297 922
CHROMIUM
Ambient Water Quality Criteria
Criteria and Standards Division
Office of Water Planning and Standards
U.S. Environmental Protection Agency
Washington, D.C.
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CRITERION DOCUMENT
CHROMIUM
CRITERIA
Aquatic Life
For trivalent chromium the criterion to protect freshwater
aquatic life as derived using the Guidelines is "e(0-83*ln
(hardness )+2.94).. as a 24-hour average (see the figure
"24-hour average trivalent chromium concentration vs. hardness")
and the concentration should not exceed "e(°•83* In(hardness)
+3.72)« (See the figure "maximum trivalent chromium concen-
tration vs. hardness") at any time.
For hexavalent chromium the criterion to protect freshwater
aquatic life as derived using the Guidelines is 10 \ig/l as a
24-hour average concentration and the concentration should not
exceed 110 ug/1 at any time.
For saltwater aquatic life, no criterion for trivalent chro-
mium can be derived using the Guidelines, and there are insuff-i-/'
cient data to estimate a criterion using other procedures.
For hexavalent chromium the criterion to protect saltwater
aquatic life as derived using the Guidelines is 25 ug/1 as a
24-hour average and the concentration should not exceed 230 ug/1
at any time.
Human Health
For the protection of human health from the toxic properties
of chromium (except hexavalent chromium) ingested through water
and contaminated aquatic organisms, the recommended water quality
criterion is 50 ug/1.
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For the maximum protection of human health from the potential
carcinogenic effects of exposure to hexavalent chromium through
ingestion of water and contaminated aquatic organisms, the ambient
water concentration is zero. Concentrations of hexavalent chro-
mium estimated to result in additional lifetime cancer risks rang-
ing from no additional risk to an additional risk of 1 in 100,000
are presented in the Criterion Formulation section of this docu-
ment. The Agency is considering setting criteria at an interim
target risk level in the range of 10""^, 10~^, or 10"^ with corres-
ponding criteria of 8 ng/1, 0.8 ng/1, and v.08 ng/1, respectively.
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CHROMIUM
Introduction
Chromium is a metallic element which can exist in sev-
eral valence states. However, in the aquatic environment
it virtually is always found in valence states +3 or +6.
Hexavalent chromium is a strong oxidizing agent which reacts
readily with reducing agents such as sulfur dioxide to give
trivalent chromium. Cr III oxidizes slowly to Cr VI, the
rate increasing with temperature. Oxidation progresses
rapidly when Cr III absorbs to MnO, but is interfered with
by Ca II and Mg II ions. Thus, accumulation would probably
occur in sediments where chemical equilibria favor the forma-
tion of Cr III, while Cr VI, if favored, would presumably
dis.sipate in soluble forms. Hexavalent chromium exists
in solution as a component of an anion, rather than a cation,
and therefore, does not precipitate from alkaline solution.
The three important anions are: hydrochromate, chromate,
and dichromate. The proportion of hexavalent chromium pre-
sent in each of these forms depends on pH. In strongly basic
and neutral solutions the chromate form predominates. As
pH is lowered/ the hydrochromate concentration increases.
At very low pH the dichromate species predominates. In
the pH ranges encountered in natural waters the proportion
of dichromate ions is relatively low. In the acid portion
of the environmental .range, the predominant form is hydrochro-
mate ion (63.6 percent at pH 6.0 to 6.2) (Trama and Benoit,
1960). In the alkaline portion of the range, the predominant
form is chromate ion (95.7 percent at pH 8.5 to 7.8) (Trama
A-l
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and Benoit, 1960). The anionic form of chromium can affect
its toxicity.
Trivalent chromium in solution forms numerous types
of hexacoordinate complexes (Cotton and Wilkinson, 1962).
The best known and one of the most stable of these is the
amine class (complexes include aquo ions, acido complexes
(which are anionic), and polynuclear complexes. Complex
formation can prevent precipitation of the hydrous oxide
or other insoluble forms at pH values at which it would
otherwise occur.
Chromium salts are used extensively in the metal finish-
ing industry as electroplating, cleaning, and passivating
agents, and as mordants in the textile industry. They also
are used in cooling waters, in the leather tanning industry,
in catalytic manufacture, in pigments and primer paints,
and in fungicides and wood preservatives. Kopp reported
a mean surface water concentration in the United States
of 9.7 ;ug/l, based on 1,577 samples. Trivalent chromium
is recognized as a essential trace element for humans.
Hexavalent chromium in the workplace is suspected of being
carcinogenic.
In the freshwater environment, hexavalent chromium has
been shown acutely toxic to invertebrates at concentrations
as low as 22 jag/1 (Baudouin and Scoppa, 1974) and 17,600
;ug/l for vertebrates (Pickering and Henderson, 1966). For
marine waters the figures are 2,000/ag/l for invertebrates
(Eisler and Hennekey, 1977) and 30,000/jg/l for vertevrates
(Mearns, et al. 1976).
A-2
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For trivalent chromium the figure is 2,000 jug/1 in
freshwater (Biesinger and Christensen, 1972) and no data
on marine organisms are available. Hexavalent chromium
has been shown chronically toxic to freshwater organisms
at 105 jug/1 (Sauter, et al. 1976) and to marine organisms
at 38 jug/1 (Oshida, 1978). For trivalent chromium in fresh-
water the figure is 445 jug/1 (Biesinger and Christensen,
1972) and no data on the chronic toxicity of trivalent chro-
mium in marine waters are available.
Since chromium is an element, it will not be destroyed
and may be expected to persist indefinitely in the environ-
ment in some form.
Both Cr VI and ,Cr III have shown mutagenic activity (Rafetto;
et al. 1977). Occupational exposure to chromate fumes is
suspected of causing cancer in humans (Natl. Acad. Sci.
1974) .
A-3
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REFERENCES
Baudouin, M.F., and P. Scoppa. 1974. Acute toxicity of various
metals to freshwater zooplankton. Bull. Environment. Contam.
Toxicol. 12: 745.
Biesinger, K.E., and G.M. Christensen. 1972. Effects of
various metals on survival, growth, reproduction and metabo-
lism of Daphnia magna. Jour. Fish. Res. Board Can. 29: 1691.
Cotton, F.A., and G. Wilkinson. 1962. Advanced inorganic
chemistry. Interscience Publishers, John Wiley and Sons,
Inc., New York.
Cutshall, N.W. 1967. Chromium-51 in the Columbia River and
adjacent Pacific Ocean. Ph.D. thesis. Oregon State University,
Corvallis.
Eisler, R., and R.J. Hennekey. 1977. Acute toxicities of
Cd , Cr , Hg , Ni and Zn to estuarine macrofauna. Arch.
Environ. Contam. Toxicol. 6: 315.
Kopp, J.F. 1969. The occurrence of trace elements in water.
Page 59. In D. Hemphill, ed. Trace Substances in Environmental
Health III. University of Missouri, Columbia.
Mearns, A.J., et al. 1976. Chromium effects on coastal organ-
isms. Jour. Water Pollut. Control Fed. 48: 1929.
A-4
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National Academy of Sciences. 1974. Chromium. U.S. Government
Printing Office, Washington, D.C.
Oshida, P.S. 1978. A safe level of hexavalent chromium for
marine polychaete. S. Calif. Coastal Water Res. Proj. El
Segundo, Calif. Annu. Rep.
Pickering, Q.H., and C. Henderson. 1966. The acute toxicity
of some heavy metals to different species of warm water
fishes. Int. Jour. Air-Water Pollut. 10: 453.
Rafetto, G., et al. 1977. Direct interaction with cellular
targets as the mechanism for chromium carcinogenesis. Tumori
63: 503 (cited from.Toxline) .
Sauter, S., et al. 1976. Effects of exposure to heavy metals
on selected freshwater fish. Ecol. Res. Ser. U.S. Environ.
Prot. Agency, Washington, D.C.
Trama, F.B., and R.J. Benoit. 1960. Toxicity of hexavalent
chromium to bluegills. Jour. Water Pollut. Control Fed.
32: 868.
A-5
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.AQUATIC LIFE TOXICOLOGY*
FRESHWATER ORGANISMS
Introduction
Chromium is a chemically complex metal which occurs in va-
lence states ranging from -2 to +6. The hexavalent and trivalent
chromium compounds are the biologically and environmentally sig-
nificant forms of the element, but they have very different chemi-
cal characteristics. Hexavalent chromium is very soluble in
natural water. As with many other metal cations, the solubility
j ,»
of trivalent chromium in natural water is low and varies with
water quality, being less soluble at high pH, alkalinity, and
hardness.
Trivalent chromium is substantially more toxic to aquatic
life in soft than in hard water. The effect of water hardness on
the toxicity of hexavalent chromium is insignificant. As a result
of these relationships the criterion for trivalent chromium is
hardness related while that for hexavalent chromium is a single
concentration for the 24-hour average.
*The reader is referred to the Guidelines for Deriving Water
Quality Criteria for the Protection of Aquatic Life [43 PR 21506
(May 18, 1978) and 43 FR 29028 (July 5, 1978)] in order to better
understand the following discussion and recommendation. The fol-
lowing tables contain the appropriate data that were found in the
literature, and at the bottom of each table are the calculations
for deriving various measures of toxicity as described in the
Guidelines.
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Acute Toxicity
As shown in Table 1, the data base for freshwater fish and
chromium has 73 LC50 values, but about half of the values are for
goldfish and fathead minnows from one report. Values include data
for 14 species from seven families. Fifty-three percent of the
values did not need adjustment for standardization. For the LC50
values that required adjustment for test methods or duration of
the test, only four of the tests were less than 96 hours.
Adjustment was required for 34 static tests and for 26 tests in
which the concentrations were not measured.
No side-by-side static and flow-through tests or measured and
unmeasured test concentrations are available for either hexavalent
or trivalent chromium for direct comparison of these two
conditions with regard to the appropriateness of the adjustment
factors.
The adjusted 96-hour LC50 values for hexavalent chromium for
nine species ranged from 9/620 ug/1 for the fathead minnow tested
in soft water to a high of 138,500 ug/1 for the largemouth bass in
hard water. Wallen, et al. (1957) studied the toxicity of
hexavalent chromium to mosquitofish using potassium and sodium
salts of both dichromate and chromate. Based on chromium, both
dichromate salts were about half as toxic as either chromate salt.
Trama and Benoit (1960) also studied the toxicity of hexavalent
chromium using potassium dichromate and potassium chromate. The
unadjusted 96-hour LC50 values are 110,000 ug/1 for the dichromate
salt and 170,000 ug/1 for the chromate salt. They attributed the
lower LC50 value of the dichromate salt as due to its acidity
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being greater than that of the chromate salt because chromium is
slightly more toxic at lower pH values.
The variation in toxicity of hexavalent chromium due to water
hardness was less than the variation between the dichromate and
chromate salts of hexavalent chromium in soft water (Pickering and
Henderson, 1966). The unadjusted fathead minnow 96-hour LC50
values for dichromate and chromate salts in soft water were 17,600
ug/1 and 45,600 ug/1, respectively. The unadjusted 96-hour LC50
values for dichromate in soft and hard water were 17,600 ug/1 and
27,300 ug/1/ respectively. The unadjusted 96-hour LC50 value of
hexavalent chromium, using the dichromate salt, to the bluegill in
soft water was 118,000 ug/1 and in hard water was 133,000 ug/1.
For both of the species, the difference in LC50 values due to
hardness is less than a factor of 2.
The data from Adelman and Smith (1976) as shown in Tables 1
and 7 indicate that the threshold lethal concentration for hexa^
valent chromium does not occur within 96 hours. For the mean of
16 LC50 values, the ratio of 11-day to 96-hour values is 0.37 for
the fathead minnow and 0.27 for the goldfish.
The geometric mean of the adjusted values for hexavalent
chromium is 51,000 ug/1. When divided by the species sensitivity
factor (3.9), the Final Fish Acute Value obtained for hexavalent
chromium is 13,000 ug/1.
The adjusted 96-hour LC50 values for trivalent chromium for
11 species of fish ranged from 1,820 ug/1 for the guppy in soft
water to 39,300 ug/1 for the bluegill tested in hard water.
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Following the Guidelines, an exponential equation describing
the relationship of toxicity of trivalent chromium to hardness for
each species was fit by least squares regression of the natural
logarithms of the toxicity values and hardness.
For trivalent chromium, sufficient acute toxicity data and
hardness ranges were available for only two fish species to fit
regression equations. The slopes of these equations were 0.89 for
fathead minnows and 0.78 for bluegills, with a mean of 0.83.
Although these regressions were for only two LC50 values each, and
therefore not statistically significant, they were the only values
available and were in reasonable agreement.
As a measure of relative species sensitivity to trivalent
chromium, logarithmic intercepts were calculated for each species
by fitting the mean slope (0.83) through the geometric mean
toxicity value and hardness for each species. These intercepts
.varied from 5.02 for guppies to 6.22 for rainbow trout, with a
mean intercept of 5.81 for all 11 fish species. This variation in
logarithmic intercepts indicates a narrow range of species sensi-
tivity to trivalent chromium of 3.5 times when adjusted for hard-
ness effects.
When the mean intercept of 5.81 is adjusted by the species
sensitivity factor (3.9), an adjusted mean intercept of 4.45 is
obtained. Thus, the Final Fish Acute Value is given by
e(0.83«ln(hardness)+4.45) .
As shown in Table 2, the data base for freshwater inverte-
brate species has 20 LC50 values for 14 invertebrate forms of
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which eight are identified to species. All LC50 values were from
static tests. The adjusted LC50 values varied from 19 ug/1 as
hexavalent chromium for Daphnia hyalina to a high of 55,000 ug/1
as trivalent chromium for a caddisfly. The data in Table 2 in-
dicate that cladocerans are more sensitive to the lethal effects
of chromium than the aquatic insects.
Debelak (1975) studied the acute toxicity of hexavalent
chromium to Daphnia magna (Table 7) in both a reconstituted water
with a hardness of 163 mg/1 (as CaCC^) and pH value of 8.3 and
pond water with a hardness of 86 mg/1 (as CaCO^) and pH value of
8.4. The mean of five 72-hour LC50 values was 39 ug/1 in the pond
water and 73 ug/1 in the reconstituted water. Thus, hexavalent
chromium was slightly more toxic in the softer dilution water.
No data were available to indicate hardness effects on acute
toxicity of trivalent chromium to invertebrate species1since no
species has been tested over a range of water hardness. Assuming
that a similar relationship to hardness probably exists for acute
toxicity to invertebrate species as with fish, the slope from the
fish acute equation (0.83) was used to determine the logarithmic
intercepts (relative species sensitivity) for invertebrate
species.
Variation observed for invertebrate acute values for triva-
lent chromium is seen to be only slightly greater than the acute
data on fish; the calculated intercepts for invertebrate LC50
values ranged from 4.30 for mayfly larvae to 7.77 for caddisfly.
