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OCR for page 67
IV
Toxicity of
Selected Drinking
Water Contaminants
CHEMICALS EVALUATED
the health effects of a large number of contaminants found in drinking
water were evaluated in Drinking Water and Health (National Academy
of Sciences, 19771.
The compounds evaluated in this chapter were selected for the
following reasons:
1. Sufficient new data have become available to justify further
attention to several chemicals examined in the first study.
2. New contaminants have been identified in drinking water subse-
quent to the first study.
3. Several compounds were judged to be of concern because of
potential spill situations.
4. The chlorination of drinking water or the use of other disinfectants
yields compounds that require toxicological evaluation. A list of such
compounds was prepared by the Safe Drinking Water Subcommittee on
Chemistry of Disinfectants and Products. They are evaluated in this
chapter by the Subcommittee on Toxicology.
The 1977 study (National Academy of Sciences, 1977) examined the
radioactive, particulate, and chemical contaminants found in drinking
67
OCR for page 68
68 DRINKING WATER AND H"LTH
water. Radioactive contaminants are not considered in this study.
Asbestos was one of the particulates examined in the first study. A
reevaluation of this contaminant will be justified when the several studies
now underway are completed. The number of volatile organic com-
pounds identified in drinking water supplies has increased from
approximately 300 at the time of the first study to 700 at the present time
and will continue to grow. Limitations of time, manpower, and scientific
information have not permitted an in-depth evaluation of most of the
compounds recently found in drinking water. It was the belief of this
subcommittee that it could perform a more valuable service to the
Environmental Protection Agency (EPA) in the future if it evaluated
criteria documents that were prepared by the EPA or other groups
contracted to conduct these tasks. It will be necessary for the EPA to
develop a mechanism for a comprehensive search and review of the
literature in order to make in-depth hazard assessments for these
chemicals. It is the consensus of this subcommittee that this cannot be
done appropriately by the National Academy of Sciences because time
and staff requirements far exceed those available. Neither can it be
expected that the scientists who donate their services on these subcom-
mittees will have the resources or time to carry out the routine aspects of
this task.
ACUTE EXPOSURES
In addition to providing
information on chronic toxicity, the subcommit-
tee has evaluated the potential acute toxicity insofar as justified by the
available data. These data will provide a basis for making judgments of
possible health erects resulting from accidental spills of chemicals into
drinking water supplies. To this end the subcommittee has provided a
suggested no-adverse-response level (SNARL) for acute exposures of 24
hr or 7 days. These values are calculated based on the assumption that
100% of the exposure to the chemical was supplied by drinking water
during either the 24-hr or 7-day period. In those few cases where the
chemical is a known or suspected carcinogen' the potential for
carcinogenicity after an acute exposure has not been considered These
acute SNARL's were calculated only when there was human exposure
data or sublethal animal data. LD50's were not used as a basis for
calculation. Some 7-day values were derived by dividing the 2=hr
SNARL by 7, but only when the data were very good. The converse was
OCR for page 69
Toxicity of Selected Drinking Water Contaminants 69
not done nor were data obtained from studies of lifetime exposures used
to establish acute SNARL's. In some cases in which data from inhalation
exposures were used there was information on absorption/retention. The
details concerning retention and absorption are given in the monographs
for each chemical. It must be emphasized that these calculated acute
SNARL's should not be used to estimate hazard from exposures
exceeding 7 days. They are not a guarantee of absolute safety.
Furthermore, SNARL's are based on exposure to a single agent and do
not take into account possible interactions with other contaminants. In
all cases the safety or uncertainty factor used in the calculations of the
SNARL's reflect the degree of confidence regarding the data as well as
the combined judgment of the subcommittee members.
As in the previous report, the following assumptions were used when
assigning an uncertainty factor to calculate either the acute or chronic
SNARL's:
· An uncertainty (safety) factor of 10 was used when good chronic or
acute human exposure data were available and supported by chronic or
acute data in other species.
· A factor of 100 was used when good chronic or acute toxicity data
were available for one or more species.
· A factor of 1,000 was used when the acute or chronic toxicity data
were limited or incomplete.
