Dioxin: Environmental Impacts and Potential Human Health Effects

CICXIN: E N V I R 3 N M E N T A L I M P A C T S AND P O T E N T I A L H U M A N H E A L T H E F F E C T S

ISSUE BRIEF NUMBER IB83079

AUTHOR:

M i c h a e l M.

Simpson

Science Policy Research Division

T H E L I B R A R Y OF C O N G R E S S

CONGRESSIONAL RESEARCH SERVICE

MAJOR I S S U E S S Y S T E M

D A T E O R I G I N A T E D 04/18/83

DATE UPDATED 10/21/83

FOR A D D I T I O N A L I N F O R M A T I O N C A L L 2 8 7 - 5 7 0 0

CRS- 1

ISSUE DEFINITION

Animal studies indicate that dioxin is a highly toxic .compound; however,

there have been no human deaths attributed to exposure to dioxin.

Current

concerns about dioxin center around the potential adverse environmental

impacts a s well a s the possible harmful human health effects of trace dosages

encountered a s environmental contaminants.

The environmental impact a n 8

human health effects of such exposure to djoxin are not clear a t this time.

Conflicting statements regarding the effects of dioxin exposure are found

in both scientific and popular journals.

This controversy stems from the

lack of conclusive findings from well-defined exposure studies. Policymakers

are consequently confronte5 with deciding whether or not to take regulatory

cr other action t o address fears about the threat to health and the

environment, in the absence of confirmed findings on the risks associated

with dioxin.

This issue brief presents a short background

on the physical/chemical

properties of dioxin, describes several existing sources of possible human

exposure, and highlights.what is currently known about its environmental

impacts and human health effects.

Congressional interest is intense a t this

time because of large numbers of Vietnam

veterans' claims for benefits

associated with use of herbicides in that war a s well a s because of certain

incidents of potential significance to health involving disposal of wastes

Veterans'

Complaints

conraining dioxin.

(See also IB83043 -- Agent Orange:

and Studies of Health Effects.)

BACKGROUND AND POLICY ANALYSIS

The compound dioxin was identified when i t was synthesized by a research

technician in the mid-1950s.

The technician was exposed to the dioxin and

subsequently developed a severe

case

of

chloracne

which

required

hospitalization.

This event provided the first clue a s to the potential

human health effects of dioxin exposure.

There a r e many different forms of dioxin; the form most commonly r e f e r r e d (TCDD).

Dioxin is a

to a s dicxin is 2 , 3 , 7 , 8 , - t e t r a c h l o r o d i b e n z o - p - d i o x i n

(2,4,5,-trichlorophenol).

contaminant that occurs in the production of TCP

When TCP is used to make other compounds, a dioxin contaminant may be passed

along to the new substance. The compound TCP i s used in the proauction of

several

compounds,

including

the

herbicide

2,4,5,-T

(2,4,5,-trichiorophenoxyacetic acid) and

the

compound

hexachlorophene

(bis-trichoro-2-hydroxyphenol

methane),

whi.ch i s

used

in

soaps

and

disinfectants.

The level of dioxin contamination in 2,4,5-T until 1970 averaged 1-5 parts

per million (pprn) with a few samples a s high as 4-7 ppm.

After-1970, levels

of dioxin contamination were required to be reduced to less than 0.1

ppm

in

2,4,5-T. The U.S.

Pharmacopeia has established a maximum

detectable limit

of 0.05 ppm dioxin for hexachlorophene; the actual content measured

in

(A

physical/chemical

hexachlorophene has been less than 0.005

ppm.

description of the compound dioxin is provided in the appendix.)

Policymakers have often been called upon to make risk-regulating decisions

CRS- 2

in the absence of sufficient scientific data. Frequently such data a s may be

available are conflicting.

In making

such policy decisions, Congress

considers a number of factors in determining allowable risk to public health

and the environment, a s well a s the economic impact and net social benefits

involved.

Policy decisions about the regulation of dioxin may affect the

general population, several industries, and foreign trade; At present, there

are several organizations, activities, agencies, and

interest

groups

concerned about the issue of dioxin.

Their positions are reflected by their

individual policy statements.

o The Veterans Administration (VA) has a long-standing and continuing

concern over the effects of dioxin exposure, stemming from the use of Agent

Orange in Vietnam.

