NCD980602163_19890601_Warren County PCB Landfill_SERB C_2,3,7,8-Tetrachloro-Dibenzo-p-Dioxin-OCR

-,:
\ -w,...·.
2,3, 7 ,8-TETRACHLQRO-
DIBENZO-p-DIOXIN
! Agency for Toxic Substances and Disease Registry
U.S. Public Health Service
1. PUBLIC HEALTH STATEMENT
1.1 'WHAT IS DIOXIN?
1
The chlorinated dibenzo-p-dioxins are a class of compounds that are
loosely referred to as dioxins. There are 75 possible dioxins. The one
with four chlorine atoms at positions 2, 3, 7 and 8 of the dibenzo-p-
dioxin chemical structure is called 2,3,7,8-tetrachlorodibenzo-p-dioxin
(2,3,7,8-TCDD). It is a colorless solid with no known odor. 2,3,7,8-TCDD
does not occur naturally nor is it intentionally manufactured by any
industry, except as a reference standard. It can be inadvertently
produced in very small amounts as an impurity during the manufacture of
certain herbicides and germicides and has been detected in products of
incineration of municipal and industrial wastes. At the present time,
2,3,7,8-TCDD is not used for any purpose other than scientific research.
1.2 HOW MIGHT I BE EXPOSED TO 2,3,7,8-TCDD?
The main environmental sources of 2,3,7,8-TCDD are:
• Use of herbicides containing 2,4,5-trichlorophenoxy acids (2,4,5-T)
• Production and use of 2,4,5-trichlorophenol in wood preservatives
• Production and use of hexachlorophene as a germicide
• Pulp and paper manufacturing plants
• Incineration of municipal and certain industrial wastes
• Small amounts formed during the burning of wood in the presence of
chlorine
• Accidental transformer/capacitor fires involving chlorinated
benzenes and biphenyls
• Exhaust from automobiles powered with leaded gasoline
• Improper disposal of certain chlorinated chemical wastes
Although 2,4,5-T, 2,4,5-trichlorophenol and hexachlorophene are no
longer produced commercially (except for certain medical purposes),
disposal sites of past production wastes are still sources of present
exposure. 2,3,7,8-TCDD has been found in at least 28 of 1,177 hazardous
waste sites on the National Priorities List (NPL). Very low levels of
2,3,7,8-TCDD have been detected in ambient air. Detection of 2,3,7,8-
TCDD in drinking water has not been reported. 2,3,7,8-TCDD has not been
detected in most rural soils examined, but it can be present at trace
levels in urban soils. The highest concentration of 2,3,7,8-TCDD was
detected in a waste-oil-contaminated soil in Missouri that contained a
2,3,7,8-TCDD level more than one million times higher than soils from
normal urban areas. 2,3,7,8-TCDD was detected in fish obtained from the
2 Section 1
contaminated sections of Lake Ontario, Saginaw Bay, the Michigan rivers,
and several watersheds including those from Maine, Wisconsin, and
Minnesota. In human milk, minute amounts of 2,3,7,8-TCDD have been
detected in the United States and in several European countries.
Consumer sources are:
• Skin contact with surfaces such as soil or vegetation contaminated
by the chemical
• Skin contact and inhalation of wood dusts from use of
pentachlorophenol-treated woods
• Inhalation of air near improperly maintained dump sites or
municipal incinerators
• Consumption of fish and cow's milk from contaminated areas
• Consumption of breast milk containing 2,3,7,8-TCDD by babies
• Minute exposure from the use of paper towels, napkins, coffee
filters, computer papers, and other contaminated paper products
Workers at risk of contacting 2,3,7,8-TCDD are:
• Workers who have been involved in the production or use of
trichlorophenol and salts, hexachlorophene, and 2,4,5-T or other
herbicides containing this chemical. The production of 2,4,5-T and
2,4,5-trichlorophenol, however, has been discontinued in the United
States.
Workers in the p~p and paper industry
• Workers at certain municipal and industrial incinerators
• Workers involved in the high-temperature/pressure treatment of
woods with pentachlorophenol
• Workers at certain hazardous waste sites
• Workers involved in the cleanup of certain accidental
capacitor/transformer fires and in the salvaging of transformers
• Workers who have been involved in spraying of phenoxy herbicides
such as Agent Orange
1.3 HOW DOES 2,3,7,8-TCDD GET INTO MY BODY?
• Absorption through skin from contaminated soils and other materials
• Ingestion of 2,3,7,8-TCDD through the consumption of contaminated
fish, cow's milk, foodstuffs, and, in the case of small children,
soil
Breathing contaminated ambient air. This may contribute very small
amounts to total body intake; however, particulates such as fly ash
from municipal and industrial incineration may constitute a major
source of exposure.
