Environ. Scl. Technol. 1986, 20, 145-149
(23) Cabaniss, G. E.; Linton, R. W. Environ. Sci. Technol. 1984, 18, 271-275. (24) Liu, B. Y. H.; Pui, D. Y. H.; Whitby, K. T.; Kittelson, D. B.; Kousaka, Y.; McKenzie, R. L. Atmos. Enuiron. 1978, 12, 99-104. (25) Wickert, K. BWK 1959,11, 266-279. (26) Eatough, D. J.; Christensen, J. J.; Eatough, N. L.; Hill, M. W.; Major, T. D.; Mangelson, N. F.; Post, M. E.; Ryder, J. F.; Hansen, L. D.; Meisenheimer, R. G.; Fischer, J. W. Atmos. Environ. 1982,16, 1001-1015. (27) Potter, E. In “Proceedings of the 4th International Clean Air Congress”; Kasuga, S., Ed.; Japanese Union Air Pollution Assoc.: Tokyo, 1977; p 808. (28) McCarthy, J. F.; Yurek, G. J.; Elliott, J. F.; Amdur, M. 0. Am. Znd. Hyg. Assoc. J. 1982, 43, 880-886. (29) Craig, N. L.; Harker, A. B.; Novakov, T. Atmos. Environ. 1974; 8, 15-21. (30) Schlesinger, R. B.; Gurman, J. L.; Chen, L.-C. Atmos. Environ. 1980, 14, 1279-1287. (31) Lowell, P. S.; Schwitzgebel, K.; Parsons, T. B.; Sladek, K. J. Znd. Eng. Chem. Process Des. Dev. 1971, 10, 384-390. (32) Clark, W. E.; Landis, D. A.; Harker, A. B. Atmos. Environ. 1976,10,637-644. (33) Novakov, T.; Chang, S. G.; Harker, A. B. Science 1974,186, 259-261. (34) Amdur, M. 0.;McCarthy, J. F.; Gill, M. W. Am. Znd. Hyg. ASSOC.J. 1983, 44, 7-13. (35) Amdur, M. 0.;McCarthy, J. F.; Gill, M. W. Am. Znd. Hyg. ASSOC.J. 1982, 43, 887-889. (36) Amdur, M. 0.;Dubriel, M.; Creasia, D. A. Enuiron. Res. 1978,15, 418-423. (37) Lam, H. F.; Peisch, R.; Amdur, M. 0. Toxicol. Appl. Pharmacol. 1982, 66, 427-433. (38) Conner, M. W.; Rogers, A. E.; Amdur, M. 0. Toxicol. Appl. Pharmacol. 1982,66, 434-442. (39) Cross, C. E.; Parsons, G. H.; Gorin, A. B.; Last, J. A. In “Mechanisms in Respiratory Toxicology”; Witschi, H., Nettesheim, P., Eds.; C.R.C.: Boca Raton, FL, 1982; pp 219-246. (40) Castleman, W. L.; Dungworth, D. L.; Schwa&, L. W.; Tyler, W. S. Am. J. Pathol. 1980, 98, 811-840. (41) Hayes, J. A.; Snider, G. L.; Palmer, K. C. Am. Rev. Respir. Dis. 1976,113, 121-130. (42) Stephens, R. J.; Freeman, G.; Crane, S. C.; Furiosi, N. J. Exp. Mol. Pathol. 1971, 14, 1-19.
As, 7440-38-2; Cs, 7440-46-2; angiotensin converting enzyme, 9015-82-1; horseradish peroxidase, 62628-26-6.