The VA's review of available literature and ongoing

studies indicates that, as yet, no consensus exists within the scientific

community concerning the causal relationship between

dioxin exposure and

those health problems experienced by some Vietnam veterans.

o The Dow Chemical company acknowledges that dioxin i s highly toxic and

produces ill health effects in laboratory animals; however, a t concentrations

found in the environment, the company believes dioxin does not pose a health

hazard to humans.

o The American Medical Association (AMA) has not confirmed any chronic

aCverse human health effects related to environmental exposure to dioxin

other than chloracne, but has encouraged further research in this area.

o As a result of studies conducted a t sites contaminated with dioxin, the

Centers for Disease Control (CDC) has established a safe exposure limit for

dlsxin in the environment at 1.0 part per billion (ppb).

The CDC's position

is that below 1.0

ppb the individual i s not a t risk; above 1.0 ppb,

inadequate data exist to determine if any risk is present.

The exposure

limit is both site and condition specific -- i.e., this limit may vary from

location to location, depending upon the level of dioxin contamination, and

the condition of exposure. CDC is presently conducting research on Vietnam

veterans exposed to dioxin (phenoxy herbicides) to better define the health

risks from exposure.

o The National Institute for Occupational Safety and Health (NIOSH) claims

that evidence i s increasing to support a link between occupational exposure

to dioxin and soft,tissue sarcoma.

o The Veterans of Foreign Wars (VFW), in its concern for the health of

veterans in general, finds that although no confirmed relationship has been

established between dioxin exposure and specific adverse health effects,

there are sufficient trends reportea in the scientific journals to suggest

some health risk. The VFW is seeking compensation for any veteran suffering

from specific conditions reported to result from dioxin exposure.

o Also supporting the idea of compensation is the Vietnam

Veter2ns

of

America (VVA). The VVA maintains that scientific evidence supports the

association of adverse human health effects and dioxin exposure.

o The Sierra Club and the Environmental D-efense Fund

(EDF) have taken

stronger positions against dioxin.

The Club and EDF believe dioxin presents

a health hazard and recommend further research to determine the degree of

hazard to man.

They call for the removal of all uses of chemicals

contaminated with dioxin and stricter control over production of chemicals

that could have dioxin a s a contaminant.

CRS- 3

IB83079

The diversity of these pclicy positions reflects the

scientific data.

lack

UPDATE-10/21/83

of

conclusive

Dioxin Research

Dioxin research is presently being conducted in several private and

Federal research facilities. Federal agencies have budgeted over $101000,000

for dioxin research during fiscal year 1983 (FY83) and more than $50 million

is scheduled to be spent on dioxin research in FY84.

The major purp0s.e of

this research i s to determinate the human health effects and environmental

impacts associated with dioxin exposure.

In addition to Federal expenditures, the Dow Chemical Company has made

$3,000,000.00 available to researchers to identify the human health effects

resulting from Cioxin exposure.

Concern has been expressed concerning the coordination and control of

research efforts by individuals, interest groups, researchers, and Federal

agencies.

Superf crnd

At present, funds used to temporarily or permanently

relocate residents

living in dioxin-contaminated areas come from the Superfund budget.

If the

trend of buying these contaminated areas continues, additional funding of the

Superfund program will become necessary.

(See IB83D64 -Superfund:

Hazardous Waste Clean-up -- for details of the complete issues associated

with the Superfund.)

Sources of Exposure to Dioxin

Public concern about exposure to dioxin has been heightened a s a result of

increased awareness of several sources of proven or possible exposure:

1)

the use of the herbicide "Agent Orange" in aerial spraying operations during

the Vietnam conflict

(there were also occasional uses of herbicides such a s

2,4,5-T for brush control in civilian applications until 1979.

Since 1979, .

uses of 2,4,5-T have been limited to rice crops and rangelands; 2) the

from

municipal

Seveso, Italy, chemical plant accident; 3) emissions

incinerators and some fossil fuel power plants; 4) the; spreading of dioxin

contaminated oil for dust control in Missouri.

and 5) unknown

sources of

dioxin in Michigan, New Jersey, Massachusetts, and Oregon.

1. Herbicide Aerial Spraying.

From 1 9 6 2 to 1971, herbicide aerial spraying operations were conducted by

the U.S. in the Republic of Vietnam.

The peak periods of spraying were 1968

and 1969. According to the U.S. Air Force, the herbicide most eften sprayed

was "Agent Orange," a half-and-half mixture of the herbicide 2, 4,-D

( 2 , 4 - d i c h l o r o p h e n o x y a c e t i c acid) and

2,4,5-T

(2,4,5-trichlorophenoxyacetic

acid).