• Intake of 2,3,7,8-TCDD from the consumption of drinking water
should be negligible
d
j
I
I I
Public Health Statement 3
• According to one estimate of ambient exposure, breathing air
constitutes 2%, drinking water less than 0.01%, and consuming foods
98% of the total human exposure to 2,3,7,8-TCDD. No estimate of
relative intake of 2,3,7,8-TCDD due to skin absorption is
available.
1.4 HOW CAN 2,3,7,8-TCDD AFFECT MY HEALTH?
• In humans, 2,3,7,8-TCDD causes chloracne, a severe skin lesion that
usually occurs on the head and upper body. Unlike common acne,
chloracne is more disfiguring and often lasts for years after the
initial exposure.
• There is suggestive evidence that 2,3,7,8-TCDD causes liver damage
in humans, as indicated by an increase in levels of certain enzymes
in the blood, although these effects might also have resulted from
the concomitant exposure to the chemicals contaminated with
2,3,7,8-TCDD or to the solvents in which these chemicals are
usually dissolved. Animal studies have demonstrated severe liver
damage in some species.
• There is suggestive evidence that 2,3,7,8-TCDD causes loss of
appetite, weight loss, and digestive disorders in humans, although
these effects might also have resulted from the concomitant
exposure to the chemicals contaminated with 2,3,7,8-TCDD or to the
solvents in which these chemicals are usually dissolved. Animal
exposure to 2,3,7,8-TCDD results in severe loss of body weight
prior to death.
• Although not demonstrated in humans, in animal studies 2,3,7,8-TCDD
produced toxicity to the immune system. This toxicity can result in
greater susceptibility to infection.
• Although not demonstrated in humans, in some animal species
exposure to 2,3,7,8-TCDD resulted in adverse reproductive effects
including spontaneous abortions. The monkey is very sensitive to
this toxic property of 2,3,7,8-TCDD.
• Although not demonstrated in humans, in some animal species
exposure to 2,3,7,8-TCDD during pregnancy resulted in malformations
in the offspring. Low levels of 2,3,7,8-TCDD have been detected in
human milk, but the effects on infants and children are unknown.
• The human evidence for 2,3,7,8-TCDD alone is inadequate to
demonstrate or reflect a carcinogenic hazard, although certain
herbicide mixtures containing 2,3,7,8-TCDD as an impurity provide
limited evidence of causing cancer in exposed humans. Based on the
positive evidence in animal studies, 2,3,7,8-TCDD is probably
carcinogenic in humans.
1.5 IS THERE A MEDICAL TEST TO DETERMINE IF I HAVE
BEEN EXPOSED TO 2,3,7,8-TCDD?
There is no common medical test available to demonstrate
convincingly that you have been exposed to 2,3,7,8-TCDD. It is believed
that a blood test to detect certain enzymes indicating liver damage may
be helpful in determining whether exposure has occurred. These tests do
I
I .
I
I ! :,,
I "!!' I !·:
I t
75
7. POTENTIAL FOR HUMAN EXPOSURE
7.1 OVERVIEW
The human exposure pathways to 2,3,7,8-TCDD have changed since the
late 1970s. Because 2,3,7,8-TCDD was a contaminant in herbicide
preparations containing 2,4,5-T, the manufacture, use, and disposal of
these herbicides were the primary sources of exposure to 2,3,7,8-TCDD.
In 1979, EPA (1979) completely banned the use of 2,4,5-T. With the
stoppage of production of 2,4,5-T and other pesticide preparations
containing the contaminant 2,3,7,8-TCDD, both occupational and general
population exposure to 2,3,7,8-TCDD due to manufacture and use of the
herbicides ceased to exist. Presently, the important sources of
2, 3, 7, 8-TCDD exposures to the general population are cont_aminated soil,
dump sites, and municipal incinerators. 2,3,7,8-TCDD has been found in
at least 28 of 1,177 sites on the National Priorities List (View 1989).
With the change of sources, the exposure pathways have also changed over
the years (i.e., dermal and inhalation exposure from the manufacture and
use of 2,4,5-T to ingestion of foods obtained from contaminated sites).