Literature Cited (1) Comar, C. L.; Nelson, N. EHP, Environ. Health Perspect. 1975,12, 149-170. (2) National Research Council, Committee on Research Needs on Health Effects of Fossil Fuel Combustion Products, Final Report; National Academy of Sciences: Washington, D.C., 1980; pp 1-73. (3) Amdur, M. 0.;Mead, J. Am. J.Physiol. 1958,192,364-368. (4) Amdur, M. 0. In “Inhaled Particles and Vapors”; Davies, C. N., Ed.; Pergamon: Oxford, 1961; pp 281-292. (5) McJilton, C.; Frank, N. R.; Charlson, R. E. Science 1973, 182, 503-504. (6) Amdur, M. 0.;Underhill, D. W. Arch. Enuiron. Health 1968, 16,460-468. (7) Johnstone, H. F. In “Inhaled Particles and Vapors”; Davies, C. N., Ed.; Pergamon: Oxford, 1961; pp 95-108. (8) Amdur, M. 0. “Proceedings of the Conference on Health Effects of Air Pollutants”; National Academy of Sciences, U.S. Government Printing Office: Washington, D.C., 1973; pp 175-205. (9) Amdur, M. 0. Am. Znd. Hyg. Assoc. J. 1974,35,589-597. (10) Davidson, R. L.; Natusch, D. F. S.; Wallace, J. R.; Evans, C. A. Environ. Sci. Technol. 1974,8, 1107-1113. (11) Linton, R. W.; Loh, A.; Natusch, D. F. S.; Evans, C. A.; Williams, P. Science 1976, 191, 852-854. (12) Dyson, W. L.; Quon, J. E. Environ. Sci. Technol. 1976,10, 476-481. (13) Judeikis, H. S.; Stewart, T. B.; Wren, A. G. Atmos. Environ. 1978,12, 1633-1641. (14) Amdur, M. 0.;Corn, M. Am. Ind. Hyg. Assoc. J. 1963,24, 326-333. (15) Flagan, R. C.; Taylor, D. D. In “18th Symposium (International) on Combustion”; The Combustion Institute: Pittsburgh, PA, 1981; pp 1227-1235. (16) Neville, M.; Quann, R. J.; Haynes, B. S.; Sarofim, A. F. In “18th Symposium (International) on Combustion; The Combustion Institute Pittsburgh, PA, 1981; pp 1267-1274. (17) Ondov, J. M.; Ragaini, R. C.; Biermmn, A. H. Environ. Sci. Technol. 1979,13,946-953. (18) McElroy, M. W.; Carr, R. C.; Ensor, D. S.; Markowski, G. R. Science 1982,215,13-19. (19) Quann, R. J.; Neville, M.; Janghorbani, M.; Mims, C.; Sarofim, A. F. Enuiron. Sci. Technol. 1982,16, 776-781. (20) Neville, M.; Sarofim, A. F. In “19th Symposium (International) on Combustion”; The Combustion Institute: Pittsburgh, PA, 1982; pp 1441-1449. (21) Haynes, B. S.; Neville, M.; Quann, R. J.; Sarofim, A. F. J. Colloid Interface Sci. 1982, 87, 266-278. (22) Hansen, L. D.; Silberman, D.; Fisher, G. L.; Eatough, D. J. Environ. Sci. Technol. 1984, 18, 271-275.
Received for review November 26,1984. Accepted July 29,1985. This research was supported by Program Project Grant ES02429 from the National Institute of Environmental Health Sciences and by Grant R8-0910410 from the Environmental Protection Agency; it was begun under Contract R P l l l 2 from Electric Power Research Institute.
Synthesis of Mutagenic Compounds in Crankcase Oils Mohamed Abdeinasser, Mark Hyland, and Neil D. Jespersen* Chemistry Department, St. John’s University, Jamaica, New York 11439
rn Motor oils become mutagenic after use in internal combustion engines. This work has shown that the major factor involved in the production of these mutagens is nitrogen dioxide. Sulfur dioxide and other gases do not seem to cause the production of mutagens. These results may be related to the mutagenicity of diesel exhaust particulates and some synthetic fuels.
Introduction In 1978 Payne et al. (1) demonstrated that dimethyl sulfoxide (Me,SO) extracts of used crankcase oils were mutagenic. The mutagenic activity reported was not due 0013-936X/86/0920-0145$01.50/0
to benzo[a]pyrene or benzanthracene, both of which are known minor constituents of motor oil (2). A 1980 review of the carcinogenic potential of petroleum hydrocarbons, sponsored by the American Petroleum Institute, stated “The possibility of carcinogenic potential should be thus considered in planning for either the recycling or the disposal of used motor oils” (3). Since Me430 extracts of refined motor oils show no mutagenic activity (1) in the Ames test ( 4 ) and extracts of used motor oils are mutagenic, this work attempts to identify the factor(s) that contribute to the synthesis of these mutagenic substances. To do this, virgin motor oil was subjected to various conditions thought to be present
0 1986 American Chemical Society
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within the crankcase. These included high temperatures and the presence of air, sulfur dioxide, and nitrogen dioxide. Other substances such as ammonia, hydrogen sulfide, and nitrous oxide were studied since they represent other oxidation states of the two major pollutants, NO2 and SO2. This report presents the results of these experiments and the finding that only nitrogen dioxide seems to be responsible for the synthesis of mutagens in motor oil.
