Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter.
Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 90
90 DRINKING WATER AND HEALTH
mg/m3) during major organogenesis and found no adverse fetal effects.
Ungvary et al. (1978) exposed rats to 1,500 ppm (3,840 mg/m3) during
pregnancy and observed that there was increased fetal mortality but no
malformations.
Although Infante et al. (1976a,b) reported increased rates of malforma-
tions in one city where a vinyl chloride plant was located, subsequent stud-
ies by Edmonds et al. (1978) revealed that the parents of these children had
not been workers in the plant nor had they been living closer to the manu-
facturing source than had the controls. Infante et al. (1976b) reported a
significant increase in fetal loss among the wives whose husbands had been
exposed. As a "control" group, they used workers in rubber plants.
Sanotskii et al. (1980) did not find an increase in spontaneous abortions
among the wives of vinyl chloride workers.
In summary, vinyl chloride does not appear to be teratogenic in rats or
rabbits. The data on humans are not adequate for judgment to be made.
CONCLUSIONS AND RECOMMENDATIONS
A SNARL for chronic exposure was not calculated because orally adminis-
tered vinyl chloride is an established carcinogen in humans. It is also car-
cinogenic in mice, hamsters, and rats, in which angiosarcomas were
found, regardless of route. The older animals and females appeared to be
more susceptible. The cancer risk estimate for vinyl chloride can be found
in Volume 1 of Drinking Water and Health.
URANIUM (U)
Uranium was evaluated in the third volume of Drinking Water and Health
(National Research Council, 1980, pp. 173-178~. That review was devoted
exclusively to the element's chemical toxicity. In the following review, the
committee also considers its radiological effects and provides updates and,
in some instances, reevaluations of the information on chemical toxicity
contained in the previous volume. Included are some references that were
not assessed in the earlier report.
Uranium is ubiquitously distributed throughout the earth's crust. It has
a complex radioactive decay scheme resulting in the emission of different
radiations and the production of several radioactive daughter products.
Because its abundance in the crust varies geographically, uranium is a
highly variable source of contamination of drinking waters that may be
directly consumed by humans and incorporated into their diet. In this brief
review, the committee discusses the potential for radiation and chemical
toxicity from the ingestion of natural uranium and clarifies the difference
OCR for page 91
Toxicity of Selected Contaminants 91
between radiation toxicity and the rather well-studied chemical toxicity of
this element. For the purpose of brevity and conciseness, not all of the
primary references have been cited; rather, the committee has provided
several references that are representative and sufficiently broad to cover
the needs of this report.
Natural uranium is present in soils and rocks in concentrations generally
varying between 0.5 and 5 ppm. The average is approximately 1.8 ppm in
most soils. Higher concentrations are present in salic rock, in granite, and
in sedimentary shale. More than 99% of uranium is present as the isotope
uranium-238. Another 0.72870 occurs as the fissionable isotope uranium-
235, and 0.0054~o by weight of uranium as uranium-234. The half-lives
are: uranium-238, 109 years; uranium-235, 108 years; and uranium-234,
105 years. The radioactivity of the three isotopes in natural uranium aver-
ages approximately 7.35 x 105 disintegrations per minute per gram, al-
most all of which is from uranium-238 (National Council on Radiation
Protection and Measurements, 1975~.
Uranium-238 is generally found to be in equilibrium with thorium-234,
palladium-234, and uranium-234, so that a gram of natural uranium
would contain 0.33 psi of each of the four nuclides. Furthermore, ura-
nium-238 and uranium-234 are generally in disequilibrium in nature. The
fractionation of 234 from 238 is believed to occur by the displacement of
the daughter atom uranium-234 from the crystal lattice by recoil, which
renders uranium-234 potentially capable of being oxidized to the hexava-
lent stage when it is more easily leached into the water phase than the par-
ent 238. Because of the disequilibrium, the 234:238 uranium activity con-
centration ratio can vary among water samples. Reported values range
from 0.7 up to 9 (United Nations, 1977~.
The activity concentration of uranium-238 in tap water is usually re-
ported to be less than 0.03 psi/liter. Thus, the contribution of drinking
water to total dietary intake is generally small. A report by the United Na-
tions (1977), however, states that concentrations of uranium found in Rus-
sian tap water have been as high as 70 psi/liter and that concentrations of
approximately 1,000 psi/liter have been measured in several wells in Fin-
land. The highest concentration actually reported was S,OOO psi/liter. The
very high concentration of uranium in the water from those wells was at-
tributed to small, localized uranium-rich deposits (Asikainen and Kahlos,
1980; Kahlos and Asikainen, 1980~.
Although uranium may adhere to inhaled particles, inhalation is only a
minor route of entry into humans. The United Nations (1977) estimated
that the daily adult intake via inhalation is approximately 1 X 10-3 psi.
The major route of entry is ingestion.
The National Council on Radiation Protection and Measurements
OCR for page 92
92 DRINKING WATER AND HEALTH
(1975) assumed a 1.8 kg/day food intake level for a "reference man" and,
in limited measurements, determined that drinking water provides to of
the 1 psi of uranium ingested daily. Approximately 20~o of the daily in-
take is provided by grains and cereal products; 20~o by meat, fish, and
eggs; 20% by green vegetables, fruits, and pulses; and 20~o by root vegeta-
bles. As much as logo may be present in milk and dairy products.
METAB O LI S M
The data indicate that approximately 1 psi (~ 1 Age of uranium is con-
sumed daily and that from 2 % to 3 % of that amount is derived from drink-
ing water (National Council on Radiation Protection and Measurements,
1975~. To a large extent, the uptake and fate of ingested uranium are con-
trolled by the total quantity ingested and, to a lesser extent, on the particu-
lar chemical form. In general, the smaller the amount ingested, the greater
the fraction absorbed (Durbin and Wrenn, 197S). For the purposes of this
report, it will be assumed that the quantity of uranium ingested by humans
is very small and, therefore, the maximum uptake possible occurs. Hursh
and Spoor (1973) cite data indicating that between 12~o and 30~0 of the
ingested uranium is absorbed from the intestinal tract into the blood-
stream. An inte~.~ediate figure of 20~o is assumed in the following discus-
s~on.
Of the absorbed uranium, approximately 805to is excreted, logo goes to
the kidneys, and the remaining logo is deposited in the skeleton. The kid-
ney retention is believed to be brief, with a biological half-life of 1 to 2
weeks. The uranium deposited in the skeleton is divided disproportion-
ately between the spongy and compact bone compartments. Approxi-
mately 80~o of the skeletal mass is assumed to be compact bone in which
~95~o of the deposited uranium has a short effective half-life ranging
from 1 month to 1 year, whereas only ~ to of the absorbed uranium in the
remaining 20~o of the skeleton may have an average half-life of about
10 years (Roswell and Wrenn, 1980~. Because of efficient renal clearance
of circulating uranium, redistribution of uranium deposits is inefficient
and the body burden of uranium probably reflects recent dietary intakes.
Natural uranium bicarbonate complexed with proteins is filtered by the
kidney glomeruli. The plasma equilibrium is shifted from the proteinate to
the bicarbonate until all uranium not deposited in the skeleton has passed
through the glomeruli. Once in the kidney tubules, the bicarbonate com-
plex is partially dissociated to consenre sodium. With the accompanying
renal reabsorption of water, the urine becomes more acidic, the uranium
more concentrated, and further bicarbonate disassociation occurs. The
freed uranium can bind to the luminal surfaces of the cells lining the proxi-
OCR for page 93
Toxicity of Selected Contaminants 93
mal renal tubules and, with sufficient time and dosage, can cause tubular
damage (Durbin and Wrenn, 1975~. Hodge (1951) noted, "The uranium-
inhibited reaction is located on the cell surface, is rate limiting in the pres-
ence of uranium, is chemical in nature, is an enzymatic not a diffusion
process, is specific, and probably involves the reaction of uranium with the
phosphates of adenosine triphosphate." Therefore, the mechanism of tox-
icity is likely to be suppression of cellular respiration. The site of action is
invariably confined to the proximal convoluted tubules of the kidney
(Hursh and Spoor, 1973~.
HEALTH ASPECTS
Observations in Humans
The committee found no reports of radiological toxicity in humans ex-
posed to natural uranium by ingestion. Furthermore, as Hursh and Spoor
(1973) noted, "The implication that the contamination of drinking water
by uranium is an uncommon and relatively unimportant hazard is con-
finned by the dearth of precise and unambiguous information in the litera-
ture." The excellent summarized history of uranium poisoning by Hodge
(1973) indicates that renal injury occurred in uranium-treated diabetics in
the last century and early in this century. These patients were generally
given hundreds of milligrams per day over extended periods. There are no
population studies, and only specific clinical assessments have been re-
ported. Recent studies in humans are confined to those in which much
lower concentrations of uranium were used. The aim of these studies was
to determine the absorption and urinary excretion of oral doses to assist in
interpreting reports of early therapeutic administrations.
Luessenhop et al. (1958) investigated the effects of intravenous adminis-
tration of uranyl nitrate [UO2(NO3~2] in humans. Five volunteers with ter-
minal brain cancer received doses that ranged from 0.097 to 0.28 mg/kg
(average, 0.15 mg/kg). They noted the following distribution-excretion
pattern: from to to 14~o to the skeletal system, 165'o to the kidneys, and
49~o to 84~o excreted in the urine. These percentages are comparable to
those found in studies of small animals. The most sensitive indicator of
renal damage was an increase in urinary catalase. Other chemical signs
included albuminuria, urinary casts, and a suggestion that there was inter-
ference with the renal capacity for reabsorption of sodium and chloride
and the secretion of potassium. These authors concluded that, of the com-
mon laboratory animals, rats appear to correspond most closely in sensitiv-
ity to humans in regard to intravenous tolerance to uranium.