There is a paucity of data on the level of 2,3,7,8-TCDD in ambient
air due to sampling and analytical difficulties associated with
quantification of very low levels of 2,3,7,8-TCDD. The ambient level of
2,3,7,8-TCDD in urban areas in West Germany and Sweden ranged from
<0.001-0.08 pg/m3 . Although ambient air samples from several locations
in the United States have been collected for the quantification of
2,3,7,8-TCDD levels, results from these studies are not yet available.
The concentration of total tetrachlorodibenzo-p-dioxin (not
2,3,7,8-TCDD alone) in ambient air in Bloomington, Indiana, was 18 to
92 fg/m3 (femtograms per cubic meter). Assuming that the 2,3,7,8-TCDD
isomer constitutes 5% of the total tetra isomers, the concentration of
2,3,7,8-TCDD in Bloomington air would be 0.9 to 4.6 fg/m3 . The
concentration of 2,3,7,8-TCDD in the air around the stack of a municipal
incinerator has been estimated as 38 fg/m3. The accidental transformer
fire in Binghamton, New York, produced a much higher level of 2,3,7,8--~
TCDD--at 0.23 to 0.47 pg/m3. The concentration of 2,3,7,8-TCDD in the , ~~--'?
air surrounding a field after the application of Silvex containing 7 t-f('
15 ppm 2,3,7,8-TCDD was 0.62 pg/m3. Other than certain industrial 9
effluents and leachates from chemical dump sites, no 2,3,7,8-TCDD has/
ever been reported in drinking water. The concentrations of 2,3,7,8-TCDD
in most uncontaminated soils are below the detection limits of
analytical methods. In urban soils, the level of 2,3,7,8-TCDD is in the
range <0.0002 to 0.011 ng/g. Much higher levels have been detected in
soils contaminated by certain hazardous wastes, waste oils, and spillage
of 2,4,5-trichlorophenol. A soil from Shenandoah Stables in Missouri
contaminated by waste oil containing 2,3,7,8-TCDD had up to 1,750 ng/g
of 2,3,7,8-TCDD. Fish samples collected from lakes and a selected
II
76 Section 7
Michigan river contained undetectable levels to 67 pg/g 2,3,7,8-TCDD. No
2,3,7,8-TCDD was detected in rice, soybeans, and crawfish in the United
States, or in Canadian chicken and pork samples. 2,3,7,8-TCDD at a
concentration range of 0.021-0.049 ng/kg has been detected in three of
six samples of cow's milk from Switzerland. Although several other PCDDs
and PCDFs have been detected in some foods in Japan, no 2,3,7,8-TCDD has
been found in these samples at sub-ppt detection limits. Since fat is
the chief contributor.to the body burden of 2,3,7,8-TCDD in humans, it
has been analyzed by many investigators. Levels of 2,3,7,8-TCDD in
adipose tissue of exposed and control persons in Missouri have been
determined. The level of 2,3,7,8-TCDD in adipose tissue in certain
segments of the general population in the United States and Canada
ranges from undetectable to 20 pg/g, with a mean value of 5 to 7 pg/g.
Values as high as 99 pg/g were detected in an individual heavily exposed
during the spraying operation in South Vietnam. 2,3,7,8-TCDD has been
detected in human milk in the United States at 0.29 pg/g; in members of
the general population in Sweden at trace to 2.3 pg/g, with a mean value
of 0.6 pg/g; and in Germany at 1.3 to 3.3 pg/g, with a mean value of
1.9 pg/g. 2,3,7,8-TCDD was also found in human milk .in other European
countries. Although there are no data regarding exposure levels, workers
at sites of improper chemical waste disposal and the general population
residing near these sites may be susceptible to higher exposure to
2,3,7,8-TCDD. Breast-fed babies nursed by mothers residing near
improperly operated municipal incinerators may also be at higher risk.
The estimated daily human exposure to 2,3,7,8-TCDD, expressed as
picograms per kilogram of body weight (pg/kg), is 0.02 through
inhalation, 0.5 to 5 through the consumption of milk, and 20 through the
consumption of fish. The daily exposure of a 5-kg baby resulting from
the consumption of 850 mL of breast milk is 20 to 200 pg/kg. From the
estimated body burden and the half-life of 2,3,7,8-TCDD in the human
body, the daily human intake of 2,3,7,8-TCDD has been estimated as
0.05 ng in one study and in the range of 0.003-0.036 ng in another.