Experimental Section The salmonella mutagenicity test, developed by Ames et al. (41, was used to assess the mutagenic potency of samples generated in this work. This assay was run precisely as detailed in the +’methods paper” by Maron and Ames (5). Samples of tester strains TA-98, TA-100, TA1535, TA-1537, and TA-1538 were obtained directly from Ames. Liver microsome preparations (S-9) were obtained from Litton Bionetics, Kensington, MD. Two milliliters of this S-9 preparation was used in making 50 mL of the “S-9 mix” referred to below. In preliminary studies, and in agreement with other reports (1, 6, 7), it was shown that TA-98 was the most responsive strain toward mutagenic substances in Me2S0 extracts of used motor oils. Therefore, only the TA-98 strain was used in this study. The S-9 preparation was tested for effectiveness with P-naphthylamine. This test gave no excess revertants without the S-9 mix and over 2000 revertants/plate with the S-9 mix. All strains were tested for their appropriate characteristics using the methods suggested ( 4 ) . All assays used six plates/sample (i.e., each assay involved six plates for the blank, six for each of the controls, and six plates each for every dilution of every sample tested) in order to allow for adequate statistical analysis. Duplicate, and at times triplicate, runs of most assays were made to assure that the results were reproducible. Each plate contained 30 mL of minimal agar. Two milliliters of top agar, containing 100 pL of sample and 100 pL of TA-98 culture, was spread on each plate. Experiments involving microsomal activation also included 100 p L of the S-9 mix with the top agar. Plates were incubated at 37 “C for 48 h. Revertant colonies were then hand counted. Plates were checked for the presence of a “background lawn” as an indication of little or no toxicity. High concentrations of the NO2-treated samples did show some evidence of toxicity. Virgin motor oil (SAE 1OW-40 sold under the brand name of Motorcraft by Ford Motor Co.) was purchased locally. After the appropriate treatment, described later, samples were prepared by extracting the treated oil with an equal volume of Me2S0. Typically, 50 mL of oil was extracted with 50 mL of Me2S0. This 1:l extract was the basic sample from which others were prepared by quantitative dilution with Me2S0 as needed. The 1:l extract is defined as having a “concentration” of 1.00 since the actual amount of mutagenic substance is unknown at this point. All of the dose-response data are relative to this defined concentration. All samples were autoclaved just prior to assay, as a precaution against bacterial contamination. Comparisons of sterile unautoclaved samples with autoclaved samples showed that autoclaving did not alter the mutagenic characteristics observed. Autoclaving also assures that residual gases are not retained in the samples and that only nonvolatile substances were assayed. All other chemicals used were reagent grade. Glassdistilled water was used throughout, and the gases used were obtained from Matheson Gas Products, East Rutherford, NJ. 146
Environ. Scl. Technol., Vol. 20, No. 2, 1986
Table I. Average Number of Revertants/Plate for Unused and Used Oil Samples sample blank unused oil used oilb
concn’ 1.00 0.50 0.25 1.00 0.50 0.25
av revertants/plate (1std dev) without S-9 with S-9 22.2 (13) 22.3 (12.8) 22.7 (f3.6) 21.7 (12.6) 78.8 (17.2) 50.8 (f4.5) 37.2 (17.2)
22.0 (13.6) 21.0 (14.6) 23.2 (17.2) 21.8 (f1.9) 159.2 (122.1) 89.3 (f15.6) 57.4 (f16.8)
“As defined in text. bThis sample taken from an automobile after 3000 miles of use. The auto had recently passed New York State emissions testa.