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However, there also was a relatively narrower range of hardness in
the toxicity test waters (44 to 50 mg/1) as compared to the fish
acute tests. Since eight invertebrate species are represented in
the data base for trivalent chromium and the range of species sen-
sitivities is narrower than indicated by the species sensitivity
factor (21) from the Guidelines, a sensitivity factor was calcu-
lated from the variance of the logarithmic intercepts'. This fac-
tor is 1.645 times the standard deviation (1.44), which is 2.37.
The mean intercept (6.09) when adjusted by 2.37 is 3.72. Thus,
the Final Invertebrate Acute Value is given by e(0*83-ln
(hardness)+3.72). Since the invertebrate species are slightly
more sensitive to trivalent chromium than fish, the Final Inver-
tebrate Acute Value becomes the Final Acute Value.
The- data in Table 2 indicate that the freshwater invertebrate
species are also more sensitive to the lethal effects of hexa-
valent chromium than are freshwater fish. Thus the Final Inver-
tebrate Acute Value (110 u.g/1) becomes the Final Acute Value for
hexavalent chromium.
Chronic Toxicity
The data base for fish chronic values for chromium (Table 3)
is for seven species. Benoit (1976) reported on the long-term
effects of hexavalent chromium to brook trout and rainbow trout.
The maximum acceptable toxicant concentration (MATC) of 200 to 350
ug/1 was established on the basis of survival. Growth in weight
was retarded at all test concentrations during the first eight
months of the exposure. However, this was a temporary effect on
growth and was not used by the author to establish the MATC.
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Sauter, et al. (1976) studied the toxicity of hexavalent
chromium (sodium dichromate) to eggs and fry of six fish species:
rainbow and lake trout, northern pike, white sucker, channel cat- .
fish, and bluegill. The eggs and fry were continuously exposed in
soft water for a maximum of 60 days after hatching. Observations
were made of the hatchability of eggs, and the survival, length,
and weight of the fry after 30 and 60 days. The majority of the
data generated from these chromium exposures indicates a very sig-
nificant cumulative effect on fry. This was especially true for
the rainbow and lake trout since significant mortality occurred
between 30 and 60 days. This cumulative effect is consistent with
the observed low geometric mean application factor of 0.004 (Table
3) based on life cycle tests with the rainbow and brook trout
(Benoit, 1976). The chronic value for rainbow trout (Table 3) is
37 ug/1 from the embryo-larval test and 265 ug/1 from the life
cycle test. This variation is due in part to the effect on growth
that was considered to be temporary and was not used to establish
the MATC in the chronic test while in the embryo-larval test the
effect was on growth. In addition, the geometric mean of the
limits is divided by the adjustment factor of 2 for the embryo-
larval data. The chronic value for brook trout was the same as
that for the rainbow trout derived from the life-cycle tests
(Benoit, 1976).
All of the life cycle and embryo-larval tests were conducted
with hexavalent chromium in soft water with a hardness range of 34
to 45 mg/1 (as CaCO3). Since the effect of hardness on acute
toxicity of hexavalent chromium was insignificant, the same
B-7
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relationship will be assumed for chronic toxicity to fish. There-
fore, a geometric mean of the chronic values was calculated and is
177 ug/1. After division by the sensitivity factor (6.7), a Final
Fish Chronic Value of 26 ug/1 is obtained for hexavalent chromium.
No chronic data for fish and trivalent chromium are avail-
able.
The data base for the invertebrate chronic values for
trivalent chromium is limited to Daphnia magna (Table 3). The
geometric mean of the limits of the chronic values is 445 y.g/1
which is about one-fifth of the acute value.(Table 2) in the same
dilution water.
Daphnia magna is among the most sensitive species tested
(Table 2). Therefore, it would appear to be inappropriate to use
the Guidelines species sensitivity factor of 5.1 with the chronic
data for Daphnia magna. Consequently, that sensitivity factor is
not used in the calculations to derive the Final Invertebrate
Chronic Value. Since appropriate invertebrate data were not
available to establish a relationship between chronic toxicity
values and hardness, a relationship was established by using the
slope (0.83) from the Final Fish Acute Value and the trivalent
chromium value and water hardness from the Daphnia magna chronic
test. The calculated intercept for invertebrate species is 2.94.
The derived equation for invertebrate species (e(0.83-In(hardness)
+2.94)) becomes the Final Chronic Value since there are no
chronic exposure data for fish and trivalent chromium.
Trabalka and Gehrs (1977) studied the chronic toxicity of
hexavalent chromium to Daphnia magna. They found a significant
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effect on both life span and fecundity at all test concentrations
including the lowest of 10 ug/l« Because there was no concentra-
tion for the lower limit of the MATC, this datum is included in
Table 7 instead of Table 4. On the basis of these data, the Final
Invertebrate Chronic Value for hexavalent chromium would be less
than 10 ug/lf which is lower than the Final Fish Chronic Value.
Plant Effects
The data on seven species of algae and Eurasian watermilfoil
(Table 5) indicate that some algae are sensitive to the effects of
chromium. All tests were conducted with hexavalent chromium, and
reduction in growth and photosynthesis was the effect used to
measure toxicity. The concentration of chromium ranged from 10
ug/1 for a green alga to 9,900 ug/1 for Eurasian watermilfoil.
Growth of the green alga, Chlamydomonas reinhardi, was reduced at
a concentration of 10 ug/1 in Hold's basal medium. The Final
Plant Value for hexavalent chromium is 10 ug/1.
Residues
Data are available for the rainbow trout and the bioconcen-
tration factor is about one (Table 6). No maximum permissible
tissue concentration is available; therefore, no Residue Limited
Toxicant Concentration can be calculated.
Miscellaneous
The data, in Table 7 indicate that low concentrations of hexa-
valent chromium have a deleterious effect on the growth of fishes.
Olson and Foster (1956) reported a statistically significant ef-
fect on growth of Chinook salmon at 16 ug/1 and on rainbow trout
at 21 ug/1. At these concentrations, growth was reduced about ten
percent.
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Olson (1958) studied the comparative toxicity of hexavalent
and trivalent chromium to chinook salmon. As shown in Table 1,
hexavalent chromium at a concentration of 200 ug/1 was more toxic
in Columbia River water (hardness, 70 mg/1 as CaCO3) than a
similar concentration of trivalent chromium. Survival and growth
in the trivalent chromium exposure was similar to controls;
however, survival and growth in the hexavalent chromium exposure
was only about 50 percent of the control.
The lowest concentration to produce an adverse effect was re-
ported by Dowden and Bennett (1965). They reported a 48-hour LC50
for Daphnia magna of 30 ug/1 of chromic sulfate. It is not pos-
sible to determine the formula weight of the salt. If it were an-
hydrous, the 48-hour LC50 value would be 8 u.g/1- This value for
trivalent chromium is so much lower than the value of 2,000 ug/1
reported by Biesinger and Christensen (1972) that 8 ug/1 is con-
sidered to be an outlier, and the value is in doubt.
Using the data of Trabalka and Gehrs (1977) and comparing the
results with other chronic tests with hexavalent chromium, it is
estimated that a concentration of 5 ug/1 would not produce any
deleterious effects.
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CRITERION FORMULATION
Freshwater-Aquatic Life
Summary of Available Data
The concentrations below have been rounded to two significant
figures. All concentrations herein are expressed in terms of
chromium.
Hexavalent chromium
Final Fish Acute Value = 13,079 ug/1
Final Invertebrate Acute Value = 110 ug/1
Final Acute Value = 110 ug/1
Final Fish Chronic Value = 26 ug/1
Final Invertebrate Chronic Value = less than 10 ug/1
Final Plant Value = 10 ug/1
Residue Limited Toxicant Concentration = not available
Final Chronic Value = less than 10 ug/1
0.44 x Final Acute Value = 48 ug/1
Trivalent chromium
Final Fish Acute Value = e(°•83*ln(hardness)+4.45)
Final Invertebrate Acute Value = e(°•83 'In(hardness)+3.72)
Final Acute Value = e<°•83'ln(hardness)+3.72)
Final Fish Chronic Value = not available
Final Invertebrate Chronic Value - e(°-83-ln(hardness)+2.94)
Final Chronic Value = e(°•83*ln(hardness)+2.94)
Final Plant Value = not available
Residue Limited Toxicant Concentration = not available
Hexavalent chromium
The maximum concentration of hexavalent chromium is t-he Final
Acute Value of 110 ug/1 and the 24-hour average concentration is
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the Final Chronic Value of less than 10 u.g/1. No important ad-
verse effects on freshwater aquatic organisms have been reported
to be caused by concentrations lower than the 24-hour average
concentration.
CRITERION: For hexavalent chromium the criterion to protect
freshwater aquatic life as derived using the Guidelines is 10 ug/1
as a 24-hour average and the concentration should not exceed 110
ug/1 at any time.
Trivalent chromium
The maximum concentration of trivalent chromium is the Final
Acute Value of e(0•83*In(hardness) +3.72) and the 24-hour
average concentration is the Final Chronic Value of e(0«83*ln
(hardness)+2.94)t No important adverse.effects on freshwater
aquatic organisms have been reported to be caused by concentra-
tions lower than the 24-hour average concentraion.
CRITERION: For trivalent chromium the criterion to protect
freshwater aquatic life as derived using the Guidelines is "e
(0.83-ln(hardness)+2.94)" as a 24-hour average (see the figure
"24-hour average trivalent chromium concentration vs. hardness")
and the concentration should not exceed "e(0-83*ln (hard-
ness )+3.72)" (see the figure "maximum trivalent chromium concen-
tration vs. hardness") at any time.
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lOOOOr
4000
-------
loooor
4000
o
!3
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Table 1. Freshwater fish acute values for chromium
00
M
ui
Organism
American eel,
Angutlla rostrata
Rainbow trout,
Salmo gairdneri
Rainbow trout,
Salmo gairdneri
Rainbow trout,
Salmo gairdneri
Rainbow trout,
Salmo gairdneri
Brook trout,
Salvellnus fontinalis
Goldfish,
Carassius auratus
Goldfish,
Carassius auratus
Goldfish,
Carassius auratus
Goldfish,
Carassius auratus
Goldfish.
Carassius auratus
Goldfish.
Carassius auratus
Goldfish.
Carasbius auratus
Goldfish.
Carassius auratus
Goldfish.
Carabsius auratus
Bioassay Test Chemical
Method* Conc^** Description
Adjusted Hardness
Time LCiO LCio (mg/1 as
(hrs) (aq/1) (uq/ll CaCOj)
S M Trivalent 96 16.900 12,000 55
FT M Hexavalent 96 69.000 69.000 45
S U Trivalent 96 11,200 6,100
FT M Trivalent 96 ' 24,100 24.100 105***
S M Hexavalent 24 110,000 46,900 334
FT M Hexavalent 96 59,000 59,000 45
FT M Hexavalent 96 123,000 123.000 220
FT M Hexavalent 96 123,000 123.000 220
FT M Hexavalent 96 90,000 90,000 220
FT M Hexavalent 96 125.000 125.000 220
FT M Hexavalent 96 109,000 109.000 220
FT M Hexavalent 96 135,000 135.000 220
FT M Hexavalent 96 110.000 110,000 220
FT M Hexavalent 96 129,000 129,000 220
FT M Hexavalent 96 98.000 98.000 220
Reference
Rehwoldt,
et al. 1972
Benoit, 1976
Bills, et al.
1977
Hale, 1977
Schiffman &
Fromm, 1959
Benoit. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith, 1976
Adelman &
Smith. 1976
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Table 1- (Continued)
03
I
Organism
Goldfish.
Carassuis auratus
Gold'fish.
Carassius auratus
Goldfish.
Carassius auratus
Goldfish.
Carassius auratus
Goldfish.
Carassius auratus
Goldfish.
Carassius auratus
Goldfish,
Carassius auratus
Goldfish.
Carassius auratus
Goldfish.
Carassius auratus
Goldfish.
Carassius auratus
Goldfish.
Carassius auratus
Carp.
Cyprinus carpio
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Bioassay
Method*
FT
FT
FT
FT
FT
FT
FT
FT
S
S
S
S
FT
FT
FT
Test
Cone ,**
M
M
M
M
M
M
M
M
U
U
U
M
M
M
M
Chemical
Description
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Trivalent
Trivalent
Hexavalent
Hexavalent
Hexavalent
«
Time
(hrs)
96
96
96
96
96
96
96
96
24
96
96
96
96
96
96
LCbO
tuq/l>
133.000
102,000
133.000
126.000
126.000
133,000
126.000
124,000
249.000
37.500
4,100
14,300
56,000
51,000
53.000
Adjusted
LCiU
(ug/1)
133.000
102,000
133.000
126.000
126,000
133,000
126.000
124,000
89.800
20,500
2,240
10.200
56.000
51,000
53.000
Hardness
(mg/1 as
CaCO,)
j
220
220
220
220
220
220
220
220
100
20
20
55
220
220
220
Reference
Adelman &
Smith, 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith, 1976
Adelman &
Smith. 1976
Dowden &
Bennett, 1965
Pickering &
Henderson, 1966
Pickering &
Henderson. 1966
Rehwoldt,
et al. 1972
Adelman &
Smith. 1976
Adelman &
Smith
Adelman &
Smith. 1976
-------
Table 1. (Continued)
03
Of ydrnsm
Fathead minnow,
Ptmophalcs promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Method*
FT
FT
FT
FT
FT
FT
FT
FT
FT
FT
FT
FT
FT
FT
S
S
Test
Cone .**
M
M
M
M
M
M
M
M
M
M
M
M
M
M
U
U
Chemical
Debcripcioa
llexavalent
Hexavalent
llexavalent
llexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
llexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Time
(fits)
96
96
96
96
96
96
96
96
96
96
96
96
96
96
96
96
LCbU
(Uq/H
49,000
48.000
60.000
50.000
53.000
49.000
37.000
66.000
55,000
38,000
34,000
29.000
34.000
26.000
17,600
27,300
Adjusted
LCDU
49.000
48,000
60,000
50.000
53,000
49.000
37,000
66,000
55.000
38.000
34.000
29.000
34,000
26.000
9,620
14.900
Hardness
(mg/1 as
CaC03)
220
220
220
220
220
220
220
220
220
220
220
220
220
220
20
360
Reference
Adelman &
Smith. 1976
Adelman &
Smith, 1976
Adelman &
Smith. 1976
Adelman &
Smith, 1976
Adelman &
Smith, 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith. 1976
Adelman &
Smith, 1976
Pickering &
Henderson, '.
Pickering &
Pimephales promelas
Henderson, 1966
-------
Table 1. (Continued)
DO
1
I-"
00
Organism
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Fathead minnow,
Pimephales promelas
Banded killifish.
Fundulus diaphanus
Mosquitof ish,
Gambusia affinis
Mosquitof ish,
Cambusia affinis
Mosquicofish,
Gambusia affinis
Mosquitof ish,
Gambusia affinis
Guppy,
Poecilia reticulata
Guppy.