7.2 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT
7.2.1 Air
Due to sampling and analytical difficulties associated with
quantification of very low concentrations of 2,3,7,8-TCDD, very few data
are available for the levels of this compound in ambient air. The
concentration of total tetrachlorodibenzo-p-dioxin isomers in both vapor
and particulate phase in the ambient air in Bloomington, Indiana, was
approximately 18 to 92 fg/m3 . The analytical method used could not
unequivocally identify 2,3,7,8-TCDD from other tetra isomers. Using the
measured concentration in flue gases from five municipal incinerators
and an air dispersion model, the maximum ambient concentration of
2,3,7,8-TCDD in the area around the stacks was estimated as 38 fg/m3.
Since municipal incinerators are one of the prime sources of atmospheric
2,3,7,8-TCDD, there are a vast number of publications concerning the
level of these compounds in the fly ashes of the incinerators; however,
most of the publications failed to distinguish 2,3,7,8-TCDD from its
isomers. The levels of 2,3,7,8-TCDD in the flue gas of European
incinerators are 0.05 to 1.3 ng/m3; in U.S. incinerators, the levels are
a maximum of 3.5 ng/m3 (under normalized conditions of the emitted
Potential for Human Exposure 77
gases) (Barnes 1983, Eitzer and Hites 1986, EPA 1985b, Marklund et al.
1986, Nottrodt and Ballschmiter 1986). The measured concentrations of
2,3,7,8-TCDD in four locations in Hamburg, West Germany, were in the
range of 0.02-0.08 pg/m3 (Rappe and Kjeller 1987). The locations
consisted of an urban site, a traffic tunnel, a site downwind from a
municipal incinerator, and a site in the vicinity of a dump site and a
metal refinery. The levels of 2,3,7,8-TCDD in urban air in Sweden ranged
from 0.001-0.009 pg/m3 (Rappe and Kjeller 1987). Although ambient air
samples from several locations in the United States have been collected
for quantifying the levels of PCDDs and PCDFs, the results are not yet
available.
Accidents involving certain transformer/capacitor fires can release
larger amounts of 2,3,7,8-TCDD in the air. The concentration of
2,3,7,8-TCDD in the air of the State Office Building in Binghamton, New
York, following an accidental fire, was 0.23 to 0.47 pg/m3. Following an
accidental locomotive fire in Sweden, the concentration of 2,3,7,8-TCDD
was 50 pg/m3 . The concentration of 2,3,7,8-TCDD in the air surrounding a
field after the application of Silvex containing 15 ppm 2,3,7,8-TCDD was
0.62 pg/m3 , but the concentration dropped to a level of 0.18 pg/m3 on
the second day (EPA 1985b, Rappe et al. 1985, Smith et al. 1986).
7.2.2 Water
No report is available on the detection of 2,3,7,8-TCDD in drinking
water, using methods with detection limits in the pico-per-liter range;
however, 2,3,7,8-TCDD has been detected in aqueous industrial effluents,
sediments, and leachates from hazardous waste sites. The concentrations
of tetrachlorinated dibenzo-p-dioxins, including 2,3,7,8-TCDD, in
effluents from a trichlorophenol manufacturing facility ranged from none
detected (detection limit, 10 to 30 pg/g) to 100 pg/g. The discharged
wastewater effluent from Dow into the Tittabawassee River, in Michigan,
has been reported to be approximately 15 pg/L. The leachate samples from
a waste disposal site in Jacksonville, Arkansas, had a mean 2,3,7,8-TCDD
levei of 14 ng/L. The sump pump water from residences and leachates from
the Love Canal area in New York contained 2,3,7,8-TCDD ranging from none
detected to 1,560 ng/L. The concentrations of 2,3,7,8-TCDD in sediments
from storm sewers, residential sump water, and surface water around the
same site were none detected (detection limit, 10 to 100 pg/g) to 9,570
ng/g (EPA 1985b, Lamparski et al. 1986, Tiernan et al. 1985). The
concentration of 2,3,7,8-TCDD in the sludge of seven pulp and paper mill
wastewaters in the U.S. had concentration levels ranging from none
detectable (<1.0 pg/g) to 414 pg/g (Kuehl et al. 1987).
7.2.3 Soil
Concentrations of 2,3,7,8-TCDD in most soils with no obvious source
of contamination are below the detection limits of current analytical
methods. In urban soils, the level of 2,3,7,8-TCDD is in the range of
<0.0002 to 0.009 ng/g. In a national dioxin study, EPA sampled soils
from 138 rural and 221 urban sites not associated with sources of
2,3,7,8-TCDD. Only 17 of the rural and urban soils had detectable levels
of 2,3,7,8-TCDD at a concentration range of 0.2-11.2 pg/g (TMN 1987).
