EPA 560/4-76-004
SUMMARY CHARACTERIZATIONS
OF SELECTED CHEMICALS
OF NEAR-TERM INTEREST
APRIL 1976
OFFICE OF TOXIC SUBSTANCES
U.S. ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20460
-------
This Document Is available to the public through the National Technical
Information Service, Springfield, Virginia 22151
-------
EPA 560/4-76-004
SUMMARY CHARACTERIZATIONS OF SELECTED CHEMICALS
OF NEAR-TERM INTEREST
Prepared by the
OFFICE OF TOXIC SUBSTANCES
U.S. ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20460
APRIL 1976
-------
Preface
This Report includes summary characterizations of 15 chemicals of
near-term interest to EPA. There are many other chemicals of interest,
and in the months ahead, similar characterizations of other chemicals
will be prepared.
The characterizations are based on information available as of
April 1976. As additional information and interpretations of data become
available, an updating of the characterizations may be appropriate.
To this end, the Office of Toxic Substances would welcome comments on
the technical aspects of the Report.
The Report was prepared -by the Office of Toxic Substances drawing
on information provided by a number of Offices. The Office of Research
and Development was particularly helpful in supplying information concerning
platinum, hydrogen sulfide, and polynuclear aromatic hydrocarbons.
-------
Table of Contents
Preface 1
Arsenic 1
Asbestos 5
Benzene 9
Benzldlne r . i i ./ 13
f-
Cadmium
Ethylene 01 bromide 21
Hexachlorobenzene 25
Hydrogen Sulfide 29
Mercury 33
Platinum 37
Polybromlnated Blphenyls 41
Polynuclear Aromatic Hydrocarbons 45
Trlchloroethylene 49
Tr1s (2,3-dibromopropyl) Phosphate 53
Vinylidene Chloride 57
111
-------
ARSENIC
Why Should the Chemical Be of Concern at This Time?
In 1975, OSHA proposed a strict standard for workplace air exposure limits to
inorganic arsenic. Earlier EPA sampling had found that atmospheric concentrations
near two copper smelters exceeded the proposed limit (Anaconda, Montana; and Tacoma,
Washington) and closely approached it at three other smelter sites. Preliminary
results of an EPA-sponsored epidemiology study near an arsenical pesticide plant in
Baltimore reveal lung cancer rates several times the national average. Congress has
proposed that explicit attention be given to establishing an air standard by 1977 in
an amendment to the Clean Air. Act. A number of arsenical compounds are being consi-
dered for rebuttable presumption proceedings under FIFRA/FEPCA.
What Are the Health and Ecological Effects, and Environmental Behavior?
Liver, skin, lung, and lymphatic cancers, and adverse effects on the thyroid
gland have been reported in epidemiological studies of occupationally exposed in-
dividuals. The main threat of arsenic as a carcinogen is inhalation of the inorganic
forms. A preliminary mortality study of the population surrounding Allied Chemical
Company's arsenical pesticide plant in Baltimore revealed a lung cancer rate sixteen
times the national average. A previous study had shown that retired workers from
this plant suffer from lung cancer at a rate seventeen times the national average. A
Dow Chemical Company study indicated an excess of lung and lymphatic cancers among
their workers who had been exposed to arsenical compounds. Arsenic occurs in two
forms: trivalent and pentavalent. Trivalent arsenic is much more toxic
than pentavalent, both acutely and chronically. Pentavalent arsenic is often found
in metallo-arsenicals, and is of concern because it can degrade into the trivalent
form.
A 1972 outbreak of arsenic poisoning in Getchell, Nevada, is attributed to stack
effluent from a gold smelter. Studies made abroad have suggested that arsenic may be
a skin carcinogen when ingested in drinking water at levels as low as 0.3 mg/1. The
debate over the carcinogenicity of arsenic is largely due to the fact that the animal
studies conducted to date have not shown a relationship between ingested arsenic and
cancer. Organic arsenical compounds may be more hazardous than previously believed.
Carbarsone has been reported to produce liver cancer in trout through ingestion (480
mg/100g diet).
Arsenic is particularly toxic to legumes and other crop plants. Depending on
the soil type, 6 ppm arsenic can cause a 50 percent growth reduction. Phytotoxic
levels of arsenic have been found as far as two miles from the Tacoma smelter. Once
combined in soil, arsenic is extremely persistent.
What Are the Sources, Environmental Levels, and Exposed Populations?
Inorganic arsenic is emitted to the air from several sources, including copper,
lead, and zinc smelters, glass production plants, coal-burning facilities, cotton
gins, arsenical-compound (including pesticides) production plants, and pesticide
application. Organic arsen.ic discharges are associated with the manufacture and use
of pesticides. Trivalent arsenic occurs naturally, is a common contaminant of ores,
and is the major component of arsenic emissions from smelters. Based on EPA estimates,
-1-
-------
the 15 copper smelters contribute most heavily to air emissions of inorganic arsenic.
The Anaconda copper smelter in Montana, and the ASARCO copper smelter and arsenic
plant in Tacoma, Washington, have been identified as having the highest arsenic
emissions. Other industrial sources generally emit less arsenic than copper smelters.
Air levels in most urban areas for 1973 and 1974 were at or below the level of
detection (0.001 ug/m3). Levels in areas near smelters ranged from 0.003 to 4.86
ug/m3.
The land disposal of arsenical wastes can become a long-range public health
hazard. A good example is Perham, Minnesota, where eleven people were poisoned by
contaminated well water in 1972.
A 1975 survey of drinking water supplies showed that about one percent exceeded
the interim drinking water standard of 0.05 mg/1. Trivalent arsenic is found at high
levels in some ground water. Underground injection of arsenical pesticide wastes in
Philadelphia has cpntaminated a nearby stream which is being considered for use as a
drinking water supply.
Three new technologies for energy production have important arsenic implications.
Early data on coal gasification indicate that two-thirds of the arsenic present is
volatilized. Oil shale exploitation and geothermal energy development may also
release large quantities of arsenic.
What Are the Technologic and Economic Aspects?
In general, particulate control measures (multicyclones, balloon flues, and
electrostatic precipitators) are used to reduce arsenic emissions. Baghouses offer
the greatest potential for control, but have not been widely adopted by the smelting
industry because of high capital and maintenance costs. Costs and feasibility of
emission controls will vary from plant to plant. Significant control efforts are
being planned at the ASARCO smelter in Tacoma, and are underway at Anaconda. Conven-
tional water treatment technology has been shown to be effective in meeting the
arsenic drinking water standard. Arsenic concentrations of 0.1 and 1.6 mg/1 in
wastewater can inhibit waste treatment by activated sludge and anaerobic digestion
respectively. Thus, concentrations exceeding these levels can present an additional
hazard in waste waters subjected to these treatment methods. Air and water pollution
control efforts normally result in a solid waste or sludge. At present, these
materials are being stored, pending development of acceptable disposal technologies.
What Steps Have Been Taken, and What Is Being Done?
i
EPA is locating and monitoring arsenical discharges, and is conducting several
studies to determine the toxicity of various arsenical compounds. Limited epidemio-
logical studies are planned to help determine effect levels. Studies have been
initiated to determine control technologies and costs for arsenic reduction, and an
Air Pollution Assessment Report on Arsenic has been prepared. EPA is considering the
development of standards under Section 112 of the Clean Air Act. A review of the use
of arsenical pesticides has recently been completed, and research into disposal
techniques for arsenical wastes is planned. A Scientific and Technical Assessment
Report is planned upon receipt of the NAS study of health effects.
In November 1975, OSHA proposed a workplace exposure limit for inorganic arsenic
at 4 ug/m3 (8 hour, TWA). The previous standard of 500 ug/m3 for all forms of arsenic
would remain in effect only for organic forms.
-2-
-------
REFERENCES
Air Pollution Assessment Report on Arsenic; EPA, Office of Air Quality
Planning and Standards (December 1975).
Burruss, R. P. and Sargent, D. H., Technical and Microeconomic Analysis of
Arsenic and Its Compounds; EPA, Office of Toxic Substances (performed under
contract no. 68-01-2926) (September 1975).
Criteria for a Recommended Standard...Occupational Exposure to Inorganic
Arsenic, New Criteria -- 1975 (incorporating results of the Allied and Dow
Chemical worker studies); HEW, National Institute for Occupational Safety
and Health (publication no. NIOSH 75-149, 1975).
Faust, S. D., and Clement, W. H., Investigation of the Arsenic Condition at
the Blue Marsh Lake Project Site. Pennsylvania; U.S. Army Corps of Engineers
performed under contract no. DACW 67-71-C-0288 (1973).
Hazardous Waste Disposal Damage Reports (at page 1); EPA, Office of Solid
Waste Management Programs (publication no. EPA 530/SW-157, June 1975).
Helver, J. E., "Progress on Studies on Contaminated Trout Rations and Trout
Hepatoma;" NIH Report (April 12, 1962).
A Pilot Study on the Community Effects of Arsenic Exposure in Baltimore; EPA,
Office of Toxic Substances (performed under contract no. 68-01-2490, in draft).
Tseng, W. P., et. al., "Prevalence of Skin Cancer in an Endemic Area of Chronic
Arsenicism in Taiwan;" J. National Cancer Inst., 40:453 (1968).
Wands, Ralph C., Letter to APHA Panel on Arsenic Studies; National Research
Council (February 17, 1976).
-3-
-------
ASBESTOS
Why Should the Chemical Be of Concern at This Time?
OSHA has proposed lowering its workplace standard by a factor of ten on the
basis of recent epidemiological data suggesting wider spread health effects than
previously suspected. A number of major commercial sources of airborne asbestos are
limited by EPA regulations. The Agency is investigating taconite and other hard-rock
mining operations, where asbestos is a major ore contaminant. There is renewed
interest in hazards possibly presented by dust from asbestos brake linings and
interior sources. Meanwhile, EPA continues to underscore the hazard of asbestos
fibers in water supplies resulting from Reserve Mining Company's operations. EPA's
nationwide sampling program is showing levels of asbestos fibers in water supplies,
natural runoff, and discharges from manufacturing and mining sites.
What Are the Health and Ecological Effects, and Environmental Behavior?
Airborne asbestos fibers have been known to cause asbestosis, lung cancer, and
pleural and peritoneal mesothelioma. OSHA cites a number of studies showing gastroin-
testinal (61) cancer in workers exposed to asbestos. In one study of insulation
workers in the United States, seven percent of deaths could be attributed to asbestosis,
which generally appeared about 20 years after first exposure -- the same latency
period as for most cancers. Available epidemiological data show that lung cancer is
responsible for as much as 20 percent of all deaths among certain asbestos workers;
mesothelioma, 11 percent; and GI cancer, eight percent.
There are few if any data on the dose-response relationships of asbestos fibers
in either air or water. Effects of airborne asbestos are far better documented than
those of waterborne. OSHA cited workers who had developed mesothelioma at exposure
levels below the previous standard of 5 fibers per cubic centimeter in its recent
proposal to reduce the level by a factor of ten. There is some evidence that asbestos
diseases, including mesothelioma, occur in families of workers exposed to asbestos at
levels presumed to be much lower than direct occupational exposure.
Asbestos fibers are extremely resistant to degradation in the environment. Thus
far, it has been impossible to demonstrate adverse effects on plants. Some adverse
effects on animals have recently been reported.
What Are the Sources, Environmental Levels, and Exposed Populations?
The United States utilized approximately 800,000 tons of asbestos fiber in 1974.
Asbestos products are widely used in the construction industry (asbestos-cement pipe,
building and other construction products, and floor tile). Other products include
friction materials (such as brake linings), felt and paper, packings and gaskets, and
fireproof textiles. It has been estimated that 85 percent of the asbestos is tightly
bound in products and is therefore not as available to the environment as are air-
borne and waterborne asbestos fibers generated in the mining and milling of asbestos
ore, manufacture and fabrication of asbestos products, and disposal of solid wastes
from these processes. Asbestos was used in spray insulation in buildings between
1950 and 1972. This may become a major source of environmental discharge as buildings
constructed during this period are demolished.
Asbestos minerals are found throughout the United States. Significant quantities
of asbestos fibers appear in rivers and streams draining from areas where asbestos-
rock outcroppings are found. Some of these outcroppings are being mined. Asbestos
-5-
-------
fibers have been found in a number of drinking water supplies, but the health implica-
tions of ingesting asbestos are not fully documented. Emissions of asbestos fibers
into water and air are known to result from mining and processing of some minerals.
Asbestiform fibers in the drinking water of Duluth and nearby communities at levels
of 12 million fibers per liter have been attributed to the discharge of 67,000 tons
of taconite tailings per day into Lake Michigan by Reserve Mining.
Exposure to asbestos fibers may occur throughout urban environments. A recent
study of street dust in Washington, D.C., showed approximately 50,000 fibers per
gram, much of which appeared to come from brake linings. Autopsies of New York City
residents with no known occupational exposure showed 24 of 28 lung samples to contain
asbestos fibers, perhaps resulting from asbestos from brake linings and the flaking
of sprayed asbestos insulation material.
What Are the Technologic and Economic Aspects?
