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.
                             B-l

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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
                             B-2

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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.
                             B-5

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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.
                              B-6

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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
                             B-ll

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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.
                              B-12

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!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

-------
                           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



                          REFERENCES








 Adelmann,  I.R.,  and  L.L.  Smith.   1976.   Standard  test fish



 development.   Part 1.  Fathead minnows  (Pimephales promelas)



 and  goldfish  (Carrassius  auratus)  as standard  fish in bioassays



 and  their  reaction to  potential  reference  toxicants.   U.S.



 Environ. Prot. Agency,  EPA  600/3-76-061a,   Duluth,  MN.   77 p.








 Anderson,  B.C.   1948.   The  apparent  thresholds  of toxicity



 to Daphnia magna  for chlorides of  various  metals  when added



 to Lake Erie  water.  Trans. Am. Fish.  Soc.   78: 96.








 Baudouin, M.F.,  and P.  Scoppa.  1974.  Acute toxicity of



 various metals to freshwater zooplankton.   Bull.  Environ.



 Contam. Toxicol.  12:  745.








 Benoit, D.A.   1976.  Chronic effects of  hexavalent chromium



 on brook trout (Salvelinus  fontainalis)  and  rainbow trout



 (Salmo gairdneri).  Water Res.  10: 497.








 Bernhard,  M.,  and A.  Zattera.  1975.  Major  pollutants  in



 the marine environment.  In Marine Pollution and  Marine



Waste Disposal.  Pergamon Press, New York   195.








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.
                               B-43

-------
Bills, T.D., et  al.   1977.  Effects  of  residues  of  the poly-
chlorinated biphenyl  aroclor  1254  on the  sensitivity  of
rainbow trout  to selected environmental contaminants.   Prog.
Fish-Cult.  39:  150.

Buhler, D.R.,  et al.   1977.   Tissue  accumulation  and  enzymatic
effects of hexavalent  chromium  in  rainbow  trout  (Salmo gaird-
nerj.).  Jour.  Fish. Res. Board Can.   34: 9.

Buikema, A.L., Jr., et al.  1974.  Evaluation of  Philodina
acuticornis (Rotifera) as a bioassay  organism for heavy
metals.  Water Resour. Bull., Am. Water Resour. Assoc.
10: 648.

Cairns, J., Jr.,  and A. Scheier.  1969.  A comparison  of
the toxicity of  some common industrial waste components
tested individually and combined.  Prog. Fish-Cult.   30: 3.

Capuzzo, J.M., and J.J. Sasner.  1977.  The effect of  chromium
on filtration  rates and metabolic activity of Mytilus  edulis
L. and Mya arenaria L.  In Physiological Responses of Marine
Biota to Pollutants.  Academic Press, N.Y.  225.

Clendenning, K.A., and W.J.  North.   1959.   Effects of waste
on the giant kelp, Macrocystis pyrifera.  In;  Proc.  1st
Conf.  Waste Disposal Marine Environ.  Berkeley,  Calif.   82.
                               B-44

-------
 Debelak,  R.W.   1975.   Acute  toxicity of mixtures of copper,


 chromium  and  cadmium  to  Daphnia magna.   Thesis,  Miami Univ.,


 Oxford, Ohio.   54  p.






 Dowden, B.F.,  and  H.J. Bennett.   1965.   Toxicity of selected


 chemicals to  certain  animals.   Jour.  Water Pollut.  Control


 Fed.   37:  1308.






 Eisler, R., and  R.J.  Hennekey.   1977.   Acute toxicities

      2 +    L.C    4-2     -^ 2        -^ 2
 of  Cd   ,Cr  ,Hg   , Ni    and  Zn   to  estuarine macrofauna.


 Arch.  Environ.  Contamin. Toxicol.  6:  315.






 Freeman,  L.,  and I. Fowler.   1953.   Toxicity of  combinations


 of  certain  inorganic  compounds to Daphnia  magna  Straus.