Results and Discussion The results of Payne et al. (1)were verified by showing that used motor oil extracts were mutagenic while new motor oil was not. Used motor oil from three different automobiles was tested with similar results in all cases. Although the mutagenic activity of these samples varied slightly, it was evident that the results were not due to a localized defect in a particular automobile. Table I lists the appropriate data. The elevated temperature at which crankcase oil is used was the first possible cause of mutagen formation considered. It was thought quite possible that pyrolysis or oxidation processes within the engine could degrade this complex mixture into mutagenic species. Since internal combustion engines are water cooled, it was estimated that a reasonable average oil temperature would be 100 OC. A sample of new motor oil was heated at 100 “C for 100 h in a 250-mL round-bottom flask. The system was not sealed, allowing volatile components to dissipate and some oxygen to enter. Samples were taken every 8 h over the 100-h period. Neither the basic Ames assay nor the assay with microsomal activation (S-9) showed any evidence of mutagen production. The same experiment was run with the addition of primary standard iron wire to the mixture. The iron wire was a crude attempt to simulate the metal of the engine block, which may catalyze the synthesis of mutagens. Once again, the results indicated that mutagens were not produced. Another sample was heated at 100 “C while air was slowly bubbled through it to enhance oxidation processes. This mixture quickly oxidized into a solid mass. Analysis of the residue still produced no evidence of mutagen formation. These experiments suggest that neither pyrolysis nor oxidation of motor oil is responsible for the appearance of mutagenic substances in Me2S0extracts of used motor oil. A preliminary experiment was run by generation of NO2 from copper wire and nitric acid. Bubbling NOz into motor oil for even a short period of time produced a large mutagenic response. The same experiment was run with iron wire added to the oil. Figure 1gives the results of these experiments. Figure 1suggests that iron may have some catalytic effect. The differences are, however, not statistically significant, and additional work must be done to demonstrate this effect conclusively. In addition, it would be more realistic to use cast iron rather than primary standard iron wire. To study the effects of nitrogen dioxide more carefully, commercial N204was used to generate NO2. A tank of Nz04was warmed slightly (to 35-40 “C)to increase the pressure of NO2. This was regulated to a flow rate of approximately 2 mL/s. A sample of motor oil was heated
Tool v)
C
I I
2
/
P
F.
/P’
/
8
hr
7
hr.
/
4
+ 6 a
CON C E NTRATION
Flgure 1. Dose-response curves for motor oil treated with nitrogen dioxide. Open symbols are results with S-9 microsomal activation, and fllled symbols are without S-9 added. Squares represent the presence of iron, and circles are results with no iron In the mixture.
to 100 OC, and the addition of NO2 started. This process was continued for 8 h with samples taken each hour. The oil darkened appreciably during this process and the color of the MezSO extracts demonstrates this effectively. The extract of the first hour of treatment is light yellow; the second hour it is orange; and subsequent extracts are deeper shades of brown. The product of this experiment was very mutagenic and required substantial dilution to obtain a reasonable number of revertant colonies per plate. Figure 2a illustrates the linear dose-response relationships obtained with various dilutions of the MezSO extracts without microsomal activation. Figure 2b illustrates the results with microsomal activation. Greater concentrations, close to 1.0, showed evidence of toxicity toward TA-98. In parts a and b of Figure 2, error bars, indicating the standard deviation of the data points, are included on the upper two curves where space permits. Figure 3, which is a plot of the 1OO:l dilution, clearly illustrates the large, nonlinear increase in mutagenic potential of the motor oil during the experiment. Difficulty in precisely controlling the flow of NO2 may explain the sharp increase in revertants with time. Another possible explanation would be that multiply nitrated species are more mutagenic than singly nitrated compounds. Pitts et al., in experiments with atmospheric levels of NO2, have shown that nitrated species of polycyclic aromatic hydrocarbons can be produced even at very low levels of nitrogen dioxide (8). Sulfur dioxide is another common pollutant associated with the internal combustion engine. Experiments, similar to the NOz work above, with SOz show no evidence of mutagen formation after an 8-h reaction period. Hydrogen sulfide, often associated with catalytic converters, was also tested with no increase in the number of revertants observed. These results are illustrated in Figure 4. While nitrogen dioxide causes mutagen synthesis, similar experiments with ammonia and nitrous oxide do not lead to mutagen formation. Both of these compounds have nitrogen in lower oxidation states than NOP. Additionally, they do not possess the unpaired electron that makes NOz very reactive. Figure 4 illustrates the hourly results for these gases. They show no evidence of mutagen synthesis, with the number of revertants being statistically the same as the blanks. With nitrogen dioxide being the only compound, of those studied here, capable of producing mutagenic substances in motor oil, it was of interest to see if the mutagens produced by the NO2were the same as those produced by the internal combustion engine. This was done by thinlayer chromatography (TLC) as suggested by Payne et al.