Dioxin is a contaminapt of 2,4,5-T.

Average dioxin levels in "agent

orangew were estimated a t 2 ppm with a high of 4 7 ppm and a low of 0.02 ppm.

The Environmental Protection Agency (EPA) has since recommended the limit for

the contaminant dioxin in 2,4,5-T a t 0.1 ppm (May 1971).

Both U.S.

air and

ground forces were subjected to possible dioxin exposure while in specific

CRS- 4

regions of the Republic of Vietnam (see IB83043

Complaints and Studies of Health Effects).

IB83079

-- Agent

UPDATE-10/21/83

Orange:

Veterans'

2. Seveso, Italy, Chemical Plant Accident.

The Seveso, Italy, accident (July 1 0 , 1976) involved an explosion a t a

chemical plant where TCP was manufactured.

A cloud of TCP with the

contaminant dioxin escaped from the chemical plant a s a result of the

explosion.

The cloud, estimated to contain roughly 3 grams of dioxin, was

dispersed by the wind across a residential area adjacent to the plant.

Several hundred people were exposed to the, chemical cloud. Within the first

year after the accident 187 cases of chloracne were reported; 1 6 4 were

children and 23 were adults. Eight of the children with chloracne also had

severe chemical burns; eleven other children had chloracne and mild

chemical

burns.

Several other children that did not develop chloracne did develop

erythema (red skin patches).

Very few adults developed chloracne or chemical

burns.

Studies are still being conducted on the exposed population

to

determine the chronic health effects.

3. Power Plant and Incinerator Emissions.

Dioxin has also been identified a s an emission from some fossil fuel power

plants and municipal incinerators.

The dioxin is produced during the

incomplete combustion of fuel or waste that contains such compounds a s

chlorophenols, chlorinated benzenes, and biphenyl ethers.

The amount of

discharge (smoke stack emissions) is dependent upon incinerator operation,

fuel, and combustion temperature.

4. State of Missouri Contamination.

Dioxin contamination of soil in Kissouri dates back

t o 1971, when

dioxin-contaminated waste oil was applied to the soil for dust control. At a

horse arena where the dioxin-contaminated

waste oil was applied several

horses died.

Several other sites in the State also were sprayed with the

dioxin-contaminated waste oil for dust control.

Not all sites have been

positively identified or tested.

Dioxin contamination sites in the State

have been identified to have levels between 1.0

ppb-1,800 ppb.

Some

estimates for suspected dioxin contamination sites are a s high as 1.0 ppm.

The problem of dioxin site identification and cleanup has been complicated by

rainfall, surface run-off, and flooding which spreads the dioxin contaminatedsoil. At present, efforts are underway to identify all dioxin sites in the

State and either clean up the site or possibly relocate the residents.

As a result of the scil being contaminated with dioxin, the EPA has

requested the Federal Emergency Management Agency

(FEMA) to permanently

relocate the residents of Times Beach and 1 1 families of Imperial, MO.

The

EPA has also requested FEMA to temporarily relocate three St. James, MO

Families.

5.

Michigan and New Jersey Contamination.

Certain sites in Michigan and New Jersey have recently been identified a s

having been contaminated with dioxin.

Dioxin has been detected in rivers

around the Dow Chemical Plant in Midland, Michigan, and a t three sites near

the Diamond Alkali Corp. plant in New Jersey. Both plants a r e reported to

have produced Agent Orange contaminated with dioxin during the Vietnam

War.

In New Jersey

At presen-t only one site has been identified in Michigan.

there are 5 0 additional sites that are scheduled for eioxin contamination

CRS- 5

testing. The specific source or sources of dioxin contamination remain to be

determined in both States. Further investigations will be conducted in each

State to identify any additional dioxin contaminated sites.

6.

Identification of Sites Possibly Contaminated with Dioxin.

In 1980, the Environmental Protection Agency compiled a list of sites

33 States possibly contaminated with dioxin.

These sites -will be tested

determine if they are actually contaminated.

in

to

Massachusetts is one of the suspect States.

Several ponds and lakes in

the State will be tested during the summer of 1983. The ponds and lakes may

have been contaminated when herbicides were sprayed on them to control water

weeas in the 1950s and 1960s.

It has been reported that dioxin-contaminated sites also exist in Oregon,

with dioxin concentrations up to six times greater than those at Times Beach,

Mo.