CHRONIC EXPOSURES
When the chemical of concern was not a known or suspected carcinogen,
the subcommittee calculated a SNARL for chronic exposure. In most
cases, whenever chronic SNARLS's were estimated, data were available
from studies lasting a major portion of the lifetime of the experimental
animal. For these SNARL's an arbitrary assumption was made that 20~o
of the intake of the chemical of concern was from drinking water.
Because of this assumption it would be inappropriate to use these values
as though they were maximum contaminant intakes. A risk estimate
rather than a chronic exposure SNARL was provided in those cases in
which there was adequate evidence of carcinogenicity [see Drinking
Water and Health (National Academy of Sciences, 1977) for details].
Table IV-1 summarizes the acute and chronic SNARL's as well as the
carcinogenic risk estimates for the chemicals reviewed in this report.
OCR for page 70
70 DRINKING WATER AND H"LTH
TABLE IV- ~ Summation of Acute and Chronic Exposure Levels and
Carcinogenic Risk Estimates for Chemicals Reviewed
Suggested No-Adverse-Response Upper 95%
Level (SNARL), mg/liter, Confidence
by Exposure Perioda Estimate of
Lifetime Cancer
Chemical24-hour 7-day Chronic Risk per,ug/literb
Acrylonitrile1.3 x 10-6
Benzene 1 2.6
Benzene hexachloride3.5 0.5
Cadmium 0~08 0.005
Carbon tetrachloride14 2.0
Dichloro
difluoromethane350 5.6
1,2-Dichloroethane7.0 x 10-7
Epichlorohydrin0.84 0.53
Ethylene dibromide9.1 x 10-6
Methylene chloride35 5.0
Polychlorinated
biphenyl0.35 0.05
Tetrachloroethylene172 24.5 1.4 x 10-7
1, 1,1-Trichloroethane490 70 3.8
Trichloroethylene
TrichloroQuoromethane
Toluene
Uranium
Xylenes
Bromide
Catechol
Chlorine dioxide
Chlorite
Chloroform
Oi bromochloromet inane
2,4-Dichlorophenol
Hexachlorobenzene
Iodide
Resorcinol
105 15
88 8
420 35 0.34
3.5 0.21
21 11.2
1,400 224 2.3
2.2
22
18
115.5
11.7
0.38
0.21
3.2
0.03
16.5
0.5
0.7
1.19
2.9 x 10-5
a See text for details on individual compounds.
b See Drinking Water and Health (National Academy of Sciences, 1977) for details.
OCR for page 71
Toxicity of Selected Drinking Water Contaminants 71
CHEMICALS SELECTED BY EPA
Acrylonitrile (CH2=CHCN)
Acrylonitrile is an unsaturated synthetic organic compound that has a
variety of applications. Primarily it is used in the production of acrylic
and modacrylic fibers, nitrite rubber, and plastics. As a pot nt, highly
effective fumigant it is used most often to protect grain, dried fruit,
walnuts, and tobacco against insect pests. Annual production totals
approximately 682 million kg (U.S. Environmental Protection Agency,
1 978a).
Acrylonitrile, also known as 2-propenenitrile, vinyl cyanide, and
cyanoethylene, is a colorless, highly flammable liquid with a mild,
pungent odor resembling that of peach pits. It is manufactured by the
reaction of propylene with ammonia in air. Its boiling point is 77.3°C. At
20°C its solubility in water is 7.35 g/100 ml, and the specific gravity of
the liquid is 0.811 (Manufacturing Chemists Association, 19741.
The principal exposure of humans to acrylonitrile is likely to occur
through atmospheric contamination. Patterson et al. (1976) estimated
that the total emission from manufacturing processes in 1974 was 14
million kg. There is relatively little information on the movement, fate,
and persistence of acrylonitrile in water. Zabezhinskaya et al. (1962)
reported that at an initial concentration of 10 mg/liter, only 46%
remained after 24 hr. 19% after 48 hr. and 537O after 96 hr. Under some
conditions, the relatively high vapor pressure of acrylonitrile would
probably promote the escape of the compound to the atmosphere.
