THE ROLE OF MUTAGENICITY IN
DETERMINING DRINKING WATER QUALITY
Kathleen Schenck Patterson
Biologist
Systems and Field Evaluation Branch
Benjamin W. Lykins, Jr.
Chief
Systems and Field Evaluation Branch
Drinking Water Research Division
Risk Reduction Engineering Laboratory
U.S. Environmental Protection Agency
Cincinnati, Ohio 45268
INTRODUCTION
Many drinking water utilities are considering alternatives to
the exclusive use of chlorine for disinfection in order to comply
with federal regulations regarding acceptable levels of disinfec-
tion by-products (DBP). Current and proposed regulations limit DBP
on an individual basis or as a group of related compounds (e.g.,
trihalomethanes) based on an evaluation cf the human health risk
and what is technically and economically feasible. Consequently,
an evaluation is needed of the risks associated with the use of
alternative disinfectants relative to the risks associated with the
use of chlorine.
Human epidemiological studies would provide the most relevant
information on the risks associated with the use of various
drinking water disinfectants. Epidemiological studies have sug-
gested increased risks of cancer in areas with chlorinated waters,
but the evidence is inconclusive/ } Even less epidemiological
information is available concerning the potential adverse effects
of other disinfectants currently in use or for proposed treatment
options.
Another source of information on potential risk would be data
from animal studies. Unfortunately, such studies are both time
consuming and costly. In addition, due to the variable nature of
source waters, multiple studies would likely be needed to evaluate
each treatment process. Due to these and other limitations, the
routine use of animal studies to evaluate treatment options is
impractical'
Short-term in vitro tests for the detection of genotoxic
chemicals can be conducted relatively quickly and inexpensively.
Consequently, their use in the evaluation of various disinfection
processes has been recommended/2, ,4> Many of these assays are
designed to detect mutagens( ', which are substances that cause a
permanent change in the genetic material. Such changes in the re-
productive cells could be passed on to offspring and potentially
809

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lead to heritable diseases. In non-reproductive cells such damage
is thought to be involved in or at least correlated with the
processes that lead to cancer.{2) Thus, it seems prudent to try to
minimize human exposure to mutagenic compounds.
The Ames Salmonella assay is one of the most commonly used
tests for mutagenicity. The advantages of this assay are that it
is relatively easy to perform, low in cost, has been well
validated, and has an extensive literature base due to its wide-
spread use.{4) Additionally, the underlying genetics of the assay
have been well defined.' The accuracy of the Ames test for
predicting the carcinogenicity of chemicals in rodents has been
found to be comparable to that of three other commonly used
genotoxicity assays that use mammalian cells.'8'
Over 1000 organic compounds have been identified in drinking
water samples and many more have been detected but not
identified/9' However, most of these compounds are present at pg/L
levels or less. At these low concentrations most known mutagens
would not be detected in the Ames assay.(10) Consequently, it is
usually necessary to use some method of concentrating the organic
compounds present in drinking water prior to testing for muta-
genicity. One of the most popular concentration methods involves
the use of Amberlite XAD resins. The major advantage of XAO resins
is that they can be used to concentrate the large volumes of water
needed for mutagenicity testing in relatively short periods of
time.'
In the two pilot-scale drinking water plant studies presented
here, source waters were treated with a variety of disinfection
schemes, incorporating ozone, monochloramine, chlorine dioxide and
chlorine. Concentrates of the organic compounds present in the
water samples were prepared by XAD resin adsorption/ethyl acetate
elution. The concentrates were then tested for mutagenicity in the
Ames Salmonella assay in order to compare the relative mutagenic
potencies of the water samples following the different methods of
disinfection.
METHODS
Sample concentration for mutagenicity testing
The organic compounds present in the water samples were con-
centrated by adsorption on Amberlite XAD resins (Figure 1). The
resins were cleaned by consecutive 24 hour Soxhlet extractions with
methanol, ethyl acetate and methanol and stored in methanol. Prior
to use, the methanol was replaced by distilled water. The columns
contained XAD-8 resin over XAD-2 resin. Immediately prior to
passage of the water samples over the columns, the samples were
acidified to pH 2 by in-line addition of HC1 using a metering pump
and a static head mixer. Previous work showed the recovery of
mutagenic activity to .be much greater from water samples acidified
to pH 2 prior to passage over XAD columns than from water samples
concentrated at pH 8. The columns were eluted with ethyl
acetate. Residual water was removed from the ethyl acetate eluates
810