 Sewage Ind. Wastes  25:  1191.






 Fromm, P.O.,  and R.H. Schiffman.  1958.  Toxic action of


 hexavalent chromium on largemouth bass.  Jour. Wildl.  Manage.


 22: 40.






 Fromm, P.O., and R.M. Stokes.   1962.  Assimilation  and metab-


 olism of chromium by  trout.  Jour. Water Pollut.  Control


 Fed.  34:  1151.






Carton, R.R.  1972.  Biological  effects of  cooling  tower


 blowdown.   71st Nat.  Meeting.  Am. Inst. Chem. Eng.  Jour.,


Dallas, Tex.
                               B-45

-------
Hale, J.G.   1977.   Toxicity  of  metal mining wastes.   Bull.



Environ. Contain. Toxicol.  17:  66.







Hill, C.W.,  and P.O.  Fromm.   1968.   Response of  the  interrenal



gland of rainbow trout  (Salmo gairdneri)  to stress.   Gen.



Comp. Endocrinol.   11:  69.







Holland, G.A., et  al.   1960.  Toxic  effects of organic  and



inorganic  pollutants  on young salmon and  trout.  Wash.  Dept.



Fish. Res. Bull. 5.   264 p.







Hughes, J.S.  1971.   Tolerance  of striped bass, Morone  saxa-



tilis (Walbaum), larvae and  fingerlings to  nine chemicals



used in pond culture.   Proc.  24th Annu. Conf., Southeastern



Assoc.  Game Fish  Comm., 1970.  p. 431-438.







Kuhnert, P.M., et  al.   1976.   The effect of  in vivo chromium



exposure on Na/K-and  Mg-ATPase  activity in  several tissues



of the rainbow trout  (Salmo  gairdneri).  Bull. Environ.



Contamin.  Toxicol.   15:  383.







Mearns, A.J., et al.  1976.  Chromium effects on coastal



organisms.   Jour,  of Water Poll. Control Fed.  48:  1929.







Moshe, M.,  et al.   1972.  Effect of  industrial wastes on



oxidation  pond performance.  Water Res.  6:  1165.
                              B-46

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kubo, K., and T. Okubo.  1962.  Study  on  the  bioassay method
or the evaluation of water pollution.   II:  Use of the
ertilized eggs of sea urchins and  bivalves.   Bull. Tokai
egional Fish. Res. Lab.  32: 131.

Ison, K.R., and R.C. Barrel.  1973.  Effect of salinity

-------
Oshida, P., and D.J. Reish.  1975.  Effects of chromium
on reproduction in polychaetes.  So. Calif. Coastal Water
Res. Proj., 1500 E. Imperial Hwy., El Segundo, Calif. Ann.
Report  55.

Oshida, P.S., and J.L. Wright.  1978.  Effects of hexavalent
chromium on sea urchin embryo and brittle stars.  So. Calif.
Coastal Water Res. Proj., 1500 E. Imperial Hwy., El Segundo,
Calif. Ann. Report 181.

Patrick, R., et al.  1975.  The role of trace elements in
management of nuisance growth.  U.S. Environ. Prot. Agency,
EPA .660/2-75-008.  Corvallis, OR.   250 p.

Pickering, Q.H., and C. Henderson.   1966.  The acute toxicity
of some heavy metals to different species of  warm water
fishes.  Air Water Pollut.  10: 453.

Raymont, J.E.G., and J. Shields.  1963.  Toxicity of copper
and chromium in the marine environment.  Int. J. Air. Water
Pollution  7: 435.

Rehwoldt, R., et al.   1972.  The effect of  increased tempera-
ture upon the acute toxicity of some heavy metal  ions.
Bull.  Environ. Contam. Toxicol.  8: 91.