OCR for page 94
94 DRINKING WATER AND HEALTH
Observations in Other Species
Acute Effects The renal injury associated with uranium toxicity usu-
ally manifests itself several days after exposure. In rats, cellular necrosis
appears in the lower portion of the proximal convoluted tubules as demon-
strated by hyaline casts or casts containing shed necrotic cells. Accompa-
nying the pathological changes are functional changes in the kidney, char-
acterized by proteinuria, impaired Diodrast and p-aminohippuric acid
clearance, and increased clearance of amino acids and glucose (Stone et
al., 1961~.
In studies in dogs, Thompson and Nechay (1981) demonstrated that
uranium as uranyl nitrate [UO2(NO3~2] produced a 74~o inhibition of re-
nal calcium Ca2+ ATPase and an 84~o inhibition of renal magnesium
Mg2+ ATPase at concentrations of 3 X 10-s M and 1 X 10-s M, respec-
tively. They postulated that uranium dioxide (uo2+) may compete with
ATP for binding sites on the Ca2+ and Mg2+ ATPase and that this may be
a factor in its renal toxicity.
Nomiyama et al. (1974) demonstrated in rabbits that early renal injury
could be detected by increases of specific enzymes in the urine following
one intravenous injection of uranyl acetate (0.2 mg of uranium/kg bw).
Urinary alkaline phosphatase, glutamic oxaloacetic transaminase, and
glutamic-pyruvic transaminase all increased significantly before changes
were observed in routine urinalyses or renal function tests. Thus, assays for
selected urinary enzymes may be more sensitive indicators of early renal
· .
nJury.
An interesting phenomenon observed after acute exposure to uranium is
the development of tolerance (mainly in rats) to the effects of repeated ex-
posure. This tolerance may be related to the ability of "uranium-condi-
tioned" animals to excrete uranium more efficiently or to a mechanism in
which the renal tubular epithelium does not bind and retain uranium as
well as "unconditioned" epithelium (Durbin and Wrenn, 1975~.
Maynard and Hodge (1949) also studied the acquired uranium tolerance
in rats and concluded that "prolonged exposure to uranium may produce
conditions under which injection of an ordinary damaging dose of uranium
results in no appreciable renal tubular necrosis."
Chronic Effects Many studies have been conducted to compare the
toxicity of natural uranium and some of its isotopes after continuous inges-
tion. Rodents and dogs continuously fed a wide range of natural uranium
concentrations developed no radiogenic cancers. At the higher levels, renal
OCR for page 95
Toxicity of Selected Contaminants 95
damage predominates as the toxic end point. As pointed out by Durbin
and Wrenn (1975), "Because uranium has a long residence time in bone,
the radiation dose is limiting for all uranium isotopes except 23su and 238U
and all mixtures of uranium isotopes containing at least 91.5~o 238U by
weight (12-fold enrichment in 23su by the gaseous diffusion process has at
least an equal amount of 234U)."
For example, in a classic toxicity study by Finkel (1953), injections of
natural uranium in concentrations as high as 1 mg/kg induced no malig-
nant bone tumors, whereas uranium-233 doses of 1 mg/kg proved to be a
maximally effective bone carcinogen, comparable to uranium-232 at 5 X
10-4 mg/kg. More importantly, the uranium-232 activity was approxi-
mately 10 psi/kg' as was that of the uranium-233, whereas the natural
uranium contained a maximum of 7 X 10-4 ~Ci/kg.
Maynard and Hodge (1949) conducted 2-year studies in which rats were
continuously fed different uranium compounds ranging from O.l~o to
20~o of the dietary mass. The lowest dietary levels producing retardation of
growth were: uranyl fluoride, 0.1%; uranyl nitrate hexahydrate, 0.5~o;
and uranium tetrafluoride, 20~o. Uranium dioxide at 20~o, the highest
level tested, produced no effect. The only major pathological effect ob-
served as a result of chronic oral exposure was necrosis of the renal tubular
epithelium, involving predominantly the proximal convoluted tubule. The
same effects were frequently observed in dogs and rabbits exposed for only
30 days. Although chemical toxicity was observed, primarily in the kidney,
no radiogenic effects were noted.
The same authors also fed various uranium compounds at graded doses
of 0.0002 to 0.2 g/kg/day to dogs over a 1-year period. With the exception
of one dog fed the highest level (0.2 g/kg/day) of uranyl nitrate, all the
dogs survived, gained weight, and were healthy and active. Only at dietary
doses greater than 0.02 g/kg/day were any effects of uranium toxicity
noted. Moderate elevations in blood nonprotein nitrogen and urea nitro-
gen were observed as well as transient urinary sugar and proteinuria. Path-
ological effects were not described.
The investigators observed~interesting differences in response between
dogs dosed for 1 year and rats dosed for 2 years. Rats were more resistant
to the toxicity of uranyl fluoride (UO2F2) by a factor of approximately 25.
For uranyl nitrate [UO2(NO3~2-6H2O], the rats were more resistant by a
factor of about 20, and for uranium tetrafluoride (UF4), by a factor of 4.
ln summary, studies in laboratory animals have produced radiation-re-
lated cancers only when high specific-activity isotopes of uranium were
used. There have been no reports of cancers resulting from the ingestion of
natural uranium in laboratory animals.
OCR for page 96
96 DRINKING WATER AND HEALTH
Mutagenicity No data were found by the committee.
Teratogenicity No data were found by the committee.
CONCLUSIONS AND RECOMMENDATIONS
Suggested No-Adverse-Response Level (SNARL)
Chronic Exposure Because there is no evidence that naturally occur-
ring uranium-238 is carcinogenic, a chronic exposure SNARL will be cal-
culated. Two-year studies in rats and a 1-year study in dogs by Maynard
and Hodge (1949) have indicated that the dog is the more sensitive species.
In chronic exposures, the highest dietary level tolerated by dogs with no
decreases in body weight gain or symptoms of renal involvement was
1 mg/kg/day. Luessenhop et al. (1958) found 0.15 mg/kg to be the mini-
mum-observed-effect dose in humans, but this dose was administered in-
travenously. This amount is approximately the same as that absorbed (as-
suming 20% gastrointestinal absorption) following an oral dose of
1 mg/kg. Using an uncertainty factor of 100, and assuming that a 70-kg
adult consumes 2 liters of water daily and that logo of the uranium intake
is provided by the water, one may calculate a chronic SNARL as:
1.0 mg/kg X 70 kg X 0 1 = 0.035 mg/liter, or 35 ~g/liter
If one assumes that the isotopic ratios in natural uranium are in equi-
librium, then there would be 0.33 pCi/pg of uranium-238. A value of
35 ~g/liter would be equivalent to 11.6 psi/liter, which is about twice the 5
psi/liter established as the current maximum contaminant level (MCL)
for radium (U.S. Environmental Protection Agency, 1975a). Ingestion of
water containing radium at 5 psi/liter is estimated to cany a risk of be-
tween 0.7 to 3.0 fatal cancers per year per million persons exposed. There
is currently no standard for uranium.
Ike total absence of carcinogenic effects from ingested natural uranium
in either animals or humans makes it difficult to develop an appropriate
model for the radiotoxicity of that element. Furthermore, the fact that
drinking water rarely contributes more than 2~o to 5~o of the total ura-
nium ingested daily leads to the conclusion that a radiation risk model for
natural uranium is inappropriate and unjustified on the basis of present
knowledge. When natural uranium is subjected to an enrichment process
resulting in specific activity exceeding 106 disintegrations per minute per
gram, it is possible that a radiotoxicity model could be developed (U.S.
OCR for page 97
Toxicity of Selected Contaminants 97
Energy Research and Development Administration, 1976~. This assump-
tion is based primarily on the findings of Finkel (1953), who studied ura-
nium-233 and natural uranium, and on the radioactivity rather than the
mass relationships of the different uranium isotopes tested in laboratory
animals. Finkel reported that the radioactivity, in terms of alpha disinte-
gration rate, reached levels comparable to those seen in radium-226 toxic-
ity. For purposes of this discussion, the effectiveness of uranium-233 and
uranium-235 can be regarded as fairly comparable to that of radium-226,
based on ingested psi per unit time.
Because of its loo specific activity, natural uranium does not pose a
problem of radiotoxicity in drinking water. Assessment of uranium toxicity
in drinking water should be based on its chemical toxicity and not on radi-
ation toxicity. However, when the specific activity of uranium in drinking
water has been altered so that it is greater than that of natural uranium,
potential radiotoxicity should be given attention equal to that of the chemi-
cal toxicity. The committee also recommends that toxicological assessment
of uranium in cater be based solely on its renal toxicity in all instances
except when industrial processes result in a marked enrichment of shorter-
lived uranium isotopes.
Additional research should be carried out to determine with greater pre-
cision the dynamics of uranium absorption from the gastrointestinal tract
for different chemical forms of uranium.
CONCLUSIONS
Chronic Toxicity
Table II-10 lists the compounds reviewed in this volume for which there
were sufficient data to calculate either a chronic SNARL or cancer risk
estimate. The statistical methodology for the cancer risk estimate is de-
scribed for chlorobenzene on page 21. Further details on methodology can
be found in Volumes 1 and 3 of Drinking Water and Health (National
Research Council, 1977, 1980~. It is important to stress that the reader
should refer back to the discussion on individual compounds for specific
details.