METABOLISM
The metabolism of acrylonitrile has not been studied systematically with
radio-labeled material. Investigators studying the metabolism of acrylo-
nitrile have concentrated on ascertaining the fate of the cyano group of
the molecule. Brieger et al. (1952) reported that inhaled acrylonitrile is
metabolized first to the free cyano group, and then to thiocyanate. They
found high cyanate levels and high thiocyanate levels in the blood of
rats, dogs, and monkeys that had been treated with acrylonitrile. In a
study with both oral and intraperitoneal administration of acrylonitrile
in rats, mice, and Chinese hamsters, Gut et al. (1975) observed that
thiocyanate was eliminated in the urine and that acrylonitrile was bound
strongly to components of the blood. There appeared to be an
interspecific difference in the metabolic pattern: less cyanide formed in
rats than in mice. Earlier studies (Dudley and Neal, 1942; Lawton et al.,
OCR for page 72
72 DRINKING WATER AND H"LTH
1943; Paulet et al., 1966) indicated the same lack of agreement on the
principal metabolic product of acrylonitrile. Some of the studies reported
cyanide, and others, thiocyanate, as the principal breakdown product.
The fate of the remainder of the molecule has not been established. The
possibility of conjugation has been raised by Hashimoto and Kanai
(1972) who reported binding of acrylonitrile with cysteine and gluta-
thione with a concomitant decrease in sulfhydryl (SH) groups. Earlier
work by these investigators indicated that a large amount of injected
acrylonitrile was unchanged after treatment of rabbits, guinea pigs, and
rats.
HEALTH ASPECTS
Observations in Humans A recent report by the DuPont Corporation to
government regulatory agencies stated that acrylonitrile may be a
carcinogen (Anonymous, 1977~. It also stated that preliminary results of
an epidemiological study of workers in a polymerization operation with
potential for exposure to acrylonitrile indicated excess cancer incidence
and cancer mortality as compared with company and national experi-
ence. This study included about 470 males who began working in the
polymerization area of the plant between 1950 and 1955 and who are still
actively employed or have been retired from the company (Anonymous,
19771. The DuPont report emphasizes that the data are preliminary and
that more exhaustive studies are under way.
A number of incidents of illnesses and fatalities have been caused by
the industrial and structural pest control uses of acrylonitrile. The
compound is an acute poison and a severe skin and eye irritant. It may
be toxic when inhaled, ingested, or absorbed through intact skin.
Symptoms of exposure include nasal and respiratory oppression,
vomiting, nausea, weakness, fatigue, headache, and diarrhea (Patterson
en al., 19761. The symptoms of poisoning from acrylonitrile are very
similar to those from cyanide. Such poisoning generally results from
inhalation by workers of vapor in industrial settings where the concen-
tration of acrylonitrile varies from 16 to 100 ppm. No fatalities have been
reported under these conditions.
In contrast to the safety record of acrylonitrile in the chemical
industry, the use of the compound in structural pest control has resulted
in a number of fatalities (Davis, 1967; Davis e! al., 1973; Patterson et al.,
1976; Radimer et al., 1974; Sartorelli, 1966). The reported fatalities
generally resulted from direct exposure to acrylonitrile or from too rapid
a return to a building that had been fumigated with the compound.
OCR for page 73
Toxicity of Selected Drinking Water Contaminants 73
Death resulted following symptoms that are similar to those of cyanide
poisoning. However, death has also occurred as the result of toxic
epidermal necrolysis (Radimer et al., 1974~. Acrylonitnle, when used for
fumigation, is generally combined with other materials such as meth-
ylene chloride and carbon tetrachlonde. Consequently, it is somewhat
difficult to disassociate the symptoms of one compound from another.
Observations in Other Species
Acute Elects Investigating acute poisoning after intravenous injec-
tion of acrylonitrile in dogs and rabbits, Paulet et al. (1961) absented
considerable differences in interspecific response to cyanide intoxication.
Symptoms of nervous disorders dominated the picture. Electroencepha-
lographic records show that the higher nervous centers were affected.