2,3,7,8-TCDD has been detected in samples that originated from certain
industrial sites, waste disposal sites, and sites involved in accidental
!'
78 Section 7
spillage of chemicals containing 2,3,7,8-TCDD. The levels of 2,3,7,8-
TCDD in soils from different locations are given in Table 7.1. It is
apparent from Table 7.1 that the accidental or improper disposal of
still-bottom residue from the manufacture of 2,4,5-trichlorophenol
(2,4,5-TCP) may produce one of the highest levels of 2,3,7,8-TCDD in
soils.
7.2.4 Other
There are limited data that 2,3,7,8-TCDD does not bioaccumulate in
crop plants (Anonymous 1985). Crops grown in soil contaminated with
2,3,7,8-TCDD (up to 752 ppt) after the Seveso accident contained only a
few parts per trillion of 2,3,7,8-TCDD in the aboveground portions. The
roots of these plants, however, contained higher levels of 2,3,7,8-TCDD
than the surrounding soil, suggesting that a similar study using root
crops would demonstrate the contamination of the edible portion of the
plant. This could represent a significant source of dietary intake in
some areas. However, Wipf and Schmid (1983) reported that edible
portions of root vegetables contained much less 2,3,7,8-TCDD than the
surrounding soil.
Since aquatic organisms bioconcentrate 2,3,7,8-TCDD, a few
investigators analyzed fish-eating birds as an indicator of possible
pollution in the suspected water bodies. A herring gull sample from Lake
Huron contained 75 pg/g 2,3,7,8-TCDD. Similarly, herring gull eggs
collected from the Great Lakes contained 12 to 101 pg/g 2,3,7,8-TCDD.
Samples from Lake Ontario and Saginaw Bay had the maximum levels of
2,3,7,8-TCDD (Stalling et al. 1986); those from Lake Michigan and Lake
Superior had the minimum levels of contamination (Buser and Rappe 1984).
Fish samples from the Great Lakes and selected Michigan rivers were
shown to contain between undetectable amounts (detection limit, 2 pg/g)
and 67 pg/g 2,3,7,8-TCDD (Fehringer et al. 1985, Niemann 1986, Ryan et
al. 1984). Yellow perch samples from Woods Pond, Massachusetts, were
found to contain 26 pg/g 2,3,7,8-TCDD (Buser and Rappe 1984). Fish
obtained from the Androscoggin River in Maine, the Wisconsin River in
Wisconsin, and Rainy River in Minnesota, all of which received
discharges from pulp and paper mills, contained 29, 125 and 185 pg/g of
2,3,7,8-TCDD, respectively (Kuehl et al. 1987). Fish collected from
about 400 selected and random sites by EPA contained 2,3,7,8-TCDD at
levels ranging from none detected (<0.2 pg/g) to 85 pg/g (TMN 1987). No
2,3,7,8-TCDD was found in rice, soybean, and crawfish samples from
Arkansas and Louisiana at a detection limit of 10 pg/g, or in Canadian
chicken and pork samples at a detection limit of 2 to 4 pg/g (Ryan et
al. 1985a, Firestone et al. 1985). As a result of the present day
bleaching processes used in the pulp and paper industry, trace amounts
of 2,3,7,8-TCDD have been detected in paper products. Preliminary
results indicate that 2,3,7,8-TCDD is present at 3 to 4 pg/gin certain
samples of paper towels and 13 to 39 pg/gin samples of communication
papers, such as stationery, computer papers, and envelopes (TMN 1987).
