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
M i c h a e l M.
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
Animal studies indicate that dioxin is a highly toxic .compound; however,
there have been no human deaths attributed to exposure to dioxin.
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
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
(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
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
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
(2,4,5,-trichiorophenoxyacetic acid) and
whi.ch i s
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.
of dioxin contamination were required to be reduced to less than 0.1
2,4,5-T. The U.S.
Pharmacopeia has established a maximum
of 0.05 ppm dioxin for hexachlorophene; the actual content measured
hexachlorophene has been less than 0.005
description of the compound dioxin is provided in the appendix.)
Policymakers have often been called upon to make risk-regulating decisions
in the absence of sufficient scientific data. Frequently such data a s may be
available are conflicting.
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
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
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.
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
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.
The diversity of these pclicy positions reflects the
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
At present, funds used to temporarily or permanently
living in dioxin-contaminated areas come from the Superfund budget.
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:
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.
uses of 2,4,5-T have been limited to rice crops and rangelands; 2) the
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
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
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).
ground forces were subjected to possible dioxin exposure while in specific
regions of the Republic of Vietnam (see IB83043
Complaints and Studies of Health Effects).
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
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
Several other children that did not develop chloracne did develop
erythema (red skin patches).
Very few adults developed chloracne or chemical
Studies are still being conducted on the exposed population
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
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
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.
EPA has also requested FEMA to temporarily relocate three St. James, MO
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
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
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.
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.
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,
The source of the dioxin in Oregon is unknown at this time.
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,
Few studies have been conducted to determine whether dioxins
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.
soil to uncontaminated
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
danger of contamination of the rivers and streams is from dioxin-contaminated
The eroded dioxin-contaminated soil particles could Settle on
the bottom of the stream or could be carried with the flow of' the stream.
Small quantities of dioxin can be disposed of by physiochemical, chemical,
and microbiological means.
Physiochemical means include: ultraviolet light;
ultraviolet l i g h t treatment was
developed recently for commercial disposal of dioxin-contaminated
Chemical disposal i s possible
T h e treatment i s 98% efficient.
alkaline dehydrochlorination, reduction with
oxidation with ruthenium tetroxide, chloridides, and chlorolysis.
uses anhydrous a l k a l i metal
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.
Oxidation with ruthenium tetroxide i s a n acceptable method f o r destroying
i s usually
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
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
d u e to i t s high cost i t may n o t be considered practical
f o r bulk
Research i s underway to develop a better microbial degradation method.
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)
(not true disposal);
(presently permitted but may still present a n environmental hazard
this i s n o t actually
and C ) entombment (concrete mixed
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
destruction of d i o x i n ' i s only surface active
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
T h e Environmental Protection
has recommended a maximum
Agency's Scientific Advisory Panel i n 1 9 8 0 established
" 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
i n soil f o r a n y
extended periods of time.
The chemical industrial exposure limit for dioxin
weight was set by the EPA to protect workers in the
chemical industry and
Experiments on laboratory animals show interspecies differences (i.e.,
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
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
No human deaths have been reported after an acute exposure to dioxin.
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.
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.
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
have been reported include:
1) enlarged liver;
abnormality; 3 ) neuromuscular effects; 4) deranged porphyrin
in production of porphyrin -- a natural pigment produced by
spontaneous abortion; 6 )
1. Liver Enlargement.
Enlargement of the liver has been reported in some exposed individuals.
However, mortality among the dioxin-exposed
individuals who displayed an
enlarged liver w a s not statistically different from that of non-exposed
individuals (individuals with normal livers).
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.
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
exposure to hexachlorobenzene, polychlorinated biphenyls and dioxin).
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
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
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.
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.
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.
It has recently been reported that an association may exist between
stomach cancer and dioxin exposure.
Evidence in support
association i s not sufficient to make a positive confirmation of cause and
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
and the total population a t large no signi'ficant difference is observed.
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
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
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
(c) establishment of final dioxin disposal
(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
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.
Committee on Interstate and Foreign
Subcommittee on Oversight and Investigations.
exposure of Vietnam veterans.
96th Congress, 2d session. Sept. 25, 1986. Washington,
U.S. Govt. Print. Off., 1981.
Involuntary exposure to agent orange and other toxic
Hearings, 96th Congress, 1st session. June
26-27, 1979. Washington, U.S. Govt. Print. Off., 1980.
U S .
Congress. House. Committee on Veterans Affairs.
Subcommittee on Oversight and Investigations.
status of agent orange studies.
May 6 , 1981. Washington,
U.S. Govt. Print. Off., 1981.
Committee on Veterans Affairs.
Subcommittee on Medical Facilities and Benefits.
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.
Committee on Veterans Affairs.
Hoc Subcommittee. Status of Vietnam veterans in the Bay
Hearing, 96th Congress, 2d session. Apr. 1 0 ,
1980. Washington, U.S. Govt. Print., Off., 1980. 64 p.
CHRONOLOGY OF EVENTS
U.S. EPA confirmed the presence of dioxins and
furans in municipal incinerator emissions.
Contaminated sites reported in Massachusetts
Soil contamination with dioxins found in Michigan
and New Jersey.
Missouri clean up of dioxin spills begins.
P.L. 96-510, Comprehensive Environmental Re-sponse
Compensation and Liability Act 1980 (CERCLA),
clean up of hazardous waste sites.
Hearings held by Subcommittee on Oversight and
Investigations of the Committee on Energy and
Hearing on the hazards of dioxin.
P.L. 94-469, Toxic Substance Control Act, the
control of all toxic substances not covered by
other toxic substances control.
Seveso, Italy chemical plant explosion, dioxin
contaminant spread over local region.
P.L. 94-56, Hazardous Material Transportation Act.
(Amended 1976 to cover the transport of toxic
P.L. 93-523, Safe Drinking Water Act.
1977 to eliminate contaminants from discharge or
entry into water sources.)
P.L. 92-500, Clean Water Act.
Pollution Control Act.)
(Amended 1977 to cover
discharge of toxic pollutants into water.)
P.L. 94-580, Resource Conservation and Recovery
Act (RCRA), control of hazardous wastes.
Missouri sites were contaminated with Cioxin.
P.L. 91-604, Clean Air Act.
(Amended 1 9 7 7 to
cover discharge of hazardous pollutants into the
Agent orange contaminated with dioxin used in Republic of
Vietnam for aerial spraying operations.
Incinerator production of dioxin.
ADDITIONAL REFERENCE SOURCES
Axelrod D. Dioxin exposure report to the
legislative April 1982. New York State Department of
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.
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.
Chlorodioxins -- origin and fate.
Society Washington, D.C.
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.
Environmental degradation of
Science, v. 195,
Mar. 25, 1977:
Seminars in Dermatology, v. 1 , no. 4 ,
Esposito, M.P., Tierman, T.O., and Dryden, F.E.
Environmental Protection Agency, Cincinnati, OH. EPA-600
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.
quantilation in Stack-Collected coal fly ash.
v. 207, Jan. 4 , 1980:
Kriebel, David. The dioxins--toxic and still troublesome.
Environment, v. 23, no. 1 , Jan./Feb. 1981:
Kociba, R.J. and Schwetz, B.A.
Toxicity of 2,3,7,8,tetrachlorodibenzop-dioxin (TCDD).
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:
Missouri's costly dioxin lesson.
219, Jan. 28, 1983:
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,
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:
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.
Structure and physical/chemicai characteristics of
2,3,7,8-tetrachlorodibenzo-P-dioxin, 'E'DD or dioxin.
normal-oc t ano 1
lard oil '
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