Coagulation treatment and filtration are necessary to remove contaminant asbestos
from water. Filtration technologies for air, while meeting the no-visible-emission
standard, permit large quantities of asbestos fibers to escape. Fibrous glass has
frequently been substituted for applications requiring insulative properties, but
there is some debate over its safety. For some other applications, such as brake
linings, economically feasible substitutes may not be available.
There is no inexpensive, standardized analytical method for measuring asbestos,
and monitoring costs are very high.
What Steps Have Been Taken, and What Is Being Done?
An air standard has been promulgated for a number of major commercial sources of
asbestos fibers. Hard-rock mining and taconite beneficiation, where asbestos is an
ore contaminant, are being investigated. Effluent guidelines have been promulgated
under the Federal Water Pollution Control Act which, together with the NPDES permit
program, should reduce asbestos discharges.
EPA is sponsoring an extensive national asbestos monitoring program. Prelimin-
ary findings indicate that asbestos is a widespread contaminant of drinking water.
NAS is reviewing the implications of these preliminary findings. EPA's Reserve
Mining Task Force is monitoring efforts to halt the discharge of taconite tailings
into Lake Superior. Standard analytical methods are being developed for both research
and monitoring purposes. A number of epidemiology studies to further clarify the
health risks of asbestos are being sponsored by EPA.
In 1972, OSHA established a workplace exposure standard. Last October, OSHA
proposed a further reduction in the level. The National Institute of Environmental
Health Sciences (NIEHS) is conducting ingestion experiments to clarify health hazards
of this route of exposure; EPA is partially sponsoring these studies.
-6-
-------
REFERENCES
Asbestos, Its Sources, Uses, Associated Environmental Exposure and Health
Effects; EPA. Office of Toxic Substances (September 1975).
Asbestos, The Need for and Feasibility of Air Pollution Controls; National
Academy of Sciences (1971).
Biological Effects of Asbestos; HEW, National Institute of Health (February
1973)7
Castleman, B. I., and Fritsch, A. J., Asbestos and You; Washington, Center
for Science in the Public Interest (February 1973).
Effluent Guidelines for the Asbestos Manufacturing Industry: Building
Materials and Paper; 40 Federal Register 1874 (January 9, 1975).
Effluent Guidelines for the Asbestos Manufacturing Industry: Friction
Materials and Textiles; 40 Federal Register 18172 (April 25, 1975).
Haley, T. J., "Asbestosis - A Reassessment of the Overall Problem,"
J. Pharm. Science 64{9):1435 (1975).
"1975 - Review," Asbestos 57(7):12 (January 1976).
National Emission Standards for Hazardous Air Pollutants: Asbestos and
Mercury; 39 Federal Register 38064 (October 25. 1974).
National Emission Standards for Hazardous Air Pollutants: Asbestos and
Mercury (Amendment); 40 Federal Register 48292 (October 14. 1975).
Occupational Exposure to Asbestos: Proposed Rules; 40 Federal Register
47652 (October 9, 1975).
Occupational Safety and Health Standards: Subpart Z - Toxic and Hazardous
Materials; 40 Federal Register 73072 (May 28, 1975).
-7-
-------
BENZENE
Why Should the Chemical Be of Concern at This Time?
Benzene, a component in gasoline and an important feedstock for the
chemical industry, has been the subject of numerous published reports
linking leukemia with worker exposure to it. Large quantities of benzene
are discharged into the environment from automobiles, and probably from
stationary sources. The Environmental Defense Fund has been particularly
concerned about the identification of benzene in drinking water in the
parts per billion range. NIOSH has recently recommended a reduction in
workplace levels.
What Are the Health and Ecological Effects, and Environmental Behavior?
Numerous fatalities from occupational benzene poisoning have been
reported since the early 1900's. After inhalation or ingestion, benzene
is absorbed rapidly by the blood. At non-lethal concentrations, a
variety of human central nervous system disorders are observed, depending
upon the extent of exposure. These include euphoria followed by giddiness,
headache, nausea and staggering gait, as well as fatigue, insomnia,
dizziness, and unconsciousness. Observed human blood-forming system
damage includes anemia, reduction in platelet numbers, and depression of
the white blood cell count.
Chronic benzene exposure has also resulted in chromosome aberrations
in human lymphocytes. As early as the 1930's, benzene was suspected in
cases of leukemia. Available epidemiological data indicate that the
compound does induce leukemia, although the data cannot be considered to
constitute unequivocal evidence that benzene acting alone is leukemogenic.
Attempts by NCI and others to induce leukemia in animals with benzene
have not been successful. However, the results of inhalation experiments
with mice, the species most susceptible to leukemia, are not yet available.
Based on its physical properties, benzene is expected to be quite
mobile and probably persistent. Adverse effects on ecological resources
have not been reported.
What Are the Sources, Environmental Levels, and Exposed Populations?
In 1973 over 10 billion pounds of benzene were produced from petroleum
and coal in the United States. This volatile, colorless, flammable
liquid is used mostly for synthesis of organic chemicals. It has been
estimated that at least 80 million pounds of benzene may be lost to the
environment during benzene production, storage, and transport, while an
upper limit of 650 million pounds may be released during its use to
produce other organics. The latter figure was calculated from the
difference between 100% yield and the reported yield in these reactions.
Therefore, this is only a crude measure of the worst-case benzene emissions
during usage. The emissions would be concentrated in the Texas Gulf
area and the Northeast.
-9-
-------
It has been calculated that approximately one billion pounds of
benzene were released with hydrocarbon emissions from motor vehicles in
1971 in a geographical pattern similar to population distribution.
Another 22-24 million pounds of benzene may be released into the environment
each year with spilled oil. Hydrocarbon emissions from non-transportation
sources, such as coke ovens and power plants, may also contain considerable
amounts of benzene. Additionally, benzene is an active ingredient in a
number of insecticides and miticides, although the amount of release to
the environment from this source has not been calculated.
In an EPA study of organic compounds in the drinking water of 10
cities, benzene was detected in water from four cities at concentrations
ranging from 0.1-0.3 ug/1. Previous studies reported levels up to 10
ug/1. Average levels of benzene detected in air in a limited number of
studies are in the low ppb range with one high reading of 23 ppm reported
in the vicinity of a solvent reclamation plant. No data have been found
on levels of benzene in soil, wildlife, and fish. Benzene is widely
enough distributed that most people are probably exposed to very low
levels; the health implications of this type of exposure are not known.
Uhat Are the Technologic and Economic Aspects?
Reduction in organic compound emissions to achieve the National
Ambient Air Quality Standard for oxidants should also result in some
reduction in benzene emissions. As a result of lead removal from gasoline,
the average content of aromatics, including benzene, in gasoline is
likely to increase slowly. However, hydrocarbon emission controls on
motor vehicles should result in a net reduction in benzene emissions.
What Steps Have Been Taken, and What Is Being Done?
In 1974 NIOSH published a criteria document for occupational exposure
to benzene which recommended adherence to the existing Federal standard
of 10 ppm as a time-weighted average with a ceiling of 25 ppm. OSHA is
now in the final stages of reviewing its current standard. NIOSH is
conducting a retrospective study of benzene mortality and a study of
airborne benzene levels in service stations.
EPA has also initiated an air monitoring program which will determine
benzene levels in selected areas. Qualitative results obtained to date
indicate widespread low-level benzene contamination. Air regulations
are not being considered at this time; however, further studies are
planned. EPA has conducted a limited survey of drinking water supplies
in which benzene was identified in some samples, and has begun a more
extensive survey which will seek out benzene as well as a number of
other pollutants. EPA has proposed to designate benzene a hazardous
substance under section 311 of FWPCA, and ocean dumping is already
strictly regulated. A National Academy of Sciences review of the health
aspects of benzene being done for EPA should be completed soon. CPSC is
also awaiting the results of the NAS study on the health effects of
benzene, and will determine if action is appropriate when the results
have been received.
-10-
-------
REFERENCES
Browning, Ethel, Toxicity and Metabolism of Industrial Solvents;.Amsterdam,
Elsevier (1965).
Criteria for a Recommended'Standard...Occupational Exposure to Benzene; HEW, National
Institute for Occupational Safety and Health (NIOSH), (Publication No. NIOSH 74-137,
1974).
Deutsche Forschungsgemeinschaft, Benzene .in the Work Environment; Weinheim, Verlag
Chemie GmbH (1974).
Harris, Robert, The Implications of Cancer Causing Substances in Mississippi River
Water; Washington,Environmental Defense Fund (November 6, 1974).
Occupational Safety and Health Standards: Subpart Z - Toxic and Hazardous Substances
29 CFR 1910.1000, Table Z-2.
IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man
7:203j Lyon, International Agency for Research on Cancer (1974).
Moran, John B., Lead in Gasoline: Impact on Current and Future Automotive Emissions;
presented to Air Pollution Control Association meeting (June 1974).
Preliminary Assessment of Carcinogens in Drinking Water: Report to Congress; EPA,
Office of Toxic Substances (December 1975).
Development of Analytical Techniques for Measuring Ambient Atmospheric Carcinogenic
Vapors; EPA, Office of Air Quality Planning and Standards (Publication No. EPA-600/2-
75-076, November 1975).
Sources of Contamination, Ambient Levels, and Fate of Benzene in the Environment,
EPA, Office of Toxic Substances (Publication No. PB 244139, December 1974).
-11-
-------
BENZIDINE
Why Should the Chemical Be of Concern at This Time?
Benzidine, a human carcinogen, is used as an intermediate in the manufacture of
a number of azo dyes which color textile, leather, and paper products. In addition
to the Agency's long-standing concern over liquid effluent discharges containing
benzidine, recent research results suggest that some of the benzidine-derived azo
dyes may reconvert to benzidine in man, or under certain environmental conditions.
The AFL/CIO has expressed strong interest in any action taken on benzidine.
What Are the Health and Ecological Effects, and Environmental Behavior?
For a number of years, the manufacture and use of benzidine have been associated
with a high risk of bladder cancer among exposed workers. Many scientists believe
that tumors can result from ingestion, inhalation, or skin absorption. A number of
animal studies have demonstrated the carcinogenic effects of benzidine. Mice, rats,
and hamsters develop liver tumors, and dogs develop bladder cancer. Such studies
have many deficiencies for estimating the risk associated with the levels of exposure
to carcinogens likely to be encountered in the environment.
Free benzidine has been detected in the urine of monkeys fed benzidine-derived
azo dyes, establishing a potential for reconversion of azo dyes to benzidine.
Metabolism of benzidine-derived azo dyes may be similar in humans. Japanese silk
painters reportedly have a high incidence of bladder cancer, possibly resulting from
licking brushes and spatulas coated with benzidine-derived azo dyes. However, the
carcinogenicity of such dyes has not been specifically determined.
Industrial data indicate that benzidine entering a waterway dissipates and may
be degraded by naturally occurring processes. Confirmatory investigations have not
been conducted. Other aspects of environmental behavior have not been addressed. It
has been hypothesized that azo dyes can reconvert to benzidine under certain undefined
environmental conditions.
What Are the Sources, Environmental Levels, and Exposed Populations?
The three identified manufacturers (Allied, GAF, and Fabricolor) estimate that
they produce 45 million pounds of azo dyes annually from benzidine. The dyes are
used by about 300 major manufacturers of textile, paper, and leather products. The
largest manufacturer (Allied) recently announced its intention to phase out benzidine
production.
r
The principal environmental concern at benzidine production facilities has been
the amount of benzidine in the waste effluents discharged to publicly owned waste
water treatment works (POTWs). However, the only discharge measurements to date have
been made by industry, which has contended that discharges at any facility usually do
not exceed one pound per day. Benzidine is believed to be present in the sludge
removed from industrial pretreatment plants. The environmental adequacy of land
disposal of these sludges is unknown. According to industry data, discharges from
the POTW are usually below the limit of detection. However, there are occasionally
significant accidental releases to POTWs. Levels of benzidine exceeding 5 mg/1 can
inhibit anaerobic digestion wastewater treatment processes. Thus, concentrations
above this level at the POTW present a problem to POTWs using this process, and a
possible hazard to the receiving waters.
-13-
-------
Free benzidine is present in the benzidine-derived azo dyes. According to
industry, quality control specifications require that the level not exceed 20 ppm,
and in practice the level is usually below 10 ppm. Industry has estimated a total
environmental discharge at the 300 user facility sites of 450 pounds per year or
about 1.5 pounds per year per facility, assuming all of the free benzidine is discharged
in the liquid effluent.
No measurements for benzidine in ambient air, surface water, or drinking water
have been reported. Further, no measurements for free benzidine in finished products
containing azo dyes have been reported.
What Are the Technologic and Economic Aspects?
The principal liquid effluent control technology currently being used is the
reaction of benzidine with nitrous acid. While effective in destroying benzidine,
hazardous decomposition by-products may be formed. Industry thus far has rejected
carbon adsorption as uneconomical. The costs of treatment at the benzidine manu-
facturing plants are of far less concern than at the user plants. Thus, there is a
continuing industrial emphasis on reducing the levels of free benzidine in dyes,
which result from more complete reactions and release less benzidine into the environ-
ment.