A model to estimate 2,3,7,8-TCDD intake by humans from inhalation
of air and ingestion of drinking water and food predicted that the food
chain accounts for 98% of the daily human intake of 2,3,7,8-TCDD (Travis
and Hattemer-Frey 1987). Connett and Webster (1987) also concluded that
food could be the predominant source of 2,3,7,8-TCDD intake by far,
·----·----·--··•-······-----. 'I ! .,. ~ i, f .. i .,, .. ,t . ., JC.. t . ! ... ·:, ii,, Table 7.1. Le-vets of 2,3,7,8-TCDD in soil from different locations TCDD concentrationa,b Site Sample history (ng/g) References Love Canal, N.Y. Soils outside the dump site ND (0.001-0.020) EPA 1985b Jacksonville, Ariz. Waste disposal site ND-2.9 EPA 1985b Midland, Mich. Inside DOW facility 0.01-52 Nestrick et al. 1986 St. Louis, Mo. Urban sample of no obvious 0.12 EPA 1985b source of contamination Shenandoah Stables, Mo. Contaminated by waste oil 101-33,000 Tiernan et al. 1985, Kimbrough et al. 1977 Timberline Stables, Mo. Contaminated by waste oil 30-42 Tiernan et al. 1985 Bliss Farm, Mo. Contaminated by waste oil 382c Tiernan et al. 1985 '\l 0 Bubbling Springs Ranch, Mo. Contaminated by waste oil 76-95 Tiernan et al. 1985 rt (I) ::s Minker Resident, Mo. Contaminated by waste oil soc Tiernan et al. 1985 rt .... Ill Times Beach, Mo. Contaminated by waste oil 4.4-317 Tiernan et al. 1985 ...... Urban areas, United States Urban samples of no obvious <0.0002-0.009 Nestrick et al. 1986 t-1) 0 1-1 source of contamination ::i::: C New Jersey Spillage of 2,4,5• TCP 26,QQQC Jackson et al. 1986 i3 Ill still bottom ::s Scrap yard where used reactor l,IOOc• Jackson et al. 1986 l:l] New Jersey ~ vessels were collected 0 ti) ND(0.0007)-0.003 C Lansing, Mich. Urban sample Nestrick et al. 1986 1-1 (I) Gaylord, Miss. Urban sample ND(0.0002) Nestrick et al. 1986 -....J Detroit, Mich. Urban sample 0.0021-0.0036 Nestrick et al. 1986 I.O
Table 7.1 (continued) Site Sample history Chicago, Ill. Urban sample Akron, Ohio Urban sample Nashville, Tenn. Urban sample Pittsburgh, Pa. Urban sample Philadelphia, Pa. Urban sample Brooklyn, N.Y. Urban sample Arlington, Va. Urban sample 0ND = not detected. bValues within. parentheses are detection limits. conly one sample was analyzed. TCDD concentration°·b (ng/g) 0.0042-0.0094 0.0063 0.0008 0.0026 0.0009 0.0026 ND(0.0003) References Nestrick et al. 1986 Nestrick et al. 1986 Nestrick et al. 1986 Nestrick et al. 1986 Nestrick et al. 1986 Nestrick et al. 1986 Nestrick et al. 1986 (X) 0 Ct) (b 0 r-t .... 0 :::s '-I
I I I
!
...;_
Potential for Human Exposure 81
compared with inhalation intake. Actual data on measured levels of
2,3,7,8-TCDD in food, however, are limited. Fat specimens from three of
seven steers that were confined to a fenced pasture sprayed with 2,4,5-T
herbicide contained 3-4 ng/kg 2,3,7,8-TCDD (Karcher et al. 1978). This
result indicates that beef obtained from cattle grazing in contaminated
pastures (for example, those near municipal incinerators) may contribute
to 2,3,7,8-TCDD ingestion from contaminated food. Six samples of cow's
milk from various locations in Switzerland were analyzed for PCDDs.
Although sub-ppt (ng/kg) levels of 2,3,7,8-TCDD-substituted hepta-CDDs
were found in all samples, only three contained 2,3,7,8-TCDD at a
0.021-0.049 ng/kg range (detection limit <0.013 ng/kg) (Rappe et al.
1987). The daily intake of PCDDs by residents of Japan through
consumption of food has been estimated by several investigators (Ogaki
et al. 1987, Ono et al. 1987, Takizawa and Muto 1987). None of these
investigators, however, reported the detection of 2,3,7,8-TCDD in any
food.
Since adipose tissue appears to be the chief contributor to the
body burden of 2,3,7,8-TCDD, many investigators analyzed fat tissue from
both exposed and control populations. That fat has the highest burden is
confirmed by the tissue analysis of a woman who died 7 months after the
accident in Seveso, Italy. The following levels of 2,3,7,8-TCDD (pg/g)
were found in different organs: fat, 1,840; pancreas, 1,040; liver, 150;
thyroid, 85; brain, 60; lung, 60; kidney, 40; and blood, 6. The levels
of 2,3,7,8-TCDD in adipose tissue in certain segments of the general
population of the United States and Canada ranged from undetectable to
20 pg/g, with a mean value of 5 to 7 pg/g. In a U.S. National Human
Adipose Tissue Survey (Stanley et al. 1986), 2,3,7,8-TCDD was detected
with a frequency of 76%. In Europe, the range of 2,3,7,8-TCDD
concentration in the adipose tissue in segments of the general
population is not detectable to 9 pg/g, with a mean value of 3 pg/g.