The source of the dioxin in Oregon is unknown at this time.

Environmental Effects

1.

Biological Accumulation and Elimination.

Stadies have demonstrated that accumulation and elimination of dioxin

occurs in many animal species.

It has been reported that dioxin, at

concentrations found in the environment, does not accumulate in animal tissue

to any significant degree.

It would appear that the rates of accumulation and elimination

dependent upon the environmental concentration, conditions of exposure,

animal species.

are

and

Few studies have been conducted to determine whether dioxins

are

accumulated in plants.

Those studies that have addressed this question

appear to indicate that very little dioxin accumulation occurs in plants.

When accumulation did occur the lowest levels were recorded in the fruits and

leaves with the highest levels found on the surface of roots.

It is

interesting

to

note

that

when

plants

were

transplanted

from

dioxin-contaminated

soil to uncontaminated

soil,

the

dioxin

levelsaccumulated in the plant disappeared.

2. Soil Contamination.

Some studies have'been conducted to determine if dioxin is persistent in

most types of soils. Those studies that evaluate dioxin persistence in soil

found that over 90% of the dioxin could be detected in the soil one year

after the original contamination occurred.

This would indicate that a strong

bond is established between dioxin and most soils.

The persistence of dioxin

in the environment has been attributed to these strong bonds.

3. Water Contamination.

Dioxin is not very soluble in water

(highly insoluble).

The greatest

danger of contamination of the rivers and streams is from dioxin-contaminated

soil run-off.

The eroded dioxin-contaminated soil particles could Settle on

the bottom of the stream or could be carried with the flow of' the stream.

CRS- 6

Disposal Methods

Small quantities of dioxin can be disposed of by physiochemical, chemical,

and microbiological means.

Physiochemical means include: ultraviolet light;

gamma rays;

or hydrogen

donation.

An

ultraviolet l i g h t treatment was

developed recently for commercial disposal of dioxin-contaminated

liquid

Chemical disposal i s possible

wastes.

T h e treatment i s 98% efficient.

utilizing

alkaline dehydrochlorination, reduction with

iron

chlorides,

oxidation with ruthenium tetroxide, chloridides, and chlorolysis.

Alkaline

dehydrochlorination

uses anhydrous a l k a l i metal

salts

of

polyhydroxy alcohols to remove the chlorine from

the chlorinated dioxins.

This is accomplished by mixing dioxins, a l c o h o l , a n d a water solution of any

(alkaline) metal hydroxide.

Reduction of dioxin with iron chlorides i s being studied; this method

had limited success.

has

Oxidation with ruthenium tetroxide i s a n acceptable method f o r destroying

i s usually

used

t o destroy dioxin

small a m o u n t s o f . d i o x i n . This method

produced i n the laboratory.

Chloriodide research i s being conducted i n the hopes of using chloriodides

to destroy dicxin i n contaminated soil.

Micellar catalysts a r e used

un the

process.

being

investigated.

Final

research

Chlorolysis I S a process currently

results r e m a i n to S e determined.

M i c r o b i o l o g i c a l ~ m e a n s depend on microbes to

destroy t h e dioxin.

T h i s method has been field tested with limited

success;

d u e to i t s high cost i t may n o t be considered practical

f o r bulk

disposal.

Research i s underway to develop a better microbial degradation method.

Such

degradation has not proven successful t o date.

Larger quantities of dioxin

can be disposed of using more traditional means such as: a) incineration; b)

perpetual

repository storage

(not true disposal);

c)

secure

landfill

(presently permitted but may still present a n environmental hazard

later);

with

dioxin

this i s n o t actually

and C ) entombment (concrete mixed

disposal)

.

--

Dioxin i s easily destroyed by natural sunlight i n a very short time.

The difficulty in this form of disposal resnlts from the f a c t that natural

light

destruction of d i o x i n ' i s only surface active

(i..,

i t destroys only the

layer on the surface directly exposed to the natural sunlight.)

General Exposure Standards

Two a g e n c i e s have established exposure standards f o r dioxin and a tBird

exposure limit.

T h e Environmental Protection

has recommended a maximum

Agency's Scientific Advisory Panel i n 1 9 8 0 established

the

" n o ' observable

effect level" (NOEL) f o r dioxin a t 0.001 micrograms dioxin p e r - kilogram of

body weight. per day (mg/kg/day).

T h e NOEL i s defined a s a dose b e l o w which

no c a r c i n o g e n i c , teratogenic, o r reproductive effect i s observed.

