uses

Dicamba is mainly used as herbicide to control weeds,

dock, bracken, and brush. Dicamba is frequently

applied with other herbicides including atrazine,

glyphosate, imazethapyr, ioxynil, and mecoprop.

Chronic Toxicity (or Exposure)

Animal

Prolonged dietary dicamba exposure at high dosages

in rats led to changes in liver and decreased body

weights. Dicamba was negative in reproductive, tera-

togenic, and carcinogenic tests.

Exposure Routes and Pathways

Dicamba is available as an odorless, white or brown,

crystalline solid. Exposure to dicamba may occur

through oral, dermal, or inhalation route.

Human

Little is known regarding chronic effects of dicamba

in humans but animal studies suggest little potential

for chronic toxicity.

Toxicokinetics

Dicamba is known to be well absorbed orally. Min-

imal absorption occurs through the skin. Following

ingestion in animals, dicamba is readily distributed in

all organs and systems. When given as a food sup-

plement to rats, most dicamba was excreted un-

changed in the urine while a small proportion was

metabolized into glucuronic acid conjugates. The

half-life of elimination in rats was estimated to be

0.83 h.

In Vitro Toxicity Data

Dicamba is not mutagenic.

Clinical Management

There is no specific antidote; therefore, the treatment

is symptomatic and supportive. Skin decontamina-

tion should be done with repeated washing with

soap. Exposed eyes should be irrigated with copious

amounts of water (at room temperature) for at least

15min. Emesis can be induced if initiated within

30min of ingestion. Ipecac can be used to induce

emesis. Emesis is not encouraged if the patient is

comatose or convulsing. Activated charcoal slurry

with or without saline cathartic and sorbitol may be

used.

Mechanism of Toxicity

There is little evidence of dicamba toxicity in mam-

mals. In plants its primary action is to act as a growth

regulator.

Acute and Short-Term Toxicity

(or Exposure)

Environmental Fate

Dicamba is moderately persistent in soil (half-life is

1–4 weeks). Microbial degradation is predominant.

Degradation increases with temperature, increasing

moisture, and low pH. When soil moisture increases

above 50%, however, dicamba degradation is

reduced. Photodegradation occurs to a limited

extent. Some dicamba residues volatilize from

plant surfaces. Dicamba does not bind to soil parti-

cles and is highly water soluble and therefore mobile.

Groundwater contamination is possible. In sur-

face waters, microbial degradation is predominant.

Animal

The oral LD 50 for dicamba is 757–1707mg kg 1 in

rats, 1190mg kg 1 in mice, 2000mg kg 1 in rabbits,

and 566–3000mg kg 1 in guinea pigs. In rabbits, the

dermal LD 50 is greater than 2 g kg 1 while the inha-

lation LC 50 in rats is greater than 200mg l 1 .

Human

Symptoms of poisoning with dicamba include loss of

anorexia, vomiting, muscle weakness and spasms,

bradycardia, shortness of breath, central nervous

4 Dichlone

Photodegradation can also occur. Dicamba does not

signiﬁcantly bioaccumulate.

Exposure Standards and Guidelines

The reference dose for dicamba is 0.045mg kg 1

day 1 .

Ecotoxicology

Dicamba is practically nontoxic to birds (LD 50 in

mallard ducks was 42gkg 1 ). The 8 day dietary

LC 50 in mallards and quail was 410 000 ppm. Di-

camba is also of low toxicity to ﬁsh. The LC 50 (96 h)

for dicamba was 100–135mg l 1 in rainbow trout,

bluegill, grass shrimp, ﬁddler crab, and sheeps-

headminnow. The LC 50 (48 h) was 110mg l 1

See also: Pesticides; Pollution, Water.

Relevant Websites

http://extoxnet.orst.edu – Extension Toxicology Network,

Oregon State University.

http://www.epa.gov – US Environmental Protection Agency

and National Pesticide Information Center.

Daphnia magna . Dicamba is not toxic to bees.

Dichlone

Xun Song

Toxicokinetics

Toxicokinetic data for dichlone are limited. It has

been demonstrated that dichlone is poorly absorbed

from the gastrointestinal tract.

This article is a revision of the previous print edition article

by Todd A Bartow, volume 1, p. 461, & 1998, Elsevier Inc.

* C HEMICAL A BSTRACTS S ERVICE R EGISTRY N UMBER :

CAS 117-80-6

* S YNONYMS : Dichloronaphthoquinone; 2,3-Dichloro-

1,4-naphthoquinone; Phygon; Algistat; Quintar;

Sanquinon; Miraclear

* C HEMICAL /P HARMACEUTICAL /O THER C LASS : Naph-

thoquinone

* C HEMICAL S TRUCTURE :

Mechanism of Toxicity

The exact mechanism of toxicity is not clear. In vitro

studies suggested that incubation of dichlone with

normal human erythrocytes induced rapid loss of in-

tracellular potassium, increased the osmotic fragility,

and inhibited the Na þ ,K þ -ATPase. Dietary dichlone

exposure caused inhibition of glycolysis in rat liver.

Dichlone can inhibit pyruvate and succinate dehy-

drogenases. Dichlone was also reported to cause

oxidative stress and swelling of mitochondria.

Acute and Short-Term Toxicity

(or Exposure)

Uses

Dichlone is primarily used as a fungicide. It is espe-

cially effective for brown rot of stone fruit and scab

on apples and pears. Dichlone is also used to control

blue algae. There are no registered uses for dichlone

in the United States.

Animal

The acute dermal LD 50 in rabbits was 5 g kg 1 . The

oral LD 50 in rats was 1.3 g kg 1 . Dichlone is a skin

irritant.

Human

Dichlone has relatively low toxicity in humans. It is

irritating to the skin and mucous membranes. Irrita-

tion of the cornea may occur. Ingestion of large doses

usually results in prompt emesis. Large doses may

cause central nervous system depression, coma, and

death.

Exposure Routes and Pathways

Exposure to dichlone may occur through oral and

dermal routes.

Dichlorobenzene 5

Chronic Toxicity (or Exposure)

Animal

Contaminated clothing should be removed and

discarded.

Little toxicity was noted in rats given a diet of

1500 ppm dichlone for 2 years. Dietary exposure of

dogs to dichlone (500 ppm) for 1 year elicited slight

liver changes.

Ecotoxicology

Dichlone is toxic to ﬁsh. Dichlone is relatively non-

toxic to bees. The LC 50 in Daphnia magna is

0.014 ppm.

Human

Based on animal studies, dichlone exposure is

not expected to lead to chronic toxicity. Little is

known, however, regarding long-term exposures in

humans.

Exposure Standards and Guidelines

The reference dose for dichlone is 0.08mg kg 1

day 1 .

Clinical Management

If a poisoning is suspected, one should not wait

for symptoms to develop. Immediate medical atten-

tion should be sought. Emesis may be indicated

in recent substantial ingestion unless the patient is

or could rapidly become obtunded, comatose,

or convulsing. Emesis is most effective if initiated

within 30min. An activated charcoal cathartic

may also be employed. Use of any fat should be

avoided since these agents may increase the irritant

effects If contaminated with dichlone the affected

area should be washed vigorously with soap.

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