Instances of higher levels in adipose tissue have been reported in
individuals exposed to this chemical either during spraying herbicides
containing 2,4,5-T or during accidental capacitor or transformer fires.
For example, the adipose tissue of a few exposed individuals in the
State Office Building fire in Binghamton, New York, had 2,3,7,8-TCDD
concentrations in the range 11.6 to 28.3 pg/g, with a mean value of
17.4 pg/g. The adipose tissue of a few heavily exposed individuals
involved in spraying operations in Vietnam had 2,3,7,8-TCDD levels
ranging from undetectable (detection limit, 3 pg/g) to 99 pg/g, with a
mean value of 37 pg/g; however, no difference in the level of 2,3,7,8-
TCDD was found in lightly exposed, possibly exposed, and other Vietnam
veterans who sought medical help compared with the control population
group (EPA 1986a; Graham et al. 1986; Gross et al. 1984; Nygren et al.
1986; Patterson et al. 1987c; Schecter et al. 1985, 1986; Stanley et al.
1986; Weerasinghe et al. 1986; Young 1984). The median concentrations of
2,3,7,8-TCDD (concentration range in parentheses) in control and exposed
populations in Missouri have been reported to be 6.4 pg/g (1.4 to
20.2 pg/g) and 17 pg/g (2.8 to 750 pg/g), respectively (Patterson et al.
1986). The levels of 2,3,7,8-TCDD in human serum have been reported by
researchers from Centers for Disease Control (Patterson et al. 1987b,
Patterson et al.). On a lipid-adjusted basis, the levels of 2,3,7,8-TCDD
in human serum of certain members of the general population was reported
to range from 4 pg/g to 7.6 pg/g. Determination of 2,3,7,8-TCDD levels
82 Section 7
in blood may be used as an indicator of body burden. The advantage of
this method is that it requires a noninvasive technique for withdrawing
sample specimens.
Human breast milk has also been analyzed for 2,3,7,8-TCDD. It has
been reported that human breast milk is the largest contributor to the
body intake of 2,3,7,8-TCDD in breast-fed babies (Rappe et al. 1986,
Schecter and Gasiewicz 1987). The following levels (the detection limits
are given in parentheses) of 2,3,7,8-TCDD have been determined in human
breast milk from different countries: United States, none detected (0.1
to 6.0 pg/g) in mothers from 2,4,5-T-exposed areas and in control areas;
none detected (<0.2 pg/g) and 0.29 pg/gin two mothers' milk collected
in 1986 from Binghamton, New York; Canada, 0.17 pg/gin a single pooled
sample of 200 mothers' milk collected in 1980-81; Seveso, Italy, 2.3 to
28.0 pg/g from mothers near accident area; South Vietnam, none detected
(0.5 pg/g) to 40 to 50 pg/g from mothers in sprayed areas; Sweden, trace
to 2.3 pg/g, with a mean of 0.6 pg/g; and Germany, 1.3 to 3.3 pg/g, with
a mean of 1.9 pg/g. 2,3,7,8-TCDD was also detected in human milk
obtained from Denmark, the Netherlands, and Yugoslavia (EPA 1985b, Heath
et al. 1986, Jensen 1987, Nygren et al. 1986, Patterson et al. 1986,
Rappe et al. 1986, Schecter et al. 1987, Young 1984). There is a large
unexplainable difference in the values of 2,3,7,8-TCDD concentrations in
milk from South Vietnamese mothers analyzed by two groups of
investigators (Schecter et al. 1987, Young 1984).
According to a statement by CDC (1986), "Contamination of breast
milk with trace amounts of a variety of chlorinated compounds should not
discourage women from breastfeeding except under unusual circumstances
which have to be evaluated on an individual basis .... Substitutes used
for human milk are not entirely free of these compounds and may have
high metal levels .... Avoiding breastfeeding would deprive the infant
of immunological-protection and psychological benefits for the infant
and mother."
Other human tissues, obtained from the autopsy of two subjects in
Canada, were analyzed for 2,3,7,8-TCDD with the following results:
liver, none detected to 2.5 pg/g; muscle, none detected; and kidney,
none detected. The detection limit in these determinations were in the
range of 1 to 4 pg/g (Ryan et al. 1985b). No 2,3,7,8-TCDD was detected
in the blood of exposed workers following the accident in Binghamton,
New York, at a detection limit of 1 to 2 pg/g (Schecter et al. 1985).