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by using separatory funnels to drain off the water layers followed
by the addition of sodium sulfate. The eluates were then
concentrated by rotary vacuum evaporation and dissolved in dimethyl
sulfoxide (DMSO) to give 8000-fold concentrates.
Assay for mutagenic activity
Mutagenic activity was determined in Salmonella tvphimiirium
using the standard plate method of Maron and Ames. stain-
specific genetic markers were verified for each strain prior to
use. Spontaneous and positive control responses and appropriate
solvent controls were included with each assay. In assays
employing metabolic activation, the methods for preparation of the
liver homogenate (S9) from Aroclor 1254-pretreated male, Sprague-
Dawley rats and the S9 cofactor mix were as described in Maron and
Ames. The S-9 concentration in the S-9 mix was 5% (v/v), and 0.5
ml of S-9 mix was added per plate. The samples were assayed at
doses equivalent to 0.05L to 1.6L per plate, using duplicate or
triplicate plates per dose. Mutagenic activity was calculated from
the initial slopes of the dose-response curves using the method of
Bernstein, et al / 5)
Chemical Analyses
Total organic carbon (TOC) concentrations were determined
using the persufate-ultraviolet oxidation method and the
adsorption-pyrolysis-titrimetric method was used for total organic
halide (TOX) analyses.0"
JEFFERSON PARISH. LOUISIANA. PILOT PLANT STUDY
Ozone (0j) and monochloramine (NH2C1) are among the primary
alternatives to chlorine (Cl2) disinfection being considered for
widespread use in the drinking water industry. Although 03 is an
effective disinfectant, its short half-life in water at pH 8,
necessitates the use of a secondary disinfectant to ensure a
disinfectant residual throughout the distribution system. In the
present study, water samples were disinfected with CI, or NH,C1
alone or following ozonation. These samples were evaluated in the
Ames assay in order to compare the relative levels of mutagenic
activity present in drinking waters prepared by these different
methods of disinfection.
Treatment Process
At a pilot-scale drinking water treatment plant in Jefferson
Parish, LA, three studies were conducted in which clarified and
sand filtered Mississippi River water was treated with either Cl2,
NH2C1, Oj or was not disinfected (Figure 2). Each treatment stream
consisted of a contact chamber followed in series by a sand column
and a 55-gallon, stainless-steel drum fitted with a spiral,
stainless-steel baffle. The modified drum served as an additional
contact chamber. The non-disinfected treatment stream was similar
except that the initial contact chamber was omitted. The contact
811

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time in the contact chamber was approximately 30 min. for each of
the disinfected streams. The stream treated with 0, was split
after the sand column and post-disinfected with either u2 or NH2C1.
As a result of stream splitting the flow rate to the two post-
disinfected drums was decreased. Therefore, the contact time for
the post-disinfected drums was approximately 150-180 min. while the
contact time in the drums for the streams treated initially with
CIj or KHjCl and the non-disinfected stream was approximately 85-100
min. Sufficient CI, or NHjCl was added during post-disinfection so
that the residual levels of disinfectant in the ozonated samples
were approximately equal to those of the water samples disinfected
initially with CI, or NH,C1. The final residual levels of Cl2 and
NH2C1 were 0.5 - f.O mg/l and 0.8 - 1.5 mg/l respectively.
Sample Collection and Analyses
Samples were collected from each of the five treatment streams
in September, 1989, March, 1990 and July, 1990. The water samples
were concentrated by adsorption on XAD resins for mutagenicity
testing as described in the methods. Columns contained 5L of XAD-8
resin followed by columns containing 51 of XAD-2 resin. Water
(1500L) from each treatment stream was passed through the two
columns in series at a flow rate of 60L/hr. Following sample
collection, each column was filled with sufficient ethyl acetate to
provide a standing head. The columns were then agitated to
completely wet the resin and allowed to equilibrate for 15 minutes.
Each column pair was then eluted serially with 151 of ethyl
acetate. The final concentrates were assayed for mutagenicity as
described in the methods using Salmonella strains TA100, TA98, TA97
and TA102, with and without metabolic activation.
Results and Discussion
In the Ames assay, genetic damage is indicated by the
induction of mutations that cause the histidine-requiring
Salmonella tester strains to become histidine independent.
Mutation to histidine independence is demonstrated by the growth of
bacterial colonies on minimal agar plates. These bacterial
colonies are referred to as revertants. A mutagenic response is
indicated by a dose-related increase in the number of revertant
colonies.
Figure 3 shows the dose-response curves, in strain TA100
(-S9) for each of the five water samples collected in September,
It can be seen from the figure that mutagenic activity was detected
in all of the water samples,including a very low level in the non-
disinfected water. Table 1 shows the mutagenic activities,
expressed as revertants per liter equivalent (i.e. the slope of the
dose-response curve), for the water samples collected in September
under each of the assay conditions used.
In this study, the addition of a metabolic activating system
(+S9) resulted in decreased levels of mutagenic activity in all of
the tester strains used. Thus the mutagens in the disinfected
water samples appear to be direct-acting (do not require metabolic
activation). Decreased levels of mutagenic activity in the
812