Poecilia reticulata
White perch,
Morone araericana
Striped bass,
Morone saxatilis
Striped bass,
Morone saxatilis
Striped bass.
Morone saxatilis
Biodssay
Method*
S
S
S
FT
FT
S
S
S
S
S
S
S
S
S
S
S
Test
Cone.**
U
U
U
M
M
M
U
U
U
U
U
U
M
U
U
M
Chemical
Description
Hexavalent
Trivalent
Trivalent
Hexavalent
Hexavalent
Trivalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Trivalent
Trivalent
Hexavalent
Hexavalent
Trivalent
Time
(hra)
96
96
96
96
t
96
96
96
96
96
96
96
96
96
96
96
96
LCbO
(uq/H
45,600
5,070
67,400
52.000
37,000
16.900
107,000
99.000
135,000
92,000
30.000
3.330
14,400
35,000
26.500
17.700
Adjusted
LCio
(uq/1)
24,900
2,770
36,800
52,000
37.000
12,000
58.500
54.100
73,600
50.400
16,400
1,820
10.200
19.100
14.500
12,600
Hardness
(rag/1 as
CaCO,)
20
20
360
231***
231***
55
" 100***
•? 100***
< 100***
< 100***
20
20
55
35
35
55
Reference
Pickering &
Henderson, 1966
Pickering &
Henderson, 1966
Pickering &
Henderson, 1966
Rue sink &
Smith, 1975
Rue sink &
Smith. 1975
Rehwoldt.
et al. 1972
Uallen, et
al. 1957
Wallen, et
al. 1957
Wallen, et
al. 1957
Wallen, et
al. 1957
Pickering &
Henderson, 1966
Pickering &
Henderson, 1966
Rehwoldt,
et al. 1972
Hughes, 1971
Hughes, 1970
Rehwoldt.
et al. 1972
-------
Table I. (Continued)
03
I
M
VO
Organism
Pumpkinseed,
Lepomis gibbosus
Bluegill.
Lepomis macrochlrus
Bluegill,
Lepomis roacrochirus
Bluegill.
Lepomis macrochirus
Bluegill.
Lepomis macrochirus
Bluegill,
Lepomis macrochirus
Bluegill.
Lepomis macrochirus
Bluegill,
Lepomis macrochirus
Bluegill.
Lepomis macrochirus
Bluegill.
Lepomis macrochirus
Largemouth bass,
Micropterus salmotdes
Bioassay Test
Method* Cone.**
M
S
S
S
S
S
S
S
S
S
U
u
u
u
u
u
u
u
M
Chemical
Description
Trivalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Trivalent
Trivalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Time
Adjusted
LCbO LCbU
(mi/1) (uq/l)
96 17.000 12.100
96 113,000 61,800
24 261,000 94.200
96 118.000 64.500
1
96 133,000 72,700
96 7.460 4.100
96 71.900 39,300
96 110.000 60,100
96 170,000 92,900
48 213,000 94.300
96 195.000 138.500
Hardness
(mg/1 as
CaC03)
55
44
100
20
360
20
360
45
45
120
334
Reference
Rehwoldt,
et al. 1972
Cairns &
Scheier, 1969
Dowden &
Bennett, 1965
Pickering &
Henderson, 1966
Pickering &
Henderson, 1966
Pickering &
Henderson, 1966
Pickering &
Henderson, 1966
Trama &
Benoit, 1960
Trama &
Benoit, 1960
Turnbull,
et al. 1954
Fromm &
Schiffman. 1958
* S = static, FT = flow-through
•'>•«• U = unmeasured, M = measured
•v»»- Alkalinity
-------
Table 1. (Continued)
Organism
BicMssay Test
Method cope,
Chemical
Description
Time
Adjusted
LC50
Hardness
(rag/1 as
CaCO,
Reference
DO
I
10
o
Hexavalent chromium:
Geometric mean of adjusted values = 51,007 pg/1 30 = 13,079 yg/1
Lowest value from a flow-through test with measured concentrations •» 26,000 ug/1
Trivalent chromium:
Adjusted LC50 vs. hardness:
Fathead minnow: slope » 0.89, intercept = 5.25, r = 1.0, not significant. N <• 2
Bluegill: slope - 0.78. intercept «• 5.98, r =• 1.0, not significant, N - 2
Geometric mean slope " 0.83
Mean intercept for 11 species *> 5.81
Adjusted mean intercept ° 5.81 - In(3.9) - 4.45
Final Fish Acute Value - e(0.83-ln(hardness)+4.45) -
-------
Table 2. Freshwater invertebrate acute values for chromium
Organism
Rotifer.
Philodina acuticornis
Rotifer,
Philodina roseola
Rotifer,
Philodina roseola
Rotifer.
Philodina roseola
Rotifer.
Philodina roseola
Rotifer.
Philodina roseola
00
1 Annelid.
fy Nais sp
l~~*
Snail.
Amnicola sp.
Snail.
Amnicola sp.
Cladoceran.
Daphnia hyalina
Cladoceran,
Daphnia magna
Cladoceran,
Daphnia magna
Copepod,
Cyclops abyssorum
Copepod,
Cyclops padanus
Scud,
Canmiarui. sp
BlOaSbay
Method*
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
Tetit
conc_..**
U
M
M
M
M
M
M
M
M
U
M
U
U
U
M
Clienueai
Description
Hexavalent
Uexavalent
Hexavalent
Hexavalent
Hexavalent
Hexavalent
Trivalent
Trivalent
Trivalent
Hexavalent
Trivalent
Hexavalent
Hexavalent
Hexavalent
Trivalent
Time
itirgj
96
96
96
1
96
96
96
96
96
96
48
48
48
48
48
96
LCbO
(ug/ii
3.100
12.000
8.900
7,400
5.500
4.400
9,300
12,400
8,400
22
2.000
6,400
10.000
10.100
3.200
Adjusted
LCJU
(Uq/1)
2.600
13,200
9.800
8,100
6.100
4.800
10,200
13,600
9.200
19
2.200
5,400
8,500
8,600
3,500
Hardness
(mg/1 as
CaCO,)
25
_
.
.
50
50
50
66
45
_
66
66
50
Reference
Buikema ,
et al. 1974
Schaefer &
Pipes, 1973
Schaefer &
Pipes. 1973
Schaefer &
Pipes. 1973
Schaefer &
Pipes. 1973
Schaefer &
Pipes. 1973
Rehwoldt .
et al. 1973
Rehwoldt,
et al. 1973
Rehwoldt,
et al. 1973
Baudouin &
Scoppa, 1974
Biesinger &
Christensen,
1972
Dowden &
Bennett, 1965
Baudouin &
Scoppa, 1974
Baudouin &
Scoppa, 1974
Rehwoldt,
et al. 1973
-------
Table 2. (Continued)
to
1
M
M
Orgdniam
Mayfly,
Ephemerella subvaris
Damselfly.
Unidentified
Caddisfly.
llydropsyche betteni
Caddisfly.
Unidentified
* S = static
** U » unmeasured, M =
Hexavalent chromium:
Geometric mean of ac
Bioassay Test
Metfiod* cone,
S U
S M
S U
S M
measured
ijusted values =
Chemical
,_** Description
Trivalent
Trivalent
Trivalent
Trivalent
2,315 i.g/1 ^
Time
(hrs)
96
96
96
96
- » 110 u
Adjusted Hardness
LCbO LCbo (mg/1 as
(uq/l) fug/1) CaCCO
2.000 1.700 44
43.100 47.400 50
64.000 54.500 44
50,000 55,000 50
R/l
Reference
Warnick &
Bell. 1969
Rehwoldt,
et al. 1973
Warnick &
Bell. 1969
Rehwoldt,
et al. 1973
Trivalent chromium-.
Adjusted LC50 vs. hardness:
No hardness relationship could be derived for any invertebrate species.
Using the geometric mean slope (0.83) from the fish acute values, the mean intercept for 8 vertebrate
species = 6.09, with a standard deviation of 1.44.
Adjusted mean intercept = 6.17-(1.645-1.44)=3.72
Final Invertebrate Acute Value = e(°-83-ln(hardness)+3.72
-------
Table 3. Freshwater fish chronic values for chromium
00
I
NO
CO
Organism
Rainbow trout,
Salmo gairdneri
Rainbow trout,
Salmo pairdneri
Brook trout,
Salvelinus fontinalis
Lake trout,
Salvelinus namaycush
Northern pike,
Esox lucius
White sucker,
Catostomus commersoni
Channel catfish.
Ictalurus punctatus
Bluegill,
Lepomis macrochirus
Limits
Test* (uq/i)
E-L 51 - 105
LC 200 - 350
LC 200 - 350
E-L 105 - 194
E-L 538 - 963
E-L 290 - 538
E-L 150 - 305
E-L 522 - 1122
Chronic Haioness
Value (OKJ/I as
(uq/1) CaCO,)
37 34
265 45
265 45
72 34
\
360 38
. 198 39
107 ' 36
368 38
Reference
Sauter. et al. 1976
Benoit. 1976
Benoit. 1976
Sauter. et al. 1976
Sauter, et al. 1976
Sauter, et al. 1976
Sauter. et al. 1976
Sauter, et al. 1976
* LC = life cycle or partial life cycle, E-L - embryo-larval
** All data are for hexavalent chromium.
No chronic data are available for trivalent chromium.
Geometric mean of chronic values = 177 iig/1 i— j = 26 yg/1
Lowest chronic value = 37 wg/1
Application Factor Values (Benoit. 1976)
Species
Rainbow trout,
Salmo gairdneri
96-hr LC50 MATC
(PR/1) (MR/1)
69.000 265
AF
0.004
Brook trout, 59,000
Salvelinus fontinalis
265
0.004
-------
Organism
Cladoceran,
Daphnia maj-na
Chronic
Limits Value
Teat* (uq/JLI (uq/1)**
LC 330-600 445
Hardness
(mg/1 as
CaC03)
45
* LC = life-cycle or partial life-cycle
** TrivalenC chromium
Geometric mean of chronic values = 445 wg/1 -•- » 87 pg/1
Lowest chronic value = 445 pg/i
Trivalent chromium:
Invertebrate chronic value vs. hardness:
gj No hardness relationship could be derived for any invertebrate species.
M Using the geometric mean slope (0.83) from the fish acute values, the intercept for Daphnia
*"• magna (only species tested) = 2.94
Final Invertebrate Chronic Value - e<°'83'ln
-------
Table 5. Freshwater plant effects for chromium*
Organism
Effect
Concentration
(uq/1)
Reference
Green alga,
Chlamydomonas
reinhardi
Green alga,
Chlorella pyrenoidosa
Green alga,
Chlorella sorokiniana
Green alga,
Selenastrum
capricornucum
Green alga,
Scenedesmus sp.
Diatom,
Cx) Nitzschia palea
1
£j> Did torn,
Nitzschia palea
Alga.
Natural algae
population
Eurasian watermilfoil,
Myriophyllum sptcaturo
Eurasian watermilfoil,
Myriophyllum spicatum
Reduction in 10 Zarafonetis & Hampton, 1974
growth
50% inhibition 5,000 Wium-Andersen, 1974
in photosynthesis
44% inhibition 1,000 Moshe. et al., 1972
in growth
Inhibition in 45 Carton, 1972
growth
Inhibition in 500 Staub. et al. 1973
growth
50% inhibition 800 Wium-Andersen, 1974
in photosynthesis
Growth 150 Wium-Andersen, 1974
32% inhibition 20 Zarafonetis 6, Hampton, 1974
in photosynthesis
50% root weight 1,900 Stanley, 1974
inhibition
50% root weight 9,900 Stanley, 1974
inhibition
* All data are for hexavalent chromium.
Lowest plant value = 10 Mg/1
-------
CO
I
N)
CTi
Table 6- Freshwater residues for chromium
Organism
Rainbow trout,
Salmo gairdneri
Rainbow trout,
Salmo gairdneri
Rainbow trout,
Salmo gairdneri
Time
Bioconcentration Factor (days)
<1 22
1 36
1 30
Keterence
Duhler, et al.
Fromm & Stokes,
Fromm & Stokes,
1977
1962
1962
-------
Table 7. Other freshwater data for chromium
Organism
Algal community
Algal community
Algal community
Protozoa,
Colptdium campylum
Protozoa,
CO Blephartsma sp.
^l Protozoa,
Opercularia sp.
Protozoa,
Vorticella micros toma
Cladoceran,
Daphnta magna
Cladoceran,
Paphnia magna,
Cladoceran,
Daphnia magna
Cladoceran,
Daphnia magna
Cladoceran,
Daphnia magna
Cladoceran,
Daphnta magna
Cladoceran,
Test
Duration
1 mo
1 mo
1 mo
48 hrs
3 hrs
48 hrs
48 hrs
64 hrs
72 hrs
72 hrs
72 hrs
72 hrs
72 hrs
72 hrs
Hardness
(rag/1 as
Ettect CaC03}
Diatoms re-
duced blue
green algae
dominant
Diversity of
diatoms
reduced
Bioconcentra-
tion of chrom-
ium: 8,500
507. inhibi-
tion of
growth
Some "
living
50% inhibi-
tion of
growth
50% inhibi-
tion of
growth
LC50 -160
LC50 163
LC50 163
,
LC50 • 163
LC50 163
LC50 163
LC50 86
Result
400*
100*
400*
12,900*
32,000*
21,200*
530*
1,200**
64*
72*
73*
74*
81*
31*
fteterencfe
Patrick, et al.
Patrick, et al.
Patrick, et al.
1975
1975
1975
Subo & Aiba, 1973
Ruthven & Cairns
, 1973
Sudo & Aiba, 1973
Sudo £, Aiba, 1973
Anderson, 1948
Debelak, 1975
Debelak, 1975
Debelak, 1975
Debeiak. 1975
Debelak. 1975
Debelak, 1975
-------
Organism
Test
Ouration Fttect
Hardness
(mg/1 as Result
Reference
03
1
N)
00
Cladoceran,
Daphnia magna
Cladoceran,
Daphnia magna
Cladoceran,
Daphnia magna
Cladoceran,
Djphnia magna
Cladoceran,
Daphnia magna
Cladoceran,
Daphnia magna
Cladoceran,
Daphnia magna
Cladoceran,
Daphnia magna
72 hrs
72 hrs
72 hrs
72 hra
48 hrs
100 hrs
100 hrs
96 hrs
Cladoceran. Life span
Daphnia magna >
Midge,
Chironomus sp.
Stonefly,
Acroneuria lycorias
Coho salmon,
Oncorhynchus kisutch
Chinook salmon.
Oncorhynchus tshawytscha
Chinook salmon.
Oncorhynchus tshawytscha
Chinook salmon.