The investigators also found hyperglycemia and a decrease in the
concentration of plasma inorganic phosphate. Acute oral toxicity values
(LDso's) for acrylonitrile range from 27 to 128 mg/kg for mice (Benes
and Cerna, 1959; Zell!e,r et al., 1969) and from 78 to 93 mg/kg for rats
(Benes and Cerna, 1959; Smyth and Carpenter, 1948~.
Acrylonitrile has also been characterized as a serious hazard in
inhalation studies conducted by the Union Carbide Corporation in rats
(Union Carbide Corporation, 1970~. After breathing saturated air for 5
min. all exposed animals died. After breathing 100 ppm for 4 hr. all of six
rats died; for 2 hr. one of six; and for 1 hr. none of six. After breathing
500 ppm for 4 hr. none of six died, and for 8 hr. one of six died (Union
Carbide Corporation, 19701. Roudabush et al. (1965) reported that acute
dermal LDso values from acrylonitrile were 0.28 mg/kg when applied to
the abraded skin of rabbits, 0.46 mg/kg on the intact skin of guinea pigs,
and 0.84 mg/kg on the abraded skin of guinea pigs.
Subchronic and Chronic Effects There are surprisingly few long-term
studies on the toxicity of acrylonitrile in laboratory animals. None of the
few studies in the literature was designed to establish a no-adverse-e~ect
or minimal-effect dosage level.
Dudley et al. (1942) conducted a three-part study of the inhalation
toxicity of acrylonitrile. In a preliminary series, they exposed four rhesus
monkeys and two dogs for 4 hr/day, 5 days/week for 4 weeks to an
average concentration of 0.12 mg/liter (56 ppm) of acrylonitrile in air.
These experiments indicated that dogs are more susceptible to acryloni-
trile than are monkeys and that repeated exposure to concentrations of
0.12 mg/liter produces no signs of cumulative action. In the second part
of their study, they exposed 16 rats, 16 guinea pigs, 3 rabbits, and 4 cats
OCR for page 74
74 DRINKING WATER AND H"LTH
in the same manner for 8 weeks to an average concentration of 0.22
mg/liter (100 ppm) of acrylonitrile in air. These experiments show that
rats, guinea pigs, and rabbits tolerate repeated exposures to 0.22 mg/liter
acrylonitrile in air over a period of 8 weeks; that cats are definitely more
sensitive to acrylonitrile than are rodents; and that there is no evidence
of cumulative action of acrylonitrile. In the third part of the study, they
exposed 16 rats (8 adult, 8 young animals), 16 guinea pigs, 4 rabbits, 4
cats, and 2 rhesus monkeys in the same way to an average concentration
of 0.33 mg/liter (153 ppm) acrylonitrile in air. These experiments showed
that repeated exposures to 153 ppm were definitely toxic to guinea pigs,
rats, and rabbits and were much more toxic to monkeys and cats. The
exposures produced irritation of eyes and nose, loss of appetite,
gastrointestinal disturbances, and incapacitating weakness of hind legs
from which the animals recovered relatively rapidly. Even after exposure
to such high concentrations no definite evidence of cumulative action
was observed.
In a study on the ejects of acrylonitrile on rats Barnes (1970) noted no
adverse ejects. Six rats were given 15 successive oral doses of 30 mg/kg,
followed by seven doses of 50 mg/kg, and then 13 doses of 75 mg/kg
over a period of 7 weeks. The investigators supplied no details on the
types of observations that were made to assess toxicity.
Studies have also been conducted on the toxicity of acrylonitrile to
adult rats following daily intraperitoneal administration of the com-
pound (Knobloch et al., 19711. Daily injection of 50 mg/kg for 3 weeks
produced a statistically significant loss of body weight; leucocytosis;
signs of damage and functional disturbances of liver and kidneys;
increase in the weight of liver, kidneys, and heart; and histological
damage. Microscopic examination of the organs of these animals showed
slight damage of neuronal cells of the cortex and brain stem and
parenchymal degeneration of liver and kidneys. Unfortunately, no other
dosage rates were included in this study.