Mutagenicity As described in Chapter 1, a chemical was judged to be a
mutagen when it could be shown that it was mutagenic in any one short-
term test. The data summary in Table Il-11 is based on this criterion. It is
important to stress that the reader should refer back to the discussion on
individual compounds for specific details.
OCR for page 98
98 DRINKING WATER AND HEALTH
TABLE II-10 Summation of Chronic Exposure Levels and
Carcinogenicity Risk Estimate for Chemicals Reviewed
Chemical
Suggested No-Adverse-Response
Level (SNARL), mg/liter, for
Chronic Exposure
Upper 95%
Confidence Estimate
of Lifetime Cancer
Risk per ~g/liter
Aldicarb
Chlorobenzene
o-Dichlorobenzene
p-Dichlorobenzene
1, 1 -Dichloroethylene
Dinoseb
Hexach lorobenzene
Methomyl
Picloram
Rotenone
Tetrachloroethylene
1,1, 1 -Trichloroethane
Trich loroethylene
Uranium
o. oo7a
0.3`
0.094a- C
0.10
0.039
0.175
1.05
0.014
0.035
2.13 x 10 - 7b
I .85 x l o ha
d
2.98 x 10 8b
3.3 X 10 7b
aThis is the suggested no-adverse~effect level calculated in Volume I of Drinking Water and [health (lsia-
tional Research Council, 1977) and continues to be the recommended SNARL.
bBased on limited evidence (see Chapter 1) from ongoing studies being conducted by the National Toxicol-
ogy Program ( I 982a.d,e). The studies on these compounds have undergone peer review and the results are
. . . .
In press at t lIS Writing.
This SNARL must be reviewed when the cancer bioassay is completed and reviewed (see text for details).
dNeither a SNARL nor a cancer risk estimate has been calculated by the committee pending the outcome of
an ongoing study being conducted by the National Toxicology Program (1982d).
Teratogenicity The only compound reviewed in this volume that
showed teratogenic potential following oral exposure was hexachloroben-
zene. Dinoseb was teratogenic following intraperitoneal, but not oral expo-
sure. The data for rotenone and trichloroethylene are inconclusive.
RE SEARCH REC OMMENI)ATION S
Although specific research recommendations are given for many of the
compounds reviewed, the major areas are summarized here.
1. The most urgent need is for comparative data on various aspects of
metabolism in laboratory animals and humans. Only with such data can
relevant animal models be used to predict more accurately the potentially
adverse health effects in humans.
2. In conjunction with the above recommendation, these kinds of data
ultimately need to be included in the mathematical models now used to
estimate cancer risk.
OCR for page 99
Toxicity of Selected Contaminants 99
TABLE II-11 Mutagenicity Studies of Chemicals
Reviewed in this Volume
Chemical
Mutagenicitya
Aldicarb
Carbofuran
Carbon tetrachloride
Chlorobenzene
o-Dichlorobenzene
p-Dichlorobenzene
1 .2-Dichloroethane
1, l-Dichloroethylene
cis- 1 ,2-Dichloroethylene
trans- 1 ,2-Dichloroethylene
Dichloromethane
Dinoseb
Hexachlorobenzene
Methomyl
Picloram
Rotenone
Tetrach loroethylene
1,1, 1 -Trichloroethane
Trichloroethylene
Vinyl chloride
Uranium
NDb
_ c
ND
+
+
_ c
+
ND
aScc text for details.
bND = no data.
Inconclusive data, see text for details.
3. Data on reproductive effects including teratogenicity should be gen-
erated for the majority of the compounds reviewed.
REFERENCES
Abdel-Aal, Y.A.I., and T.Y. Hclal. 1980. Relative toxicity and a~ticholinesterase activity of
phosfolan and carbofuran to four rodent species. Int. Pest Control 22:4Y)~41.
Adams, C.E., M.B. Hay, and C. Lutwak-MaDn. 1961. The action of various agents upon the
rabbit embryo. J. Embryol. Esp. Morphol. 9:468491.
Ahdaya, S.M., R.J. Monroe, and F.E. Guthne. 1981. Absorption and distribution of intuba-
ted insecticides in fasted mice. Pestic. Biochem. Physiol. 16:3W6.
Ahmed, A.E., V.L. Kubic, J.L. Stevens, and M.W. Anders. 1980. Halogenated methanes:
Metabolism and to~cicity. Fed. Proc. 39:3150-3155.
Ahmed, B.E., R.W. Hart, and N.J. Lewis. 1977. Pesticide induced DNA damage and its
repair in cultured human cells. Mutat. Res. 42:161-174.
Ahr, H.J., L.J. King, W. Nastainczyk, and V. Ullrich. 1980. The mechanism of chloroform
and carbon monoxide formation from carbon tetrachloride by microsomal cytoebrome
P-450. Biochem. Pharmacol. 29:2855-2861.
OCR for page 100
100 DRINKING WATER AND HEALTH
Al'pert, A.E., A.V. Arkhangel'skii, A.M. Lunts, and N.P. Panina. 1972. Experimental he-
patopathies and carcinoma of the breast in rats. Byull. Eksp. Biol. Med. 14(10):78-81.
(Russ.)
Alumot E., E. Nachtomi, E. Mandel, and P. Holstein. 1976. Tolerance and acceptable daily
intake of chlorinated fumigants in the rat diet. Food Cosmet. To~cicol. 14:105-110.
American Conference of Governmental Industrial Hygienists. 1981. Threshold Limit Values
for Chemical Substances and Physical Agents in the Workroom Environment with In-
tended Changes for 1981. Cincinnati, Ohio: American Conference of Governmental Indus-
trial Hygienists. 94 pp.
Anders, M.W., and J.C. Livesey. 1980. Metabolism of 1,2-dihaloethanes. Pp. 331-341 in B.
Ames, P. Infante, and R. Reitz, eds. Banbury Report 5. Ethylene Dichloride: A Potential
Health Risk? Cold Spring Harbor, N.Y.: Cold Spring Harbor Laboratory.
Andersen, K.J., E.G. Leighty, and M.T. Takahashi. 1972. Evaluation of herbicides for pos-
sible mutagenic properties. J. Agric. Food Chem. 20:649-656.
Andersen, M.E., and L.J. Jenkins, Jr. 1977. Oral toxicity of 1,1-dichloroethylene in the rat:
Effects of sex, age, and fasting. Environ. Health Perspect. 21:157-163.
Andersen, M.E., J.E. French, M.L. Gargas, R.A. Jones, and L.J. Jenkins, Jr. 1979. Satura-
ble metabolism and acute toxicity of 1,1-dichloroethylene. Toxicol. Appl. Phall~lacol.
47:385-393.
Anderson, D., M.C.E. Hodge, and I.F.H. Purchase. 1977. Dominant lethal studies with the
halogenated olefins vinyl chloride and vinylidene dichloride in male CD-1 mice. Environ.
Health Perspect. 21:71-78.
Anderson, D., C.R. Richardson, T.M. Weight, I.F.H. Purchase, and W.G.F. Adams. 1980.
Chromosomal analyses in vinyl chloride exposed workers. Results from analysis 18 and 42
months after an initial sampling. Mutat. Res. 79:151-162.
Anderson, D., C.R. Richardson, I.F.H. Purchase, H.J. Evans, and M.L. O'Riordan. 1981.
Chromosomal analysis in vinyl chloride exposed workers: Comparison of the standard
technique with the sister-chromatic exchange technique. Mutat. Res. 83:137-144.
Anderson, M.W., D.G. Hoel, and N.L. Kaplan. 1980. A general scheme for the incorpora-
tion of pharmacokinetics in low-dose risk estimation for chemical carcinogenesis: Exam-
ple—~rinyl chloride. Toxicol. Appl. Pharmacol. 55:154-161.
Antal, M., M. Bedo, G. Constantino~rits, K. Nagy, and J. Szopvolgyi. 1979. Studies on the
interaction of methomyl and ethanol in rats. Food Cosmet. To~cicol. 17:333-338.
Apfeldorf, R., and P.F. lnfante. 1981. Re~riew of epidemiologic study results of vinyl chlo-
ride-related compounds. Environ. Health Perspect. 41:221-226.
Ariyoshi, T., K. Ideguchi, K. Iwasaki, and M. Arakaki. 1975. Relationship between chemi-
cal structure and acti~rity. II. Influences of isomers in dichlorobenzene, trichlorobenzene,
and tetrachlorobenzene on the activities of drug-metabolizing enzymes. Chem. Phann.
Bull. 23:824-830.
Ariyoshi, T., M. Eguchi, Y. Muraki, H. Yasumatsu, N. Suetsugu, and K. Anzono. 1981.
Effccts of chlorinated benzencs on the acti~nties of b-aminole~rulinic acid synthetase and
heme osygenase and on the content of hemoprotein in the li~rer of rats. J. Phann. Dyn.
4:69-76.
Ashack, R.J., L.P. McCarty, R.S. Malek, F.R. Goodman, and N.P. Peet. 1980. Evaluation
of rotenone and related compounds as antagonists of slow-reacting substance of anaphy-
lasis. J. Med. Chem. 23:1022-1026.
Asikainen, M., and H. Kahlos. 1980. Natural radioactivity of drinking water in Finland.
Hcalth Phys. 39:77-83.