Oncorhynchus tshawytscha
32 days
96 hrs
7 days
13 days
4 mos
12 wks
12 wks
LC50
LC50 86
LC50 86
LC50 86
LC50
LC50 100
LC50 100
LC50
Life span re-
duced fecundity
reduced
LC50 50
LC50 44
LC50***
Growth 70
Mortality and 70
growth
No effect on 70
mortality or
growth
1--- • 1_ - Lfl _ ••
• 38*
39*
42*
44*
'4-8*
140*
130*
50*
10*
11,000
32,000**
25,000*
16*
200*
200**
Debelak, 1975
Debelak, 1975
Debelak. 1975
Debelak, 1975
Dowden & Bennett
Dowden & Bennett
Freeman & Fowler
Trabalka & Gehrs
Trabalka & Gehrs
Rehwoldt, et al.
. 1965
. 1965
, 1953
. 1977
. 1977
1973
Warnick & Bell, 1969
Holland, et al. 1960
Olson & Foster, 1956
Olson. 1958
Olson. 1958
Rainbow trout,
Salmo gairdneri
14 wks Growth
70
21* Olson & Foster. 1956
-------
Table 7. (Continued)
03
I
N)
VO
Organism
Rainbow trout,
Salmo gairdneri
Rainbow trout,
Salmo gairdneri
Rainbow trout,
Salmo gairdnert
Goldfish,
Carassius auratus
Fathead minnow,
Pimephalea promelas
Test
Duration Ettect
7 days Plasma
"cortisol"
2 days Inhibition
Na/K- ATPase
24 hrs Hematocrits
11 days LC50****
11 days LC50****
Largemouth bass, 36 hrs Pathology of 334
Micropterus salmoides intestine
Hardness
(mg/1 as Result
CaC00) (uq/ii
• i J * '' ™ ~ ™
70 20*
2,500*
334 2,000*
220 30,400*
220 17,300*
94,000*
Reference
Hill & Frorara, 1958
Kuhnert, et al. 1976
Schiffman & Fronan, 1959
Adelman & Smith, 1976
Adelman & Smith, 1976
Frorara & Schiffman, 1958
* Hexavalent chromium.
** Trivalent chromium.
*** Calculated from data
**** Geometric mean of 16 tests
-------
SALTWATER ORGANISMS
Introduction
All available toxicity data are for hexavalent chromium, and
all bioconcentration data are for trivalent chromium. Studies
which reported toxicity data for trivalent chromium used static
\
test conditions and stated that a precipitate formed. This has
been interpreted as meaning that actual exposure levels were not
known. The only bioconcentration data reported here were derived
from two flow-through studies using trivalent chromium where no
precipitation was reported. The kinetics of the precipitation of
trivalent chromium in saltwater systems is complex, but regardless
of its form, it may still be ingested and bioconcentrated.
Acute Toxicity
Acute toxicity data for hexavalent chromium and saltwater
fishes are limited to two species (Table 8) and all studies were
conducted with adult fish. The experiments on Fundulus heterocli-
tus performed at 20° and 20 °/oo salinity (Eisler and Hennekey,
1977) resulted in a higher acute toxicity value than in those with
Citharichthys stigmaeus in full strength saltwater at 11.7 to
12.7°C (Sherwood, 1975). Adjustment of the fish acute toxicity
data gives a Final Fish Acute Value of 7,800 ug/1.
Saltwater invertebrate species are more sensitive to hexa-
valent chromium than saltwater fishes. Adjusted acute toxicity
values ranged from 1,694 ug/1 for the polychaete worm, Nereis
virens to 88,935 ug/1 for the mud snail Nassarius obsoletus,
(Eisler and Hennekey, 1977). Larvae of Capitella capitata were
found to be slightly less sensitive than adults, with adjusted
B-30
-------
acute toxicity values of 6,776 ug/1 and 4,234 ug/l» respectively
(Table 9). The sensitivity of the brackish water clam, Rangea
cuneata, to acute hexavalent chromium poisoning was dependent on
salinity, with acute toxicity values of 35,000 and 14,000 ug/l» in
water of salinities of 22 and 5.5 °/oo, respectively. Acute
toxicity values for the bivalve molluscs were between those for
the relatively insensitive gastropods (mud snails).and the an-
nelids (polychaete worms). Within the invertebrate species, the
arthropods demonstrated the widest range of adjusted LC50 values
from 4,338 ug/1 for sea urchin larvae, Strongylocentrotus pupura-
tus, (Oshida and Wright, 1978), to 44,044 ug/1 for zoea of the
crab, Sesarma haemotocheir (Okubo and Okubo, 1962). The Final
Invertebrate Acute Value of 230 ug/1/ derived by using the Guide-
lines, is lower than any value in Table 9 and thus protects 95
percent of the species represented. Since this value is lower
than the Final Fish Acute Value of 7,800 v.g/1, the Final Acute
Value for chromium is 230 ug/1.
Chronic Toxicity
There are no life cycle or embryo-larval" chronic toxicity
data with chromium and saltwater fishes. There are chronic toxic-
ity data for hexavalent chromium and three species of saltwater
polychaete worms (Table 10). All these studies use reproductive
success as a measure of chronic toxicity, and all were tests with
renewed solutions and unmeasured (except Oshida, 1978) toxicant
concentrations. The chronic values for Neanthes arenaceodentata
ranged from 25 ug/1 to 71 ug/1 with a geometric mean of 40 ug/1.
The chronic toxicity of chromium to Capitella capitata of 71 ug/1
while similar to Neanthes is an order of magnitude less than that
B-31
-------
reported for Ophryotrocha diadema (707 ug/D« The chronic toxic-
ity of hexavalent chromium to these species ranges from 9 to 89
times greater than the reported acute toxicity. The geometric
mean of the chronic values is 126 which, divided by the species
sensitivity factor (5.1)/ results in a chronic value of 25 ug/l«
This value is identical to the lowest chronic value reported and
the Final Invertebrate Chronic Value is 25 ug/1. Since there is
no Fish Chronic Value or suitable Residue Limited Toxicant Concen-
tration, the Final Invertebrate Chronic Value becomes the Final
Chronic Value of 25 ug/l«
Plant Effects
The data available on sensitivity of plants to chromium poi-
soning is limited to the algal species Macrocystis pyrifera.
Hexavalent chromium has been shown to inhibit photosynthesis in
this alga at 1,000 ug/1 (10 to 20 percent inhibition in 5 days)
and 5,000 ug/1 (50 percent inhibition in 96-hours). Therefore the
Final Plant Value is 1,000 ug/1.
Bioconcentration
The only bioconcentration data available are for trivalent
chromium from studies with three different species of bivalve mol-
luscs. A bioconcentration factor of 84 was reported for Mytilus
edulis, 116 for Crassostrea virginica, and 152 for Mya arenaria.
No data are available to calculate the Residue Limited Toxicant
Concentration (RLTC) for chromium.
Miscellaneous
Hexavalent chromium seems to be a cumulative toxicant (Table
13). For example, the 96-hour LC50 for the polychaete worm,
Capitella capitata, is 4,235 ug/l» whereas the 28-day LC50 value
B-32
-------
is 280 ug/1. The 96-hour LC50 is 48,279 ug/1 and the 7-day LC50
is 8,000 ug/1 for the soft shell clam. For the starfish, Asteria
forbesi, the 96-hour LC50 is 27,104 ug/1, whereas the 7-day LC50
is 10,000 ug/1. The 96-hour LC50 for the speckled sanddab is
16,948 ug/1 but the 21-day LC50 is 5,400 ug/1.
In addition to the chronic mortality data reported in Table
13, there are two sublethal measures of chromium toxicity. Oshida,
et al. (1976) reported a reduction in brood size of Neanthes
arenaceodentata exposed to 12.5 ug/1. Although this value is
slightly lower than the Final Chronic Value of 25 ug/1 it does not
warrant lowering the latter. Oshida and Reish (1975) reported in-
hibition of tube building in the same species after a 14-day expo-
sure to 79 ug/1. This concentration is 43 times lower than the
96-hour acute toxicity .value and is similar to a chronic value of
71 ug/1 (Table 10). Thus tube building may be a potential predic-
tor of chronic reproductive effects.
B-33
-------
RITERION FORMULATION
Saltwater-Aquatic Life
ummary of Available Data
The concentrations below have been rounded to two significant
'igures. All concentrations herein are expressed in terms of
:hromium.
lexavalent chromium
Final Fish Acute Value = 7,800 ug/1
Final Invertebrate Acute Value = 230 ug/1
Final Acute Value = 230 ug/1
Final Fish Chronic Value = not available
Final Invertebrate Chronic Value = 25 ug/1
Fina.! Plant Value = 1,000 ug/1
Residue Limited Toxicant Concentration = not available
Final Chronic Value = 25 U9/1
0.44 x Final Acute Value = 100 ug/1
The maximum concentration of hexavalent chromium is the Final
Acute Value of 260 ug/1 and the 24-hour average concentration is
the Final Chronic Value of 25 ug/1- No important adverse effects
on saltwater aquatic organisms have been reported to be caused by
concentrations lower than the 24-hour average concentration.
CRITERION: For hexavalent chromium the criterion to protect
saltwater aquatic life as derived using the Guidelines is 25 ug/1
as a 24-hour average and the concentration should not exceed 230
ug/1 at any time.
For saltwater aquatic life, no criterion for trivalent chro-
mium can be derived using the Guidelines, and there are insuffi-
cient data to estimate a criterion using other procedures.
B-34
-------
Table 8 Marine fibh acute values for chromium
(33
I
Ul
U1
flioassay
Organism Method*
Speckled sanddab, S
Citharichthyb sti^maeus
Speckled banddab, S
Citharichthys stigniaeus
Mummichog, S
Fundulus heteroclitus
Adjusted
Teat Time LCbO LC50
Cone.** (hra) (ug/1) . fuq/1) Reference
U 96 31,000 16,948 Sherwood
U 96 30,000 16.401 Mearns.
U 96 91,000 49.750 Eisler &
1977 '
. 1975
et al. 1976
llennekey,
* S = static
** U = unmeasured
Geometric mean of adjusted values = 28,800 wg/1
28,800
7.800 ng/1
-------
Table 9. Marine invertebrate acute values for chromium
Biodseay
0£3ajl!2ffi Method*
Polychaete worm (larvae) ,
Capitella capitata
Polychaete worm (adult).
Capitella capitata
, Polychaete worm,
Ctenodrilus serratus
Polychaete worm,
Neanthes arenaceodentata
Polychaete worm,
. Neanthes arenaceodentata
Polychaete worm.
Nereis virens
03
Jj I Polychaete worm,
Ophryotrocha diadema
Soft shell clam,
Mya arenaria
' Brackish water clam,
' Rangea cuneata
Brackish water clam,
Rangea cuneata
Mud snail,
'. Nast.ari.us obsoleutus
Hermit crab,
Pagurus longicarpus
Crab (zoea) ,
Sesanna haemotocheir
Starfish,
S
S
S
S
S
S
S
S
S
S
S
S
S
S
Test
Cone.**
U
U
U
M
M
U
U
U
U
U
U
U
U
U
Time
(hra)
96
96
96
96
96
96
96
96
96
96
96
96
24
96
LC50
(uq/ll
8,000
5,000
4,300
3,100
2.220-4,300
2.000
7,500
57,000
14,000
35,000
105,000
10,000
200,000
32.000
• Adjusted
LC50
(uq/H
6,776
4.235
3.642
3,410
3.399***
1.694
6.352
48,279
11,858
29,645
88.935
8.470
44.044
27.104
Reterence
Reish, et al. 1976
Reish, et al. 1976
Reish & Carr. 1978
Mearns, et al. 1976
Oshida & Reish, 1975
Eisler & Hennekey. 1977
Reish &-Carr, 1978
Eisler & Hennekey, 1977
Olson & Harrel, 1975
Olson & Harrel. 1975
Eisler & Hennekey. 1977
Eisler & Hennekey, 1977
Okubo & Okubo, 1962
Eisler & Hennekey, 1977
Abterias forbesi
-------
Table 9. (Continued)
CD
I
ui
Qrqanianj
Sea urchin (larvae),
Strongylocentrotus
purpuratus
Bioassay Test Time LC50
Method* Cone.** (hrs) (uq/i\
M 48
2,900 -
29.000
Adjusted
LC50
luq/1) Reference
4,338*** Oshida & Wright, 1978
* S •» static
** ' U = unmeasured, M = measured
*** Corrected geometric mean of LC50 range
Geometric mean of adjusted values = 11,101 ng/1
11,101 oan M
—j^— - 230 pg/1
-------
Table 10. Marine invertebrate chronic values for chromium
00
Chronic
Limits Value
Organism
Polychaete worm,
Capital la capitata
Polychaete worm,
Ophryotrocha diadema
Polychaete worm,
Neanthes arenaceodentata
Polychaete worm,
Neanthes arenaceodentata
Polychaete worm,
Neanthes arenaceodentata
CD
' * I.C = lifp rvelp fir narl-ij
Teat *
LC
LC
LC
LC
LC
al 1 i f «» cvi
(uq/1) (uq/1)
50-100 71
500-1000 707
25-50 35
50-100 71
17-38 25.2
r»l A i i £
Reference
Reish, 1977
Reish & Carr,
Oshida & Reish
Oshida, et al.
Oshida, 1978
1978
, 1975
1976
Geometric mean of chronic values = 126 wg/1 = 25 pg/1
Lowest chronic value = 25 Mg/1
-------
00
I
OJ
vo
Table 11. Marine plant effects for chromium
Concentration
Organism Ettect (uq/H Reference
Alga, 96-hr EC50 5,000 Clendenning & North, 1959
Macrocystis pyrifera 50% inhibition of
photosynthesis
Alga, 10-20% inhibition 1.000 Bernnard &'Zattera. 1975
Macrocystis pyrifera of photosynthesis
in 5 days
Lowest plant value = 1,000 ug/1
-------
Organism
Bioconcentration Factoi
(days)
weterence
American oyster,
Crassostrea virginica
Soft shell clam.
Mya arenarla
Blue mussel,
Mytilus edulis
116
152*
84*
140
168
168
Shuster & Prlngle,
Capuzzo ft Sasner,
Capuzzo & Sasner,
1969
1977
1977
* Dry to wet weight conversion '
** All bioconcentration data is based on trivalent chromium.
Geometric mean bioconcentration factor for all species = 114
CO
I
-------
Table 13. Other marine data for chromium
DO
I
Organism
Polychaete worm,
Ctenodrilus serratus
Polychaete worm,
Ophryotrocha diadema
Polychaete worm
(juvenile)
Neanlhes arenaceodentata
Polychaete worm
(adult),
Neanthes arenaceodentata
Polychaete worm,
Neanthes arenaceodentata
Test
Duration
21 days
21 days
28 days
28 days
7 days
Result
(uu/H
Polychaete worm, 440 days
Neanthes arenaceodentata
Polychaete worm, 56 days
Neanthes arenaceodentata
Polychaete worm, 14 days
Neanthes arenaceodentata
Polychaete worm, 59 days
Neanthes arenaceodentata
Polychaete worm, 7 days
Neanthes arenaceodentata
Polycahete worm, 350 days
Neanthes arenaceodentata
Polychaete worm
(adult)
Captuella capi tata
Polychaete worm,
Nereis virens
Polychaete worm.