Following the reports of epidemiological evidence of the carcinogeni-
city of acrylonitrile, Norris ( 1977) initiated a 2-year feeding and
inhalation study in rats. In the ingestion study, acrylonitrile was
incorporated into the drinking water of laboratory rats at concentrations
of 0, 35, 100, and 300 mg/liter (corresponding to 0, 4, 10, and 30
mg/kg/day). In the inhalation study, male and female rats were exposed
to 0, 20, and 80 ppm acrylonitrile for 6 hr/day' 5 days/week. In April
1977, interim results of the 2-year studies were reported (National
Institute for Occupational Safety and Health, 1977; Norris, 1977~. Rats
ingesting 35 mg/liter acrylonitrile exhibited mild signs of toxicity while
OCR for page 75
Toxicity of Selected Drinking Water Contaminants 75
those ingesting lOO and 300 mg/liter showed marked signs of toxicity.
Norris (1977) reported that both male and female rats that ingested lOO
or 300 mg/liter acrylonitrile for 12 months developed stomach papillo-
mas (1 of 20 rats at lOO mg/liter and 12 of 20 at 300 mg/liter); central
nervous system tumors (2 of 20 at 35 mg/liter, 2 of 20 at 100 mg/liter,
and 3 of 20 at 300 mg/liter); and Zymbal gland carcinoma (2 of 20 at lOO
mg/liter, and 2 of 20 at 300 mg/liter). No such tumors were seen in
control animals. In the inhalation study, after 1 year of exposure to 80
ppm acrylonitrile. 26 rats died and three developed central nervous
system tumors that were comparable to those reported in the ingestion
study. Gross examination of other rats in this study, who were also
exposed to 80 ppm acrylonitrile by inhalation, revealed an increased
incidence of ear canal tumors and mammary region masses. In animals
exposed to 20 ppm, there was an apparent increase in subcutaneous
masses of the mammary region, although no ear canal or central nervous
_ 1 ~.1 ~1
system tumors were observed. (other than neoplasms, signs of toXlClty
were limited to decreased water and food consumption and decreased
body weight gain.
Mutagenicity The mutagenicity of acrylonitrile has been demon-
strated in the Salmonella typhimurium test (Milvy and Wolff, 1977) and in
E. cold WP2 strains (Venitt and Bushell, 1977~. In the Ames (Salmonella)
assay, acrylonitrile was active in the presence of a mouse liver
homogenate, producing mutations in three tester strains. Bacteria were
exposed by spotting the acrylonitrile on a lawn of Salmonella; by shaking
a reaction mixture consisting of bacteria, liver homogenate, and
acrylonitrile; and by exposing the homogenate and bacteria to an
atmosphere containing acrylonitrile. By the latter method mutagenicity
was observed at exposures as low as 57 mg/liter. Acrylonitrile was also
mutagenic in various DNA-repair strains of E. cold WP-2. The effects
were weak in plate incorporation tests, but assays using a simplified
fluctuation test showed acrylonitrile to be significantly mutagenic at
doses that were 20 to 40 times lower than those giving significant results
in the plate test. Use of the different DNA-repair strains indicated that
acrylonitrile causes DNA damage of the type that is exemplified by
methyl methanesulfonate.
Carcinogenicity Acrylonitrile has given positive results in a rat
feeding study. Epidemiological evidence also contributes strong evidence
to implicate acrylonitrile as a carcinogen. These studies are discussed
above.
OCR for page 76
76 DRINKING WATER AND H"LTH
Reproduction The subcommittee found no studies on reproductive
effects of acrylonitrile.
Teralogenicity The subcommittee noted no studies reporting the
teratogenicity of acrylonitrile.
Carcinogenic Risk Estimate The interim results of a 2-year ingestion
study with acrylonitrile in the drinking water of rats give evidence of
what appears to be an increase in cancer at several sites (Norris, 1977~.
Dose-response data (Norris, 1977) were used to estimate both the
lifetime risk and an upper 957 confidence bound on the lifetime risk at
the low dose level. These are estimates of lifetime human risks which
have been corrected for species conversion on a dose/surface area basis.