If limitations were imposed on benzidine production or use, the vacuum would
probably be filled by imported benzidine-derived dyes and substitute dyes. However,
some of the possible substitutes, such as o-toluidine, are also of environmental and
occupational health concern. Industry estimates that adequate substitutes would be
three to five times more expensive. In some highly specialized uses, particularly
for the halogenated benzidine dyes, a technically adequate substitute may not be
available.
What Steps Have Been Taken, and What Is Being Done?
The stringent work place standards required by OSHA because of the carcinogenic
nature of benzidine reduce environmental discharges resulting from inadequate house-
keeping procedures at benzidine manufacturing sites.
EPA proposed a toxic pollutant effluent standard in December 1973 and is plan-
ning to repropose such a standard and a pretreatment requirement during the next few
months. The results of current animal experiments at the National Center for Toxico-
logical Research, addressing carcinogenicity and metabolic behavior, should be available
within one year. Benzidine is also being examined in the expanded EPA drinking water
survey.
-14-
-------
REFERENCES
Benzidine: Wastewater Treatment Technology; EPA, Office of Water and Hazardous
Materials (June 1974).
Cranmer, Morris, Dr., General Considerations in Setting a Benzidine Standard?
Testimony to EPA, Office of Water and Hazardous Materials.
EPA/SOCMA*, Stipulation of Fact; EPA, Office of Water and Hazardous Materials
(Hearings, May 30, 1974).
Haley, Thomas J., "Benzidine Revisited: A Review of the Literature and
Problems Associated with the Use of Benzidine and Its Congeners," Clinical
Toxicology, 8:13 (1975).
Hazard Review of Benzidine,* HEW, National Institute for Occupational Safety
and Health (July 1973).
Occupational Safety and Health Standards: Subpart Z - Toxic and Hazardous
Materials (Benzidine); 39 Federal Register 20 (January 29. 1974).
Rinde, Esther and Troll, Walter, "Metabolic Reduction of Benzidine Azo Dyes
to Benzidine in the Rhesus Monkey"; J. National Cancer Inst., 55:181 (1975).
SOCMA, Comments on Production and Use of Benzidine; submitted to EPA, Office
of Water and Hazardous Materials (March 9, 1973).
SOCMA, Affidavit of Mr. Kelvin H. Ferber; submitted to EPA, Office of Water
and Hazardous Materials (May 13, 1974).
SOCMA, Benzidine Effluent Data; submitted to EPA, Office of Water and Hazardous
Materials (June 6, 1974).
SOCMA, Industrial Hygiene and Environmental Control; submitted to EPA, Office
of Water and Hazardous Materials (May 30, 1975).
SOCMA, Submission; submitted to EPA, Office of Water and Hazardous Materials
(June 5, 1975).
SOCMA, Second Submission; submitted to EPA,Office of Water and Hazardous
Materi als (August 5, 1975).
*Synthetic Organic Chemical Manufacturers Association
-15-
-------
Bis(Chloromethyl) Ether (BCME)
Why should the chemical be of concern at this time?
BCME was first documented as a human carcinogen in 1972. Since
then, the results of animal testing studies have shown this substance to
be a potent carcinogen with a very short latent period. While no monitoring
data are currently available to document an environmental problem, there
is some concern about the potential formation of BCME from environmental
contaminants (formaldehyde and chloride ion).
What are the health and ecological effects, and environmental behavior?
Several studies indicate that workers exposed to BCME as a conta-
minant of chloromethyl methyl ether (CMME) have a markedly increased
risk of developing respiratory tract cancer, generally oat cell carcinoma.
Exposure periods of two to fourteen years (average, ten) by inhalation
of vapors at undefined concentrations, and an average latent period of
15 years, have been reported. In the most detailed epidemiological
study of workers, a control population having similar smoking habits was
identified. Comparing nonsmoker controls to nonsmoker workers, and
controls who smoked with workers who smoked, cancer occurrence was
determined to be at least eight times greater for the exposed workers in
either instance.
The toxic properties of BCME were known in the early years of the
20th Century. In 1917-1918, Germany produced 200 tons of this substance
for potential use in chemical warfare.
Animal experiments indicate that BCME and CMME produce similar
effects, but that BCME is much more toxic. A seven-hour inhalation
exposure of about eight parts per million BCME is 100% lethal to rats
and hamsters within 14 days. All animals exhibited significant increases
in lung weight/body weight ratios. At three ppm, BCME is a potent
respiratory irritant; 100 ppm incapacitates test animals and results in
fatal lung damage within one or two minutes. Rats exposed for six hours
to inhalation of 0.1 ppm developed respiratory cancers as early as seven
months after exposure (average latency, 13 months). In dermal experiments,
BCME was shown to be a moderate initiator and a potent promoter of cancer.
Available experimental data show that BCME has a half-life in water
of 10-40 seconds, and that it hydrolyzes rapidly. BCME has a half-life
in air of about 25 hours, and its ability to spread in that medium may
be influenced by humidity.
What are the sources, environmental levels, and exposed populations?
BCME is known to be a contaminant of CMME, at concentrations rang-
ing from one to seven percent. Because CMME is produced solely as an
intermediate for chemical production, manufacturing data are not recorded.
CMME is used in the manufacture of ion exchange resins by four companies
in as many states. A fifth manufacturer of CMME is listed, but no
information on its capacity or purposes was found. Because of its
contaminant nature, BCME was suspected to have been contained in manufac-
tured resins; however, tests using C radio-tracers failed to confirm
this.
-1-
-------
it has Deen hypothesized that inadvertent formation of BCME could
occur in the environment if high concentrations of formaldehyde and
ionic chloride are present; however, monitoring data have not been
collected.
Formaldehyde is a high volume chemical (six billion pounds) with
major applications in the production of phenolic, urea and melamine
resins. The production and use of these resins can result in release of
formaldehyde to the environment. The major emission sources of formaldehyde
are combustion processes which are estimated to release about 690 million
pounds annually. Chloride ions are common environmental contaminants.
Analysis of air samples taken inside textile plants where formal-
dehyde and chloride are present has found concentrations of approximately
two parts per billion BCME. Concentrations of 210-1500 ppb have occurred
above some laboratory formalin slurries. Environmental monitoring has
not been performed.
Should BCME be released from an industrial plant, it has been
estimated that an exposure risk might be presented to persons living
within twenty miles of the site. Additional people could be exposed if
the potential for formation of BCME from formaldehyde and chloride ion
is realized.
What are the technologic and economic aspects?
BCME has no commercial use. Patent applications for minor uses in
cellulose crosslinking, in preparation of three-block styrene-butadiene-
styrene polymers, and in treatment of vulcanized rubber to improve epoxy
resin adhesion have been filed. Because of the well-known hazards
presented by BCME, it is unlikely that these uses will become of eco-
nomic importance.
CMME containing BCME as a contaminant is used almost exclusively in
the production of ion exchange resins. No other use is reported. CMME
could theoretically be produced free of BCME contamination; however, it
would probably be neither technologically or economically feasible. A
more reasonable approach might be to develop control technology capitalizing
on the ease with which BCME and CMME hydrolyze.
What steps have been taken, and what is being done?
In 1972, the American Conference of Governmental Hygienists proposed
a threshold limit value of one part per billion for BCME, which was
adopted in 1974. In 1974, OSHA established stringent workplace standards
for BCME and CMME. The standards are stated in terms of engineering
controls, rather than a maximum time-weighted-average concentration.
The standard further provides for medical surveillance and record keeping.
NIOSH is studying industrial facilities where formaldehyde and
ionic chloride are used to determine if BCME is inadvertently formed.
If this is found to occur, that agency will recommend standards to OSHA.
Because environmental modeling has predicted air concentrations
below the detection limit, no air standards are contemplated. Should
monitoring reveal detectable levels, this decision will be reviewed.
-2-
-------
REFERENCES
Investigation of Selected Potential Environmental Contaminants:
Haloethers; Final Report under EPA contract No. 68-01-2996
(available NTIS-PB 246356, September, 1975).
Review of the Environmental Fate of Selected Chemicals; Final
Report under EPA contract No. 68-01-2681 (available NTIS-
PB 238-908, January, 1975).
Brown, S.M. and Selvins, S. (1973), "Lung Cancer in Chloromethyl
Methyl Ether Workers", N. Engl. J. Med. 289: 693-4.
Drew, R.T., Laskin, S., Kuschner, M. and Nelson, N. (1975) "Inhalation
Carcinogenicity of Alpha Halo Ethers. I. Acute Inhalation Toxicity
of Chloromethyl Methyl Ether and Bis(chloromethyl) Ether", Arch.
Environ. Health 30, 2, 61-9.
Figueroa, W.G., Raszokowski, R. and Weiss W. (1973), "Lung Cancer in
Chloromethyl Methyl Ethyl Workers", N. Engl. J. Med. 288, 21_,
1096-7.
I ARC (1974) Monographs on the Evaluation of the Carcinogenic Risk of Chemicals
to Man, Bis (Chloromethyl)ether, Vol. 4. 231-238.
Kallos, G.J. and Solomon, R.A. (1973), "Formation of Bis(Chloromethyl)
Ether in Simulated Hydrogen Chloride-Formaldehyde Atmospheric
Environments", Amer. Ind. Hyg. Assn. J., 34, 11, 469-73.
Kuschner, M. Laskin, S., Drew, R.T., Cappiello, V.P. and Nelson, N.
(1975), "Inhalation Carcinogenicity of Alpha Halo Ethers. III.
Lifetime and Limited Period Inhalation Studies with Bis(chloro-
methyl) ether at 0.1 ppm", Arch. Environ. Health, 30, 2, 73-7.
Laskin, S., Kuschner, M., Drew, R.T., Cappiello, V.P. and Nelson, N.
(1971), "Tumors of the Respiratory Tract Induced by Inhalation
of Bis(Chloromethyl) Ether", Arch. Environ. Health. 23, 2, 135-6.
Laskin, S., Drew, R.T. Cappiello, V., Kuschner, M. and Nelson, N.
(1975), "Inhalation Carcinogenicity of Alpha Halo Ethers. II.
Chronic Inhalation Studies with Chloromethyl Methyl Ether", Arch.
Environ. Health, 30_, 2, 70-2.
OSHA (1973), "Emergency Temporary Standard on Certain Carcinogens", Fed.
Regist. 38, 10929-30.
OSHA (1974) "Rules and Regulations: Bis(Chloromethyl) Ether", Fed. Regist.
39, 23559-23561.
Sakabe, H. (1973), ".Lung Cancer Due to Exposure to Bis(Chloromethyl) Ether",
Ind. Health.. ]_1_, 3» 145-8-
Tou, J.C. and Kallos, G.J. (1974), "Aqueous Hydrochloric Acid and For-
maldehyde Mixtures for Formation of Bis(chloromethyl) Ether",
Amer. Ind. Hyg. Assn.. J, 35_, 7, 419-22.
-3-
-------
CADMIUM (Cd)
Why Should the Chemical Be of Concern at This Time?
As evidence that cadmium levels in the environment may be increasing emerges,
concern mounts over this substance's ability to accumulate in the body at low
level exposures. Cadmium, which is used in a variety of commercial and consumer
products, is believed to reach man through a number of routes, particularly as a
contaminant of fish and other foods. There is recent concern over the presence
of Cd in sludge which might reach the food chain as a result of leaching from
disposal sites or its use as a soil conditioner. A proposed amendment to the
Clean Air Act calls for explicit EPA attention by 1977 to a possible air standard
for cadmium.
What Are the Health and Ecological Effects, and Environmental Behavior?
Cadmium accumulates in the kidney cortex, where it can cause damage to the
renal tubules at levels on the order of 200 ppm. The results of autopsy studies
show current levels of 15-50 ppm in the kidneys of people over the age of 50 who
were not occupationally exposed; the higher levels generally reflect those found
in individuals who had been smokers. Autopsy data on the occupationally exposed
are inconclusive because samples have been too small.
At high levels of Cd exposure, other effects, such as bone brittling, have
been observed, mainly in Japan, where widespread occurrence of Itai-Itai disease
caused nearly 100 deaths. These effects resulted from an estimated intake of
600 ug/day. The average American diet contains 50-75 ug/day. Heavy fish eaters
receive a higher dose, but well below the levels observed in Japan. About five
percent of ingested Cd is retained in the body, and its biological half-life in
humans is estimated to be at least 15 years.
Prolonged exposure to cadmium dust can cause emphysema. Recent epidemiological
studies indicate abnormally high rates of several forms of cancer due to occupational
exposure. Hypertension has been developed in laboratory animals after prolonged
exposure to low levels. The presence of Cd in human fetal tissues during prenatal
life shows -that the metal traverses the placenta. Experimental studies in
laboratory animals have confirmed this observation and have also shown that Cd
is a potent teratogen.
Cadmium particulate in air falls out into water and soils. Plants take it
up from the soil, and people and animals ingest Cd from these sources. Uptake
from contaminated water has not been so well documented; it is suspected that
this is the significant route of exposure for fish.
What Are the Sources, Environmental Levels, and Exposed Populations?