Rehwoldt, R., et al.   1973.  The  acute  toxicity  of  some
heavy metal ions toward benthic organisms.   Bull.  Environ.
Contam. Toxicol.   10:  291.
                              B-48

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Reish, D.  J.    1977.   Effects of chromium on the life history

of Capitella capitata (Annelida:Polychaeta).  In Vernberg,

F.J.,  A. Calabrese,  P.P.  Thurberg,  and W.B.  Vernberg (eds).

Physiological Responses of Marine Biota to Pollutants.

Academic Press.  N.Y.   119.


Reish, D.J.,  and R.S. Carr.  1978.   The effect of heavy

metals on the survival/ reproduction, development and life

cycles for two species of polychaetous annelids.  Mar.  Pollut,

Bull.   9:  24.


Reish, D.J.,  et al.   1976.  The effect of heavy metals on

laboratory populations of two polychaetes with comparisons

to the water quality conditions and standards in southern

California marine waters.  Water Res.  10: 299.


Ruesink, R.G., and L.L. Smith, Jr.   1975.  The  relationship

of the 96-hour LC50  to the lethal threshold concentration

of hexavalent chromium, phenol and sodium pentachlorophenate

for fathead minnows.   Trans. Am. Fish Soc.  3:  567.


Ruthven, J.A., and J. Cairns.  1973.  Response  of  freshwater

protozoan artificial communities to metals.  Jour.  Protozool.

20: 127.


Sauter, S. , et al.   1976.  Effects of exposure  to  heavy

metals on selected freshwater fish--Toxicity of  copper,

cadmium, chromium and lead to eggs and fry of several  fish

species.  U.S. Environ. Prot. Agency, EPA 600/3-76-105,

Duluth, MN.  75 p.
                               B-49

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Schaffer, E.D., and W.O. Pipes.   1973.  Temperatures  and



the toxicity of chromate and  arsenate  to  the  rotifer,  Philodina



roseola.  Water Res.   7: 1781.







Schiffman, R.H.,  and P.O.  Fromm.   1959.   Chromium  induced



changes  in the  blood of rainbow  trout, Salmo  gairdneri.



Sewage  Ind. Wastes.  31: 205.







Sherwood, M.J.  1975.  Toxicity  of  chromium  to  fish.   Ann.



Rep. S.  Calif.  Coas. Water Res.  Proj.  El  Segundo,  Calif.   61.







Shuster, C.N.,  Jr.,  and B.J.  Pringle.  1969.  Trace metal



accumulation by the  American  oyster, Crassostrea virginica.



1968 Proc. Nat. Shellfish  Assoc.   59:  91.







Stanley, R.A.   1974.   Toxicity  of heavy metals  and salts



to  Eurasian  watermilfoil  (Myriophyllum spicatum L.).   Arch.



Environ. Contam.  Toxicol.   2:  331.







Staub,  R.J.,  et al.   1973. Effects of industrial  effluents



on  primary  phytoplankton  indicators.   Tenn.  Water  Resources



Res. Center.   Res.  Rep.  26.  16 p.







Sudo,  R.,  and  S.  Aiba.  1973.   Effect  of  copper and  hexavalent



 chromium on the specific  growth rate of  ciliata isolated



 from activated-sludge.  Water Res.   7: 1301.
                                B-50

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 Trabalka, J.R.,  and C.W. Gehrs.   1977.  An  observation  on



 the  ttsxicity  of  hexavalent  chromium  to Daphnia  magna.   Toxicol.



 Letters   1: 131.








 Trama, F.B.,  and R.J. Benoit.   1960.  Toxicity  of  hexavalent



 chromium  to bluegills.  Jour. Water  Pollut. Control Fed.



 32:  868.








 Turnbull, H., et al.  1954.  Toxicity of various  refinery



 materials to  freshwater fish.   Ind.  Eng. Chem.  46: 324.








 Wallen, I.E., et al.  1957.  Toxicity to Gambusia  affinis



 of certain pure chemicals in turbid  waters.   Sewage Ind.