T h e F e d e r a l Food and Drug Administration (FDA) set the dioxin levels i n

edible f i s h a s not to exceed a l i m i t of 5 0 . p p t (parts per trillion).

I t has

(CDC) that individuals

beer, recommended by t h e Centers for Disease Control

not be exposed t o l e v e l s of dioxin greater

than

1 ppb

i n soil f o r a n y

CRS- 7

IB83079

UPDATE-10/21/83

extended periods of time.

The chemical industrial exposure limit for dioxin

weight was set by the EPA to protect workers in the

related fields.

Biological Effects

of 0.0007

mg/kg

body

chemical industry and

-- Animals

Experiments on laboratory animals show interspecies differences (i.e.,

no

two species react in the same way) in response to a high concentration acute

exposure to dioxin.

This response would i'ndicate that dioxin has a different

acute toxic effect in each animal species.

However, when exposure levels a r e

high enough to cause death, the length of time between exposure and death

(the latent period) i s similar for each species. How the dioxin causes death

in experimental animals is not known. When laboratory animals are exposed t o

lower concentrations of dioxin, where death i s not expected to occur, two

sets of symptoms are generally observed. The first set of symptoms, common

to all species, includes:

a) chloracne; and b) the development of horny skin

layer (hyperkeratosis).

The second set of symptoms which i s specific to each

individual species includes: a) in pregnant female mice, dioxin exposure

results in the production of some abnormal offspring (teratogenic effect); b)

in pregnant female mice and some other species, dioxin exposure causes the

death of some of the unborn offspring (fetotoxic effect); c) in chickens a

unique lesion is developed (hydropericordium); d) in some animal species a n

infiltration of tissues with fluid occurs

(edema); e) in rabbits liver

disturbances are common; f) in monkeys conversion of the meibomian gland

occurs (the gland in the eyelid changes from a sebaceous fluid producer to a

keratin producer); and g) in guinea pigs suppression of the immune system

occurs. Although reproductive disorders were observed in female mice, n o

reproductive disorders were observed in male mice exposed to dioxin a t

identical concentrations.

Biological Effects

-- Man

No human deaths have been reported after an acute exposure to dioxin.

The

most prominent effect observed in man from a n acute or chronic exposure t o

dioxin is chloracne.

Chloracne can range in severity and extent.

The more

severe cases may involve extensive acne-li-ke eruptions of blackheads,.

abcesses, and cysts initially on the face, giving the appearance of grayish

sheets. The most severe cases may involve the total body.

Chloracne is not

a condition that is unique to dioxin exposure;

it may a.lso occur from

expcsure to many

other chlorinated compou'nds.

The chronic effects of

exposure to dioxin (other than chloracne) a r e not well understood.

Although

several symptoms, diseases, and conditions have been described by individuals

chronically exposed to dioxin, there is not sufficient information t o

establish a cause-and-effect association.

The diseases or conditions .that

2)

liver

function

have been reported include:

1) enlarged liver;

(a disturbance

abnormality; 3 ) neuromuscular effects; 4) deranged porphyrin

in production of porphyrin -- a natural pigment produced by

tae body);

5)

spontaneous abortion; 6 )

congential malformation;

7) cancer;

and

8)

chromosomal aberrations.

1. Liver Enlargement.

Enlargement of the liver has been reported in some exposed individuals.

However, mortality among the dioxin-exposed

individuals who displayed an

CRS- 8

enlarged liver w a s not statistically different from that of non-exposed

individuals (individuals with normal livers).

Any

relationship between

dioxin exposure a n d the liver enlargements i s unclear a t this time.

2. Liver Function Abnormality.

Liver dysfunction has been observed i n s o m e individuals who a l s o were

accidently exposed to dioxin.

Individuals exposed to l o w l e v e l s o f dioxin

may have an abnormal liver f u n c t i o n , yet n o temporary o r permanent d a m a g e may

occur. Exposures to very high levels o f dioxin may cause a n a b n o r m a l liver

function with s o m e signs of permanent damage.

Any relationship between

dioxin exposure a n d liver function abnormality i s unclear a t this time.

3. Neuromuscular Effects.

Some individuals exposed t o dioxin r e p o r t a weakness i n their l o w e r limbs.

T h i s effect has n o t been observed i n a n y animal trials.

The impairment

reported seems to be slight, affecting muscular coordination without a n y

other apparent s i d e effects.