6 hr.
W
>
5
W LL
4 hr.
hr.
3 3 hr. 2 hr. I hr. 0
0.01 0.02
0.05
CONCENTRATION
IO.
lS-91
7 hr.
6 hr
5 hr
4 hr. 3 hr. 2 hr I hr. W
’
0 01
0 02
CONCENTRATION
Figure 2. (a) Dose-response curves for hourly samples of motor oil reacted with nitrogen dioxide at 100 O C . Error bars, representing one standard deviation, are shown only for hours 7 and 8. (b) Same as Figure 2a except results obtained with S-9 microsomal activation.
( I ) . Me2S0 extracts of new motor oil, heated motor oil, used oil, heated oil with iron, heated oil with NOz, and heated oil with NOz and iron were chromatographed on silica gel using benzene as the mobile phase. Visually the chromatograms of three of the above samples (the used motor oil and the two samples with NOz)were similar with five distinct bands. Equal areas of each band were scraped from the TLC plates, eluted with methylene chloride, dried and redissolved in Me2S0, and subjected to the Ames assay. Only direct-acting mutagens were assayed. The pattern for these three samples is very similar in the Ames assay also. Band four contains most of the mutagenic potential in the used motor oil and the NO2-treated samples. Band three is the next most active fraction. Table I1 lists the data for all six of the above samples while Figure 5 is a histogram comparing the fraction of revertants found in each TLC band for the three active samples. Although the number of revertants found for each sample varies Environ. Sci. Technol., Voi. 20, No. 2, 1986
147
Table 11. Average Number of Revertants (rev) Obtained f r o m the Five TLC Bands o f Six O i l Samples
new oil rev %" 14.7 0 16.3 0 0 18.0 16.7 0 17.3 0
band 1 2 3 4 5
used oil rev % 16.0 0 27.0 13.0 34.3 22.1 67.0 64.9 21.7 5.2
heated oil rev % 14.7 0 19.0
0 0 0 0
16.0 14.0 16.4
heated oil + Fe rev % 15.0 15.3 16.3 16.5 19.7
0 0 0 0 0
heated oil + NO2 rev % 17.0 50.0 175.0 524.7 35.3
0
4.5 22.1 71.2 2.5
heated oil + NOp + Fe rev % 15.6 40.7 208.0 606.7 30.0
0
2.8 23.4 72.7 1.5
"All percentages were calculated after substracting the blank (17.8) from each sample. A value less than zero was taken to be zero. Percentages for new oil, heated oil, and heated oil with Fe were not calculated since the results did not differ statistically from the blank.
I
3
2
TLC 0
1
2
3
4
5
6
7
8
HOURS
Figure 3. Plot of revertants found each hour at 1:lOO dilution of the orlglnal Me,SO extract. Circles represent results without S-9, while x's represent results with S-9 microsomal activation.
2oi
w
a 12.
2
3
4
5
6
HOURS OF TREATMENT
7
8
Flgure 4. Results showing that ammonia, hydrogen sulfide, sulfur dioxide, and nitrous oxide do not react with heated motor oil to form mutagens. Dashed lines represent the values for the blanks in each of these experiments.
greatly as shown in Table 11, it is the pattern of these results that strongly suggests that the species produced by the NOz treatment are similar to those found in used motor oil.