 Wastes  29: 695.








 Warnick, S.L., and H.L. Bell.   1969.  The acute toxicity



 of some heavy metals  to different species of  aquatic  insects.



 Jour. Water Pollut. Control Fed.  41: 280.








Wium-Andersen, S.  1974.  The effect of chromium on the



 photosynthesis and growth of diatoms and green  algae.   Physiol.



 Plant  32: 308.








 Zarafonetis, J.H.,  and R.E.  Hampton.  1974.   Some  effects



 of small concentrations of chromium  on growth and  phytosyn-



 thesis in algae.   Mich.  Academician  6:  417.
                              B-51

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                          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.

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    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
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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

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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

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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

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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

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     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

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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

-------
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

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     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

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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

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 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

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     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

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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

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                                         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

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 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

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                                     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

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     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

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 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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                          REFERENCES

Anwar, R.A., et al.  1961.  Chronic  toxicity  studies:   III.
Chronic toxicity of  cadmium and chromium  in  dogs.  Arch.
Environ. Health. 3:  456.

Baetjer, A.M. 1950.  Pulmonary carcinoma  in  chromate workers:
I. A review of the literature and report  of  cases.  AMA
Arch. Hyg. Occup. Med.  2: 487.

Baetjer, A.M., et al. 1959a.  The distribution and retention
of chromium in men and  animals.  AMA Arch. Ind. Health 20:
136.  -

Baetjer, A.M., et al.   1959b.  Effect of  chromium on incidence
of lung tumors in mice  and rats.  AMA Arch.  Ind. Health
20:  124.

Bidstrup, B.L., and  R.A.M. Case. 1956.  Carcinoma of the
lung in workmen in the  bichromates-producing industry in
Great Britain.  Br.  Jour. Ind. Med.   13:  260.

Bigalief, A.B., et al.  1976.  Chromosome aberrations induced
by chromium compounds in somatic cells of mammals.   Tsitol.
Genet. 10: 222.  (cited from Toxline) .

Bigalief, A.B., et al.  1977.  Evaluation of the mutagenous
activity of chromium compounds.   Gig.  Tr.  Prof. Zabol.
6:  37.   (cited from Toxline)
                                 C-38

-------
 Bloomfield,  J.J.,  and W.  Blum.  1928.   Health hazards in
 chromium plating.   Pub.  Health  Rep.   43:  2330.   Cited in
 Natl.   Acad.  Sci.  (1974).

 Bonatti, S.f  et al.  1976.   Genetic  effects of potassium
 dichromate in schizosaccharomyces Pombe.   Mutat.  Res. 38:
 147.

 Bovett,  P.,  et al.  1977.   Spirometric alterations in workers
 in the  chromium electroplating  industry.   Int.  Arch. Occup.
 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
 L.  and Mya arenaria L.  In  Physiological Responses of Marine
 Biota to Pollutants.   Academic  Press,  N.Y.  225.

 Casto, B.C., et  al. 1977.   Development of  a  focus assay
 model for  transformation of hamster cells  In  vitro by chemical
 carcinogens.   Proc. Am. Assoc. Cancer Res.   18: 155.

Collins, R.J., et al.  1961.  Chromium excretion in the dog.
Am. Jour.  Physiol.  201: 795.
                                 C-39

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Cordle, F., et al. 1978. Human exposure  to polychlorinated
biphenyls and polybrominated biphenyls.  Environ. Health.
Perspec. 24: 157.

Davids, H.W., et al. 1951.  Underground  water contamination
by chromium wastes.  Water Sewage Works  98: 528.

Davidson, I.W.F., et al. 1974.  Renal Excretion of trace
elements: chromium and copper.  Proc. Soc. Exp. Biol.  Med.
147: 720.

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
human subjects - normal, elderly and diabetic subjects.
Page 123.  Ir\  W, Mertz and W.E. Cornatzer, eds. Newer Trace
Elements in Nutrition.  Marcel Dekker, New York.