Cadmium is produced in conjunction with zinc refining. In 1974, the total
U.S. consumption of cadmium was about 6300 metric tons, at a cost of about $8500
per metric ton. About one-third was imported. By 1985, demand is expected to
reach 9600 metric tons.. Of the total use in 1975, about 55 percent went to
electroplating, 21 percent to plastic stabilization, 12 percent to pigments, 5
percent to batteries, and 7 percent to a variety of other uses. Major growth is
expected in the nickel-cadmium battery industry.
-17-
-------
An EPA-sponsored study estimated that a total of 1800 metric tons of Cd
were released to the environment in 1974. Of this, about 20 percent was from
zinc mining and smelting, via air, water, and tailings; fifty percent was from
such indirect sources as fossil fuel combustion, fertilizer use, and disposal of
sewage sludge; and thirty percent was from industrial uses, such as remelting of
cadmium-plated scrap, incineration of plastics containing Cd, and electroplating.
The major sources of human exposure are food and tobacco contamination,
while direct water and air intake appear to be very minor contributors. Groundwater
contamination as a result of waste disposal, however, is common. FDA's marketbasket
survey has been identifying low levels of Cd in most composite class samples.
Thus, virtually everyone is exposed to trace levels of Cd. Recent studies
indicate that, in Sweden, Cd concentrations in wheat may be increasing at a rate
roughly proportional to levels of industrial use. Increasing soil levels may
result from airborne fallout, fertilizer use, and cadmium in irrigation waters.
Cadmium has been identified in soils at several locations at levels of 0.55 to
2.45 ppm.
Cadmium levels of 1 to 10 ug/1 have been found in 42 percent of available
ambient water samples, with more than 10 ug/1 in four percent. Fifty-four
percent of the samples did not contain measurable amounts. The annual release
of Cd to the air at one copper smelter was estimated to be 250 tons per year.
Ambient air levels averaged .031 ug/m3. Soil levels of Cd were about 1.6 ppm,
between one and five miles from the smelter, and were reflected by average
findings of 4.7 ppm in leafy vegetables.
What Are the Technologic and Economic Aspects?
Substitutes are or will soon be available for most but not all electro-
plating uses and for plastic stabilizer use at comparable cost and efficacy.
A Cd level of 0.02 mg/1, has been shown to inhibit wastewater treatment by
anaerobic digestion. Should Cd concentrations exceeding that level reach a
wastewater treatment plant using anaerobes, a hazard may be presented to the
receiving water. Trace contamination of air and water by Cd is common. Removal
of such components is usually extremely costly.
What Steps Have Been Taken, and What Is Being Done?
NIOSH is expected to submit a criteria document to OSHA this year, at which
time the existing workplace standard will be reviewed. FDA has banned certain
uses of Cd pigments and cadmium-containing materials.
Epidemic!ogical studies are being conducted by the World Health Organization
to determine whether cadmium may be a factor in hypertension and cardiac disease
in humans. NCI is sponsoring studies to investigate the carcinogenic potential
of Cd metal, Cd oxide, and Cd sulfide.
EPA has prohibited the ocean dumping of cadmium, except as trace contamination.
The effluent guidelines for the electroplating industry address Cd released from
this segment of the economy, and hazardous spill regulations include some cadmium
compounds among the substances for which spill penalties have been established.
An-Interim Primary Drinking Water Standard has been issued and pesticides containing
Cd are being reviewed for possible Rebuttable Presumption Against Registration
proceedings. A Scientific and Technical Assessment Report on Cd has documented
health and technological concerns for EPA.
-18-
-------
REFERENCES
Chauve, S., et. al., "Zinc and Cadmium in Normal Human Embryos and Fetuses;"
Archiv Environmental Health 26:237 (1973).
Cadmium and the Environment: Toxicity, Economy,.Control; Paris, Environment
Directorate, Organization for Economic Cooperation and Development (1975).
Ferm, V. H., "Developmental Malformations Induced by Cadmium;" Biol Neonate
19:101 (1971).
Friberg, Lars, et al, Cadmium in the Environment, 2nd ed.; Cleveland, Ohio,
CRC Press (1974).
Fulkerson, William et al, Cadmium: The Dissipated Element; Oak Ridge National
Laboratory, (reoort no. ORNL NSF-EP-21, January 1973).
National Inventory of Sources and Emissions: Cadmium-1968; EPA, Office of
Air and Water Programs (report no. APTD-68, February 1970).
Regulations for Rebuttable Presumption Against Registration, 40 CFR 162.11.
Scientific and Technical Assessment Report on Cadmium; EPA, Office of Research
and Development (publication no. EPA 600/6-75-003, March 1975).
Technical and Microeconomic Analysis of Cadmium and Its Compounds. EPA, Office
of Toxic Substances (Report No. EPA 560/3-75-005, June 1975).
Webb, M., "Cadmium;" Br. Med. Bull, 31(3):246-250 (1975).
-19-
-------
ETHYLENE DIBROMIDE (EDB)
Why Should the Chemical Be of Concern at This Time?
Ethylene dibromide, which is used primarily as an additive in leaded gasoline,
has been identified by the National Cancer Institute (NCI) as an extremely potent and
fast-acting carcinogen when administered at high dose levels to animals. Recent
monitoring data reveal very low concentrations in air collected from urban and rural
areas, and near production and storage facilities. EOF has petitioned EPA to cancel
all registered pesticides containing this chemical.
What Are the Health and Ecological Effects, and Environmental Behavior?
EDB is an extremely strong irritant. Chronic exposure can result in liver and
kidney damage. High levels of exposure cause immediate depression of the central
nervous system, usually resulting in death of laboratory animals. Laboratory animals
survive only a few hours of exposure to 200 ppm EDB in air; adverse effects have been
noted at exposures as low as 30 ppm. The exposure of domestic animals to EDB has
revealed severe reproductive effects. In 1974, NCI issued a memorandum of alert
citing preliminary findings of strong carcinogenesis in rats and mice. This document
cites a high incidence of squamous cell carcinoma of the stomach in both rats and
mice, with tumors observed after only six weeks of exposure. EDB is also mutagenic
and teratogenic in animals. In humans, weakness and rapid pulse have been associated
with EDB exposure, and, less commonly, cardiac failure leading to death.
The freshwater toxicity of EDB is indicated by the 48-hour Median Tolerance
Limit for pan and game fish (15 to 18 ppm). The environmental behavior of 2DB is
poorly understood. EDB is reportedly short lived in the atmosphere. In -soil, EDB is
persistent for at least two weeks; however, within a two-month period, it is converted
to other compounds. Ethylene, one of these, can reduce yields of fruits, vegetables,
and flowering plants.
What Are the Sources, Environmental Levels, and Exposed Populations?
In 1973, approximately 175,000 tons of EDB were produced in the United States.
Since sales appear higher than production figures, a small amount of EDB is probably
imported. The major producers of EDB are: Houston Chemicals, Ethyl, Dow, PPG,
Northwestern, and Great Lakes Chemical. Four of the manufacturing sites are located
in Arkansas, one in Texas, and another in Michigan. Eighty to ninety percent of EDB
produced in the United States is used as a lead scavenger in gasoline, and it is also
registered for use as an insect fumigant and a soil nematocide. The pesticidal use
of EDB is less than 1,000 tons per year. EDB is also used as an intermediate in the
synthesis of dyes and Pharmaceuticals, and as a solvent for resins, gums, and waxes.
A small amount of EDB is used in the production of vinyl bromide.
The limited amount of monitoring data available indicates the presence of EDB
residues throughout the environment. A Dutch study examining EDB residues in wheat,
flour, and bread showed that flour made from wheat treated 13 weeks before analysis
contained from 2 - 3 ppm of EDB. Bread made from this flour was found to contain
about 0.02 -0.12 ppm of EDB. The fumigation of apples reportedly results in detectable
residues on the skin and in the outer pulp for from 4-28 days. Low levels of EDB
have also been found in the ambient atmosphere of urban and rural areas. Ambient air
collected in the vicinity of gasoline stations along highly trafficked arteries in
Phoenix, Los Angeles, and Seattle has shown EDB concentrations of 0.07 - 0.11 ug/m3.
-21-
-------
EDB also escapes into the environment during the production and storage/transfer of
gasoline products at oil refineries. Concentrations of EDB in the vicinity of manu-
facturing plants located in Arkansas ranged from 90 - 115 ug/m3, while concentrations
around a bulk transfer site in Kansas City were 0.2 - 1.7 ug/m3. Since fully validated
monitoring techniques are not yet available, these results should be considered
qualitative rather than quantitative indicators.
Although few people live immediately adjacent to production plants where the
ambient levels of EDB are the highest thus far recorded, very large populations
frequent or live near highly trafficked areas of the type where EDB has been detected.
What Are the Technologic and Economic Aspects?
The elimination of most pesticidal uses for EDB will not result in significant
reduction in media exposure, since less than 10 percent of production goes to this
use. However, residues in food, which may pose a serious problem, have not been well
studied. USDA uses EDB to fumigate certain types of exported and imported grains and
produce. Effective substitutes are probably not readily available for some uses, and
may be more costly for others. Strict control of EDB emissions from production
plants should pose few problems since production is basically a closed system. Major
EDB emissions into the environment occur during packaging, and the recycling or
capturing of vapors would seem practical. At present, the elimination of EDB from
leaded gasoline is not being undertaken by manufacturers. Ethylene dichloride (EDC),
which is being used in conjunction with EDB in leaded gasoline could be increased in
concentration, and EDB eliminated; however, the environmental impacts of EDC are not
clear.
>
What Steps Ha^e Been Taken, and What Is Being Done?
Actions have been taken to phase out the use of leaded gasoline and are expected
to result in a concurrent reduction of exposure to EDB. Gasoline transfer vapor
recovery and vehicle evaporative emission controls should further reduce EDB emissions.
Monitoring efforts have been initiated to define the zones of impact associated with
various stationary and mobile sources of EDB. EPA will gather information on the
quantities of EDB, EDC, and other gasoline additives produced, as a result of recently
promulgated fuel and fuel additive regulations. Pesticides containing EDB are under-
going special review to determine whether they should be considered candidates for
Rebuttable Presumption Against Registration procedures.
OSHA has established a standard for ethylene dibromide to guard against irrita-
tion and cumulative hepatic injury; however, the existing standard does not consider
the new evidence on carcinogenicity. NIOSH and OSHA are currently reviewing the new
evidence to determine whether more rapid action should be taken to revise the standard.
-22-
-------
REFERENCES
Alumot, (Olomucki), E. and Hardof, Z., "Impaired Uptake of Labelled Protein
by the Ovarian Follicles of Hens Treated with Ethylene Dibromide;" Comp. Biochem.
Physiol. 39B:6168 (1970).
Amir, D., "Sites of Spermicidal Action of Ethylene Dibromide in Bulls;"
J. Reprod. Fert. 35(3):519-525 (1973).
Olson, et. al., "Induction of Stomach Cancer in Rats and Mice with Halogenated
Aliphatic Fumigants;" J. National Cancer Inst. 51(6) 1993-1995 (1973).
Occupational Safety and Health Standards: Subpart Z - Toxic and Hazardous
Substances. 20 CFR 1910.100, Table 1-2.
Memorandum of Alert: Ethylene Dibromide, National Cancer Institute
(October 4, 1974).
Regulations for Fuels and Fuel Additives; 40 Federal Register 51995-52337
(November 7, 1975).
Regulations for Rebuttable Presumption Against Registration; 40 CFR 162.11.
Review of Selected Literature on Ethylene Dibromide; EPA, Office of Toxic
Substances (November 1974).
Sampling and Analysis of Selected Toxic Substances. Task II -- Ethylene
Dibromide; EPA, Office of Toxic Substances (performed under Contract No.
68-01-2646) (Publication No. EPA-560/6-75-001, September 1975).
Toxicological Studies of Selected Chemicals. Task II: Ethylene Dibromide;
EPA, Office of Toxic Substances (performed under Contract No. 68-01-2646,"
Preliminary findings, personal communication by C. C. Lee, Project Director)
(March 1976).
-23-
-------
HEXACHLOROBENZENE (HCB)
Why Should the Chemical Be of Concern at This Time?
Despite recent steps by several States and several companies to
reduce environmental discharges of HCB, environmental contamination persists.
Recent reports of the occurrence of HCB in human adipose tissues (95 percent of
those sampled), the food supply, effluents, drinking water, and pesticides (in
addition to registered pesticidal use) add to earlier concerns of EPA, USDA,
FDA, and other organizations. In 1973, EPA made a public commitment in response
to a petition from USDA to set an HCB food tolerance in 1976.
What Are the Health and Ecological Effects, and Environmental Behavior?
The death of breast-fed infants and an epidemic of skin sores and skin
discoloration were associated with accidental consumption of HCB-contaminated
seed grain in Turkey in the mid-19501s. Doses were estimated at 50 to 200 mg/day
for several months to two years. Clinical manifestations included weight loss,
enlargement of the thyroid and lymph nodes, skin photosensitization, and abnormal
growth of body hair. HCB levels of up to 23 ppb in blood are believed to have
contributed to enzyme disruptions in the population of a small community in
southern Louisiana in 1973.