Astolfi, E., A.H. Alonso, A. Mendizabal, and E. Zubiz~arreta. 1974. Chlonnated pesticides
OCR for page 107
Toxicity of Selected Contaminants 107
of the Carcinogenic Risk of Chemicals to Humans: Some Monomers, Plastics and Syn-
thetic Elastomers, and Acrolein, Vol. 19. Lyon: International Agency for Research on Can-
eer. S13 pp.
International Agency for Research on Caneer. 1979b. Tetrachloroethylene. Pp. 491-514 in
IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans:
Some Halogenated Hydrocarbons, Vol. 20. Lyon: International Agency for Research on
Caneer.
Ivanetieh, K.M., and L.H. Van den Honert. 1981. Chloroethanes: Their metabolism by he-
patie eytoehrome P-450 in vitro. Careinogenesis 2:697-702.
Ivie, G.W., and H.W. Dorough. 1968. Furadan-C ]4 metabolism in a lactating cow. J. Agric.
Food Chem. 16:849-855.
Jackson, J.B. 1966. Toxicologic studies on a new herbicide in sheep and cattle. Am. J. Vet.
Res. 27:821-824.
Jacobs, S. 1957. The Handbook of Solvents. New York: Van Nostrand.
Jaeger, R.J., R.B. Conolly, and S.D. Murphy. 1974. Effect of 18 hr fast and glutathione
depletion on 1,1-diehloroethylene-induced hepatotoxieity and lethality in rats. Exp. Mol.
Pathol. 20:187-198.
Jakoby, W.B., W.H. Habig, J.H. Keen, J.N. Ketley, and M.J. Pabst. 1976. Glutathione
S-transferases: Catalytic aspects. Pp. 189-211 in I.M. Arias and W.B. Jakoby, eds. Glu-
tathione: Metabolism and Function. New York: Raven Press.
Jenkins, L.J., Jr., and M.~. Andersen. 1978. 1,1-Diehloroethylene nephrotoxieity in the rat.
To~cieol. Appl. Pharmaeol. 46:131-141.
Jenkins, L.J., Jr., M.J. Trabulus, and S.D. Murphy. 1972. Bioehemieal effects of 1,1-diehlo-
roethylene in rats: Comparison with carbon tetraehloride and 1,2-diehloroethylene. Tox-
ieol. Appl. Pharmaeol. 23:501-510.
Jenssen, D., and C. Ramel. 1980. The micronucleus test as part of a short-term mutagenicity
test program for the prediction of eareinogenieity evaluated by 143 agents tested. Mutat.
Res. 75:191-202.
John, J.A., F.A. Smith, and B.A. Sehwetz. 1981. Vinyl chloride: Inhalation teratology study
in mice, rats and rabbits. Environ. Health Perspeet. 41:171-177.
Johnson, J.E. 1971. The public health implication of widespread use of the phenoxy herbi-
eides and pieloram. BioSeienee 21:899-905.
Jones, B.K., and D.E. Hathway. 1978a. The biological fate of vinylidene chloride in rats.
Chem.-Biol. Interact. 20:27-41.
Jones, B.K., and D.E. Hathway. 1978b. Differences in metabolism of vinylidene chloride
between mice and rats. Br. J. Caneer 37:411~17.
Jones, B.K., and D.E. Hathway. 1978e. Tissue-mediated mutagenicity of vinylidene chloride
in Salmonella typhimurium TA1535. Caneer Lett. 5:1-6.
Jongen, W.M.F., P.H.M. Lohman, M.J. Kottenhagen, G.M. Alink, F. Berends, and J.H.
Koeman. 1981. Mutagenicity testing of diehloromethane in short-term mammalian test
systems. Mutat. Res. 81:203-213.
Kahlos, H., and M. Asikainen. 1980. internal radiation doses from radioaeti~qty of drinking
water in Finland. Health Phys. 39:108-111.
Kaplan, A M., and H. Sherman. 1977. To~cieity studies with methyl N-ll(methylamino)ear-
bonyl~oxylethanimidothioate. Toxieol. Appl. Pharmaeol. 40:1-17.
Karlog, O., P. Nielsen, and F. Rasmussen. 1978. Toxieokineties. Toxieologieal Aspects of
Food Safety. Arch. Toxieol. Suppl. 1:55-67.
Kerklasn, P.R.M., J.J.T.W.A. Strik, and J.H. Koeman. 1979. Toxicity of hexaehloroben-
zene with special reference to hepatie glutathione levels, liver necrosis, hepatie porphyria
OCR for page 108
108 DRINKING WATER AND HEALTH
and metabolites of hexachlorobenzene in female rats fed hexachlorobenzene and treated
with phenobarbital and diethylmaleate. Pp. 151-160 in J.J.T.W.A. Strik and ].H.
Koeman, eds. Chemical Porphyria in Man. New York: Elsevier/North-Holland.
Khera, K.S. 1974. Teratogenicity and dominant lethal studies on hexachlorobenzene in rats.
Food Cosmet. To~cicol. 12:471-477.
Khera, K.S., C. Whalen, and G. Angers. 1982. Teratogenicity study on pyrethrum and ro-
tenone (natural ongin) and ronnel in pregnant rats. J. Toxicol. Environ. Health 10:111-
119.
Kluwe, W.~., C.L. Herrmann, and J.B. Hook. 1979. Effects of dietary polychlorinated bi-
phenyls and polybrominated biphenyls on the renal and hepatic toxicities of several chlon-
nated hydrocarbon solvents in mice. 1. Toxicol. Environ. Health 5:605-615.
Konietzko, H., and G. Reill. 1980. The effect of trichloroethylene on some serum-enzymes,
on the cytoenzymological activity in leucocytes, and on the acid-base equilibrium. Int.
Arch. Occup. Environ. Health 47:61-67.
Koss, G., S. Seubert, A. Seubert, W. Koransky, and H. Ippen. 1978. Studies on the toxicol-
ogy of hexachlorobenzene. III. Observations in a long-term expenment. Arch. Toxicol.
40:285-294.
Koss, G., W. Koransky, and K. Steinbach. 1979. Studies on the toxicology of hexachloro-
benzene. IV. Sulphur-containing metabolites. Arch. Toxicol. 42:19-31.
Koss, G., S. Seubert, A. Seubert. W. Koransky, P. Kraus, and H. Ippen. 1980. Conversion
products of hexachlorobenzene and their role in the disturbance of the porphynn pathway
in rats. Int. J. Biochem. 12:1003-1006.
Kramer, C.G., and J.E. Mutchler. 1972. The comlation of clinical and environmental mea-
surements for workers e~cposed to ~rinyl chloride. Am. lnd. Hyg. Assoc. J. 33:19-30.
Kneger, R. 1., P.U. Lee, M.A.H. Fahmy, M. Chen, and T.R. Fukuto. 1976. Metabolism
of 2,2-dimethyl-2,3-dihydrobenzofuranyl-7-N-dimethoxyphosphino-thioyl-N-methylcarba-
mate in the house fly, rat, and mouse. Pest. Biochem. Phys. 6:1-9.
Kubinski, H., G.E. Gutzke, and Z.O. Kubinski. 1981. DNA-cell-binding (DCB) assay for
suspected carcinogens and mutagens. Mutat. Res. 89:9S-136.
Lake, B.G., M.A. Collins, R.A. Harris, C.R. Stubberfield, P. Caciola, and S.D. Gangolli.
1980. Studies on the induction of hepatic ~cenobiotic metabolism in the guinea pig. Bio-
chem. Soc. Trans. 8:9S-96.
Land, P.C., E.L. Owen, and H.W. Linde. 1981. Morphologic changes in mouse spennatozoa
after exposure to inhalational anesthetics during early spermatogenesis. Anesthesiology
54:S3-56.
Lane, R.W., B.L. Riddle, andJ.F. Bonelleca. 1982. Effects of 1,2-dichlorocthane end 1,1,1-
trichlorocthane in drinking water on reproduction and de~relopment in mice. To~cicol.
Appl. Phanncol. 63:409~421.
Leber, A.P., and R.L. Persing. 1979. Carcinogenic Potential of Rotenone. Phase I. Dietary
Administration to Hamsters. EPA-600/1-79~ 4a. Research Triangle Park, N.C: U.S. En-
~rironmental Protection Agency, Hcalth Effects Research Laboratory. 43 pp.
Leber, A.P., and D.C. Thake. 1979. Carcinogenic Potential of Rotenone. Phase II: Oral and
lotrapentoneal Administration to Rats. EPA-600/1-79-004b. Research Triangle Park,
N.C.: U.S. Environmental Protection Ageng, Health Effects Research Laboratory. 49 pp.
Lee, C.C., J.C. Bhandan, J.M. Winston, W.B. House, R.L. Dixon, and J.S. Woods. 1978.
Ca~ogenicXy of ~nnyl chlonde and nnylidene chlonde. J. Tosicol. En~ron. Health 4:
1S-30.
Lcibman, K.C., and E. Ortiz. 1977. Metabolism of halogenated ethylenes. En~riron. Health
Perspect. 21:91-97.
Leighty, E.G., and A.~. Fentiman, Jr. 1981. In ~niro conjugation of the trichloroethylene
OCR for page 109
Toxicity of Selected Contaminants 109
metabolite trichloroethanol to a fatty acid. Res. Commun. Chem. Pathol. Pharmacol.
32:569-572.
Levine, B., M.F. Fierro, S.W. Goza, and J.C. Valentour. 1981. A tetrachloroethylene fatal-
ity. J. Forensic Sci. 26:206-209.
Liddle, J.A., R.D. Kimbrough, L.L. Needham, R.E. Cline, A.L. Smmek, L.W. Yert, and
D.D. Bayse. 1979. A fatal episode of accidental methomyl poisoning. Clinical Toxicol.