Any relationship between dioxin exposure and

the neuromuscular effect i s unclear a t this time.

4. Deranged Porphyrin.

Porphyrin derangement, which may result i n spotting of the s k i n , i s known

to have a genetic a s well a s a n environmental cause

(e.g.,

environmental

exposure to hexachlorobenzene, polychlorinated biphenyls and dioxin).

Any

relationship between d i o x i n - e x p o s u r e and t h e porphyrin effect i s unclear a t

this time.

5. Spontaneous Abortions.

Spontaneous abortions have been reported a s a possible a d v e r s e health

effect of dioxin exposure. A review of r e c e n t studies indicates that there

appears to be n o difference between the r a t e of spontaneous abortions within

the Cioxin-exposed populations a n d the non-exposed populations.

6. Congenital Malformations.

It has been reported that a s a result of dioxin exposure congenital

malformations h a v e occurred.

There appears to be no difference i n t h e number of congenital malformations

occurring i n dioxin exposed and non-exposed

populations.

T h i s was confirmed in a comparison made between the r a t e of

congenital ma,lformations observed after the S e v e s o , I t a l y , accident and t h e

estimated world rate.

7. Cancer.

Cancer has been suggested a s a n e f f e c t of dioxin exposure.

It. i s

difficult to demonstrate a cause-and-effect

relationship between dioxin

exposure and cancer. There a p p e a r s to be n o difference i n the o v e r a l l cancer

eeatt! rate between the dioxin-exposed

a n d the n o n - e x p o s e d - populations.

According to s o m e studies, there does a p p e a r t o be s o m e increase i n the

incieence of soft tissue sarcoma in dioxin-exposed populations.

NIOSH claims

evidence i s increasing to support a link between occupational exposures t o

dioxin and soft tissue sarcoma.

Other s t u d i e s , conducted both

i n this

country and o v e r s e a s , have shown no increase in soft tissue sarcomas r a t e s a s

a result of dioxin exposure.

CRS- 9

IB83079

UPDATE-10/21/83

It has recently been reported that an association may exist between

stomach cancer and dioxin exposure.

Evidence in support

of

either

association i s not sufficient to make a positive confirmation of cause and

effect.

8. Chromosomal Aberrations.

Cytogenetic stuCies (those relating to the function and structure of t h e

cell) to date do not indicate an increase in the frequency of chromosomal

aberrations a s . a result of dioxin exposure.

When the prevalence of

chromosomal aberrations is compared between the dioxin-exposed

individuals

and the total population a t large no signi'ficant difference is observed.

Summarv

Studies indicate that dioxin is a highly toxic chemical that may persist

for many years in the environment.

Plants do not appear to accumulate great

amounts of dioxin. . A n i m a l s appear to accumulate and eliminate dioxin a t

different rates depending on environmental conditions and animal speciesBodies of water generally become contaminated from dioxin-contaminated soil

run-off a s a result of erosion.

Soil forms a strong bond with dioxin which

is mainly responsible for the persistence of the dioxin in the environment.

Dioxin may be disposed of by traditional methods

such a s incineration,

perpetual storage, landfill, and entombment.

Dioxin molecules a r e destroyed

by sunlight on exposed surfaces.

Animal exposure studies demonstrate species differences for the effects of

dioxin.

Chronic exposures appear to result in specific health effects for

each animal species.

Chloracne i s the most consistent condition of dioxin exposure in humans.

Other symptoms have been reported, yet no cause-and-effect

association has

been confirmed.

Points for Further Consideration

Future issues w.hich may confront policymakers include: (a) identification

of cause-effect relationships with rega,rd to the human health effects of

dioxin exosure; (b) proposed establishment of dioxin industrial discharge

requirements;

(c) establishment of final dioxin disposal

requirements

(changing the chemical character of dioxin);

(d) initiation of further

chronic exposure studies with a ~ i m a l s ; (e) development of new waste discharge

methodologies; (f) requirement for extensive acute and chronic testing of new

chemicals prior to marketing; ( g ) identification of one Federal agency t o

coordinate all dioxin and Agent Orange research efforts; (h) examination of

the need for some form of a victim compensation program, based upon a chosen

level of acceptable risk, to protect the individual from environmental

sources of dioxin (a hazard insurance program); and (i) examination of the

need for the development of a risk analysis program for all hazardous waste

sites.

HEARINGS

U.S.

Congress. House.

Committee on Energy and Commerce.