Conclusions This work has shown that NOz is the only compound, of those studied, that causes the synthesis of mutagens in motor oil. It is quite possible that the mutagens formed are nitrated po€ycyclicaromatic hydrocarbons (8). Thinlayer chromatography of the samples indicates that the 148 Environ. Sci. Technol., Voi. 20,No. 2, 1986
4
5
BAND
Figure 5. Histogram illustrating the similar dlstrlbution of mutagenic compounds in five thin-layer chromatogram bands. Open bars represent used motor 011; diagonal crosshatching represents heated motor 011 treated with nibogen dioxide, and horizontal crosshatching represents heated 011 treated wlth nitrogen dioxide in the presence of iron.
substances produced in these experiments are similar in character to those produced in the internal combustion engine. These findings may be related to two other areas of current interest. One of these is the mutagenicity of diesel exhaust particulates (9, 10). Since diesel fuel is a close relative of motor oil, it is reasonable to suggest that nitrogen dioxide is one factor in this mutagenic activity. Another is the mutagenic activity of synthetic fuels, many of which are more mutagenic than natural crude oils (11-14). Those synthetic fuels produced by in situ retorting have a great potential for interacting with nitrogen dioxide and thus becoming more mutagenic. Finally, there seems to be an interest among automobile manufacturers to increase the service life of motor oils. This work indicates that the mutagenic hazard of motor oils may increase almost exponentially with time. New motor oils or engine conditions may have to be developed in order to extend the service life of motor oils significantly. Additional work in this area should include the determination of the exact species responsible for the mutagenic activity. This work suggests they are nitrated polycyclic aromatic hydrocarbons. This information can then be correlated with the large body of data already available from the diesel exhaust particulate studies. Further work on the possible catalytic effect of iron and the effect of temperature on mutagen formation is in progress. Studies involving additional tester strains and a mamallian cell transformation assay, which may be more indicative of true carcinogenicity, are also being conducted.
Acknowledgments The efforts of Cathy Jonson, Jeannie Posthauer, Anthony DeBenedetto, Tommy Kahn, Diane Schaefer, and
Environ. Scl. Technol. 1988, 2 0 , 149-155
(7) Hermann, M.; Chaude, 0.;Weill, N.; Bedouelle, H.; Hofnung, M. Mutat. Res. 1980, 77, 327-339. (8) Pitts, J. N.; Van Cauwenberghe, K. A,; Grosjean, D.; Schmid, J. P.;Fritz, D. R.; Belser, W. L., Jr.; Knudson, G. B.; Hynds, P. M. Science 1978,202, 515-519. (9) Shuetzle, D.; Lee, F. S.-C.;Prater, T. J.; Tejada, S. B. Znt. J . Environ. Anal. Chem. 1981, 9, 93-144. (10) Lofroth, G. Environ. Sci. Res. 1981, 22, 319-336. (11) Pelroy, R. A.; Sklarew, D. S.; Downey, S. P. Mutat. Res. 1981,90, 233-245. (12) Lockard, J. M.; Prater, J. W.; Viau, C. J.; Enoch, H. G.; Sabbarwal, P. S. Mutat. Res. 1982, 102, 221-235. (13) Sheppard, E. P.; Wells, R. A.; Georghiou, P. E. Environ. Res. 1983, 30, 427-441. (14) Guerin, M. R.; Rubin, I. B.; Rao, T. K.; Clark, B. R.; Epler, J. L. Fuel 1981, 60, 282-288.
Terry Vdokales as undergraduate research assistants is acknowledged. We are indebted to B. N. Ames for the donation of the tester strains. "3,
Registry NO. NO2,10102-44-0; SOZ, 7446-09-5; H2S, 7783-06-4; 7664-41-7; N20, 10024-97-2.
Literature Cited (1) Payne, J. F.; Martins, I.; Rahimtula, A. Science 1978,200, 329-330. (2) Guerin, M. R.; Ho, C. H.; Clark, B. R.; Epler, J. L. Znt. J . Environ. Anal. Chem. 1980,8, 217-225. (3) Bingham, E.; Trosset, R. P.; Warshawsky, D. J . Environ. Pathol. Toxicol. 1980,3, 483-563. (4) Ames, B. N.; McCann, J.; Yamasaki, E. Mutat. Res. 1975, 31, 347-364. (5) Maron, D. M.; Ames, B. N. Mutat. Res. 1983,113,173-215. (6) Rao, T. K.; Allen, B. E.; Ramey, D. W.; Epler, J. L.; Rubin, I. B.; Guerin, M. R.; Clark, B. R. Mutat. Res. 1981,85,29-39.