15:159-167.
Loose, L.D., J.B. Silkworth, S.P. Mudzinski, K.A. Pittman, K.-F. Benitz, and W. Mueller.
1979. Modification of the immune response by organochlorine xenobiotics. Drug Chem.
Toxicol. 2:111-132.
Loprieno, N., R. Barale, S. Baroncelli, C. Bauer, G. Bronzetti, A. Cammellini, G. Cer-
cignani, C. Corsi, G. Gervasi, C. Leporini, R. Nieri, A.M. Rossi, G. Stretti, and G.
Turchi. 1976. Evaluation of the genetic effects induced by vinyl chloride monomer (VCM)
under mammalian metabolic activation: Studies in vitro and in viw. Mutat. Res. 40:85-96.
Lowrey, K., E.A. Glende, Jr., and R.O. Recknagel. 1981. Rapid depression of rat liver mi-
crosomal calcium pump activity after administration of carbon tetrachloride or bromo-
trichloromethane and lack of effect after ethanol. Toxicol. Appl. Phannacol. 59:389-394.
Luessenhop, A.J., J.C. Gallimore, W.H. Sweet, E.G. Struxness, and J. Robinson. 1958. The
toxicity in man of he~cavalent uranium following intravenous administration. Am. J.
Roentgenol. 79:83-100.
Lukaszewski, T. 1979. Acute tetrachloroethylene fatality. Clin. Toxicol. lS:411-415.
Malcolm, A.R., B.H. Pringle, and H.W. Fisher. 1973. Chemical toxicity studies with cul-
tured mammalian cells. Pp. 217-230 in G.E. Glass, ed. Bioassay Techniques and En~ron-
mental Chemistry. Ann Arbor, Mich.: Ann Arbor Science Publishers.
Maltoni, C. 1977. Recent findings on the carcinogenicity of chlorinated olefins. En~nron.
Health Perspect. 21:1-5.
Maltoni, C., G. Lefemine, A. Ciliberti, G. CoKi, and D. Carretti. 1981. Carcinogenicity bio-
assays of ~nnyl chloride monomer: A model of risk assessment on an experimental basis.
En~riron. Health Perspect. 41:3-29.
Marshall, L.E., and R.H. Himes. 1978. Rotenone inhibition of tubulin self-assembly. Bio-
chim. Biophys. Acta 543:590-594.
Marshall, T.C., and H.W. Dorough. 1979. Biliary e~ccretion of carbamate insecticides in the
rat. Pestic. Biochem. Physiol. 11:56-63.
Maynard, E.A., and H.C. Hodge. 1949. Studies of the to~cicity of ~rarious uranium com-
pounds when fed to e~cperimental animals. Pp. 309-376 in C. Voegtlin and H.C. Hodge,
cds. Pharmacology and Toxicology of Uranium Compounds. National Nuclcar Energy Se-
nes, Division VI, Vol. 1. New York: McGraw-Hill.
McCarthy, J.F., O.K. Fancher, G.L. Kcnnedy, M.L. Kcplinger, and J.C. Calandra. 1971.
Reproduction and teratology studies w~th the insecticide Carbofuran. To~cicol. Appl. Phar-
macol. 19:370. (abstr. 24)
McCormack, K.M., A. Abuelgasim, V.L. Sanger, and J.B. Hook. 1980. Postnatal morphol-
ogy and functional capacity of the kidney following prenatal trcatmcnt ~rith dinoseb in
rats. J. Toxicol. En~iron. Health 6:633-643.
McKc~a, M.J., and J.A. Zempel. 1981. Thc dose-dependent metabolism of l '~Cl methyl-
cne chlonde following oral administration to rats. Food Cosmet. Tosicol. 19:73-78.
McKcnDa, M.J., J.A. Zempel, E.O. Madrid, W.H. Braun, and P.J. Gehring. 1978. Metabo-
lism and phannacokinetic profile of ~rinylideDe chloride in rats follo~ring oral administra-
tiou. Toxicol. Appl. Pharmacol. 45:821-835.
Mcisocr, H.M., and L. Sorensen. 1966. Metaphase a:Test of Chinese hamster cells with rm
tenone. Exp. Cell Res. 42:291-295.
OCR for page 110
110 DRINKING WATER AND HEALTH
Mendoza, C.E., and H. Watanabe. 1978. Enhancement of the UDP glucuronyltransferase
activity and biliary excretion rate of 17,6-estradiol in the female rat fed hexachlorobenzene.
J. Agric. Food Chem. 26:458-460.
Mensik, D.C., R.V. Johnston, M.N. Pinkerton, and E.B. Whorton, Jr. 1976. The Cy~oge-
netic Effects of Picloram on the Bone Marrow Cells of Rats. Freeport, Tex.: Occupational
Health and Medical Research, Toxicology Research Laboratory, Health and Environmen-
tal Research, Dow Chemical Co. (unpublished) [11 pp.]
Merchan, J., J. Diaz-Gil, M.A. Figueras, M.A. Navarro, P. Viladiu, and he. Gosalvez. 1978.
Morphological study of rotenone-induced breast tumors in Wistar rats. Rev. Esp. Oncol-
ogia 25:107-120.
Metcalf, R.L., T.R. Fukuto, C. Collins, K. Borck, S.A. El-Aziz. R. Munoz, and C.C. Cassil.
1968. Metabolism of 2,2-dimethyl-2,3-dihydrobenzofuranyl-7-N-methylcarbamate (Fura-
dan) in plants, insects, and mammals. ]. Agric. Food Chem. 16:300-311.
Monster, A.C. 1979. Differences in uptake, elimination, and metabolism in exposure to
trichloroethylene, 1, 1,1-trichloroethane and tetrachloroethylene. Int. Arch. Occup. Envi-
ron. Health 42:311 -317.
Monster, A.C., G. Boersma, and W.C. Duba. 1976. Pharmacokinetics of trichloroethylene
in volunteers, influence of workload and exposure concentration. Int. Arch. Occup. Env~-
ron. Health 38:87-102.
Moore, L. 1980. Inhibition of liver-microsome calcium pump by in vivo administration of
CCl 4, CHCI 3 and 1,1 -dichloroethylene (vinylidene chloride). Biochem. Pharmacol.
29:2505-2511.
Morse, D.L., E.L. Baker, R.D. Kimbrough, and C.L. Wisseman. 1979. Propanil-chloracne
and methomyl toxicity in workers of a pesticide manufacturing plant. Clin. Toxicol.
15(1):13-21.
Murray, F.J., K.D. Nitschke, L.W. Rampy, and B.A. Schwetz. 1979. Embryotoxicity and
fetoto~cicity of inhaled or ingested vinylidene chloride in rats and rabbits. Toxicol. Appl.
Phannaeol. 49:189-202.
Myhr, B.C. 1973. A screen for pesticide toxicity to protein and RNA synthesis in HeLa cells.
1. Agric. Food Chem. 21:362-367.
Nakajima, T., and A. Sato. 1979. Enhanced activity of liver drug metabolizing enzyTnes for
aromatic and chlorinated hydrocarbons following food deprivation. Toxicol. Appl. Phar-
macol. 50:549-556.
National Cancer institute. 1976. Carcinogenesis Bioassay of Trichloroethylene. Carcinogene-
sis Tech. Rep. Ser. No. 2. DHEW Publ. No. (NIH) 76-802. Bethesda, Md.: U.S. Depart-
ment of Health, Education, and Welfare, Public Health Service, National Institutes of
Health. 197 pp.
National Cancer Institute. 1977a. Bioassay of Tetrachloroethylene for Possible Carcinogenic-
ity. Carcinogenesis Tech. Rep. Ser. No. 13. DHEW Publ. No. (NIH) 77-813. Bethesda,
Md.: U.S. Department of Health, Education, and Welfare, Public Health Service, Na-
tional Institutes of Health. 79 pp.
National Cancer Institute. 1977b. Bioassay of 1, 1,1-Trichloroethane for Possible Carcinoge-
nicity. Carcinogenesis Tech. Rep. Ser. No. 3. DHEW Publ. No. (NIH) 77-803. Bethesda,
Md.: U.S. Department of Health, Education, and Welfare, Public Health Senrice, Na-
tional Institutes of Health. 70 pp.
National Caneer Institute. 1978. Bioassay of Picloram for Possible Carcinogenicity. Carcino-
genesis Tech. Rep. Ser. No. 23. DHEW Publ. No. (NIH) 78-823. Bethesda, Md.: U.S.
Department of Health, Education, and Welfare, Public Health Service, National institutes
of Health. 91 pp.
National Cancer Institute. 1979. Bioassay of Aldicarb for Possible Carcinogenicity. Carcino-
OCR for page 111
Toxicity of Selected Contaminants 111
genesis Tech. Rep. Ser. No. 136. DHEW Publ. No. (NIH) 79-1391. Bethesda, Md.: U.S.
Department of Health, Education, and Welfare, Public Health Service, National Institutes
of Health. 106 pp.
National Council on Radiation Protection and Measurements. 1975. Natural Background
Radiation in the United States. NCRP Report No. 45. Bethesda, Md.: National Council on
Radiation Protection and Measurements. 163 pp.
National Research Council. 1977. Drinking Water and Health. Report of the Safe Drinking
Water Committee, Advisory Center on Toxicology, Assembly of Life Sciences. Washing-
ton, D.C.: National Academy of Sciences. 939 pp.