The risk estimates are expressed as a probability of cancer after a lifetime
consumption of 1 liter/day of water containing 1 ~g/liter of the
compound under study. For example, a risk of 1 x 10-6 implies a lifetime
probability of 2 x 10-5 of cancer if 2 liters/day were consumed and the
concentration of the carcinogen was 10 ,ug/liter. This means that at a
concentration of 10 ~g/liter during a lifetime exposure this compound
would be expected to produce one excess case of cancer for every 50,000
persons exposed. If the population of the United States is taken to be 220
million people this translates into 4,400 excess lifetime deaths from
cancer or 62.8 per year.
For acrylonitrile at a concentration of I ~g/liter, the estimated lifetime
risk for humans is 6.7 x 10-7. The upper 95% confidence estimate is
1.3 x 10-6. Both of these estimates are the averaged risks calculated from
the male and female rats. They are based on preliminary data of Norris
(1977) and are subject to change when the study is completed.
CONCLUSIONS AND RECOMMENDATIONS
Based on toxicological investigations, the Food and Agriculture Organi-
zation/World Health Organization (FAD/WHO, 1965) concluded that
an acceptable daily intake of acrylonitrile for humans could not be
determined. Both epidemiological and controlled feeding and inhalation
studies since 1965 indicate that acrylonitrile is a carcinogen. Therefore, it
would not seem possible to establish a long-te~ acceptable level for this
compound in drinking water. Unfortunately, since LD50 studies indicate
only the level of short-term toxicity, short-te~ exposure limits cannot be
calculated.
OCR for page 77
Toxicity of Selected Drinking Water Contaminants 77
Antimony (Sb)
Antimony is a metal that is chiefly a by-product of base metal and silver
ores. It has oxidation states of + 3 (trivalent) and + 5 (pentavalent) and
forms compounds with halides, oxygen, sulfur, and organic anions such
as tartrate, thioglycollate, and thioglycollamide. It is used industrially in
flameproofing textiles, in vulcanizing of rubber, and in the manufacture
of paint pigments, electronic semiconductors, thermoelectric devices,
and fireworks (National Institute for Occupational Safety and Health,
1978; Robert and Boston, 1974~. Antimony compounds also have
medical application (Gross, 1974; Harvey, 1975~. Organic antimonial
compounds are used as parasiticides to treat different forms of
schistosomiasis, bilharziasis, and leishmaniasis.
Most exposure of humans to antimony compounds occurs in industrial
settings. Schroeder (1970) has estimated the human daily intake from all
sources to be about 100 ,ug.
METABOLISM
Trivalent and pentavalent antimony are differently distributed and
excreted. Trivalent compounds have a great affinity for erythrocytes and,
therefore, give low plasma concentrations. Pentavalent compounds tend
to remain in the plasma. The trivalent form is excreted at a much slower
rate in the urine than pentavalent antimony probably because it collects
at much lower levels in plasma (National Institute for Occupational
Safety and Health, 1978; Robert and Boston, 1974~. After administration
of a single therapeutic dose of trivalent antimony only logo was
recovered in 24 hr. whereas 5097O of the pentavalent form was recovered
in 24 hr (Harvey, 19751.
Most trivalent antimony (tartar emetic) is excreted in the feces,
whereas the pentavalent forms are excreted mainly in the urine. The
distribution of antimony to the tissues has not been thoroughly studied.
However, in guinea pigs the trivalent compounds are found in high
concentration in the thyroid and liver while the pentavalent forms are
found in the liver and spleen after oral dosing. Abdallah and Saif (1962),
in their studies of humans, showed that the highest concentrations of
antimony occur in the liver, followed by the thyroid and heart. They
administered sodium antimony dimercaptosuccinate (~24Sb) intra-
venously. The liver, heart, and thyroid retained antimony for 20 days.
When three 100-mg doses of antimony were administered intramuscular-
ly over 9 days there was still considerable antimony in these tissues 53
days later.