Fortes, P.A.G. 1977.  Membrane transport in red cells.  Page
175. ^n J.C. Elling and V.L. Lew, eds. Acad.  Press.  London

Foulkes, E.G. 1974.  Excretion and retention  of cadmium,
zinc, and mercury by rabbit kidney.  Am. Jour.  Physiol.
227:  1356.

Fromm, P.O., and R.M. Stokes.  1962.  Assimilation and metabolism
of chromium by trout.  Jour. Water Pollut.  Control Fed.
34: 1151.
                                 C-40

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Gray, S.J., and K.  Sterling.  1950.   The tagging of red cells



and plasma proteins with radioactive chromium.   Jour.  Clin.



Invest.  29:  1604.







Guthrie, B.E., et al.  1979.   Background correction and



related problems in the determination of chromium in urine



by graphite furnace atomic absorption spectrometry.  Anal.



Chem.  (In press)







Hedenstedt, A., et al. 1977.   Mutagenicity of fume particles



from stainless steel welding.  Scand. Jour. Work Environ.



Health  3: 203.







Hueper, W.C. 1971.  Public health hazards from environmental



chemical carcinogens, mutagens and teratogens.  Health Phys.



21: 689.







Imbus, H.R., et al.-1963.  Boron, cadmium, chromium, and



nickel in blood and urine.  Arch. Environ. Health 6: 112.







Kopp, J.F. 1969.  The occurrence of trace elements in water.



Page 59.  I
-------
  ngard,  S.,  and T. Norseth.  1975.  A cohort study of bronchial
  cinomas in  workers producing chromate pigments.  Br.
  r.  Ind. Med.   32: 62.

 ;kin,  S., et al. 1970.  Studies in pulmonary carcinogenesis.
 ,e 321.  In Hanna, et al. eds. Inhalation Carcinogenesis.
 >. Atomic Energy Comm.

 n, T.H.   1978.  The kinetics of the trace element chromium
 II)  in the human body.  Paper presented at 2nd Int. Congress
  nuclear medicine and biology.  Washington, D.C.

 cKenzie, R.D., et al. 1958.  Chronic toxicity studies.
    Hexavalent and trivalent chromium administered in drinking
 tter to  rats.  AMA Arch. Ind. Health 18: 232.
                                                     X
 mcuso,  T.F. 1951.  Occupational cancer and other health
 izards in a chromate plant: A medical appraisal.  II. Clinical
 \d toxicologic aspects.  Ind. Med. Surg.  20: 393.

 ancuso,  T.F.,  and  W.C. Hueper. 1951.  Occupational cancer
 nd other  health  hazards  in  a chromate plant: A medical
 ppraisal:  I.  Lung cancers  in chromate workers.  Ind. Med.
 urg.   20:  358.

lertz,  W.  1969.   Chromium occurrence and function in biological
systems.   Physiol.  Rev.   49: 163.
                               C-42

-------
 Mertz,  W.,  et al.  1965.   Biological  activity and fate of



 trace quantities of intravenous  chromium (III)  in the rat.



 Am.  Jour.  Physiol.   209:  489.







 National Academy of Sciences  and National  Academy of  Engineer-



 ing.   1972.   Water  quality  criteria.   U.S.   Environ.  Prot.



 Agency.  Washington,  D.C.







 National Academy of Sciences.  1974.  Medical and Biological



 effects  of  environmental  pollutants:   Chromium.  Washington,



 D.C.







 Nation-al Institute  of- Occupational Safety  and Health.   1975.



 Occupational  exposure to  chromium (IV).  Criteria document



 HEW  (NIOSH)-76-129.







 National Institute  of Occupational Safety  and Health.  1977.



 Publ. HEW  (NIOSH)-77-149.