National Research Council. 1980. Drinking Water and Health, Vol. 3. Report of the Safe
Drinking Water Committee, Board on Toxicology and Environmental Health Hazards,
Assembly of Life Sciences. Washington, D.C.: National Academy Press. 415 pp.
National Research Council. 1982. Possible Long-Term Health Effects of Short-Term Expo-
sure to Chemical Agents, Vol. 1. Anticholinesterases and Anticholinergics. Report of the
Committee on Toxicology, Board on Toxicology and Ens ironmental Health Hazards, As-
sembly of Life Sciences. Washington, D.C.: National Academy Press. 289 pp.
National Toxicology Program. 1982a. Carcinogenesis Bioassay Experimental and Status Re-
port. March 1, 1982. Research Triangle Park, N.C:National Toxicology Program.
National Toxicology Program. 1982b. NTP Technical Report on the Carcinogenesis Bioassay
of Vinylidene Chloride in F344/N Rats and B6C3F ~ /N Mice. (Gavage Study) Tech. Rep.
Ser. No. 228. NTP-80-82. NIH Publ. No. 82-1784. Bethesda. Md.: U.S. Department of
Health and Human Services, Public Health Service, National institutes of Health. 184 pp.
National Toxicology Program. 1982c. Bioassay of Methylene Chloride for Possible Carcino-
genicity. (Final Report in Preparation) Bethesda, Md.: U.S. Department of Health and
Human Services, Public Health Service. National institutes of Health.
National Toxicology Program. 1982d. Bioassay of Tetrachloroethylene for Possible Carcino-
genicity. (Final Report in Preparation) Bethesda, Old.: U.S. Department of Health and
Human Services, Public Health Service, National institutes of Health.
National Toxicology Program. 1982e. Bioassay of 1, 1,1-Trichloroethane for Possible Carci-
nogenicity. (Final Report in Preparation) Bethesda, Md.: U.S. Department of Health and
Human Services, Public Health Service. National institutes of Health.
Nelson, B.K., BJ. Taylor, J.V. Setzer. and R.W. Hornung. 1979. Behavioral teratology of
perchloroethylene in rats. ]. Environ. Pathol. Toxicol. 3:233-2S0.
Nestmann, E.R., E.G.-H. Lee, T.I. Matula, G.R. Douglas, and ].C. Mueller. 1980. Muta-
genicity of constituents identified in pulp and paper mill effluents using the Salmonella/
mammalian-microsome assay. Mutat. Res. 79:203-212.
Nestmann, E.R., R. Otson, D.T. Williams, and DJ. Kowbel. 1981. Mutagenicity of paint
removers containing dichloromethane. Cancer Lett. 11 :295-302.
Nilsen, O.G., and R. Toftgaard. 1980. The influence of organic solvents on cytochrome
P~50-mediated metabolism of biphenyl and benzda)pyrene. Pp. 1235-1238 in MJ. Coon,
A.H. Conney, and R. W. Estabrook, eds. Microsomes, Drug Oxidation , Chemical Carcin-
ogenesis, Vol. 2. (4th International Symposium on Microsomes and Drug Oxidation) New
York: Academic Press.
Nolan, R.J., F.A. Smith, C.J. Muller, and T.C. Curl. 1980. Kinetics of 14 C-labeled picloram
in male Fischer 344 rats. Midland, Mich.: Toxicology Research Laboratory, Health and
Environmental Science, Dow Chemical Co., U.S.A. (unpublished) 34 pp.
Nomiyama, H., and K. Nomiyama. 1979a. Host and agent factors modifying metabolism of
trichloroethylene. Ind. Health (Japan) 17:21-28.
Nomiyama, H., and K. Nomiyama. 1979b. Pathway and rate of metabolism of trichloroethy-
lene in rats and rabbits. lnd. Health (]apan) 17:29-37.
OCR for page 112
112 DRINKING WATER AND HEALTH
Nomiyama, K., A. Yamamoto, and C. Sato. 1974. Assay of urinary enzymes in toxic ne-
phropathy. Toxicol. Appl. Pharmacol. 27:484-490.
Norris, J.M. 1977. Toxicological and pharmacokinetic studies on inhaled and ingested vinyli-
dene chloride in laboratory animals. Pp. 45-50 in 1977 Paper Synthetics Conference, Sept.
26-28, The Drake, Chicago, Ill. Atlanta: Technical Association of the Pulp and Paper In-
dustry.
Noviakovia, V., J. Musil, D. Buckiovia, O. Tiaborskiy, H. Solloiva, and P. Viyborniy. 1981.
Effect of tetrachloromethane and other chlorinated hydrocarbons on the hepatic metabo-
lism in the isolated perfused rat liver. J. Hyg. Epidemiol. Microbial. Immunol. 25:369-383.
Ott, M.G., W.A. Fishbeck, J.C. Townsend, and E.J. Schneider. 1976. A health study of
employees exposed to vinylidene chloride. J. Occup. Med. 18:735-738.
Parke, D.V., and R.T. Williams. 1955. Studies in detoxication 63. The metabolism of halo-
genobenzenes. (a) Meta-dichlorobenzene. (b) Further observations on the metabolism of
chlorobenzene. Biochem. J. 59:415-422.
Parry, AM. 1973. The induction of gene conversion in yeast by herbicide preparations. Mu-
tat. Res. 21 :83-91.
Peoples, S.A., K.T. Maddy, and C.R. Smith. 1978. Occupational exposure to Temik (aldi-
carb) as reported by California physicians for 1974-1976. Vet. Hum. Toxicol. 20:321-324.
Pessayre, D., J.C. Wandscheer, V. Descatoire. 1.Y. Artigou, and J.P. Benhamou. 1979a.
Formation and inactivation of a chemically reactive metabolite of vinyl chloride. Toxicol.
Appl. Pharmacol. 49:S05-515.
Pessayre, D. , H. Allemand, J.C. Wandscheer, V. Descatoire, J.Y. Artigou, and J. P. Benha-
mou. 1979b. Inhibition, activation, destruction, and induction of drug-metabolizing en-
zymes by trichloroethylene. Toxicol. Appl. Pharmacol. 49:355-363.
Pessayre, D., J.C. Wandscheer, V. Descatoire, A. Dolder, C. Degott, and J.P. Benhamou.
1980. Cumulative effects of repeated doses of compounds transformed into reactive metab-
olites. Biochem. Pharmacol. 29:1041-1047.
Plea, G.L., and R.E. Larson. 1965. Relative nephroto~cic properties of chlorinated methane,
ethane, and ethylene derivatives in mice. Toxicol. Appl. Pharmacol. 7:3744.
Politzer, P., P. Trefonas III, I.R. Politzer, and B. Elfman. 1981. Molecular properties of the
chlorinated ethylenes and their epo~cide metabolizes. Ann. N.Y. Acad. Sci. 367:478-492.
PoDomarkov, V., and L. Tomatis. 1980. Long-tenn testing of ~rinylidene chloride and chloro-
prene for carcinogenicity in rats. Oncology 37:136-141.
Poole, D.C., Vet. Simmon, and G.W. Newell. 1977. In vitro mutagenic activity of fourteen
pesticides. Toxicol. Appl. Pharmacol. 41:196. (abstr. 155)
Preache, M.M., and J.E. Gibson. 1975. Effects in mice of high and low environmental tem-
perature on the maternal and fetal toxicity of 2-sec-butyl-4,6-dinitrophenol (dinoseb) and
on disposition of 114 C]-dinoseb. Teratology 12:147-156.
Prendergast, J.A., R.A. Jones, L.J. Jenkins, Jr., and J. Siegel. 1967. Effects on experimental
animals of long-tenn inhalation of trichloroethylene, carbon tetrachloride, 1,1,1-trichlo-
roethane, dichlorodifluoromethane, and 1,1-dichloroethylene. Topical. Appl. Pharmacol.
10:270-289.
Probst, G.S., and L.E. Hill. 1980. Chemically-induced DNA repair synthesis in primary rat
hepatocytes: A correlation with bacterial mutagenicity. Ann. N.Y. Acad. Sci. 349:405406.
Putcha, L., J.V. Bruckner, and S. Feldman. 1982. Phannacokinetics of orally and intraven-
ously administered 1,1-dichloroethylene in the rat. Toxicologist 2:32. (abstr. 113)
Quarles, J.M., M.W. Sega, C.K. Schenley, and W. Lijinsky. 1979a. Transfo'.llation of ham-
ster fetal cells by nitrosated pesticides in a transplacental assay. Cancer Res. 39:4525-4S33.
Quarles, J.M., M.W. Sega, C.K. Schenley, and R.W. Tennant. 1979b. Rapid screening for
OCR for page 113
Toxicity of Selected Contaminants 113
chemical carcinogens: Transforming activity of selected nitroso compounds detected in a
transplacental host-mediated culture system. Natl. Cancer Inst. Mono~. 51:2S7-263.
Quast, J.F., C.G. Humiston, B.A. Schwetz, M.F. Balmer, L.W. Rampy, J.M. Noms, and
P.1. Gehnng. 1977. Results of 90-day toxicity studies in rats given vinylidene chloride in
their drinking water or exposed to VDC vapors by inhalation. Toxicol. Appl. Pharmacol.
41:187. (abstr. 134)
Radike, M.J., K.L. Stemmer, and E. gingham. 1981. Effect of ethanol on vinyl chloride
carcinogenesis. Environ. Health Perspect. 41:S9-62.
Radwan, Z., and D. Henschler. 1977. Uptake and rate of metabolism of vinyl chloride by the
isolated perfused rat liver preparation. lint. Arch. Occup. Environ. Health 40:101-110.