Nereis virens
21 days
7 days
100% mortality
100% mortality
50% mortality
50% mortality
50% mortality
Brood size decreased
50% mortality
50,000
50,000
700
Reterei.cfc
Reish & Carr, 1978
Reish & Carr, 1978
Reish, et al. 1976
550 Reish, et al. 1976
1,440-1,890 Oshida, et al. 1976
12.5 Oshida, et al. 1976
200 Oshida & Reish, 1975
Inhibition-tube building 79 Oshida £, Reish. 1975
50% mortality
50% mortality
Brood size decrease
28 days 50% mortality
50% mortality
50% mortality
200 Mearns. et al. 1976
1,630 Mearns, et al. 1976
12.5 Mearns, et al. 1976
280 Reish, et al. 1976
1,000 Raymont & Shields, 1963
700 Eisler & llennekey, 1977
-------
Table 13 (Continued)
Organx sm
Soft shell clam.
Mya arenaria
Mudsnail,
Nassarius obboletus
Hermit crab.
Pagurus longicarpus
Shore crab,
Carcinus maenas
Prawn (juvenile),
Leander squilla
Prawn (adult) .
Leander squilla
03 Brittle star.
1 Ophiothrix spiculata
10 Starfish.
Asterias forbesi
Mummichog,
Fundulus heteroclitus
Speckled sanddab.
Citharichthys stigmaeus
Speckled sanddab,
Citharichthys stigmaeus
Speckled sanddab.
Citharichthys stigmaeus
Silver salmon,
Oncorhynchus kisutch
Silver salmon,
Oncorhynchus kistuch
Test
nutation Ettect
7 days
7 days
7 days
12 days
7 days
7 days
7 days
7 days
7 days
21 days
21 days
21 days
5 days
11 days
50% mortality
50% mortality
50% mortality
50% mortality
Toxic threshold
Toxic threshold
50% mortality
50% mortality
50% mortality
50% mortality
EC50-feeding response
50% mortality
33% mortality
100% mortality
Result
(ug/ll
8,000
10,000
2.700
60.000
5,000
10.000
1.700
10,000
44.000
5,400
2.200
5.000
31.8
31.8
RetereiiCfe
Eisler & Hennekey, 1977
Eisler & Hennekey, 1977
Eisler & Hennekey, 1977
Raymont & Shields, 1963
Raymont & Shields, 1963
Raymont & Shields, 1963
Oshida & Wright, 1978
Eisler & Hennekey, 1977
Eisler & Hennekey. 1977
Sherwood, 1975
Sherwood, 1975
Mearns, et al. 1976
Holland, et al. 1960
Holland, et al. 1960
-------
CHROMIUM
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Bills, T.D., et al. 1977. Effects of residues of the poly-
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B-45
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B-51
-------
CHROMIUM
Mammalian Toxicology and Human Health Effects
Introduction
Chromium is a common element, present in low concentra-
tions throughout nature. Its toxicity has long been recog-
nized, but detailed analysis of toxic effects is complicated
by the occurrence of many different compounds of the metal;
these may contain Cr in different valence states and are
distinguished by their chemical, physical and toxicological
properties.
This document briefly considers some relevant chemical
and physical properties of Cr compounds to which man may
be exposed, and attempts to evaluate possible health hazards
associated with such exposures. The general area of environ-
mental effects of chromium compounds was recently reviewed
by the U.S. Environmental Protection Agency (1978); a valuable
discussion of the medical and biological effects of Cr in
the environment is found also in a volume published by the
National Academy of Sciences (1974). Occupational hazards
of chromium were assessed in a Criteria Document prepared
in 1975 (Natl. Inst. Occup. Safety Health, 1975). Mertz
(1969) provided a valuable survey of the biochemical properties
of Cr compounds.
To avoid unnecessary duplication, previously reviewed
material will not be considered at great length except when
it impinges directly on present critical considerations.
Detailed documentation for most of the available information
can be found in the earlier reviews.
C-l
-------
There is little need to discuss here the detailed chem-
stry.of chromium, as this subject has been adequately reviewed
n the recent past (U.S. EPA, 1978). However, an evaluation
f the significance of various routes of exposure to Cr-
ontaining compounds, and of the factors determining rates
>f uptake and toxicity of such compounds, requires an under-
tanding of their physical properties and of their chemical
nd biochemical reactions.
The metallic element Cr belongs to the first series
f transition elements, and occurs in nature primarily as
•ompounds of its trivalent (Cr III) or hexavalent (Cr VI)
"orms. Generally speaking, the hexavalent compounds are
elatiyely water-soluble and readily reduced to the more
nsoluble and stable forms of Cr III by reaction with organic
•educing matter. Because large amounts of Cr VI are pro-
luced and utilized in industry (primarily as chromates and
lichromates), and because of their ready solubility, traces
>f such compounds are frequently found in natural waters.
As pointed out, Cr VI is rapidly reduced when in con-
:act with biological material. The reverse reaction is
lot known to occur in the human body. Trivalent Cr forms
stable hexacoordinate complexes with many molecules of bio-
:hemical interest. Interaction of Cr III with such compounds
nay involve binding to carboxy groups of proteins or smaller
netabolites, coordination with certain amino acids, and
Dinding to nucleic acids and nucleoproteins. This last
reaction is of special significance in the consideration
Df the carcinogenic potential of Cr compounds. The field
C-2
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was reviewed by Mertz (1969) and it suffices here to emphasize
the stability of these Cr complexes, and the fact that the
element is found combined with both RNA and DNA; an effect
of Cr on the tertiary structure of nucleic acids is clearly
indicated. In general, it may be concluded that reduction
of Cr VI to Cr III and its subsequent coordination to organic
molecules of biochemical interest explain in large measure
the biological reactivity of Cr compounds. Thus, the well-
known reaction of Cr with skin proteins (i.e., the tanning
process) involves coordination sites of Cr III. For reasons
of solubility, however, uptake of compounds of Cr VI by
the living organism generally exceeds that of Cr III compounds
(see saction on "Acute, Sub-acute, and Chronic Toxicity").
A good illustration of the behavior of Cr compounds
in biological systems is furnished by the reaction of Cr
with erythrocytes (Gray and Sterling, 1950) . These cells
do not react to any significant extent with Cr III; in con-
trast, they rapidly take up anions of hexavalent Cr compounds,
utilizing presumably the broadly specific anion transport
facilitation in erythrocytes reviewed by Fortes (1977).
Thus we may invoke as a likely explanation for the greater
toxicity of Cr VI than of Cr III compounds their more rapid
uptake by tissues due to their solubility and to the facili-
tation of their translocation across biological membranes.
Once within cells, the Cr VI is likely to be reduced to
the trivalent state before reacting with cell constituents
such as proteins and nucleic acids. In the case of red
cells, it is such an intracellular reaction of Cr III with
C-3
-------
hemoglobin which explains the essentially irreversible uptake
of the metal and permits use of chromium-51 as red cell
marker.
Stable and soluble compounds of Cr III are found in
many biological systems. Among these is the so-called glucose
tolerance factor (GTF) (Mertz, 1969), a compound of unknown
structure whose absence is believed responsible for symptoms
of chromium deficiency. In the form of GTF and perhaps
of other similar complexes Cr III can also cross biological
membranes with relative ease; thus it is readily absorbed
from the intestine in this form (Doisy, et al. 1971). One
may recall in this connection the general importance of
netal ligands in determining movement of heavy metals within
the body (Collins, et al. 1961; Foulkes, 1974). It is not
surprising therefore that distribution of Cr in the body
also critically depends on the presence of specific ligands
(Mertz, 1969).
Chromium plays a role in human nutrition. Because
of this fact, lowering of ambient Cr levels to a value where
total uptake might lead to overt Cr deficiency must be avoided.
Indeed, effects of Cr-deficiency in man and experimental
animals have been described (Mertz, 1969). Levels of Cr
compounds required for optimal nutrition fall greatly below
those which have been reported to cause toxic effects (see
"Acute, Sub-acute, and Chronic Toxicity" section); therefore
normal nutritional levels need not be considered further
here. It must be pointed out, however, that the American
diet may be potentially deficient in Cr so that some increased
C-4
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Cr uptake might be beneficial.
Sources of chromium in the environment have been recently
reviewed (U.S. EPA, 1978). Although Cr is widely distri-
buted, with an average concentration in the continental
crust of 125 mg/kg, it is rarely found in significant concen-
trations in natural waters. Air levels in non-urban areas
usually fall below detection limits and may be as low as
5 pg/m . Much of the detectable Cr in air and water is
presumably derived from industrial processes, which in 1972
consumed 320,000 metric tons of the metal in the United
States alone. A significant fraction of this amount entered
the environment; additional amounts are contributed by com-
bustion of coal and other industrial processes (U.S. EPA,
1974). As a result, levels of Cr in air exceeding 0.010
/jg/m have been reported from 59 of 186 urban areas examined
(U.S. EPA, 1973). Mean concentration of Cr in 1577 samples
of surface water were reported as 9.7 >ig/l (Kopp, 1969).
The significance of 9.7 jug/1 as a mean value is questionable
because only 25 percent of the samples tested contained
any detectable Cr. Occasional values of total Cr (Cr III
and Cr VI) exceeded 50 jjg/1, a fact which must be noted
in relation to the recommended standard for domestic water
supplies (see section on "Existing Guidelines and Standards").
It is important to reemphasize at this time the analy-
tical difficulties attending estimation of low concentra-
tions of Cr, especially in biological materials. Addition-
ally, the different chemical species of Cr which may be
C-5
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present often cannot be clearly separated. Considerable
uncertainty attaches to the significance of some results,
particularly those obtained with some of the older techniques,
This topic was considered in detail recently (U.S. EPA,
1978) .
C-6
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Ingestion from Food and Water
At an average concentration of approximately 10 jul
Cr/1 drinking water (Kopp, 1969), and a daily water consump-
tion of 2 L, about 20 ;ug Cr would be ingested in water per
day compared to about 50 to 100 jig per day in the American
diet (Tipton, 1960). On the basis of the levels of Cr reported
for food and water in the general environment of the United
States, average oral intake will seldom exceed 100 /ag/day
(Tipton, 1960). Fractional absorption of such an oral load
from the intestine depends on the chemical form in which
the element is presented (see "Introduction"). In addition,
even though mechanisms involved in the movement of Cr com-
pounds across intestinal epithelial barriers are not under-
stood, it is likely that the extent of this absorption will
be greatly influenced by the presence of other dietary consti-
tuents in the intestinal lumen (MacKenzie, et al. 1958),
as has frequently been observed in the case of other dietary
metals.
For a variety of reasons, therefore, net fractional
absorption of Cr from the intestine is low and may amount
to only a few percent or even less (Mertz, 1969), depending
especially on the chemical form in which the element is
ingested. Intake of Cr from the air normally amounts to
less than 1 jug/day (see "Inhalation"), and thus does not
contribute significantly to normal Cr balance. Average
urinary excretion of Cr has been reported as 5 to 10 ug
per day (Volkl, 1971); recent work suggests that because
C-7
-------
of analytical difficulties, actual values may be somewhat
lower (Guthrie, et al. 1979). In any case it follows that
the American diet may become marginally deficient in this
element, unable to provide the optimum level required for
normal function (see "Introduction" section). This conclusion
is supported by the finding that Cr levels in tissues generally
decrease with age (Mertz, 1969). The situation is not greatly
altered by application of Cr-containing fertilizers or sewage
sludges to agricultural land. Indeed, uptake of Cr by plants
from soil is generally low. However, biomagnification factors
for Cr have been reported in rainbow trout of 1 and below
and are quoted in "Freshwater Residues for Chromium" of
the ecological effects chapters.
A bioconcentration factor (BCF) relates the concentration
of a chemical in water to the concentration in aquatic organisms,
Since BCF's are not available for the edible portion of
all four major groups of aquatic organisms consumed in the
United States, some have to be estimated. A recent survey
on fish and shellfish consumption in the United States (Cordle,
et al. 1978) found that the per capita consumption is 18.7
g/day. From the data on the nineteen major species identified
in the survey, the relative consumption of the four major
groups can be calculated.
Several bioconcentration tests have been conducted
with chromium:
C-8
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Bioconcentration
Organisms factor Valence Reference
American oyster, 116 +3 Shuster &
Crassostrea virginica Pringle, 1969
Soft shell calm, 152 +3 Capuzzo &
Mya arenaria Sasner, 1977
Blue mussel, 84 +3 Capuzzo &
Mytilus edulis Sasner, 1977
Rainbow trout, 1 -t-6 Buhler, et al.
Salmo gairdneri 1977
Rainbow trout, 1 +6 Fromm & Stokes,
Salmo gairdneri 1962
These data result in geometric means of 114 for saltwater
molluscs and 1 for freshwater fish. Because these data
are not inconsistent with those for other metals, it seems
reasonable to use the values for the two valence states
of chromium interchangeably, and to assume that saltwater
fishes and decapods would have values comparable to that
for freshwater fishes.
Consumption Bioconcentration
Group (Percent) factor
Freshwater fishes 12 1
Saltwater fishes 61 1
Saltwater molluscs 9 114
Saltwater decapods 18 1
Using the data for consumption and BCF for each of these
groups, the weighted average BCF is 11 for consumed fish
and shellfish.
Inhalation
Levels of Cr in air have been carefully monitored.
In the United States in 1964 an average value of 0.015 jug/m
C-9
-------
was reported, with a maximum of 0.35 jug/m . More recent
values show levels below detection limits in most non-urban
and some urban areas (U.S. EPA, 1973); yearly averages exceeded
0.01 jug/rn in only 59 of 186 urban areas.
The chemical form of Cr in air will vary, depending
primarily on its source. There is little information on
the size distribution of the particles, but it is safe to
assume that a significant portion will be in the respirable
range. Uptake, of course, depends on the aerodynamic diameter
of the particles. Assuming an average alveolar ventilation
of 10 m /day, with an alveolar retention of 50 percent of
Cr present at a level of 0.015 jug/m , alveolar uptake would
only amount to approximately O.ljug/day. Additional Cr
could also be deposited in the upper respiratory passages
and contribute ultimately to the intestinal load of Cr.
In any case, however, inhalation under normal conditions
does not contribute significantly to total Cr uptake.
Even in the non-occupational environment the concentra-
tion of Cr in air may rise significantly above normal back-
ground levels. Thus, increased ambient concentrations of
Cr have been reported in the vicinity of industrial sites
(U.S. EPA, 1978). In the proximity of water cooling towers,
for instance, where Cr was employed as a corrosion inhibitor,
air levels of Cr as high as 0.05 jug/m have been reported.
However, even such a relatively high level is not likely,
to alter greatly total Cr uptake. The possibility that
smoking might contribute to the pulmonary load of Cr has
not been fully evaluated.