Long-term (up to 3 years) animal ingestion studies show a detectable
increase in deaths at 32 ppm, cellular alteration at 1 ppm, biochemical effects
at .5 ppm, and behavioral alteration between .5 and 5 ppm. Apparently, the
effective dosage to offspring is increased by exposure to the parent. A 12
percent reduction in offspring survival resulted when exposure to very low
levels had been continuous for three generations. Teratogenic effects appear
minimal.
While HCB appears to have little effect on aquatic organisms, a bioaccumulation
factor of 15,000 has been demonstrated in catfish. HCB is toxic to some birds.
Eighty ppm caused death, and 5 ppm caused liver enlargement and other effects
in quail. The half life of HCB in cattle and sheep is almost 90 days. HCB is
very stable. It readily vaporizes from soil into the air; emissions to air in
turn contaminate the soil.
What Are the Sources, Environmental Levels, and Exposed Populations?
About 90 percent of the estimated 8 million pounds of HCB produced annually
in the United States is as a by-product at 10 perchloroethylene, 5 trichloro-
ethylene, and 11 carbon tetrachloride manufacturing plants. HCB is commonly
detected in solid wastes and liquid effluents. Most of the remaining production
is as a by-product at more than 70 other sites producing chlorine and certain
pesticides. About 45,000 pounds per year are released into the evironment
during pesticide use. HCB has also been found in the waste tars from vinyl
chloride and other chlorine-product plants.
In 1975, forty-six percent of the soil samples collected at 26 locations
along a 150-mile transect in Louisiana were contaminated with HCB at levels from
20 to 440 ppb. Parallel sampling of aquatic sediments revealed concentrations
of 40 to 850 ppb. Although water samples were generally below 3 ppb, one sample
below an industrial discharge contained 90 ppb. Air immediately adjacent to
production facilities has shown concentrations from 1.0 to 23.6 ug/m3. Most of
-25-
-------
the HCB appeared to be associated with participate, but low levels were found in
the gaseous phase as well, which might result from volatization from solid
wastes. Samples collected from pastureland near a known HCB production site
revealed concentrations in the vegetation from 0.01-630 ppm and in the soil from
0.01-300 ppb.
HCB residues have been found in soil, wildlife, fish,and food samples
collected from all over the world. In the United States, HCB residues have been
reported in birds and bird eggs collected from Maine to Florida, duck tissue
collected from across the country, and fish and fish eggs from the East Coast
and Oregon. Animal foods, including chicken feed, fish food, and general laboratory
feeds, have been found to contain HCB residues. The frequency of detection of
HCB residues in domestic meats has been steadily increasing since 1972, in part
because of closer scrutiny. HCB has been detected in trace amounts in only two
drinking water supplies.
EPA's monitoring of human adipose tissues collected from across the
United States reveals that about 95 percent of the population has trace HCB
residues.
What Are the Technologic and Economic Aspects?
If a food tolerance is established by EPA at about .5 ppm (the interim
tolerance), there is no reason to believe that substantial numbers of animals or
crops will be held off the market. However, a level of .3 ppm or lower would
probably prevent the marketing of some products. The feasibility and costs of
air emission and water effluent controls, particularly the effectiveness of
particulate reduction and of better houskeeping practices, have not been estimated.
Effective incineration of wastes has been demonstrated. Proper landfill practice
may serve this purpose; however, studies indicate that soil and other covers
only delay volatilization.
What Steps Have Been Taken, and What Is Being Done?
In the wake of widespread HCB contamination of cattle in Louisana in 1973,
and concern over possible contamination of sheep in California, EPA established
an interim tolerance of .5 ppm. Concurrently, the State of Louisiana and several
companies took immediate steps to tighten up solid waste practices from manu-
facturing through disposal. Also, supplies of Dacthal containing 10 percent HCB
as an inert ingredient were voluntarily withdrawn from the California market.
Several toxicological, monitoring, economics, and related projects were initiated
by EPA to provide a better basis for further actions, including the establishment
of a tolerance. Also, additional toxicological efforts were undertaken
by USDA.
As soon as the needed toxicological data are available, a food tolerance
will be established. Also, all pesticidal uses of HCB, including pesticides
which contain HCB as a contaminant, will be reviewed. Studies of land and other
disposal methods have been completed. Ocean dumping of HCB-laden tars is prohibited.
Although not directly addressed by the NPDES permit program, provisions relating
to suspended solids, and oil and grease may provide some degree of control if
HCB enters the effluent stream.
-26-
-------
REFERENCES
Assessing Potential Ocean Pollutants (p 188-208); National Academy of Sciences
(1975). :
Burns, J. E. and Miller, F. M. "Hexachlorobenzene Contamination: Its Effects
on a Louisiana Population"; Arch. Environ. Health, 30:44-48 (1975).
Cam. C. and Nygogosyan, G. "Acquired Prophyria Cutanea Tarda Due to Hexachloro-
benzene"; J. Am. Med. Assoc.. 183:88-91 (1963).
An Ecological Study of Hexachlorobenzene and Hexachlorobutadiene; Final Report
under EPA Contract No. 68-01-2689 (to be published at NTIS April' 1976).
Environmental Contamination from Hexachlorobenzene". EPA, Office of Toxic
Substances, (July 1973), (to be published at NTIS April 1976).
Industrial Pollution of the Lower Mississippi River in Louisiana; EPA, Office
of Water and Hazardous Materials (April 1972).
Sampling and Analysis for Selected Toxic Substances - Task 1, HCB and HCBD; EPA,
Office of Toxic Substances (performed under Contract No. 68-01-2646) (to be
published at NTtS, April 1976).
Survey of Industrial Processing Data, Task 1 - Hexachlorobenzene and Hexachloro-
butadiene Pollution from Chlorocarbon Processes; (EPA. Office of Toxic Substances,
Report No. 560/3-75-003, June 1975) (NTIS Publication No. PB 2436441/AS).
Survey of Methods Used to Control Wastes Containing Hexachlorobenzene; EPA,
Office of Solid Waste Management (performed under Contract No. 68-01-2956)
(November 1975).
Vos, J. G., et al. "Toxicity of Hexachlorobenzene in Japanese Quail with Special
Reference toTorphyria, Liver Damage, Reproduction and Tissue Residues"} Toxicol
Appl. Pharmacol. 18:944-957 (1971).
Z1tko, V., and Choi, P. M. K., "HCB and P,P' - DDE in Eggs of Cormorants, Gulls
and Ducks from the Bay of Fundy, Canada"^ Bull. Env. Contam. and Toxicology,
7(51):63-64 (1972).
-27-
-------
HYDROGEN SULFIDE (H2$)
Why Should the Chemical Be of Concern at This Time?
Hydrogen sulfide, a colorless gas characterized by its rotten-egg
odor, is an emission product from a large number of industrial processes
such as kraft paper mills, as well as a naturally occurring chemical.
Recently, H2S has been identified in the exhaust of improperly adjusted
catalyst-equipped motor vehicles. This has resulted in considerable
public concern because of its strong odor. It has also been identified
in emissions from prototype stationary source NOX reduction catalyst
systems. As more and more vehicles become equipped with catalysts, and
as the Agency begins to regulate NOX emissions from stationary sources,
H2$ may become a pollutant of greater concern because of its acute
toxicity.
What Are the Health and Ecological Effects, and Environmental Behavior?
HpS is readily absorbed into the blood, with the chief exposure
route being inhalation. Test animals exposed to concentrations over 700
ppm exhibited no H2S in exhaled breath. Systemic poisoning is characterized
by respiratory paralysis, occurring when H2S concentrations in the blood
exceed the oxidation capacity. Despite the substance's characteristic
odor, which is detectable at levels as low as 0.025 ppm, high concentrations
producing toxic effects can be reached almost without warning, because
of olfactory fatigue at levels above 50 ppm. Exposures in excess of 400
ppm are considered dangerous, and over 700 ppm, life threatening.
The subacute effects of H2S exposure are manifested as irritation
of the respiratory tract and eyes. Pulmonary edema or pneumonia may
result from prolonged exposure to concentrations over 250 ppm. Such
exposures over a shorter term may produce temporary symptoms, such as
headache, excitment, nausea, dizziness, and painful sensations in the
nose, throat, and chest. Chronic exposure to levels of 20 to 30 ppm can
lead to conjunctivitis, and 50 to 300 ppm may result in corneal clouding
or blurred vision.
What Are the Sources, Environmental Levels, and Exposed Populations?
The primary natural source of H2S is anaerobic microbial action on
organic materials using naturally occurring sulfates. It is also encountered
in natural gases and geothermal exhausts, sewers and sewage treatment
plants, waters of some natural springs, volcanic gases, and certain
mining operations. Because H2S is soluble in both water and petroleum,
it can be transported considerable distances before it is released.
A variety of industrial activities result in the release of H2S.
It is a well-known pollutant at kraft paper mills, oil refineries, coke
ovens, natural gas plants, chemical plants, rayon production facilities,
rubber production plants, and sugar beet refineries. Fatal and near-
fatal H2$ concentrations have been reported at industrial landfills.
Environmental levels outside the workplace have not been adequately
documented, although there have been a number of reports of odor intensity
near plants where reduced sulfur compounds are emitted.
-29-
-------
Recent studies show that HoS is emitted from maladjusted vehicles
with catalytic converters. With adequate oxygen, these catalysts normally
convert some of the sulfur dioxide emitted from the system into sulfuric
acid; these same catalysts reduce SO;? into H^S in the absence of adequate
oxygen, usually caused by a malfunctioning air injection pump or a
maladjusted carburetor. As more sophisticated catalytic control devices
are employed to achieve automotive emission standards, particularly
those for NOX, the potential for H2S emissions may increase.
Several catalytic reduction processes have been proposed to limit
NOX emissions at stationary sources to achieve the Ambient Air Quality
Standard for N02- Laboratory tests of prototype systems demonstrate
increased production of H2S. Thus, an increased potential for widespread
human exposure to low levels of this substances exists, but the levels
cannot be predicted at this time.
What Are the Technologic and Economic Aspects?
Current evidence is that H2S is emitted in significant quantities
from catalyst-equipped automobiles only when such vehicles are defective
or maladjusted. Conditions leading to H2$ formation will also result in
high levels of carbon monoxide and hydrocarbon emissions. Thus, efforts
to ensure proper maintenance of vehicle emission control systems (such
as state inspection/maintenance programs) should control automotive H2S
emissions as well, at no additional cost, at least for the 1975/77
model-year vehicles.
Desulfurization of fuels or stack gas feeds could largely eliminate
the H2S problem, but at very high cost and resulting in the generation
of large quantities of troublesome sludge.
What Steps Have Been Taken, and What Is Being Done?
H2S has been, and continues to be, assessed in exhausts from catalyst-
equipped automobiles. A fact sheet on current findings has been released
to the public. New Source Performance Standards for total reduced
sulfur from pulp mills are being developed. These should result in
lowered H2S emissions.
EPA recently contracted with NRC's Committee on Medical and Biologic
Effects of Environmental Pollutants to assess the potential environmental
problems of H2S. This study will focus upon effects on man, plants, and
animals, and, in addition, will define control technology and areas
needing additional research.
OSHA has a health standard of 20 ppm as a ceiling level with a
maximum of 50 ppm for 10 minutes once per day only if no other measurable
exposure occurs. NIOSH has scheduled HpS for FY 77 Criteria Document
development. The current American Conference of Governmental Industrial
Hygienists has recommended an 8-hour TWA of 10 ppm to guard only against
conjunctivitis.
-30-
-------
REFERENCES
Annual Catalyst Research Program Report; EPA, Office of Research and
Development (Publication No. EPA-600/3-75-010, September 1975).
Assessment of Catalysts for Control of NOX from Stationary Power Plants,
Phase I, Volume 1 - Final Report; EPA, Office of Research and Development
(Publication No. EPA-650/2-75-001a, January 1975).
R. L. Klimisch, and J. 6. Larson. The Catalytic Chemistry of Nitrogen
Oxides; New York, Plenum Press, (1975).
News Report; National Academy of Sciences,Vol. XXVI (March 1976).
Objectionable Odors from Catalyst-Equipped Vehicles; EPA, Office of Mobile
Source Air Pollution Control (Publication MSAPC fact sheet, FS-35,
February 1976).
-31-
-------
MERCURY (Hg)
Why Should the Chemical Be of Concern at This Time?
Despite recent action by EPA to limit mercury discharges during
sludge incineration and through pesticidal use, and earlier Agency
efforts to control air emissions and liquid effluent discharges, mercury
continues to enter the environment. While more stringent enforcement of
existing regulations should be helpful, discharges of mercury from
fossil fuel plants, especially those that have shifted to coal from
other less contaminated fuels, leaching of mercury from land-disposal
sites, particularly into ground water,-and urban runoff, are among the
currently uncontrolled problems.
What Are the Health and Ecological Effects, and Environmental Behavior?