Rampy, L.W., J.F. Quast, C.G. Humiston, M.F. Balmer, and B.A. Schwetz. 1977. Interim
results of two-year toxicological studies in rats of vinylidene chloride incorporated in the
drinking water or administered by repeated inhalation. Environ. Health Perspect. 21:33-
43.
Rannug, U., and B. Beije. 1979. The mutagenic effect of 1,2-dichloroethane on Salmonella
typhimurium. II. Activation by the isolated perfused rat liver. Chem. Biol. Interact.
24:265-285.
Rao, K.S., J.S. Murray. Mad. Deacon, J.A. John, L.L. Calhoun, and ].T. Young. 1980.
Teratogenicity and reproduction studies in animals inhaling ethylene dichloride. Pp. 149-
166 in B. Ames, P. Infante, and R. Reitz, eds. Banbury Report 5. Ethylene Dichloride: A
Potential Health Risk. Cold Spring Harbor, N.Y.: Cold Spring Harbor Laboratory.
Recknagel, R.O. 1967. Carbon tetrachloride hepatotoxicity. Phannacol. Rev. 19:145-208.
Recknagel, R.O., and E.A. Glende, fir. 1973. Carbon tetrachloride hepatoto~cicity: An e~cam-
ple of lethal cleavage. CRC Crit. Rev. To~cicol. 2:263-297.
Reichert, D., H.W. Werner, M. Metzler, and D. Henschler. 1979. Molecular mechanism of
1,1-dichloroethylene toxicity: Excreted metabolites reveal different pathways of reactive
intermediates. Arch. To2cicol. 42:159~169.
Reid, W.D., G. Krishna, J.R. Gillette, and B.B. Brodie. 1973. Biochemical mechanism of
hepatic necrosis induced by aromatic hydrocarbons. Pharmacology 10:193-214.
Renner, G., E. Richter, and K.P. Schuster. 1978. N-Acetyl-S-(pentachlorophenyl)cysteine, a
new urinary metabolite of he~cachlorobenzene. Chemosphere 7:663-668.
Reynolds, E.S., and M.T. Moslen. 1977. Damage to hepatic cellular membranes by chlori-
nated olef~ns with emphasis on synergism and antagonism. Environ. Health Perspect.
21:137-147.
Reynolds, E.S., M. T. Moslen, S. Szabo, R.1. Jaeger, and S.D. Murphy. 1975. Hepatoto~cic-
ity of vinyl chloride and 1,1-dichloroethylene: Role of minced function oxidase system. Am.
1. Pathol. 81:219-236.
Richter, E., and S.G. Schafer. 1981. Intestinal excretion of he~cachlorobenzene. Arch. To~c-
icol. 47:233-239.
Rickard, R.W. 1980. Chemical properties and potential toxicological significance of N-nitro-
socarbamates. Diss. Abstr. Int. 40B:559S-B.
Rimington, C., and G. Ziegler. 1963. Experimental porphyria in rats induced by chlorinated
benzenes. Biochem. Pharmacol. 12:1387-1397.
Robens, J.F. 1978. Tests for possible carcinogenicity of 20 pesticides in Osborne-Mendel rats
and B6C3F' mice. Topical. Appl. Pharmacol. 4S:236. (abstr. 40)
Roschlau, G., and H. Rodenkirchen. 1969. Histological examination of the diaplacental
action of carbon tetrachloride and allyl alcohol in mice embryos. Exp. Pathol. 3:255-263.
Rossner, P., R.J. Sram, J. Novakova, and V. Lambl. 1980. Cytogenetic analysis in workers
occupationally deposed to Vinyl chloride. Mutat. Rcs. 73:425-427.
OCR for page 114
114 DRINKING WATER AND HEALTH
Roswell, R.L., and M.E. Wrenn. 1980. Model for uranium metabolism in man. In Annual
Report, Radiobiology Laboratory. Salt Lake City: University of Utah.
Rozman, K., T. Rozman, arid H. Greim. 1981. Enhanced fecal elimination of stored hexa-
ehlorobenzene from rats and rhesus monkeys by hexadeeane or mineral oih Toxieology
22:33-44.
Rueber, M.D. 1981. Careinogenieity of pieloram. J. Toxieol. Environ. Health 7:207-222.
Sanotskii, I.V., R.M. Dawyan, and V.I. Glushehenko. 1980. Study of the reproductive func-
tion in men exposed to chemicals. Gig. Tr. Prof. Zabol. 5:28-32.
Santi, R., and C.E. Toth. 1965. Toxieology of rotenone. Farmaeo 20:270. [Food Cosmet.
Toxieol. 4:108, abstr. 937, 1966]
Sasaki, M., K. Sugimura, Mitsuaki, A. Yoshida, and S. Abe. 1980. Cytogenetie effects of 60
chemicals on cultured human and Chinese hamster cells. Senshokutai (La Kromosomo)
20:574-584.
Sathaiah, V., G.A. Sastry, and P. Venkat Reddy. 1974. Cytological effects of 2,3-dihvdro-
2,2-dimethyl-7-benzofuranyl methylearbamate "Carbofuran.'' Curr. Sei. 43:53-54. (letter
to the editor)
Schumann, A.M., J. F. Quast, and P.G. Watanabe. 1980. The pharmacokineties and mac-
romolecular interactions of perehloroethylene in mice and rats as related to oncogenicity.
Toxicol. Appl. Pharmaeol. 55:207-219.
Schumann, A.M., T.R. Fox, and P.G. Watanabe. 1982. 114ClMethyl chloroform (1,1.1-
trichloroethane): Pharmaeokineties in rats and mice following inhalation exposure. Tox-
ieol. Appl. Pharmaeol. 62:390-401.
Sehwetz, B.A., B.K.J. Leong, and Pal. Gehring. 1974. Embryo and fetotoxieity of inhaled
carbon tetrachloride, 1,1-diehloroethane and methyl ethyl ketone in rats. Toxieol. Appl.
Pharmaeol. 28:452-464.
Sehwetz, B.A., B.K.J. Leong, and P.J. Gehring. 1975. The effect of maternally inhaled tri-
ehloroethylene, perehloroethylene, methyl chloroform, and methylene chloride on embryo-
nal and fetal development in mice and rats. Toxieol. Appl. Pharmaeol. 32:84-96.
Seller, J.P. 1977. Nitrosation in vitro and in biro by sodium nitrite, and mutagenicity of ni-
trogenous pesticides. Mutat. Res. 48:225-236.
Shelton, D.W., and L.J. Weber. 1981. Quantification of the joint effects of mixtures of hepa-
totoxie agents: Evaluation of a theoretical model in mice. Environ. Res. 26:33-41.
Shimkin, M.B., and G.D. Stoner. 1975. Lung tumors in mice: Application to eareinogenesis
bioassay. Adv. Cancer Res. 21:1-58.
Short, R.D., J.L. Minor, J.M. Winston, and C.C. Lee. 1977. A dominant lethal study in male
rats after repeated exposure to vinyl chloride or vinylidene chloride. ]. Toxieol. Environ.
Health 3:965-968.
Simmon, V.F., K. Kauhanen, and R.G. Tardiff. 1977. Mutagenic activity of chemicals iden-
tified in drinking water. Pp. 249-258 in D. Scott, B.A. Bridges, and F.H. Sobels, eds.
Progress in Genetic Toxieology. Proceedings of the Second international Conference on
Environmental Mutagens, Edinburgh, July 11-15. New York: Elsevier/North-Holland.
Simon, G.S., R.G. Tardiff, and 3.~. Borzelleea. 1979. Failure of hexaehlorobenzene to in-
duce dominant lethal mutations in the rat. Toxieol. Appl. Pharmacol. 47:415-419.
Sipes, I.G., and AJ. Gandolfi. 1980. In vitro comparative bioact*ation of aliphatic hydrog-
enated hydrocarbons. Pp. 501-506 in B. Holmstedt, R. Lauwerys, M. Mereier, and M.
Roberfroid, eds. Mechanisms of Toxicity and Hazard Evaluation. Proceedings of the Sec-
ond International Congress on Toxieology, Brussels, July 6-11. New York: Elsevier/North-
Holland.
Slaeilc-Erben, R., R. Roll, G. Franke, and H. Uehleke. 1980. Triehloroethylene vapours do
not produce dominant lethal mutations in male mice. Arch. Toxicol. 45:37-44.
OCR for page 115
Toxicity of Selected Contaminants 115
Smith, A.G., J.E. Francis, and F. DeMatteis. 1980. Lobes of rat liver respond at different
rates to challenge by dietary hexachlorobenzene. Biochem. Phaunacol. 29:3127-3131.
Smith, D.M. 1977. Organophosphorus poisoning from emergency use of a handsprayer.
Practitioner 218:877-883.
Smith, W.D.L. 1981. An investigation of suspected dinoseb poisoning after the agricultural
use of a herbicide. Practitioner 225:923-926.
Soderlund, ED., S.D. Nelson, and E. Dybing. 1979. Mutagenic activation of tris(2,3-dibro-
mopropyl)phosphate: The role of microsomal osidative metabolism. Acta Pharmacol.
Tosicol. 45:112-121.
Spencer, H.C., V.K. Rowe, E.M. Adams, and D.D. Irish. 1948. Toxicological studies on
laboratory animals of certain alkyldinitrophenols used in agriculture. J. Ind. Hyg. Toxicol.
30:10-25.