C-10
-------
Of course, to the extent that the lungs represent a
target organ for Cr, additional pulmonary loads may assume
significance even though total body Cr may not have been
materially increased by the inhalation exposure. Although
such exposure can lead to significantly increased urinary
excretion of Cr, it is not clear to what extent the Cr added
to systemic pools originated in the lungs or was alterna-
tively absorbed from the intestines following pulmonary
clearance of the Cr-containing particles. In any case,
pulmonary Cr does not appear to be in full equilibrium with
other Cr pools in the body. This conclusion is based on
the fact that the Cr content of the lungs, unlike that of
the rest of the body,' may actually increase with age (Mertz,
1969). Prolonged pulmonary retention of inhaled Cr is also
reflected by the fact that the pulmonary concentration of
the element usually exceeds that of other organs. The rela-
tively slow clearance of Cr from the lungs was also noted
by Baetjer, et al. (1959), who found that 60 days after
intratracheal instillation into guinea pigs, 20 percent
of a dose of CrCl^ remained in the tissue.
Dermal
Compounds of Cr permeate the skin fairly readily when
applied in the hexavalent form; trivalent Cr compounds react
directly with epithelial and dermal tissue. Cutaneous expo-
sure is primarily a problem of the workplace: many lesions
have been described under these conditions, including ulcer-
ation and sensitization reactions. There is little evidence,
however, to suggest that cutaneous absorption significantly
C-ll
-------
contributes to the total body load of Cr in the normal environ-
ment.
The three previous sections review briefly the uptake
of Cr by ingestion, inhalation, and cutaneous absorption.
None of the three routes of entry will lead to harmful levels
of Cr in the body when exposure involves only the low levels
of the element normally found in food, water and air. Indeed,
it may be recalled ("Ingestion" section) that the average
American may actually suffer from mild Cr deficiency. The
major fraction of body Cr originating in the general environ-
ment is contributed by ingestion. In industrial surroundings,
by contrast, other routes of exposure may become more signi-
ficant *. Uptake of Cr-by inhalation may pose special risks
here. This conclusion follows from the fact that the lungs
tend to retain Cr more than do other tissues (see "Inhala-
tion" section). The "Carcinogenicity" section deals further
with pulmonary effects of exposure to Cr in air.
Under normal conditions of exposure, considerable varia-
bility has been observed in the Cr concentrations of different
tissues. It is difficult to assess to what extent the wide
range of values reported reflects analytical problems rather
than true individual variations. As a first approximation,
an average level of around 2 jug Cr/g ash may be derived
from the work of Tipton and Cook (1963) and of Imbus, et
al. (1963) for most soft tissues and for whole blood of
non-exposed humans. Levels of Cr in the lungs may be ten
times higher; there is no evidence to suggest that Cr is
a bone-seeking element. If we further assume that the aver-
C-12
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age ash content of soft tissues approximates 1 percent of
fresh weight, a total body burden in the adult of the order
of 2 mg may be calculated. Results of Schroeder, et al.
(1962) showed values of Cr in human tissues of the order
of 0.05 jug/g fresh weight, which would correspond to a total
adult body burden of around 3 to 4 mg; Schroeder (1965)
suggested an upper limit of 6 mg Cr in a 70 kg man. These
values are presented here to indicate the net result of
Cr uptake by ingestion, inhalation and cutaneous absorption
under normal conditions. As pointed out, this body burden
may actually represent a marginally deficient state.
PHARMACOKINETICS
Absorption, Distribution, Metabolism, and Excretion
Analysis of the movement of Cr through various body
pools, and determination of the size and turnover rates
of these pools, are complicated by several facts. In the
first place it is likely that different Cr compounds will
exhibit different kinetic characteristics in the body; this
is well illustrated by the wider body distribution of Cr
injected in the form of the glucose tolerance factor than
when administered as CrCl., (Mertz, 1969). Second, the chemical
methods employed for the estimation of biological Cr concent-
rations do not adequately distinguish between different
forms of Cr present in the original sample. The results
of Schroeder, et al. (1962) do suggest, however, that both
hexavalent and trivalent Cr may occur in the ash of biological
materials. Precise conclusions on this point are difficult
because the chemical forms of Cr may be changed during the
C-13
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ashing. Third, difficulties of interpretation arise from
the fact that one chemical species of Cr may be transformed
into another in the body, for instance as by reduction of
Cr VI to Cr III.
The complexity of the pharmacokinetics of Cr to be
predicted from such considerations is observed both in man
and in experimental animals. This situation may be illustrated
by reference to the urinary excretion of Cr under normal
conditions. In man the kidneys account for 80 percent or
more of Cr excretion by non-exposed individuals (Natl. Acad.
Sci., 1974); urinary excretion amounts on the average to
5 to 10 pg/day or less (see "Ingestion from Water and Foods"
section). Such a value corresponds to less than 1 percent
of the total body burden as estimated in the section on
"Evaluation of Relative Contribution of Different Exposure
Routes to Body Burden"; it also approximately equals the
average daily retention of Cr (see section on "Ingestion
from Water and Foods"). The body thus appears roughly to
be in steady state with regard to Cr. It would not be correct
to infer, however, that the turnover rates of the various
Cr pools in the body all fall below 1 percent/day; this
would be true only if Cr taken in by one of the routes of
entry discussed in the section on "Exposure" always equilibrated
evenly with different body pools.
Although unfortunately little information is available
on changes in specific radioactivities of Cr in different
body compartments following administration of Cr, there
is strong evidence to show that different compartments exhi-
C-14
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bit distinctly different turnover kinetics. Lim (1978)
reports the kinetics of radiochromium III distribution in
humans. Three major accumulation and clearance components
were found for liver, spleen, and thigh; liver and spleen
contained the higher concentrations. Normally in man, the
highest concentration of Cr is found in the lungs, and pulmonary
levels tend to rise with age while the Cr content of other
tissues falls. Apparently the lung obtains most of its
Cr from the air, not from oral loads, and pulmonary Cr does
not come into equilibrium with other body pools of Cr (see
"Inhalation" section).
Similar conclusions on non-equilibration of body pools
can be drawn from measurements on the excretion kinetics
of Cr III injected into rats. At least three kinetic
compartments were observed in this case (Mertz, et al. 1965),
with half-lives respectively of 0.5, 5.9 and 83.4 days.
A slowly equilibrating Cr compartment in man was estimated
to possess a half-life of 616 days (U.S. EPA, 1978) . Injec-
tion of 1 mg of unlabeled Cr into rats, a very large dose
compared to the presumptive body burden as calculated in
the section on "Evaluation of Relative Contributions of
Different Exposure Routes to Body Burdens" exerted little
effect on the rate of tracer excretion from the slow compart-
ment. The finding that even a very large excess of Cr does
not affect this compartment further indicates that ingested
or injected Cr does not necessarily pass through every body
compartment on its way to excretion. Finally, this conclusion
is supported by the observation that the pool from which
C-15
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Cr (at least in some systems) enters plasma following adminis-
tration of glucose is not readily labeled by injected Cr
(administered as CrCl3) (Mertz, 1969).
As is the case with other metals, chromium normally
circulates in plasma primarily in a bound, non-diffusible
form (Mertz, 1969). At low levels of Cr III the iron-binding
protein siderophilin complexes most of the Cr present, but
at higher levels of Cr other plasma proteins also become
involved. The high affinity of Cr III for siderophilin
presumably reflects the fact that this protein provides
the normal mechanism of transport for Cr to the tissues.
A small fraction of plasma Cr is also present in a more
diffus-ible form, complexed to various small organic mole-
cules which are filtered at the glomerulus and partially
reabsorbed in the renal tubule. The suggestion that this
reabsorption may involve an active transport process (Davidson,
et al. 1974) is not supported by the evidence presented.
Chromium very tightly bound in low-molecular weight complexes
such as Cr-EDTA may serve as a glomerular indicator, being
freely filtered but not at all reabsorbed (Stacy and Thor-
burn, 1966).
The half-life of plasma Cr is relatively short, and
cells tend to accumulate the element to levels higher than
those present in plasma. Presumably this accumulation results
from intracellular trapping of Cr compounds which penetrate
cells in the hexavalent form and then react with cell consti-
tuents, such as hemoglobin in the case of the erythrocyte.
Within the cells, Cr VI will be reduced to Cr III and remain
C-16
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trapped in this form. In any case, the lack of equilibration
of Cr between plasma and cells renders invalid the use of
plasma levels as indicators of total exposure.
Another reason for the limited usefulness of plasma
Cr levels as measure of body burden is the likelihood that
plasma Cr can be identified with one of the rapidly excreted
Cr compartments discussed above. This is suggested by the
finding that even though the rise in plasma Cr reported
by some authors to occur after administration of a glucose
load is not derived from a rapidly labeled pool, it is followed
by increased urinary excretion of Cr (Mertz, 1969). In
summary, little can be concluded definitely at this time
about nature, size or- location of the various body pools
of Cr whose existence was inferred from tracer equilibration
and excretion studies.
The importance of the chemical form of Cr in determining
distribution of various compounds between pools is further
illustrated by the observation that while inorganic Cr III
does not appreciably cross the placental barrier, Cr III
injected into pregnant rats in the form of natural complexes
obtained from yeast can readily be recovered from the fetuses
(see section on "Mutagenicity").
As further considered in the Effects sections, compounds
of Cr VI may act as acute irritants whereas those of Cr
III exert little acute toxic action. Presumably, this fact
reflects primarily the poor intestinal absorption of the
trivalent compounds, and the strong oxidizing power of Cr
VI. The lungs, however, may accumulate and retain relatively
C-17
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insoluble Cr III from respired air although even in this
case'Cr VI appears to be much more toxic than Cr III. Here
again-toxicity is determined as much by the chemical form
of Cr as by its concentration. The additional factor of
length of exposure to Cr is apparent in the need to implant
the test compound or to inject it intramuscularly before
sarcomas are produced at those sites (see "Carcinogenicity"
section). In terms of human exposure such routes of adminis-
tration possess little relevance except to emphasize the
importance of long-term Cr concentrations in specific body
compartments as major determinants of toxicity.
EFFECTS
Acute,. Sub-acute, and- Chronic Toxicity
Because Cr is generally accepted to be an essential
element, the effects of exposure to low levels may be beneficial
in deficiency states; such an action of Cr would of course
have to be separated from the harmful consequences of exposure
to higher concentrations. This can be readily achieved
because the amounts of Cr required to produce toxic effects
are very much higher than those involved in the correction
of possible deficiencies. Thus, the LD^Q for Cr III following
its intravenous administration (10 mg/kg weight) exceeds
by at least four orders of magnitude the dose needed to
relieve impairment of glucose tolerance in Cr-deficient
rats (U.S. EPA, 1978). Still higher levels of Cr III must
be fed by mouth before toxic symptoms appear, a fact related
to the relative insolubility and poor intestinal absorption
of most compounds of trivalent chromium.
C-18
-------
Unlike compounds of Cr III, those of Cr VI tend to
cross biological membranes fairly easily and are somewhat
more readily absorbed from the gut or through the skin.
The strong oxidizing power of hexavalent Cr explains much
of its irritating and toxic properties.
That the concentrations of chromium normally encountered
in nature barely meet the requirements for this element
in the American diet underlines the fact that natural levels
do not constitute a human health hazard. However, acute
and chronic toxicity problems associated with exposure to
Cr are of concern in the industrial environment or in areas
potentially polluted by industrial sources. Such toxic
effects are reviewed in detail by the National Institute
for Occupational Safety and Health (1975); they include
systemic actions of Cr compounds, in addition to primary
lesions at the level of the skin, the respiratory passages
and the lungs. It must be emphasized again that the findings
of lesions following exposure to high concentrations of
Cr compounds under experimental conditions, or as a result
of accidental or deliberate human exposure, may bear little
relevance to the probability of Cr exerting similar actions
at more normally encountered levels.
Exposure to relatively high levels of Cr has been studied
in some detail. Thus, when Cr in the form of K2Cr04 was
administered to dogs over a period of 4 years at a level
of 0.45 mg/1 in drinking water, increases in the Cr concen-
tration of liver and spleen were reported; at exposure levels
25 times higher, accumulation in the kidneys also became
C-19
-------
apparent (Anwar, et al. 1961). However, there were no signifi-
cant pathological changes associated with such exposures.
Similarly, a concentration of 0.45 mg Cr/1 did not lead
to any overt effects in four cases of prolonged human exposure
(Davids, et al. 1951). Rats tolerated 25 mg of Cr III or
of Cr VI per liter drinking water for one year (MacKenzie,
et al. 1958); exposure to Cr VI, however, led to a nine
times higher concentration of Cr in tissues, than Cr III,
a fact reflecting the more ready intestinal absorption of
the hexavalent form. These findings support the conclusion
that few systemic changes would be expected to result from
even moderately elevated oral exposure to Cr. On that basis
the standard of Cr established for drinking water (see section
"Existing Guidelines and Standards") should provide adequate
protection against general systemic effects. The question
of the safety of such a level in terms of possible carcinogenic
effects is considered in the section on "Carcinogenicity".
On the other hand, evidence for systemic lesions following
more massive exposure, is well documented (U.S. EPA, 1978;
Natl. Acad. Sci. 1974).
Renal damage is caused by high concentrations of Cr.
Thus intraarterial injection of dichromate has been used
for the experimental production of lesions restricted to
the first portion of the proximal tubule (Nicholson and
Shepherd, 1959). Similarly, tubular necrosis has repeatedly
been observed following massive accidental or deliberate
exposure (suicide attempts) to Cr (Natl. Acad. Sci. 1974).
These cases, however, represent acute effects of very high
C-20
-------
doses and their significance to environmental considerations
is small.
In only one instance was an association between occupa-
tional chromium exposure and hepatic lesions reported.
A small number of workers were excreting large amounts of
Cr in their urine. Hepatic changes were observed in biop-
sies although no overt clinical symptoms were seen. Among
other systems shown to respond to high doses of Cr is the
dog intestine (quoted in U.S. EPA, 1976) . Although the
possibility of more subtle and long range systemic effects
of high Cr exposure cannot be excluded, there is no evidence
to support its likelihood.
Dermal effects h-ave been reviewed in considerable detail
(Natl. Acad. Sci. 1974). The effects of Cr compounds on
the skin were recognized over 150 years ago. Since that
time they have been studied in depth by many investigators.
The earlier cases were ulcerative changes developing from
contact with various compounds of Cr VI. Later studies
emphasized that workers exposed to Cr VI can develop allergic
contact dermatitis; sensitivity also appears to develop
to higher levels of Cr III. No evidence could be found
for an association between chromium exposure and skin cancers.
In general, these reports concern relatively massive
exposures, unlikely to occur outside the occupational environ-
ment, and made even less likely at the present time because
of generally improved industrial hygiene practices, (Natl.