Hg in many forms is highly toxic to man and other living things. In
terms of toxicity, mercury and its compounds can be divided into three
categories: 1) alkyl mercury compounds; 2) elemental Hg; 3) inorganic Hg
salts and phenyl and methoxy ethyl compounds. Alkyl compounds, particularly
methyl mercury, are the most toxic. Over 90 percent of ingested methyl
mercury is absorbed in the gastrointestinal tract, and its whole-body
biological half life is 70-90 days. Methyl mercury is transported in
blood cells to, and concentrates in, brain and other central nervous
system tissues where it can cause irreversible damage. In addition, it
can cross the placental barrier and cause abnormalities in fetal tissues
and irreversible damage to the fetus at levels that appear to cause no
symptoms in the mother. Elemental mercury, phenyl and methoxy ethyl
compounds, and inorganic mercury salts are far less dangerous than
methyl mercury, because less are ingested and the rates of excretion are
higher.
The FDA action level of 0.5 ppm of Hg for fish and shellfish, both
raw and processed, is based on a 30 ug/day maximum intake of methyl
mercury. This is one tenth of the 300 ug/day average intake resulting
in a blood level of 0.2 ppb in adults, the lowest level at which neurological
symptoms have been observed.
Hg is readily transported to water by leaching from soil and fallout
from air; most forms of Hg soil and water can be biologically or chemically
transformed to methyl mercury.
What Are the Sources, Environmental Levels, and Exposed Populations?
In 1973, United States use of mercury was slightly less than 1900
metric tons, at an estimated cost of $8800 per metric ton. The chief
uses were for battery manufacture (29.9 percent) and chlor-alkali production
(24.1 percent). Use in 1965 had been approximately 2700 metric tons;
the reduction of use resulted largely from a recognition of the hazards
of the substance. In the period 1965 - 1973, several uses (particularly
as preservatives and in gold recovery) were eliminated. Hg is also used
to make paints and industrial instruments.
-33-
-------
NIOSH estimates that 150,000 workers are exposed to mercury.
Because the vapor is colorless and odorless, overexposures can easily go
unnoticed until symptoms appear. Of a total of 1900 metric tons used, it
has been estimated that as much as 80 percent is discharged into the
environment. Distribution of Hg discharges from man-related sources to
the environment is about 31 percent to the air, 6 percent to water, and
36 percent to land. Concentrations in the various media are measured in
terms of total Hg, rather than the more hazardous methyl forms; thus,
the data collected do not represent the true hazard.
Mercury is also a contaminant of coal, and may be a slag runoff
problem. In addition, landfills are a source of leaching Hg; this
problem may be particularly severe in areas where drinking water supplies
are drawn from ground water. Exposure to Hg is widespread, but inadequate
documentation of levels of methyl mercury makes estimates of risk difficult.
What Are the Technologic and Economic Aspects?
Because most mercury losses occur in use and disposal of products,
recycling may provide the best method for reducing environmental discharges
from batteries and instruments. Mercury emissions from the chlor-alkali
industry would still be significant, even if state-of-the-art controls
are applied to the production stream. Diaphram-cell technology could
eliminate mercury emissions, but might add to problems associated with
asbestos and lead. New developments in this technology are reducing use
of lead and eliminating asbestos; thus increased future reliance on new
diaphragm cells may offer the desired reduction in mercury emissions,
without the added environmental burden.
What Steps Have Been Taken, and What Is Being Done?
FDA has proposed an action level for Hg in fish and shellfish. As
a result of NIOSH recommendations, OSHA is considering revised workplace
standards for inorganic and alkyl mercury.
EPA has set a hazardous air pollutant standard for mercury under
section 112 of the Clean Air Act, and is considering New Source Performance
Standards to require zero emissions of Hg from new chlor-alkali plants.
EPA has addressed the problem through effluent guidelines for a few
industrial categories and may expand this coverage in the future. The
National Interim, Primary Drinking Water Standard for Hg is 2 ppb. Ocean
dumping is tightly controlled.
The EPA Administrator recently ordered an end to the registrations
of most pesticides containing Hg, and particularly those used in paints,
although the decision has been stayed pending completion of judicial
review.
-34-
-------
REFERENCES
Clarkson, T. W., "The Transport of Elemental Mercury into Fetal Tissue";
Biolheoncke 21:239 (1972).
Decision of the Administrator on the Cancellation of Pesticides Containing
Mercury (FIFRA Dockets No. 256 et al.) (February 17, 1976).
"Materials Balance and Technology Assessment of Mercury and Its Compounds
on National and Regional Bases"; EPA, Office of Toxic Substances (Publication
No. EPA 560/3-75-007, October 1975).
National Emission Standards for Hazardous Air Pollutants, Asbestos and
Mercury; 39 Federal Register. 38064. (October 25, 1974).
National Emission Standards for Hazardous Air Pollutants: Asbestos and
Mercury (amendments); 40 Federal Register, 48292 (October 14, 1975).
News Item (untitled), Environmental News. February 18, 1976.
News Item (untitled), Toxic Materials News, January 14, 1976.
Notice of Suspension of Mercurial Pesticides for Use on Rice Seeds, in
Laundry, and in Marine Antifoul ing paints; Federal Register, April 6, 1973.
Proposed designations and effluent standards under Sec. 307(a), FWPCA;
Federal Register, December 1973.
Pathological, Chemical and Epidemiological Research About Minamata Disease,
Ten Years After (2nd Year) TR-509-75T^
-35-
-------
PLATINUM (Pt)
Why Should the Chemical Be of Concern at This Time?
EPA research efforts nearing completion indicate that platinum is
more active biologically and toxicologically than previously believed.
It methylates in aqueous media, establishing a previously unrecognized
biotransformation and distribution mechanism. Because platinum complexes
are used as antitumor agents, the potential for carcinogenic activity is
present; tests to clarify this aspect should be completed within several
months. While low levels of emissions of platinum particulate have been
observed from some catalyst-equipped automobiles, the major potential
source of Pt is from the disposal of spent catalysts.
What Are the Health and Ecological Effects, and Environmental Behavior?
Prior to EPA's research efforts, the literature cited platinosis as
the only known adverse health effect. Platinosis is an allergenic re-
spiratory sensitization to the substance, resulting in a severe asthma-
like reaction to low concentrations by sensitized individuals. It is of
particular concern to industrial users of Pt, as 50 percent of the workers
have shown this syndrome; there is no way to predetermine if individuals
are susceptible to it.
Other literature sources indicated that metallic and insoluble
forms of Pt were toxicologically inert. Organic complexes of Pt have
been used on a limited scale as antitumor treatments, sometimes resulting
in toxic effects to the liver.
The health research program has determined the following:
-Metallic Pt and insoluble Pt compounds accumulate in many
animal organ tissues, causing various abnormalities.
-Pt methylates in aqueous systems in much the same fashion
as does mercury, suggesting a similar, but heretofore un-
known, ecosystem transport mechanism for Pt.
-Although Pt is not found in urban or rural air, water,
or soil, autopsies have found it in human fat at low
levels. It has been hypothesized that this phenomenon
may derive from Pt used in dental fillings, thus
establishing that Pt may be soluble in human tissue,
primarily lipid, and possibly by methylation.
-37-
-------
-Pt in automotive exhaust is principally associated with
large particulates coming off the catalyst.
What Are the Sources, Environmental Levels, and Exposed Populations?
Sources of Pt in the United States have been extremely limited,
being principally associated with two Pt refining plants and Pt metal
fabricators for electrical, chemical, refining, dental, jewelry, and
glass industries. Total production and use was about 1.4 million troy
ounces (52 tons) in 1971; the projection for 1981 is 2.7 million troy
ounces (92.5 tons). Recent introduction of the automotive catalytic
converter may result in nationwide exposure to Pt should Pt leach from
discarded catalysts. Each catalyst contains 2-5 grams of Pt. Monitoring
data to date have revealed virtually no Pt in air, water, or soil.
What Are the Technologic and Economic Aspects?
Should the results of current EPA research efforts to document
health hazards of Pt suggest a need to control these exposures, disposal
controls would be the most promising, since catalyst disposal is expected
to be the largest contributor of Pt to the environment. In addition,
the value of the metal would help to offset the cost of reclaiming the
Pt from discarded catalysts. If direct vehicular emissions of Pt are
found to be significant, particulate traps, which are available at
reasonable cost, may provide a technological solution. Other noble
metals have been suggested as Pt substitutes; however, even less is
known about their potential for hazard.
What Steps Have Been Taken, and What Is Being Done?
An extensive health-effects research program is in progress in EPA,
and efforts to characterize platinum in vehicular exhausts are also
underway.
OSHA has established a standard for soluble salts of Pt as 0.002
mg/m3 total Pt, 8-hour TWA. This standard was designed to prevent
development of platinosis in workers exposed to airborne Pt.
-38-
-------
REFERENCES
Annual Catalyst Research Program Report; EPA, Office of Research and
Development (Publication No. EPA-650/3-75-010, September 1975).
Brubaker, P. E., et al., "Noble Metals: A Toxicological Appraisal of
Potential New Environmental Contaminants;" Environmental Health Perspective
Vol. 10 (1975).
Duffield, F. V. P., et al., "Determination of Human Body Burden Baseline
Data of Platinum through Autopsy Tissue Analysis;" EPA, Office of Research
and Development (accepted for publication in Environmental Health Perspectives,
March 1976).
A Literature Search and Analysis of Information Regarding Sources, Uses,
Production, Comsumption, Reported Medical Cases, and Toxicology of Platinum
and Palladium; EPA, Office of Research and Development (publication no.
EPA 650/1-74-008, April 1974).
Occupational Safety and Health Standards: Subpart Z - Toxic and Hazardous
Substances.29 CFR 1910.1000, Table Z-l.
-39-
-------
POLYBROMIMATED BIPHENYLS (PBB's)
Why Should the Chemical Be of Concern at This Time?
In 1973, one to two tons of PBB's, a highly toxic flame retardant, were
accidentally mixed into an animal feed supplement and fed to cattle in Michigan.
Contamination also resulted from traces of PBB's being discharged into the environ-
ment at the manufacturing site and at other facilities involved in handling PBB's.
Approximately 250 dairy and 500 cattle farms have been quarantined, tens of
thousands of swine and cattle and more than one million chickens have been
destroyed, and law suits involving hundreds of millions of dollars have been
instituted. Before the nature of the contamination was recognized, many of the
contaminated animals had been slaughtered, marketed, and eaten, and eggs and milk
of the contaminated animals also consumed. Thus, large numbers of people have been
exposed to PBB's. While commercial manufacture and distribution of PBB's have
currently ceased, the full extent of the problem has not yet been assessed.
What Are the Health and Ecological Effects, and Environmental Behavior?
Among the 10,000 people who have been identified as having consumed PBB-
contaminated meat, milk products, poultry, and eggs, no overt symptoms have been
reported to date. Health effects can only be extrapolated from animal data.
Based on experimental data, PBB's may be much more toxic than PCB's.
Although no long term toxicity data are available, short term rat, mice,
and cattle studies have shown that PBB's may interfere with reproduction and
liver functions, promote nervous disorders, and react as a teratogenic agent in
tissues. PBB's have produced pathological changes in the livers of rats, mice,
guinea pigs, cows, and rabbits. In an experiment with guinea pigs, the chemical was
demonstrated to be an immuno-suppressant agent. About 400 cows in herds fed
contaminated feed for about 16 days exhibited anorexia, decreased milk production,
increased frequency of urination, some lameness, abnormal hoof growth, and shrinking
of the udder. Later signs of toxic effects included bloody blebs, malformed or dead
fetuses, abscesses, weight loss, and high susceptibility to stress. Non-1actating
cows died within six months while the lactating animals survived and gradually
improved. Massive liver abscesses were found in dead animals.
Fish taken from streams known to have been contaminated by PBB's have
demonstrated that PBB's can bioaccumulate 20,000 to 30,000 times the ambient levels.
PBB's are believed to be quite persistent in the environment, with perhaps one-half
the lifetime of PCB's. PBB's readily vaporize.
What Are the Sources, Environmental Levels, and Exposed Populations?
PBB's have been used commercially as flame retardant additives in synthetic
fibers and molded thermoplastic parts. PBB's have been incorporated into the plastic
housings of many commercial products, such as typewriters, calculators, and microfilm
readers, and consumer products, such as radio and television parts, thermostats,
shavers, and hand tools.
Michigan Chemical Corporation produced approximately 11 million pounds of PBB's
from 1970 to 1974. The White Chemical Corporation produced approximately 100,000
pounds of the closely related compounds, octabromobiphenyl and decabromobiphenyl, from
-41-
-------
1970 through 1973. In addition nine companies have been suppliers of laboratory
quantities of PBB's, each producing about five pounds per year. There is no indication
of importation of the material.
Monitoring in the Pine River near the facility where PBB's were produced
indicated that levels diminished from 3.2 ppb in the ambient stream near the effluent
discharge to .01 ppb eight miles downstream. Fish obtained in this eight miles
stretch had levels of .09 to 1.33 ppm.
Detailed data are available on PBB levels found in cattle and hogs, with the
highest level detected being 2.27 ppm. Data are not yet available on the levels
found in any of the 10,000 or more exposed persons.
What Are the Technological and Economic Aspects?
Michigan Chemical Corporation reportedly has paid $20 million in settling
a $270 million suit, with claims of.$500 million still outstanding. However,
the financial dimensions of the incident are still not known.