 Nettesheim, P.,  et  al. 1970.  Effects  of chronic exposure



 to air pollution on  the respiratory tracts of mice: histopatho-



 logical  findings.   Page 437. In  Nettesheim and Deatherage,



 eds. Morphology of Experimental  Respiratory  Carcinogenesis.



 U.S. Atomic Energy Comm.







Nicholson,  T.F., and G.W. Shepherd. 1959.  Movement of  elec-



 trolytes across the wall of the  urinary bladder.   Can.  Jour.



Biochem.  Physiol.  37:  103.





                                 C-43

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Petrilli, F.L., and S.  De Flora.  1977.  Toxicity  and mutageni-



city of hexavalent chromium on Salmonella Typhimurium.



Appl. Environ. Microbiol.  33: 805.







Rafetto, G., et al. 1977.  Direct interaction with cellular



targets as  the mechanism for chromium carcinogenesis.  Tumori



63: 503.   (cited from Toxline)







Ridgway, L.P., and D.A. Karnofsky. 1952.  Effects of metals



on the chick embryo - toxicity and production of abnormalities



in development.  Ann. N.Y. Acad.  Sci.  55: 203.







Schroeder, H.A. 1965.-  The biological trace elements or



peripatetics through the periodic table.  Jour.  Chron.  Dis.



18: 217.







Schroeder, H.A., et al. 1962.  Abnormal trace metals in



man-chromium.  Jour. Chron. Dis.  15: 941.







Shuster, C.N., Jr., and B.J.  Pringle. 1969.   Trace  metal



accumulation by the American oyster,  Crassostrea virginica.



1968 Proc. Nat. Shellfish Assoc. 59:  91.







Stacy, B.D., and G.D. Thorburn.  1966.  Chromium-51  ethylenedi-



aminetetraacetate for estimation of  glomerular  filtration



rate.  Science  152: 1076.
                                 C-44

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Steffee, C.H./ and A.M.  Baetjer.  1965.   Histopathologic
effects of chromate chemicals.   Arch.  Environ.  Health 11:
66.

Taylor, F.H. 1966.  The  relationship of mortality and duration
of employment as reflected by a cohort of chromate workers.
Am. Jour. Pub. Health  56: 218.

Tipton, I.H. 1960.  The  distribution of trace metals in
the human body. Page 27. In M.J.  Seven, ed. Metal Binding
in Medicine. Lippincott, Philadelphia.

Tipton, I.H./ and M.J. Cook. 1963.  Trace elements in human
tissue Part II. Adult subjects from the United States.
Health Phys.  (Engl.) 9:  103.

U.S. EPA. 1973.  Air quality data for metals 1968 and 1969.
Document APTD 1467.

U.S. EPA. 1974.  National emissions inventory of sources
and emissions of chromium. Document 450/3-74-012.

U.S. EPA. 1976.  Quality criteria for water. Off. of Plan.
Stand. Document 440/9-76-023. Washington, D.C.

U.S. EPA. 1978.  Reviews of the environmental effect of
pollutants.  Chromium document 600/1-78-023.
                                C-45

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U.S. Public Health Service.  1953.  Publ. No. 192. Fed. Security



Agency, Washington, D.C.







U.S. Public Health Service.  1962.  Publ. No.  956.







Venitt, S., and L.S. Levy. 1974.  Mutagenicity of chromates



in bacteria and its relevance to chromate carcinogenesis.



Nature  250: 493.







Volkl, A.  1971.  Tages-Chromausseheidung von Normalpersonen



 (The daily excretion of chromium in normal persons).  Zentralbl.



Arbeitsmed.  21: 122.







Wild,  D.  1978.  Cytogenic  effects in the mouse of 17 chemical



mutagens  and carcinogens evaluated by the micronucleus test.



Mutat. Res.  56: 319
                                 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.
                              C-47

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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) .
                              C-48

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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
                             C-49

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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.)
                               C-50

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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.





                              C-51

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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
                              C-52

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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).
                              C-53

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