Subcommittee on Oversight and Investigations. Defining

health emergencies under the superfunded statute: - r e c e n t

PCB and dioxin cases. Hearing, 97th Congress, 2d session.

Nov. 1 9 , 1982. Washington, U.S. Govt.

Print. Off.,

1983.

370 p.

U.S.

Congress. House.

Committee on Interstate and Foreign

Commerce.

Subcommittee on Oversight and Investigations.

Agent orange:

exposure of Vietnam veterans.

Hearing,

96th Congress, 2d session. Sept. 25, 1986. Washington,

U.S. Govt. Print. Off., 1981.

249 p.

----- Involuntary exposure to agent orange and other toxic

spraying.

Hearings, 96th Congress, 1st session. June

26-27, 1979. Washington, U.S. Govt. Print. Off., 1980.

256 p.

U S .

Congress. House. Committee on Veterans Affairs.

Subcommittee on Oversight and Investigations.

Current

status of agent orange studies.

May 6 , 1981. Washington,

U.S. Govt. Print. Off., 1981.

385 p.

U.S.

Con'gress. House.

Committee on Veterans Affairs.

Subcommittee on Medical Facilities and Benefits.

Scientific

community report on agent orange. Hearings, 96th Congress,

2d session. Sept. 1 6 , 1980. Washington, U.S. Govt.

Print. Off., 1981. 145 p.

----- Oversight hearing to receive testimony on agent orange.

Hearing, 96th Congress, 2d session. Feb. 25, 1980.

Washington, U.S. Govt. Print. Off., 1980. 121 p.

----- Oversight hearing to receive testimony on agent orange.

Hearing, 96th Congress, 2d session.

July 22, 1980.

Washington, U.S. Govt. Print. Off., 1981. p. 4 5 9 p.

U.S.

Congress. House.

Committee on Veterans Affairs.

Ad

Hoc Subcommittee. Status of Vietnam veterans in the Bay

area.

Hearing, 96th Congress, 2d session. Apr. 1 0 ,

1980. Washington, U.S. Govt. Print., Off., 1980. 64 p.

CHRONOLOGY OF EVENTS

10/20/83

-- U.S. EPA confirmed the presence of dioxins and

furans in municipal incinerator emissions.

07/00/83

-- Contaminated sites reported in Massachusetts

and Oregon.

06/00/83

-- Soil contamination with dioxins found in Michigan

and New Jersey.

-- Missouri clean up of dioxin spills begins.

11/19/82 -- Hearings held by Subcommittee on Oversight and

02/00/83

Investigations of the Committee on Energy and

Commerce.

Hearing on the hazards of dioxin.

12/03/80

-- P.L.

96-510, Comprehensive Environmental Re-sponse

Compensation and Liability Act 1980 (CERCLA),

clean up of hazardous waste sites.

"Superfundw

--

10/21/76

-- P.L.

10/11/76

-- P.L.

07/10/76

-- Seveso, Italy chemical plant explosion, dioxin

94-580, Resource Conservation and Recovery

Act (RCRA), control of hazardous wastes.

94-469, Toxic Substance Control Act, the

control of all toxic substances not covered by

other toxic substances control.

contaminant spread over local region.

07/19/75

-- P.L.

'2/16/74

-- P.L. 93-523, Safe Drinking Water Act.

10/18/72

-- P.L. 92-500, Clean Water Act.

OC/CO/71

-- Missouri sites were contaminated with Cioxin.

12/31/70

-- P.L.

1960-70

--

00/00/56

-- Dioxin identified.

Unknown

-- Incinerator production of dioxin.

94-56, Hazardous Material Transportation Act.

(Amended 1976 to cover the transport of toxic

materials. )

(Amended

1977 to eliminate contaminants from discharge or

entry into water sources.)

(Federal Water

Pollution Control Act.)

(Amended 1977 to cover

discharge of toxic pollutants into water.)

91-604, Clean Air Act.

(Amended 1 9 7 7 to

cover discharge of hazardous pollutants into the

air. )

Agent orange contaminated with dioxin used in Republic of

Vietnam for aerial spraying operations.

ADDITIONAL REFERENCE SOURCES

over nor

and

Axelrod D. Dioxin exposure report to the

legislative April 1982. New York State Department of

Health.

1982.

Barnes, D.G.

Human health aspects of accidental chemical

exposure of dioxin -- strategy for environmental reclamation

and community protection.

International Academy of

Environmental Safety, International Society of Ecotoxicology

and Environmental Safety. Oct. 5-7, 1981.