Among the substitutes for PBB's are the more expensive decabromobiphenyl oxide
and several halogenated aliphatic compounds. However, the environmental acceptability
of these compounds has not been assessed.
Monitoring methods for PBB's are in the developmental stage. Air monitoring
has not yet been attempted.
What Steps Have Been Taken and What Is Being Done?
The State of Michigan has been the focal point for responding to the
contamination incident. In addition, USDA, HEW (including FDA, NCI, and CDC), EPA,
Michigan State University, and the University of Michigan support a wide array
of epidemiological, toxicological, analytical, and related projects to clarify the
effects of PBB's on humans and animals and to assess the extent of contamination. The
HEW Toxicology Coordinating Committee is preparing a synthesis of available health
effects information and will issue a report by June 1975. EPA is providing assistance
in monitoring environmental levels of PBB's.
FDA has set temporary action levels for PBB's in contaminated foods and in animal
feed. The State of Michigan has issued warnings to sport fishermen along the Pine
River.
-42-
-------
REFERENCES
1. Survey of Industrial Processing Data, Task II - Pollution Potential
of Polybrominated Biphenyls; EPA 560/3-75-004, NTIS PB 243-690,
Prepared by Midwest Research Institute, June 1975.
2. Hesse, John L., Water Pollution Aspects of Polybrominated Biphenyls
Production: Results of Initial Surveys in thePine River in Vicinity
of St. Louis, Michigan, Presentation to the Governor's Great Lakes
Regional Interdisciplinary Pesticide Council, October 17, 1974.
3. "Michigan's PBB incident: Chemical Mix-up Leads to Disaster,"
Science, April 16, 1976.
4. The Contamination Crisis in Michigan, Polybrominated Biphenyls.
A report from the Michigan State Senate Special Investigating
Committee, July 1975.
5. Head, James D., A Case Study: Polybrominated Biphenyls, National
Academy of Sciences, 1975.
-43-
-------
POLYNUCLEAR AROMATIC HYDROCARBONS (PNA'S)
Why Should the Chemicals Be of Concern at This Time?
Increased exposure to polynuclear aromatic hydrocarbons (PNA's) and other air
pollutants has been implicated by some researchers in increased rates of cancer,
especially of the lung. Over 30 PNA's have been identified as urban air pollutants,
including several carcinogens. PNA's are emitted during fossil fuel combustion, in
natural combustion processes, and as a result of a variety of human activities. A
proposed amendment to the Clean Air Act calls for explicit attention by 1977 to a
possible air standard for PNA. PNA's have been found at low levels in liquid ef-
fluents, some drinking water supplies, and food.
What Are the Health and Ecological Effects, and Environmental Behavior?
Certain PNA's which have been demonstrated as carcinogenic in test animals at
relatively high exposure levels are being found in urban air at very low levels.
Various environmental fate tests suggest that PNA's are photo-oxidized, and react
with oxidants and oxides of sulfur. Because PNA's are adsorbed on particulate
matter, chemical half-lives may vary greatly, from a matter of a few hours to several
days. One researcher reports that photo-oxidized PNA fractions of air extracts also
appear to be carcinogenic. Environmental behavior/fate data have not been developed
for the class as a whole.
It has been observed that PNA's are highly soluble in adipose tissue and lipids.
Most of the PNA's taken in by mammals are oxidized and the metabolites excreted.
Effects of that portion remaining in the body at low levels have not been documented.
Benzo[a]pyrene (BaP), one of the most commonly found and hazardous of the PNA's
has been the subject of a variety of toxicological tests, which have been summarized
by the International Agency for Research on Cancer. 50-100 ppm administered in the
diet for 122-197 days produced stomach tumors in 70 percent of the mice studied. 250
ppm produced tumors in the forestomach of 100 percent of the mice after 30 days. A
single oral administration of 100 mg to nine rats produced mammary tumors in eight of
them. Skin cancers have been induced in a variety of animals at very low levels, and
using a variety of solvents (length of application was not specified). Lung cancer
developed in 2 of 21 rats exposed to 10 mg/m3 BaP and 3.5 ppm S02 for 1 nour per/day,
five days a week, for more than one year. Five of 21 rats receiving 10 ppm S02 for 6
hr/day, in addition to the foregoing dosage, developed similar carcinomas. No car-
cinomas were noted in rats receiving only SO^. No animals were exposed only to BaP.
Transplacental migration of BaP has been demonstrated in mice. Most other PNA's have
not been subjected to such testing.
What Are the Sources, Environmental Levels, and Exposed Population?
PNA's can be formed in any hydrocarbon combustion process and may be released
from oil spills. The less efficient the combustion process, the higher the PNA
emission factor is likely to be. The major sources are stationary sources, such as
heat and power generation, refuse burning, industrial activity, such as coke ovens,
and coal refuse heaps.- While PNA's can be formed naturally (lightning-ignited forest
fires), impact of these sources appears to be minimal. It should be noted, however,
that while transportation sources account for only about one percent of emitted PNA's
iOn a national inventory basis, transportation-generated PNA's may approach 50 percent
of the urban resident exposures.
-45-
-------
Diesel powered vehicles produce more participate emissions than gasoline powered;
the nature of the fuel is such that the emissions would be expected to contain greater
amounts of PNA's, and limited studies have confirmed this. EPA has tested gasoline-
powered passenger vehicles to determine the amount of PNA's in the exhaust. However,
this characterization is of particulate-associated PNA's; little is known of vaporous
components.
PNA's have been detected in urban water supplies at low levels. PNA's in water
and soils are adsorbed on minerals or organic particulate matter. Algae and inverte-
brates contain concentrations as high as 200 times those of the surrounding waters.
Levels detected in plants, on the other hand, are slightly lower than soil levels.
Sludge samples taken near a steel refinery showed combined benzo[ej- and benzo[ajpyrene
levels of 0.91-19.0 mg/kg (dried weight). Liquid effluents did not appear to contain
these substances.
Although a variety of PNA's have been observed in particulates from urban air
samples, these are not now routinely monitored. Atmospheric concentrations of PNA's
are generally represented by measurements of Benzo|_a]pyrene (BaP) concentrations. In
heavily industrialized areas, BaP levels have been as high as 20 nanograms (ng)/m3.
Urban BaP levels are generally 2-7 ng/m3; and rural, 0.3 ng/m3. In 1971-73, nationwide
annual emissions of BaP were estimated at 900 tons. It has been estimated that BaP
represents 2-5 percent of the total PNA's emitted from automobiles; a similar and as
yet undetermined relationship may exist for stationary source emissions.
Because of the large number of sources, most people are exposed to very low
levels of PNA's. BaP has been detected in a variety of foods throughout the world.
A possible source is mineral oils and petroleum waxes used in food containers and as
release agents for food containers. FDA's studies have indicated no health hazard
from these sources.
What Are the Technologic and Economic Aspects?
Good particulate emission controls can substantially reduce PNA emissions.
However, the costs that would be incurred in further limiting PNA emissions from
stationary and vehicular combustion sources are not known. The application of
oxidation catalyst exhaust treatment has been effective in dramatically reducing PNA
emissions from automobiles when such systems are operating properly. Similar controls
at stationary sources may have a similar effect.
What Steps Have Been Taken, and What Is Being Done?
Limitation of carbon monoxide and hydrocarbon emissions from motor vehicles have
simultaneously and dramatically reduced PNA emissions. A 1974 analysis of stationary
source problems concluded that control regulations designed specifically for BaP or
PNA were not warranted or practical, but noted that compliance with existing regulations
for incinerators, open burning, coal combustion, and coking operations could signifi-
cantly reduce PNA emissions. Additional efforts to document stationary source emissions,
atmospheric chemistry, and human exposure have been initiated on a limited scale.
EPA's STAR document and an NAS report for EPA have detailed much of the hazard and
technologic aspects of this class of compounds.
-46-
-------
REFERENCES
Begeman, C. R., and Colucci, J. M-. Polynuclear Aromatic Hydrocarbon Emissions
from Automotive Engines; Warrendale, PA, Society of Automotive Engineers, Inc.
(Publication No. 700469, 1971).
Gross, Herbert, Hexane Extractables and PAH in the Black River (Ohio); EPA,
Office of Enforcement and General Counsel (October 1974).
IARC Monographs on the Evaluation of Carcinogenic Risk of the Chemical to Man:
Certain Polycyclic Aromatic Hydrocarbons and Heterocyclic Compounds (Volume 3);
Lyon, International Agency for Research on Cancer (1973).
Moran, J. B., Assuring Public Health Protection as a Result of the Mobile Source
Emission Control Program; Warrendale, PA, Society of Automotive Engineers, Inc.
(Publication No. 740285, March 1974).
Moran, J. B., Lead in Gasoline: Impact of Removal on Current and Future
Automotive Emissions; for the Air Pollution Control Association (APCA)(June 1974)
Moran, J. B., Colucci, A., and Finklea, J. F., Projected Changes in Polynuclear
Aromatic Hydrocarbon Exposures from Exhaust and Tire Wear Debris of Light Duty
Motor VehicTislInternal Report, ERC - RTP (May 1974).
Particulate Polycyclic Organic Matter; National Academy of Sciences (1972).
Preferred Standards Path Report for Polycyclic Organic Matter; EPA, Office of
Air Quality Planning and Standards (October 1974)7
Scientific and Technical Assessment Review of Particulate Polycyclic Organic
Matter; EPA, Office of Research and Development, (1975).
-47-
-------
TRICHLOROETHYLENE
Why Should the Chemical Be of Concern at This Time?
Trichloroethylene (commonly referred to as tri), has been identified
by NCI as a carcinogen in laboratory animals. It is widely used for
vapor degreasing of fabricated metals and, to a lesser extent, in cleaning
fluids. In addition to extensive worker exposure, tri has been detected
in ambient air and water in industrial areas, in food, and in human
tissues.
What Are the Health and Ecological Effects, and Environmental Behavior?
Tri induces tumors irr mice at high dose levels, predominantly liver
cancer with some metastases (transfer) to the lungs, according to NCI.
Tri is absorbed rapidly by the lungs; only a small amount is eliminated
by exhalation, 58-70% being retained. This is slowly eliminated in the
urine as trichloroacetic acid (TCA) or trichloroethanol. The first
major review of tri poisoning studied 284 cases, including 26 fatalities,
in European plants where tri vapors were inhaled. Results indicated
that toxic action involves the central nervous system. A number of
short-term studies indicate that exposure to a concentration of 100 ppm
in air may interfere with psychophysiological efficiency. In one study,
six students exposed to 110 ppm for two four-hour periods separated by
1-1/2 hours showed significantly lower levels of performance in perception,
memory, and manual dexterity tests. A confirmatory test using six tri
workers produced almost identical results. There is a reported case of
a man operating a metal degreaser who lost his sense of taste after one
month's exposure to concentrations of tri which "occasionally escaped in
sufficient quantities to be visible". Two months later he lost facial
mobility and sensation, and developed EE6 changes which did not clear up
during the following two years.
Tri has been frequently detected in the environment; however, the
behavior and transport have not been documented. Adverse ecological
effects have not been reported.
Because of its low solubility, high vapor pressure, and high photode-
gradation rate at sea level (half life in air is about eight hours), tri
is not expected to accumulate in the atmosphere. Its half life in water
is on the order of months.
What Are the Sources, Environmental Levels, and Exposed Population?
Domestic tri production in 1974 was about 215,000 tons by five
producers. Over 90% is used for vapor degreasing of fabricated metals.
Ambient concentrations in the atmosphere of industrialized areas have
been estimated by industry to be 2-16 ppt. Water concentrations are
about 0.1 ppt. .The character of the water was not defined, but trace
amounts of tri have been identified in drinking water by EPA.
-49-
-------
Over 200,000 workers are exposed to tri. The general public is
exposed via inhalation of cleaning fluids and ingestion of foods, spices,
and medicines from which undesirable components have been removed by
extraction with tri. Residues ranging from 0.02 to 22 ppt have been
detected In foodstuffs, and concentrations of up to 32 ppt have been
detected in human tissue.
There is only one reference to degreasing equipment which concerns
control of vapor emissions. In those cases where both an exhaust system
and a degreaser vapor condensation system were in use, the average
concentration of tri in air near the operation dropped from 105 ppm to
30 ppm.
What Are the Technologic and Economic Aspects?
Both methyl chloroform and perchloroethylene should be considered
as possible substitutes for tri as degreasing agents. Both appear less
damaging to air quality. However, methyl chloroform may adversely
impact the ozone layer. All three are comparably priced and, since many
users have already made this change, the economic impact should be
minor. Closed loop systems could permit recovery of tri; however, this
may represent a higher cost factor than use of substitutes. Preliminary
NCI studies indicate that perchloroethylene may also present health
hazards.
What Steps Have Been Taken, and What Is Being Done?
In October 1975, OSHA proposed a reduction in the workplace standard,
and is currently reviewing the proposal, together with possible standards
for methyl chloroform and perchloroethylene. CPSC is preparing a monograph
on consumer exposures and possible hazards.
Tri producers are undertaking epidemiological studies, long-term
animal studies, long-term animal inhalation studies, and an in-depth
literature survey which have recently been started for the Manufacturing
Chemists Association.