Serum 2,3,7,8-TCDD levels in veterans who were heavily exposed to Agent
Orange in Vietnam during 1967-1968 have been reported by the Centers for
Disease Control to range between none detected (0.0013 pg/g) and
25 pg/g, with a median value of 3.8 pg/g. The same study reported serum
2,3,7,8-TCDD levels in a group of non-Vietnam veterans to range between
none detected (0.0013 pg/g) and 12 pg/g, with a median value of
3.9 pg/g. Serum levels in a group occupationally exposed to 2,3,7,8-TCDD
prior to 1970, however, have been reported to be 30-fold higher in the
same study (MMWR, 1987). Using an environmental partitioning model to
estimate the concentration levels of 2,3,7,8-TCDD in various
environmental media, Travis and Hattemer-Frey (1987) estimated the
following average daily intake (with the per cent of the total intake in
parenthesis): air, 0.001 ng (2%); water, 6.5 x 10-6 ng (<0.01%); and
food, 0.046 ng (98%). It is likely that the secondary source of
I
i
I
I . .
Potential for Human Exposure 83
2,3,7,8-TCDD in foods is atmospheric emissions. EPA (1988c) estimated
the human exposure to 2,3,7,8-TCDD from a variety of exposure scenarios
resulting from contaminated soils, various land disposal situations, and
municipal waste incineration. The highest exposure was attributed to the
food chain, i.e., ingestion of contaminated fish, beef, dairy products,
and other foods. Ingestion of contaminated soil, especially by children
with pica tendencies; dermal contact with contaminated soil, dust, and
sediment; and inhalation of contaminated dust and vapor further
contribute to human exposure. EPA (1988c) estimated an upper limit value
for the average 2,3,7,8-TCDD concentration in adipose tissue to be 6.72
ppt in the U.S. population. From this adipose tissue burden and
pharmacokinetic considerations, it was estimated that the upper bound
2,3,7,8-TCDD daily intake ranges from 0.04 to 0.51 pg/kg. These
estimates apply to ambient exposure and not to exposure scenarios
related to accidents.
7.3 OCCUPATIONAL EXPOSURES
Occupational exposures to 2,3,7,8-TCDD occured in the past during
the production and use of hexachlorophene, trichlorophenol, and
herbicides containing 2,4,5-T. The potential for heaviest exposure is
likely to occur during the step that is used to purify 2,4,5-
trichlorophenol from its contaminants, since these products contain much
higher levels of 2,3,7,8-TCDD than the purified products. Detection of
the highest level of 2,3,7,8-TGDD (1.1 µg/wipe) in wipe samples taken
from different trichlorophenol production and purification areas of a
production facility also confirms this (Ott et al. 1987). Few data on
the occupational exposure to 2,3,7,8-TGDD during the manufacture of
these chemicals are available (Rappe 1984). The indirect evidence of
occupational exposure to 2,3,7,8-TCDD is the significantly higher
adipose tissue levels of the compound in heavily exposed Vietnam
veterans and in certain workers at the State Office Building in
Binghamton, New York, following the transformer fire. The adipose
tissues of nine workers from a former trichlorophenol manufacturer in
Missouri showed a mean 2,3,7,8-TGDD level of 246 pg/g compared with a
mean value of 8.7 pg/g for nonexposed workers at the same site. The
lipid-adjusted mean 2,3,7,8-TGDD level in serum of the same exposed
workers was 363 pg/g compared with a value of 47.1 pg/g for nonexposed
workers (Patterson et al. in press).
7.4 POPULATIONS AT HIGH RISK
From the monitoring data discussed in Sects. 7.2 and 7.3, it is
possible to predict the segments of the general population and of
occupational groups that may be exposed to higher levels of 2,3,7,8-
TCDD. Among the occupational groups, workers involved in the production
or use of trichlorophenol or its salts, hexachlorophene, and 2,4,5-T or
other herbicides containing 2,4,5-T have the potential for exposure to
higher levels of 2,3,7,8-TGDD than the general population. 2,4,5-T and
2,4,5-trichlorophenol and its salts, however, are no longer manufactured
in the United States (SRI 1987). Workers in the wood treatment industry
have the potential for 2,3,7,8-TCDD exposure due to the possibility of
2,3,7,8-TCDD formation as a result of catalytic dechlorination of higher
chlorinated dibenzodioxins during pressure treatment of wood with