Inst. Occup. Safety Health, 1975). It is worth noting
that the standard set for permissible levels of Cr in drinking
C-21
-------
water (see section on "Existing Guidelines and Standards")
is much lower than those reported to affect the skin. No
evidence was found to suggest that presently permissible
concentrations of Cr in domestic water supplies possess
much significance in terms of skin disease.
Subtle changes in pulmonary dynamics have been observed
among workers employed in the chromium electroplating industry
(Bovett, et al. 1977) . The major effect of Cr on respiratory
passages consists of ulceration of the nasal septum, with
subsequent perforation, and of chronic rhinitis and pharingitis,
The incidence of such effects may become remarkably high
at elevated Cr levels in air. Thus, Mancuso (1951) observed
nasal septal perforations in 43 to 85 percent of workers
exposed in a chromate plant to both tri- and hexavalent
Cr in concentrations as high as 1 mg/m . The reported incidence
of rhinitis and pharingitis was even higher. In another
survey (U.S. Pub. Health Serv. 1953), 509 out of 897 chromate
workers were found with nasal septal perforations. Bloomfield
and Blum (1928) had concluded that daily exposure to chromic
acid concentrations exceeding 0.1 mg/m causes injury to
nasal tissue. Effects of lower concentrations have not
been carefully studied, so no accurate conclusions on dose-
effect relationships can be drawn.
An additional difficulty in interpreting these results
arises from the fact that the exposure of the workers dis-
cussed here may not have been associated primarily with
air-borne Cr: poor work practices leading to local contact
almost certainly caused a high proportion of the nasal lesions
C-22
-------
(Natl. Inst. Occup. Safety Health, 1975). All nasal effects,
however, presumably reflect, the irritating action of soluble
compounds of Cr VI. There is no evidence to suggest that
the ulcerative lesions can give rise to cancerous reactions.
In an average concentration of 68 jug/m , Cr VI caused
some irritation to eyes and throat in a chromate-producing
plant (U.S. Pub. Health Serv. 1953). Information avail-
able does not permit derivation of meaningful dose-effect
relationships. Nevertheless, current evidence indicates
that the presently permissible standard for the concentra-
tion of non-carcinogenic compounds of Cr VI in air will
protect most workers against irritation of the respiratory
passages. This standard permits a time-weighted average
exposure to 25 /ig Cr/m of ambient air for a 40-hour week,
with a maximum exposure to 50 jag/m of breathing zone air
for any 15-minute period.
Teratogenicity
Although the mutagenic properties of certain compounds
of Cr are well established, little evidence could be found
for fetal damage directly attributable to such compounds.
This is somewhat unexpected in light of placental permea-
bility to at least some forms of Cr (Mertz, 1969). Embryonic
abnormalities were produced in the chick when Na-,Cr9O7 or
^ +» i
Cr(NO3)2 were injected into the yolk sac or onto the chorioal-
lantoic membrane (Ridgway and Karnofsky, 1952). The signifi-
cance of these data in relation to ingestion of chromium
compounds is questionable.
C-23
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Mutagenicity
Because of the close correlation emerging between carcin-
ogenicity of chemicals and their mutagenic properties in
suitable test systems, it is of interest to refer to the
work of Venitt and Levy (1974), who reported that soluble
chromates of Na, K and Ca stimulated mutagenesis in E. coli.
Negative results were obtained with soluble salts of the
two metals closest to Cr in the periodic table (tungsten
and molybdenum), as well as with a soluble compound of Cr
III. Earlier reports (Hueper, 1971) classifying Cr salts
under the heading of carcinogenic chemicals without mutagenic
properties appear to have been in error.
In" recent years much evidence has accumulated to show
that compounds of Cr possess the definite ability to cause
transformation and mutation. Both Cr III (as CrClq) and
Cr VI (as K^C^Oy) in concentrations equitoxic to mice produced
similar morphologic changes in tertiary cultures of mouse
fetal cells (Rafetto, et al. 1977); it is interesting to
note that Cr VI caused more extensive chromosomal aberrations
than did Cr III. Wild (1978) reported that potassium chromate
produces a dose-dependent cytogenetic effect on bone marrow
in mice. Hexavalent Cr has also been suspected of being
responsible for the mutagenic effects of welding fumes (Hedenstedt,
et al. 1977). Bigalief, et al. (1976) observed a significant
increase in the frequency of bone marrow cells with chromosome
aberrations in rats acutely or chronically poisoned with
potassium dichromate. Further, aerosols of Cr VI have been
held responsible for mutagenic effects found in a group
C-24
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of workers engaged in the production of chromium (Bigalief,
et al. 1977). The full significance of these results could
not be evaluated in the absence of the detailed publications.
In bacterial test systems, compounds of Cr VI caused
mutations in Salmonella typhimurium (Petrilli and De Flora,
1977) . Two compounds of Cr III tested were neither toxic
nor mutagenic for this organism. The conclusion may be
recalled that the major risk of carcinogenicity for humans
arises from Cr VI compounds (see "Carcinogenicity" section).
In concentrations as low as 10" M, potassium dichromate
significantly increased gene conversion in a strain of yeast
(Bonatti, et al. 1976). The transformation frequency of
simian adenovirus in Syrian hamster cells was raised by
calcium chromate (Casto, et al. 1977).
Carcinogenicity
In addition to the many acute and chronic effects dis-
cussed in preceeding sections, Carcinogenicity of various
Cr compounds has been well documented, at least in man.
A series of Cr compounds was listed by the National Insti-
tute of Occupational Safety and Health (1977) under the
heading of suspected or identified carcinogens in humans.
Inclusion in this list was largely based on results of animal
experimentation. If, however, one excludes sarcoma production
at the site of implantation or injection of the suspected
carcinogen, the evidence for cancer production in experimental
animals is not convincing.
C-25
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In spite of the demonstration that Cr compounds can
cause tumors at various sites in experimental animals, the
only well-documented evidence for cancers associated with
Cr exposure of humans involves the lungs. The relatively
high incidence of lung cancer in the chromate industry has
been well documented (Natl. Acad. Sci. 1974). Industrial
exposure, as discussed below, greatly exceeds that
attributable to food, water, and air under normal conditions.
In considering the risks of pulmonary carcinogenesis in
man, the low systemic levels of Cr originating from the
diet or from drinking water can be ignored; unlike the pul-
monary load of Cr, which does not appear to be in equilibrium
with other body storeys of the element (see "Pharmacokinetic"
section), ingested Cr is poorly absorbed and presents no
risks at normal ambient levels.
The primary emphasis in this field must be placed on
the problems associated with pulmonary exposure; no evidence
has been adduced for an association in humans between Cr
and initiation of cancer at sites other than the lungs.
The literature on respiratory cancer in humans up to 1950
has been reviewed by Baetjer (1950): 109 cases had been
reported up to that date in the chromate-producing industry,
and an additional 11 cases were reported from chromate pigment
plants. It seems likely that in all instances Cr VI was
involved in the effect. In any case, the incidence of res-
piratory cancer among these work populations significantly
exceeded expected values.
C-26
-------
Further work on this subject after 1950 is considered
in the review prepared by the National Academy of Sciences
(1974). Of particular interest is the study of Taylor (1966)
on a large group of chromate workers who were followed over
a period of 24 years on the basis of records from the U.S.
Social Security Administration. Death rate from lung cancer
in this group exceeded expected values by a factor of 8.5.
Excess incidence of all other cancers amounted only to a
factor of 1.3, in agreement with the conclusion stated above
that respiratory cancers constitute the major cancer risk
associated with Cr exposure in humans. Taylor further reported
that the age-adjusted death rate from respiratory cancer
increased with the period of exposure, a finding suggesting
the existence of a definite dose-response relationship.
Little predictive use can be made of this fact as no informa-
tion on the concentration of potential carcinogens in these
studies was available.
An additional difficulty arises in attempts to inter-
pret this information because the specific carcinogen (or
carcinogens) responsible for the increased incidence of
cancer found in the chromate industry has not been fully
identified. Several compounds of Cr are likely to be present
in industrial surroundings. Further, a significant portion
of workers investigated must have been exposed to other
potential or actual carcinogens used in the chemical industry.
Finally, the lung cancers observed in industry generally
resulted from prolonged exposure. Initial exposure levels
are often not known and the only information available refers
C-27
-------
to Cr levels in air at the time of the final survey. All
these factors make it difficult to extract from data on
human subjects conclusions concerning any significant relation-
ship between degree of Cr exposure and the incidence of
lung cancer.
This problem may be illustrated by Table 1, based on
the work of Mancuso and Hueper (1951). In this study an
incidence of cancer of the respiratory system of 66.7 percent
of all cancers was observed, compared with a figure of 11.4
percent in a control group. Details of the six Cr workers
concerned, with the addition of one worker who died of res-
piratory cancer outside of the county and who was not included
in the- above calculation, are shown in the table. As clearly
emerges from these data, lung cancer arises only after a
prolonged exposure and latency period (Bidstrup and Case,
1956) . A second point apparent from the table is that the
reported levels of Cr in air (average 0.74 mg Cr03/m ) were
very high. These exposure levels were calculated for each
individual with adjustments for the occupational history,
and show that in each case the major exposure involved water-
insoluble Cr. It is not certain to what extent compounds
of Cr VI were included under the heading of water-insoluble
Cr. The suggestion that carcinogenicity in these cases
could be attributed to Cr III is probably not justified
(U.S. Pub. Health Serv. 1953); this is further borne out
by more recent work with Cr VI.
C-28
-------
TABLE 1
Deaths Due to Lung Cancer in Chromate Workers
(adapted from Mancuso & Hueper, 1951)
o
t
K)
VO
SUBJECT
CB
TG
FJ
JK
EL
ESM
WDS
Mean
YEARS OB1
EXPOSURE
9.0
14.5
12.5
7.5
9.2
2.0
7.2
8.8
LATENT
PERIOD
(years)
10.0
14.3
12.5
9.0
14.0
7.2
7.2
10.6
WATER
INSOLUBLE
' 0.37
0.37
0.19
0.92
1.12
0.19
1.12
0.61
EXPOSURE LEVELS
(mg CrO_/m )
WATER
SOLUBLE
0.17
0.08
0.02
0.29
0.15
0.02
0.15
0.13
TOTAL
0.54
0.45
0.21
1.21
1.27
0.21
1.27
0.74
The exposure levels were calculated for each individual on the basis of his occupa-
tional history, and are expressed in terms of CrO.,.
-------
Thus, Davies (1978) reported that among workers exposed
to Zn chromate in three British factories, an increased
mortality due to lung cancer was seen after an induction
time as short as one year. Concentrations of Cr were not
given. Similarly, Langard and Norseth (1975) observed an
increased cancer rate among workers in a Zn chromate plant
where no trivalent Cr was utilized. Pulmonary cancer was
identified in three workers who had been exposed to levels
of 0.5 to 0.9 mg Cr/m for 6 to 9 years. In addition, a
single case of adenocystic carcinoma of the nasal cavity
was also reported. Attention must again be drawn to the
fact that such exposures involve Cr concentrations which
are relatively massive when compared to recommended standards
(see "Existing Guidelines and Standards" section). The
standard for occupational exposure in air mandates levels
of poorly soluble mono- or dichromates not exceeding 1 ug/m .
Attempts to produce lung cancers in experimental animals
by inhalation exposure or by feeding Cr compounds have not
been successful. Inhalation did cause, however, a variety
of pulmonary symptoms (Steffee and Baetjer, 1965). Permit-
ting animals to breathe air from a chromate factory, 1 to
3 mg Cr/m , produced no bronchogenic carcinomas (Baetjer,
et al. 1959). Nettesheim, et al. (1970) exposed mice to
Cr2O3 dust (25 mg/m ) for 5% hours per day, five times each
week, for as long as 18 months with similarly negative results.
Distribution and elimination of Cr from the lungs were affected
by simultaneous infection of the animals with influenza
virus. This underscores the importance of factors other
C-30
-------
than Cr itself in determining possible effects. In any
case, not even the relatively prolonged retention of inhaled
Cr in the lungs (see "Inhalation" section) suffices to assure
an inhalation exposure adequate for the production of lung
cancer under experimental conditions. Experimental lung
tumors could only be observed following implantation of
pellets prepared from Cr VI compounds dispersed in an equal
quantity of cholesterol carrier (Laskin, et al. 1970).
As was already stated above in reference to the data gathered
in epidemiological surveys of lung cancer in humans, such
results do not lend themselves to the derivation of dose-
effect relationships, nor to extrapolation down to acceptable
levels- by a linear or any other model.
In the very high concentrations employed for the experi-
mental production of cancer, compounds of Cr may also possess
some cocarcinogenic properties. As illustrated by the observa-
tion of Lane and Mass (1977), 2.5 mg of chromium carbonyl
acted mildly synergistically with 2.5 mg benzo(a)pyrene
in producing carcinomas in tracheal grafts in rats. No
further reports on the possible cocarcinogenicity of Cr
compounds were found. It is conceivable, however, that
in the very high concentrations employed experimentally,
other Cr compounds might also possess cocarcinogenic proper-
ties. Especially likely in view of the recognized risks
associated with smoking is the probability that smoking
increases the incidence of lung cancer following pulmonary
exposure to Cr.
C-31
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CRITERION FORMULATION
Existing Guidelines and Standards
A variety of standards have been recommended for permis-
sible Cr VI levels in water and air. Table 2 provides infor-
mation on standards presently established in the United
States, as formulated by various agencies. The high accept-
able level of Cr in livestock water is based on the poor
absorption of Cr compounds in general from the gut ("Ingestion"
section). Because of this low fractional absorption, and
in view of the fact that the sensitivity of the lungs to
Cr appears to exceed that of other tissues, as discussed
in the "Carcinogenesis" section, standards for Cr in air
are much lower than those for water.
Current Levels of Exposure
Although lower Cr limits have been prescribed for air
than for water, the standard for non-carcinogenic Cr VI
in air permits significantly greater uptake of Cr than does
that for Cr VI in drinking water designed for human consump-
tion. Thus, if we assume a daily consumption of 2 liters,
with a fractional gastrointestinal absorption of 5 percent,
total uptake from that source would amount to 10 jag/day.
In contrast, the criteria discussed in the section on "Inhala-
tion", i.e., an alveolar ventilation of 10 m /24 hours with
50 percent alveolar retention of inhaled Cr, would lead
to Cr uptake through the lungs of around 40 /ig during an
8 hour exposure to levels of 25 jug/m . The upper limit
for carcinogenic Cr VI would similarly cause retention of
1 to 2 jug Cr under these conditions.
C-32
-------
TABLE 2
Recommended or Established Standards for Cr in the United States
MEDIUM CHEMICAL
SPECIES
Drinking Water Cr VI
total
Ambient Cr VI
water
REFERENCE
U.S.
Serv.
U.S.
Pub. Health
(1962)
EPA (1976)
STANDARD
50 jag/1
50 jug/1
Total
Fresh water
(aquatic life)
Livestock water
Work place
air
total
chromium
Cr VI
carcinogenic3
non-carcino-
genic
Cr VI
U.S. EPA (1976)
Natl. Acad. Sci.