Since trichloroethylene contributes to photochemical smog, State
Implementation Plans provide a mechanism for limiting emissions. Detailed
health, environmental, and economic analyses are planned. NPDES permits
limiting 8005, COD, and suspended solids also provide some control over
effluent discharges of tri.
-50-
-------
REFERENCES
Air Pollution Assessment of Trichloroethylene; EPA, Office of Air Quality
Planning and Standards (September, 1975, Draft).
Criteria Document: Occupational Exposure to Trichloroethylene; HEW, National
Institute for Occupational Safety and Health (June 1973).
Memorandum of Alert: trichloroethylene; HEW, National Cancer Institute
(March 21, 1975).
Mitchell, A. B. S., and Parsons-Smith, B. G., "Trichloroethylene Neuropathy";
Br. Med. J.. 1:422-23 (1969).
News item (untitled), Chemical and Engineering News (May 19, 1975).
Preliminary Study of Selected Potential Environmental Contaminants -- Optical
Brighteners, Methyl Chloroform, Trichloroethylene. Tetrachloroethylene. Ion
Exchange Resins; EPA, Office of Toxic Substances (Publication No EPA-560/2-
75-002, July 1975).
Stuber, K., "Injuries to Health in the Industrial Use of Trichloroethylene and
the Possibility of Their Prevention," Arch Gewerbepathol Gewerbehyg (Ger.)
2:398-456 (1932).
Trichloroethylene (Background Report); HEW, National Institute for Occupational
Safety and Health (June 6, 1975).
Trichloroethy1ene (data sheet 389) (revised); Chicago, National Safety Council
(1964).
-51-
-------
TRIS (2,3-DIBROMOPROPYL) PHOSPHATE (TBPP)
Why Should the Chemical Be of Concern at This Time?
TBPP is presently the most popular flame retardant additive for
acetate and polyester fabrics which are widely used in children's sleepwear.
Recent EPA-funded experiments have shown that TBPP is a mutagen in a
microbial assay that is also being considered for use as a screen for
carcinogenic potential. Crude experiments have suggested that TBPP is
present in the waste water from home laundry of such sleepwear. The
Environmental Defense Fund recently requested the Consumer Product
Safety Commission (CPSC) to take steps to reduce the hazards associated
with TBPP and Ralph Nader has asked the Senate Commerce Committee to
hold hearings. Both CBS and NBC have raised the issue of continuing use
of TBPP in their National news coverage.
What Are the Health and Ecological Effects, and Environmental Behavior?
TBPP is mutagenic in the "Ames bioassay" which is regarded by some
toxicologists as a screen for carcinogens. This has been confirmed by
two independent investigators.
In feeding experiments, dose-related accumulations of TBPP, or its
metabolites, were found in rats given 100 to 1000 ppm for 28 days. Six
weeks after withdrawal, no residues were found and no histopathology was
detected. A degradation product (2,3-dibromopropanol) was found in the
urine of rats after oral administration or dermal exposure, indicating
that TBPP reaches a number of organs.
Laboratory experiments have shown that aqueous extracts of fabrics
containing TBPP at extremely low levels are lethal to fish even after
the fabric had been laundered. Erratic behavior, possibly resulting
from central nervous system involvement, was noted before death. Full
confirmation of these findings has not yet been performed. Environmental
biodegradation occurs, but the rate is not known.
TBPP is also a mild sensitizing agent in humans. However, no
allergic responses have been reported from consumer or occupational
exposure.
What Are the Sources. Environmental Levels, and Exposed Populations?
About 65% of the 10 million pounds of TBPP produced annually in the
United States by six manufacturers are applied to fabrics used for
children's clothing, with the remainder used as a flame retardant in
other materials, such as urethane foams. A significant portion of the
total, perhaps ten percent, reaches the environment from textile finishing
plants and laundries. Most of the rest will eventually find its way
into solid wastes (manufacturing waste and used clothing). Environmental
levels of TBPP near manufacturing plants, dumps, mills, and laundries
have not been measured.
TBPP is added to fabrics used for children's garments to the extent
of 5-10 percent by weight. A child wearing such a garment and chewing
on a sleeve or collar could easily ingest some TBPP, particularly if the
-53-
-------
garment had not been laundered before use. The effects of saliva,
urine, or feces on the extractabi.lity of TBPP or on its absorption
through the skin have not been measured.
What Are the Technologic and Economic Aspects?
At current production levels, TBPP gross sales are about 10 million
dollars per year. Substitute materials or methods for meeting the
flammability requirements for children's sleepwear are probably available.
However, quantitative data on the cost, performance, and safety of
substitute materials and methods are not available. The major costs
would be in the product development and application areas.
What Steps Have Been Taken, and What Is Being Done?
The mutagenicity of TBPP was originally discovered in a small EPA
screening program. The limited available data on the environmental
effects of TBPP have been compiled and transmitted to the Consumer
Product Safety Commission, the National Institute for Occupational
Safety and Health, the Toxicology Coordinating Committee of the Department
of Health, Education, and Welfare, the NAS committee on the Fire Safety
Aspects of Polymeric Materials, and several other groups concerned with
flame retardants, including some TBPP manufacturers and users. The
National Cancer Institute is currently conducting carcinogenicity tests
on TBPP in rats and mice; results are expected in early 1977.
-54-
-------
REFERENCES
Harris, Robert H., and Manser, Philip J., Petition Pursuant to 15 USC
2059 to the Consumer Product Safety Commission to Commence a Proceeding
for the Issuance of a Consumer Product Safety Rule; Washington,
Environmental Defense Fund (March 24, 1976).
Nader, Ralph, Letter to Chairman, Senate Commerce Committee (undated)
(Copy received by Consumer Product Safety Commission March 25, 1976).
Prival, Michael J., Information Available to Date Relevant to the
Mutagenicity of Tris (2.3-dibromopropyl) Phosphate; EPA, Office of.Toxic
Substances (internal memorandum December 2, 1975).
A Study of Flame Retardants for Textiles; EPA, Office of Toxic Substances
(Report No. EPA-560/1-76-004, December 31, 1975).
-55-
-------
VINYLIDENE CHLORIDE (VDC)
Why Should the Chemical Be of Concern at This Time?
Vinylidene chloride (VDC), an important monomer in the manufacture
of methyl chloroform and of Saran and other plastics, is of particular
concern because the manner in which the problem is emerging is similar
to earlier developments concerning vinyl chloride. In January 1976,
NIOSH reported that about 60 percent of examined workers in a New Jersey
plant using VDC had developed liver disorders, and announced its intention
to follow up. Previous laboratory animal studies had suggested that VDC
might be a liver carcinogen, as well as produce a number of other adverse
health effects. A substantial amount of VDC is vented to the atmosphere
during production, polymerization, and fabrication.
What Are the Health and Ecological Effects, and Environmental Behavior?
Vinylidene chloride has recently been reported to cause liver
impairment. Twenty-seven of forty-six workers examined at the BASF
Wyandotte VDC polymerization plant in South Kearny, New Jersey, showed
50 percent or greater loss in liver function. Other examinations
indicate that VDC is biochemically altered in the body and may form
intermediates similar to the cancer-producing metabolites of vinyl
chloride.
Inhaled VDC is reported to produce liver tumors in rats at 200 ppm.
Inhalation experiments with animals showed that VDC causes liver and
kidney damage. When rats were pre-exposed to vinyl chloride and then
tested with VDC, the acute toxicity of VDC was greatly enhanced. Concurrent
exposure reduces the acute effects and may potentiate the carcinogenic
effects. This is important because a significant part of polymer production
involves the use of both chemicals.
As yet, the ecological effects and environmental behavior of VDC in
either air or water have not been studied. Its highly reactive nature
would seem to support a thesis that it is relatively short-lived in air,
possibly on the order of several hours.
What Are the Sources, Environmental Levels, and Exposed Populations?
Dow Chemical and PPG Industries annually produce 270 million pounds
of VDC monomer in three Gulf Coast plants. About 50 percent is used in
the production of methyl chloroform by PPG. The remainder is polymerized
to plastic resins at 12 facilities owned by a number of companies throughout
the country. The resin is then fabricated into plastics at 60 to 75
plants. It has been estimated that about four million pounds of VDC
were lost to the air in 1974. One EPA-funded report estimates that as
much as 25 percent of the VDC used in any given Saran production run is
disposed of in landfill, primarily in polymerized form, but there are no
estimates of the levels of unreacted monomer.
-57-
-------
In the past, worker exposure has generally not been monitored.
Tests demonstrate that 20,000 ppm can easily be attained in the immediate
vicinity of a spill. In some cases, past worker exposures to VDC may
have exceeded those to vinyl chloride (which were measured at 300-1000
ppm before OSHA limits were imposed). The odor threshold of VDC is 500
ppm.
What Are the Technologic and Economic Aspects?
The primary requirement for reduction of exposure to VDC would be
to limit emissions through improved housekeeping procedures in the
industry. The type of control technology used to control vinyl chloride
should be applicable to VDC production.
What Steps Have Been Taken, and What Is Being Done?
The American Conference of Governmental Industrial Hygienists has
established a threshold limit value of 10 ppm.
NIOSH is planning to monitor the follow-up studies on workers at
the South Kearny BASF plant and will survey other VDC production sites
in 1977 to determine if a workplace standard should be recommended.
EPA is preparing an assessment of the air pollution problems associated
with VDC production and use. Fetotoxicity and embryotoxicity have been
demonstrated under EPA-funded contracts. Data on environmental effects
of VDC are also being obtained.
-58-
-------
REFERENCES
Air Pollution Assessment Report: Vinylidene Chloride; EPA, Office of Air
Quality Planning and Standards (Prepared under contract) (Report to be published
June 1976).
Jaeger, R. J., Trabulus, M. J., and Murphy, S. D., "Biochemical Effects of
1,1-Dichloroethylene in Rats: Dissociation of its Hepatotoxicity from a
Liperoxidative Mechanism;" Toxicology and Applied Pharmacology, 24:457-567
(1973).
The Merck Index. 8th edition; Rahway, NJ, Merck and Co., Inc. (1968).
Prendergast, J. A., Jones, R. A., Jenkins, L. J., Jr., and Siegel, J., "Effects
on Experimental Animals of Long-Term Inhalation of Trichloroethylene, Carbon
Tetrachloride, 1,1,-Trichloroethane, Dichlorofluoromethane and 1,1-Dichloro-
ethylene"; Toxicology and Applied Pharmacology, 10:270-289 (1967).
Vinylidene Chloride Monomer Emissions from the Monomer, Polymer, and Polymer
Processing Industries; EPA, Office of Air Quality Planning and Standards
(Prepared under contract #68-02-1332, Task 13) {Report.to.be published April
1976).
Wessling, R., and Edwards, F. 6., "Poly (Vinylidene Chloride)," Kirk-Othmer
Encyclopedia of Chemical Technology, 2nd edition, (21:275-303); New York,
Interscience Publishers (1967).
-59-
-------
TECHNICAL REPORT DATA
(Please read Instructions on the reverse before completing}
1. REPORT NO.
EPA 560/4-76-004
3. RECIPIENT'S ACCESSION* NO.
4. TITLE AND SUBTITLE
5. REPORT DATE
April 1976
Summary Characterizations of Selected Chemicals of
Near-Term Interest
6. PERFORMING ORGANIZATION CODE
7. AUTHOR(S)
8. PERFORMING ORGANIZATION REPORT NO
Office of Toxic Substances
9. PERFORMING ORGANIZATION NAME AND ADDRESS
U.S. Environmental Protection Agency
Office of Toxic Substances
401 "M" Street, SW
Washington, DC 20460
10. PROGRAM ELEMENT NO.
11. CONTRACT/GRANT NO.
12. SPONSORING AGENCY NAME AND ADDRESS
U.S. Environmental Protection Agency
Office of Toxic Substances
401 "M" Street, SW
Washington, DC 20460
13. TYPE OF REPORT AND PERIOD COVERED
Final
14. SPONSORING AGENCY CODE
15. SUPPLEMENTARY NOTES
16. ABSTRACT
This report includes summary characterizations of 15 chemicals of near-term
concern to EPA. The report summarizes (a) health and ecological effects and
environmental behavior, (b) sources, environmental levels and exposed populations,
(c) technologic and economic aspects and (d) steps that have been taken and are
being taken.
17.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
b.lDENTIFIERS/OPEN ENDED TERMS
c. COSATI Field/Group
Arsenic, Asbestos, Benzene, Benzidine,
Cadmium, Ethylene Dibromide, Hexachloro-
benzene, Hydrogen Sulfide, Mercury,
Platinum, Polybrominated Biphenyls,
Polynuclear Aromatic Hydrocarbons, Tri-
chloroethylene, Tris (2,3-dibromopropyl)
Phosphate, Vinylidene Chloride
13. DISTRIBUTION STATEMENT
Release Unlimited
19. SECURITY CLASS (This Report)
Unclassified
21. NO. OF PAGES
65
20. SECURITY CLASS (Thispage)
Unclassified
22. PRICE
EPA Form 2220-1 (9-73)
------- |