OCR for page 254
254 DRINKING WATER AND HEALTH
Pomerantz, I., J. Burke, D. Firestone, J. McKinney, J. Roach, and W. Troffcr. 1978.
Chemistry of PCBs and PBBs. Environ. Health Perspect. 24:1333-1346.
Potts, C. L. 1965. Cadmium proteinuna-the health of battery workers exposed to
cadmium oxide dust. Ann. Occup. Hyg. 8:55~1.
Prendergast, J. A., R. A. Jones, L. J. Jenkins, Jr.? and J. Siegel. 1967. Effects on
experimental animals of long-term inhalation of tnchloroethylene, carbon tetrachlonde,
1, 1,1-trichloroethane, dichlorodifluoromethane, and I,1-dichloroethylene. Toxicol.
Appl. Phannacol. 10:27~289.
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28:983-987. (In Russian.)
Pyykko, K., H. Tahti, and H. Vapaatalo. 1977. Toluene concentrations in various tissues of
rats after inhalation and oral administration. Arch. Toxicol. 38:169-176.
Radimer, G. F., J. H. Davis, and A. B. Ackerman. 1974. Fumigant-induced toxic cpidermal
necrolysis. Arch. Dermatol. 1 10:13~104.
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Raipta, C., K. Husman, and A. Tossavainen. 1976. Lens changes in car painters exposed to
a m~xture of organic solvents. Albrecht von Graefes Arch. Klin. Exp. Ophthalmol.
200: 149-156.
Rajamanickam, C., J. Amrutavalli, M. R. S. Rao, and G. Padmanaban. 1972. Effect of
hexachlorobenzene on haem synthesis. Biochem. J. 129:381-387.
Raleigh, R. L. 1974. Conversation and memorandum to Dr. Stanley C. Mazaleski.
Rannug, U., and C. Ramel. 1977. Mutagenicity of waste products from vinyl chloride
industries. J. Toxicol. Environ. Health 2:1019~1029.
Rannug, U., R. Gothe, and C. A. Wachtmeister. 1976. The mutagenicity of chloroethylene
oxide, chloroacetaldehyde, 2-cholorethanol and chloroacetic acid, conceivable metabo
lites of vinyl chlonde. Chem. Biol. Interact. 12:2S 1-263.
Rapoport, I. A. 1948. [Effect of ethylene oxide, glycidol and glycols on gene mutations.]
Dokl. Akad. Nauk SSSR 60(3):469-472. (Russian)
Rauws, A. G., and M. J. Van Logten. 1975. The influence of dietary chloride on bromide
excretion in the rat. Toxicology 3:29-32.
Reinhardt, C. F., L. S. Mullin, and M. E. Maxfield. 1973. Epinephrine-induced cardiac
arrhythmia potential of some common industrial solvents. J. C)ccup. Med. 15:953-955.
Renner, G., and K. P. Schuster. 1977. 2,4,5-Tnchlorophenol, a new urinary metabolitc of
hexachlorobenzene. Toxicol. Appl. Pharmacol. 39:355-356.
Rennick, B., and A. Quebbemann, 1970. Site of excretion of catechols and catcchola mine:
Renal metabolism of catechol. Am. J. Physiol. 2 1 8 :1307-13 12.
Rhudy, R. L., D. C. Lindberg, J. W. Goode, D. J. Sullivan, and E. J. Gralla. 1978. Ninety-
day subacute inhalation study with toluene in albino rats. Abstr. 150. Toxicol. Appl.
Pharmacol. 45:28~285.
Richardson, A. P. 1937. Toxic potentialities of continued administration of chlorate for
blood and tissues. J. Pharmacol. Exp. Ther. 59:101-113.
Richardson, K. E. 1973. The effect of partial hepatectomy on the toxicity of ethylene
glycol, glycolic acid, glyoxylic acid and glycine. Toxicol. Appl. Pharmacol. 24:53~538.
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biphenyls on growth and reproduction of mink. Pp. 149-154 in Proceedings of the
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OCR for page 255
Toxicity of Selected Drinking Water Contaminants 255
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Representative terms from entire chapter:
selected drinking