Bartleson, F.D., Harrison, D.D., and Morgan, J.D.

Field

Studies of Wildlife exposed to TCDD contaminated soils.

U.S. Air Force report, AFATL-TR-75-49, Mar. 1975.

Beljan, J.R. (Council of Scientific Affairs, JAMA), Health

effects of agent orange and dioxin contaminants. .Journal

of the American Medical Association, v. 248, no. 1 5 , Oct.

1 5 , 1982.

Blain, E.H.

Chlorodioxins -- origin and fate.

Society Washington, D.C.

1973.

American Chemical

Cocucci, S., DiGerolamo, F., Verderio, A., Covallaro, A.,

Colli, G., and Gorni, A., Invernizzi, G., and Luciani, L.

Absorption and translocation cf

tetrachlorodibenzo-p-dioxin by plants f r ~ mpolluted soil.

Experientin, v. 35, Fasc 4 , May 79: 482-484.

Crosby, D.G.,

Wong A.S.

Environmental degradation of

(TCDD).

Science, v. 195,

1337-1338.

2,3,7,8-tetrachlodibenzo-p-dioxin

Mar. 25, 1977:

Crow, K.D.

Chloracne.

Seminars in Dermatology, v. 1 , no. 4 ,

December 1982:

305-314.

Esposito, M.P., Tierman, T.O., and Dryden, F.E.

Dioxin.

Environmental Protection Agency, Cincinnati, OH. EPA-600

2-80-197.

November 1980.

TCDD

Franelli, R., Cheabrando, C., and Bonaccorsi, A.

contamination in the Seveso incident. Drug Metabolism

Reviews, v. 1 3 , no. 3 , 1982: 407-422.

Kimble, E.J. and Gross, M.L.

Tetrachlorodibenzo-p-dioxin

quantilation in Stack-Collected coal fly ash.

Science,

v. 207, Jan. 4 , 1980:

59-61.

Kriebel, David. The dioxins--toxic and still troublesome.

6-13.

Environment, v. 23, no. 1 , Jan./Feb. 1981:

Kociba, R.J. and Schwetz, B.A.

Toxicity of 2,3,7,8,tetrachlorodibenzop-dioxin (TCDD).

Drug Metabolism

387-406.

Review, v. 1 3 , no. 3 , 1982:

Reggiani, G. Toxicology of 2 , 3 , 7 , 8 - t e t r a c h l o r o d i b e n z o - p - d i o x i n

(.TCDD): short review of its formation, occurrence,

toxicology, and kinetics, discussing, human health effects,

safety, measures, and disposal. Regulatory Toxicology

and Pharmacology, v. 1 , 1981:

211-243.

Sun, Marjorie.

Missouri's costly dioxin lesson.

219, Jan. 28, 1983:

367-369.

Science, v.-

Thomasson, W.A.

Deadly legacy: dioxin and the Vietnam veteran.

The Bulletin, v. 35, no. 5 , May 1979: 15-19.

Townsend, J.C., Bodner, K.M., Van Peenen, 'P.F.D., Olsen, R.D.,

and Cook, R.R.

Survey of reproductive events of wives of

employees exposed to chlorinated dioxins,

American

J o u r n a l of E p i d e m i o l o g y , v. 1 1 5 , no. 5:

695-713.

Y o u n g , A.L.,, C a l c a g n i , J.A., T h a l k e n , C.E.,

a n d T r e m b l a y , J.W.

T h e toxicology environmental fate and human risk of herbicide

o r a n g e and i t s associated dioxin.

U.S. A i r F o r c e ' R e p o r t ,

O c t o b e r 1978.

OEHL TR-78-92

APPENDIX 1

Structure and physical/chemicai characteristics of

2,3,7,8-tetrachlorodibenzo-P-dioxin, 'E'DD or dioxin.

'

Structure

Physical Characteristics

molecular weight

melting point,

decomposition point,

Chemical Characteristics

Solubility, grams/liter

ortho-dichlorobenzene

chlorobenzene

Orange Herbicide

benzene

chloroform

acetone

normal-oc t ano 1

lard oil '

me than01

water

REFERENCE:

Young, A.L., Calcagni, J.A., Thalken, C.t., and Tremblay, J.W.

The toxicology enviroumental fate and human rirk of herbicide

orange and it8 aroociated dioxin. U.S. Air Force Report,

OKHL I%-78-92, October 1982. page 1-22