(1972)
Natl. Inst. Occup.
Safety and Health
(1975)
Natl. Inst. Occup,
Safety and Health
(1975)
Natl. Inst. Occup.
Safety and Health
(1975)
100 jug/1
1 mg/1
25 jug/m3 TWA b
50 ;ag/in3 TWA b
a) Carcinogenic compounds are here taken to include all forms of Cr
VI other than Cr03 and mono- or dichromates of H, Li, Na, K, Rb, Cs
and NH4.
b) Time-weighted average.
C-33
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Special Groups at Risk
No such groups have been identified outside the occupa-
tional environment.
Basis and Derivation of Criterion
There is evidence which suggests that hexavalent chromium
(Cr VI) is a carcinogen. Based on exposure of chromium
workers to Cr VI (Mancuso and Hueper, 1951; Taylor, 1966)
the U.S. EPA Carcinogens Assessment Group has developed
a water quality criterion for Cr VI to keep the lifetime
risk level below one in 100,000 (see Appendix I).
Under the Consent Decree in NRDC vs. Train, criteria
are to state "recommended maximum permissible concentrations
(including where appropriate, zero) consistent with the
protection of aquatic organisms, human health, and recreation-
al activities." Chromium VI is suspected of being a human
carcinogen. Because there is no recognized safe concentration
for a human carcinogen, the recommended concentration of
Chromium VI in water for maximum 'protection of human health
is zero.
Because attaining a zero concentration level may be
infeasible in some cases and in order to assist the Agency
and States in the possible future development of water quality
regulations, the concentrations of Chromium VI corresponding
to several incremental lifetime cancer risk levels have
been estimated. A cancer risk level provides an estimate
of the additional incidence of cancer that may be expected
in an exposed population. A risk of 10" for example, indi-
cates a probability of one additional case of cancer for
every 100,000 people exposed, a risk of 10~6 indicates one
C-34
-------
additional case of cancer for every million people exposed,
and so forth.
In the Federal Register notice of availability of draft
ambient water quality criteria, EPA stated that it is con-
sidering setting criteria at an interim target risk level
of 10~ , 10 or 10" as shown in the table below.
Exposure Assumptions Risk Levels and Corresponding Criteria
£ 10~7 1£~6 1£~5
2 liters of drinking water 0.08 ng/1 0.8 ng/1 8 ng/1
and consumption of 18.7
grams of fish and shellfish (2)
Consumption of fish 8.63 ng/1 86.3 ng/1 863 ng/1
and shellfish only.
(1) Calculated by applying a modified "one hit" extrapolation
model described in the FR 15926, 1979 to the animal
bioassay data presented in Appendix I. Since the extrapo-
lation model is linear to low doses, the additional
lifetime risk is directly proportional to the water
concentration. Therefore, water concentrations corres-
ponding to other risk levels can be derived by multiply-
ing or dividing one of the risk levels and corresponding
water concentrations shown in the table by factors
such as 10, 100, 1,000, and so forth.
(2) Approximately one percent of the Chromium VI exposure
results from the consumption of aquatic organisms which
exhibit an average bioconcentration potential of 1.0
fold. The remaining 99 percent of Chromium VI exposure
results from drinking water.
C-35
-------
Concentration levels were derived assuming a lifetime
exposure to various amounts of Chromium VI (1) occurring
from the consumption of both drinking water and aquatic
life grown in water containing the corresponding Chromium
VI concentrations and, (2) occurring solely from the consump-
tion of aquatic life grown in the waters containing the
corresponding Chromium VI concentrations. Although total
exposure information for Chromium VI is discussed and an
estimate of the contributions from other sources of exposure
can be made, this data will not be factored into the ambient
water quality criteria. The criteria presented, therefore,
assume an incremental risk from ambient water exposure only.
Therefore, the criterion for hexavalent chromium should
be at a level of no greater than 8 ng/1 to keep the lifetime
risk of cancer below 1 in 100,000.
A water quality criterion can be set for other Cr species
on the basis of reasonable safety margins applied to the
lowest exposure observed to produce effects.
The level of 0.05 mg/1 of chromium quoted in Table
2 appears to be an acceptable risk level. This level is
500 times lower than a concentration which remained without
overt toxicological effects in rats over a period of one
year, and over 200 times lower than a level reported not
to affect dogs over four years. With the exception of hexavalent
chromium, there is no reason to believe that the level of
0.05 mg/1 (50 ug/1) permitted for ambient water poses a
significant threat to human health. As a standard, this
C-36
-------
level was set in 1962 and has in the meantime been confirmed
by several reviewing groups. Therefore, the recommended
water quality criterion for chromium, except hexavalent
chromium, is 50 ug/1. For practical purposes, it should
be noted that it is difficult to analytically distinguish
between trivalent and hexavalent chromium.
Because of the low bioconcentration of chromium, consider-
ation of the consumption of fish and shellfish does not
.change the recommended criterion:
If two liters of drinking water are ingested per day,
then a level of 50 ug/1 would correspond to an intake of
100 ug from water. To apportion this daily intake to both
drinking water and fish and shellfish consumed, the following
calculation can be used:
2 X + (0.0187) (F) (X) = 100 ug
where
2 = amount of water ingested in liter/day
X = chromium concentration in water, mg/1
0.0187 = amount of fish consumed per day, kg/day
F = bioconcentration factor, mg chromium/kg fish per
mg chromium in water. (F = 11 for chromium)
2 X + .2 X = 100 ug
2.2 X = 100 yg
X = 45 ug/1 (orxx^ 50 /ag/1)
C-37
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Bloomfield, J.J., and W. Blum. 1928. Health hazards in
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Bonatti, S.f et al. 1976. Genetic effects of potassium
dichromate in schizosaccharomyces Pombe. Mutat. Res. 38:
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Bovett, P., et al. 1977. Spirometric alterations in workers
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Environ. Health 40: 25
Buhler-, D.R., et al. -1977. Tissue accumulation and enzymatic
effects of hexavalent chromium in rainbow trout, Salmo gairdneri
Jour. Fish. Res. Board Can. 34: 9.
Capuzzo, J.M., and J.J. Sasner. 1977. The effect of chromium
on filtration rates and metabolic activity of Mytilu edulis
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Biota to Pollutants. Academic Press, N.Y. 225.
Casto, B.C., et al. 1977. Development of a focus assay
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Collins, R.J., et al. 1961. Chromium excretion in the dog.
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Davids, H.W., et al. 1951. Underground water contamination
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elements: chromium and copper. Proc. Soc. Exp. Biol. Med.
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Davies, J.M. 1978. Lung cancer mortality of workers making
chrome pigments. Lancet 1: 384.
Doisy, R.J., et al. 1971. Metabolism of chromium in
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Fortes, P.A.G. 1977. Membrane transport in red cells. Page
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Fromm, P.O., and R.M. Stokes. 1962. Assimilation and metabolism
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Gray, S.J., and K. Sterling. 1950. The tagging of red cells
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C-46
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APPENDIX 1
Summary and Conclusions Regarding
the Carcinogenicity of Chromium*
In the aquatic environment chromium is virtually always
found in the valence states +3 or +6. Cr III is an essential
trace element. The daily requirement for Cr III is provision-
ally set as a range of 50 to 200 jug Cr Ill/day (Mertz, 1979).
The evidence suggests that Cr VI is a carcinogen. Cr VI
is highly soluble in water, whereas the solubility of Cr
III is low, depending on pH, alkalinity, and water hardness.
Cr VI is a strong oxidizing agent which reacts readily with
many reducing agents including organic reducing matter,
to yield Cr III. Within the cells, Cr VI will be reduced
to Cr III and remain trapped in this form. Cr III forms
many hexacoordinate complexes in solution with carboxy groups
of proteins, or smaller metabolites, certain amino acids,
nucleic acids, and nucleoproteins; very stable bonds to
both RNA and DNA are formed by Cr III.
Almost all of the Cr VI found in the environment is
produced by industry. Chromium salts (primarily chromates
and dichromates which are compounds of Cr VI) are used exten-
sively in the metal finishing, textile, and leather tanning
industries. They are also used in cooling waters, (catalytic
manufacture, pigments, primer paints, fungicides, and wood
preservatives.
*This summary has been prepared and approved by the Carcinogens
Assessment Group of U.S. EPA in July, 1979.
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The environmental exposure to chromium occurs by inhala-
tion, ingestion from water and food, and by the dermal route.
Cr VI compounds are taken up more rapidly by tissues than
Cr III due to their greater solubility and facilitated trans-
port across cell membranes by broadly specific anion transport
mechanisms. The lung seems to be a target tissue for Cr,
as pulmonary Cr content usually exceeds that of other organs,
and Cr is cleared relatively slowly from the lungs.
Occupational exposure to CR in the air has lead to
gastric and duodinal ulcers, gastritis, ulceration, and
subsequent perforation of the nasal septum, chronic rhinitis,
and pharyngitis (Mancuso, 1951).
Hexavalent chromium has been shown to be mutagenic.
Chromates (Cr VI) 'and dichromates (Cr VI) have been mutagenic
in E. coli (Venitt and Levy, 1974), produced morphologic
changes and extensive chromosomal aberrations in tertiary
cultures of mouse fetal cells (Raffeto, et al. 1977), and
caused cytogenetic effects in mouse (Wild, 1978) and rat
(Bigalief, et al. 1976) bone marrow cell. Cr III compounds
do not produce these effects. In humans, aerosols of Cr
VI are suspected of being responsible for the cytogenetic
effects of welding fumes (Hedenstedt, et al. 1977). Cytogene-
tic effects have also been observed in a group of workers
engaged in the production of Cr (Bigalief, et al. 1977).
Furthermore, compounds of Cr VI, without metabolic activation,
caused mutations in Salmonella typhimurium, Ames strains
TA1535, TA100, TA1537, and TA98, while compounds of Cr III
were not toxic or mutagenic (Petrilli and DeFlora, 1978) .
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With metabolic activation, negative results were obtained
for Cr VI as well as Cr III. These observations indicate
that Cr VI is a direct acting mutagen capable of inducing
both frameshift errors and base pair substitutions. As little
as 10~ M potassium dichromate significantly increased gene
conversion in a strain of yeast.
Six epidemiological studies, five of which were at
different locations (Taylor, 1966, Enterine, 1974; Davies,
1978; Langard and Norseth, 1975; Mancuso and Hueper, 1951;
Baetjer, 1950), of up to 1200 chromate workers strongly indi-
cate that inhalation of Cr VI produces lung cancer. In
addition, Taylor also showed an increase in digestive cancers.
Inhalation studies using calcium chromate on rats and hamsters
have produced cancers (Laskin, 1973). The carcinogenicity
of Cr VI has not been tested by oral administration. Cr
VI has been shown to be carcinogenic when implanted in intra-
bronchial pellets and by subcutaneous as well as intramuscular
injection in mice and rats. Oral administration of 5 ppm
chromic acetate (a Cr III compound) to mice and rats has
had negative results, possibly due to the fact that it is
not absorbed in appreciable amounts from the G.I. tract.
There is no animal bioassay data for ingestion of Cr
VI on which to base a water quality criterion. A water
quality criterion based on a lifetime risk of 10~ was calcu-
lated by assuming that the chromium workers studied by Taylor
had the same exposure as those in the Mancuso and Hueper
study (see Derivation of the Water Quality Criterion for
Chromium). The result is that the water concentration of
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Cc VI should be less than 8.0 ng/1 in order to keep the
lifetime risk below 10 . Cr III, which is required in
the diet for good nutrition, does not appear to be a carcino-
gen based on the available information; consequently, no
limit is recommended by the CAG for the water concentration
of Cr III. Also, it should be noted that there was no appre-
ciable amount of hexavalent chromium present in the insoluble
crude ore (private communication, Dr. Mancuso and Dr.
Paul Urone, chemist.)
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Summary of Pertinent Data
In order to calculate a water quality criterion for
Cr VI, it was necessary to assume that the population's
exposure to Cr VI in the Mancuso and Hueper study was the
same as the exposure in Taylor's paper. Taylor's is the
only study in which the cohort is large enough (1212 people
were studied) to see the effects of Cr exposure in areas
other than the lungs, which are directly affected by inhaled
Cr. The lung cancer risk was very high in this study.
The risk of digestive cancer from Cr exposure is statistically
significant in Taylor's cohort (as shown in 1974 by Enterline);
however, the amount of Cr to which the workers were exposed
is .not available fpr Taylor's study. Mancuso and Hueper
closely studied 97 chromium workers in which they saw a
high incidence of lung cancer (however, less than Taylor's
stud-, ) . The data on exposure in the Mancuso and Hueper
study is very detailed, giving information on first exposure
date, years of exposure, latent period, amount of Cr exposure
in mg Cr/m for Cr III and Cr VI separately, and date of
death.
In order to calculate a water quality criterion for
Cr, it is necessary to know the exposure levels producing
the digestive cancer response in Taylor's study, as the
direct lung effects may not be relevant to water exposure.
The following is an account of the calculations used
in estimating the water concentration of Cr VI which would
result in a lifetime risk of dying from digestive cancer
of 10~5.
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Assuming that the average exposure in Mancuso ar-' Hueper ' s
study is 0.1 mg Cr/m (this is the mean exposure to water
soluble chromium which is Cr VI), then the concentration
in Taylor's study is also assumed to be 0.15 mg Cr/m .
The total exposure in 4.146 years (the mean exposure time
in Taylor's study) is 0.15 mg Cr/m x 10 m /working day
x 240 working days/yr x 4.146 years = 1492.56 mg. If 50
percent of this is swallowed from the respiratory tract,
then 2.018 liter/day x 365 days/year x 70 years x C mg/1
= 1492.56 x 0.5 (The bioconcentration factor in fish is
1.0)
C = 14.40 pg/1 of Cr VI
C is the estimated concentration in water necessary to produce
the observed digestive cancer incidence in the Taylor study.
The relative risk in the Taylor study is 1.533 which is
_utistically significant. The excessive risk corresponding
to a concentration ol "" = 14.40 jug/1 is .533 p, where p
s the expected population risk of digestive tract cancer.
The slope of the excessive risk curve is
B = 0.533p_ 37.01p (mg/1) ~l
0.014
The water quality criterion corresponding to a risk of 10
is given by
X = 10~^
up
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Based on the HEW Vital Statistics of the United States (1973),
the lifetime risk of dying from digestive cancer (p) is
estimated by an acturial method to be 3.5 percent.* Therefore,
the water concentration of Cr VI should be less than 8.0
ng/1 in order to keep the lifetime risk below 10~ .
Using the water concentration of 8 mg/1 for Cr VI,
the one-hit slope (Bu) may be calculated as follows:
n
B = 70 x 10"5
C(2 + RxF)
t*
R = 1.0
F = .0187 kg/day
C = 8 x 10~6 mg/1
BH = 43.345(mg/kg/day)~1 ^
*(Thus, from this data, p = .035).
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