Received for review January 23,1985. Revised manuscript received May 10,1985. Accepted October 3,1985. Research funding through St. John's University is greatly appreciated.
Important Process Variables in Chromate Ion Exchange Arup K. Sengupta
and Dennls Cllfford
Environmental Engineering Program, University of Houston-University The effects of competing ion concentrations, pH, and ionic strength on chromate selectivity have been studied in relation to chromate ion exchange. The competing effects of sulfate and chloride anions have been explained with the aid of governing chromate ion-exchange mechanism and chromate chemistry. This study also reveals that the choice of acidic pH for a conventional chromate-exchange process is due to the selectivity reversal between HCr04- and Cr042-at the prevailing ionic strength. There is a critical acidic pH; at pH lower than that, no increase in chromate removal capacity is observed.
Introduction In recirculating cooling water systems, 5-20 mg/L chromate is deliberately added as a corrosion inhibitor, while sulfate and chloride are normally present at concentrations (500-4000 mg/L) several orders of magnitude higher than chromate. Despite the severe competition from sulfate and chloride, several authors (1-4) have confirmed the viability of the chromate ion-exchange process due to chromate's very high preference for commercial styrene-dinvylbenzene (STY-DVB) anion exchange resins at acidic pH. In a binary system (i and j), the selectivity or preference of the component i is indicated by its distribution coefficient (Ai), Le., the ratio of its equivalent fraction in the exchanger phase and the aqueous phase &/xi); the higher the number is, the greater is the selectivity. yi and xi indicate equivalent fractions of component i in the exchanger phase and aqueous phase, respectively, i.e., Yi = Ci/Q (1) xi = Ci/CT (2) where Ci and Ci denote the concentrations of component i in the exchanger phase and aqueous phase, respectively. Q and CT represent the total exchange capacity of the resin and total aqueous-phase concentration, respectively. Hexavalent chromium, Cr(VI), may exist in the aqueous phase in different ionic forms with total chromate con+ Present address: Civil Engineering Department, Lehigh University, Bethlehem, PA 18015.
0013-936X/86/0920-0149$01.50/0
Park, Houston, Texas 77004
centration and pH dictating which particular chromate species will predominate. For convenience in discussion, we will describe the total chromate species as Cr(V1) or chromate, while each individual species will be represented by its chemical formula. The following are the important equilibrium reactions for different Cr(V1) species (5, 6): H2Cr04F? Hf + HCr04- log K (25 "C) -0.8 (3)
+ Cr042- log K (25 "C) -6.5 2HCr04- F? Cr2072-+ H 2 0 log K (25 "C) 1.52 HCr207-e Hf + Cr2072- log K (25 "C) 0.07 HCr04- e H+
(4)
(5)
(6) Reaction 5 does not contain any H+ terms, and therefore, in a certain pH range (2-5) this reaction is independent of pH and depends only on total Cr(V1) concentration. This may be regarded as a dimerization reaction for HCr04- at acidic pH. Since the distribution of chromate species is dependent on both pH and total Cr(V1) concentration, a predominance diagram (Figure 1) has been drawn using both pH and total Cr(V1) as variables. The solid lines on the diagram separate the areas in which the indicated species predominate. Two horizontal dashed lines on the predominance diagram indicate the range of Cr(V1) concentration (5-20 mg/L) normally encountered in cooling water. HCr04- and Cr02- are the predominant species in this total Cr(V1) concentration range, but the relative distribution of each varies with pH. One questionable aspect of many previous studies, including that of Arden and Giddings (7)) in relation to chromate ion exchange at acidic pH lies in considering Cr2072-as the only counterion in ion-exchange reactions as cited below: strongly basic
(R4N+)2S042+ Cr20T2-s (R4N+)zCr2072-+ S042- (7) weakly basic (R3NH+)zS042+ Cr2072-e (R3NH+)2Crz072-+ (8)
From the predominance diagram, however, it may be noted that HCr04- is practically the only Cr(V1) species
0 1986 American Chemical Society
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149