Stewart, R.D., H.H. Gay, D. S. Erley, C.L. Hake, and A.W. Schaffer. 1961. Human expo-
sure to tetrachloroethylene vapor. Relationship of expired air and blood concentrations to
exposure and toxicity. Arch. Environ. Health 2:516-522.
Stolzenberg, S.J., and C.H. Hine. 1980. Mutagenicity of 2- and 3-carbon halogenated com-
pounds in the Salmonella/mammalian-microsome test. Environ. Mutagenesis 2:59-66.
Stone, R.S., S.A. Bencosme, H. Latta, and S.C. Madden. 1961. Renal tubular fine struc-
ture: Studied during reaction to acute uranium injury. Arch. Pathol. 71:160-174.
Stott, W.T., J.F. Quast, and P.G. Watanabe. 1982. The pharmacokinetics and macromolec-
ular interactions of trichloroethylene in mice and rats. Tosicol. Appl. Pharrnacol. 62:137-
151.
Sundlof, S.F. 1981. The pharmacokinetics of hesachlorobenzene in male beagles. Diss. Ab-
str. Int. 41B:4084B.
Suzuki, Y. 1981. Neoplastic and nonneoplastic effects of ~rinyl chloride in mouse lung. Enn
ron. Health Perspect. 41:31-52.
S`rendsgeard, D.J., K.D. Courtucy, and J.E. Andrews. 1979. Hesachlorobenzene (HCB)
deposition in maternal and fetal tissues of rat and mouse. II. Statistical quantification of
HCB in tissues. En~riron. Res. 20:267-281.
Thompson, J.D., and B.R. Nechay. 1981. Inhibition by metals of a canine renal calcium,
magnesium-activated adenosine triphosphatase. J. TosicoJ. Environ. Health 7:901-908.
Thompson, D.J., 1.L. Emerson, R.J. Strebing, C.G. Gerbig, and V.B. Robinson. 1972.
Tcratolog~y and postnatal studies on 4-amino-3,5,6-trichloropicolinic acid (picloram) in the
rat. Food Cosmet. Tosicol. 10:797-803.
Tobin, J.S. 1970. Carbofuran: A new carbamate insecticide. J. Occup. Med. 12:16-19.
Toftgard, R., O.G. Nilsen, and J.A. Gustaf~n. 1981. Changes in rat lrver microsomal cytochrome
P~SO and enzymatic ac~ after the inhalation of n-he~cane, ylene, methyl ethyl ketone and
methylchJo~oform for four ~reeks. Seand. J. Work En~ron. Health 7:31-37.
Tomkins, D., E. Kwok, and G. Douglas. 1980. Tcsting of pesticides for induction of sister
chromatic eschangc in Chinese hamster o~rary cells. Can. ]. Genet. Cytol. 22:681. (abstr.)
Tsircl'nikov, N.I., and S.G. Dobro~rol'skaya. 1973. Morphohistochemical study of the li~rcr in
embryos during administration of carbon tetrachloride at ~rarious stages of onc~genesis.
Byull. Eksp. Biol. Med. 76:95-97.
Turner, J.C., and V. Shanks. 1980. Absorption of some organochlorine compounds by the
rat small intestine—in viva. Bull. En~ron. Contam. Tosicol. 24:652-655.
Ung~ary, G., A. Hudak, E. Tatrai, M. Ldrincz, and G. Folly. 1978. Effects of vinyl chloride
exposure alone and in combination with trypan blue—applied systematically dunng all
thirds of pregnancg on the fetuses of CFY rats. Tosicology 11:45~54.
United Nations. 1977. Sources and Effects of Ionizing Radiation. UN Pcp. No. E.77.IX.1.
Ncw York: United Nations.
OCR for page 116
116 DRINKING WATER AND HEALTH
U.S. Energy Research and Development Administration. 1976. Uranium toxicity. Pp. Ap-
pend~c IX.D 1-10 in ERDA 1541, Environmental Statement, Light Water Breeder Reactor
Program: Commercial Application of LWBR Technology, Vol. III. Washington, D.C.:
U.S. Energy Research and Development Administration.
U.S. Environmental Protection Agency. 1975a. interim Primary Drinking Water Regula-
tions. Proposed Maximum Contaminant Levels for Radioactivity. Fed. Reg. 40(158):
34324-34328.
U.S. Environmental Protection Agency. 1975b. Preliminary Assessment of Suspected Car-
cinogens in Drinking Water: Report to Congress. Report No. EPA/560/4-75-005. Wash-
ington, D.C.: U.S. Environmental Protection Agency, Office of Toxic Substances. Avail-
able from National Technical Information Service, Springfield, Va., as Publ. No.
PB-250-961. 52 - pp.
Van Duuren, B.L., B.M. Goldschmidt, G. Loewengart, A.C. Smith, S. Melchionne, I. Seid-
man, and D. Roth. 1979. Carcinogenicity of halogenated olefinic and aliphatic hydrocar-
bons in mice. J. Natl. Cancer Inst. 63:1433-1439.
Van Ryzin, I., and K. Rail 1980. The use of quantal response data to make predictions. Pp.
273-290 in H.R. Witschi, ed. The Scientific Basis of Toxicity Assessment. Developments in
Toxicology and Environmental Science, Vol. 6. New York: Elsevier/North-Holland.
Vianna, N.J., J. Brady, and P. Harper. 1981. Angiosarcoma of the liver: A single lesion of
vinyl chloride exposure. Environ. Health Perspect. 41:207-210.
Villeneuve, D.C., and S.L. Hierlihy. 1975. Placental transfer of hexachlorobenzene in the
rat. Bull. Environ. Contam. Toxicol. 13:489-491.
Villeneuve, D.C., L.G. Panopio, and D.L. Grant. 1974. Placental transfer of hexachloroben-
zene in the rabbit. Environ. Physiol. Biochem. 4:112-115.
Viola, P.L., and A. Caputo. 1977. Carcinogenicity studies on vinylidene chloride. Environ.
Health Perspect. 21:45-47.
Vos, J.G., M.J. ran Logten, J.G. Kreeftenberg, and W. Kruizinga. 1979. Hexachloroben-
zene-induced stimulation of the humoral immune response in rats. Ann. N.Y. Acad. Sci.
320:535-550.
Vozo~raya, M.A. 1976. Effect of small concentrations of benzene, dichloroethane, and their
combination on the reproductive function of animals. Gig. Sanit. 6:100-102.
Vozo~raya, M.A., and L.K. Malyaro~ra. 1975. Mechanism of the effect of dichloroethane on
the fetus of experimental animals. Gig. Sanit. No. 6:94-96.
Ware, S.A., and W.L. West. 1977. Investigation of Selected Potential Environmental Con-
taminants: Halogenated Benzenes. Final Technical Report. EPA/560/2-77/004. Wash-
ington, D.C.: U.S. Environmental Protection Agency, Office of Toxic Substances. 297 pp.
Waskell, L. 1978. A study of the mutagenicity of anesthetics and their metabolizes. Mutat.
Rcs. S7:141-153.
Watanabe, P.G., G.R. McGowan, and P.J. Gehring. 1976a. Fate of [~4Cl vinyl chloride
after single oral administration in rats. Toxicol. Appl. Pharmacol. 36:339-352.
Watanabe, P.G., G.R. McGowan, E.O. Madrid, and P.J. Gehring. 1976b. Pate of TIC]
vinyl chloride following inhalation exposure in rats. Topical. Appl. Pharmacol. 37:49-59.
Watanabe, P.G., J.D. Young, and P.J. Getnng. 1977. The importance of non-linear (dose-
dependent) phannacokinetics in hazard assessment. J. Environ. Pathol. Toxicol. 1:147-
lS9.
Wcast, R.C., and S.M. Selby. 1975. Handbook of Chemistry and Physics, 56th ed. Cleve-
land, Ohio: CRC Press.
Wilson, J.G. 1954. Influence on the offspring of altered physiologic states during pregnancy
in the rat. Ann. N.Y. Acad. Sci. 57:517-525.
OCR for page 117
Toxicity of Selected Contaminants 117
Windholz, M. 1976. The Merck Index. An Encyclopedia of Chemicals and Drugs, Ninth ed.
Rahway, N.~.: Merck and Co., Inc.
Wirthgen, B., and W. RaMce. 1977. Determination of the terminal residues of herbicides
and their toxicological importance. Nahrung 21 (5):443-4SO.
Wolfe, J.L., and R.J. Esher. 1980. Toxicity of carbofuran and lindane to the old-field mouse
(Peromyscus polionotus) and the cotton mouse (P. gossypinus). Bull. Environ. Contam.
Toxicol. 24:894-902.
Yang, K.H., R.E. Peterson, and J.M. Fujimoto. 1979. Increased bile-duct pancreatic fluid
flow in benzene and halogenated benzene-treated rats. Toxicol. Appl. Pharmacol. 47:505-
514.
Yang, R.S.H., K.A. Pittman, D.R. Rourke. and V.B. Stein. 1978. Pharmacokinetics and
metabolism of hexachlorobenzene in the rat and rhesus monkey. J. Agric. Food Chem.
26:1076-1083.
Yu, C., R.L. Metcalf, and G.NI. Booth. 1972. inhibition of acetylcholinesterase from mam-
mals and insects by carbofuran and its related compounds and their toxicities toward these
animals. J. Agric. Food Chem. 20:923-926.
Zupko, A.G.. and L.D. Edwards. 1949. A toxicological study of p-dichlorobenzene. J. Am.
Pharm. Assoc., Sci. Ed. 38:124-131.
Representative terms from entire chapter:
vinyl chloride