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presence of S3 have been previously reported for disinfected water
samples' ' ' and for chlorinated aqueous humic acid
solutions.
The individual tester strains, TA10Q, TA98, TA97 and TA102,
detect different classes of compounds based on the mechanisms by
which they cause mutations. For all of the samples, the highest
level of activity was observed in TA10Q, indicating that many of
the compounds present cause mutations by substituting one DNA base
for another.
Figure 4 shows the mutagenicity of the water samples in strain
TA100 (-S9) for all three collection times. It is obvious from the
figure that the levels of mutagenicity observed for a given
treatment varied significantly depending on the time of collection.
Seasonal variations in the levels of mutagenic activity in drinking
water have often been observed, and are addressed in a review by
Noot, et al.
In the present study, the effect of collection time is not
consistent for all of the disinfectants used. The samples treated
with Oj + CI, or Cl2 showed higher levels of mutagenic activity in
March and July than in September. Samples disinfected with 0, +
NHjCl or NHXl did not show this pattern. In an earlier study, also
done at Jefferson Parish, water treated with Cl2 in July had a
lower level of activity compared to samples treated in June or
December of the same year. The levels of activity observed for
water treated with NHXl were essentially the same for all 3
collection times. Reasons for these inconsistencies are not
clear.
In spite of variability between sampling times, the levels of
mutagenicity observed following the various disinfection treatments
show similar trends within each of the 3 collection times. The
levels of mutagenic activity of water samples disinfected with CI,
were at least twice that of water treated with NH2C1 for each of
the three collection periods (Figure 4). These results are
consistent with previous reports by Cheh et al, and Miller et
al. which showed that chlorination produced more mutagenic
activity than chloramination.
Figure 4 also shows that, for each sampling time, disinfection
with 0, prior to treatment with either Cl2 or NHjCl resulted in a
lower level of mutagenic activity than when either disinfectant was
used alone. Kriuthof et al. reported similar results when they
treated Rhine River water with Qj followed by Cl2 or Cl2 alone.
EVANSVILLE. INDIANA. PILOT PLANT STUDY
The usefulness of chlorine dioxide (C102) as a pre-
disinfectant to control the level of trihalomethanes present in
drinking water has been previously demonstrated at the Evansville
pilot plant. 1 However, due to concern over the potential
toxicity of C102 and its inorganic by-products, chlorite arid
chlorate, methods for their reduction have been investigated.
813

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Recent studies have shown that a combination of electrochemical
generation of C102 and subsequent application of the reducing
agent, ferrous chloride (FeCl2) can control the residual levels of
C102, chlorite and chlorate.<24} What impact, if any, the
incorporation of these treatment processes would have on the level
of mutagenic activity present in the finished drinking water was
evaluated.
Treatment Process
At a pilot-scale drinking water treatment plant in Evansville,
Indiana, three studies were conducted in which raw water from the
Ohio River was either treated with liquid C102, gaseous ClO^, Cl2
or was not disinfected (Figures 5-7). C102 was produced using an
electrochemical generator (Olin Corporation) and chlorination was
achieved by addition of a hypochlorous acid solution. Those
streams treated with CIO, were then clarified by the addition of
alum for coagulation followed by settling. In the April study
(Figure 5), both streams pre-disinfected with CI 02 were
subsequently treated with the reducing agent, FeCl2, to control
chlorite and CIO, concentrations. Sufficient CI, was then added to
achieve a free u2 residual of approximately 2-3 mg/L. Secondary
disinfection was followed by dual media (anthracite and sand)
filtration. In the June study (Figure 6), the reducing agent was
omitted from the liquid C102 stream. In the August study (Figure
7), NH2C1 was substituted for Cl2 as the secondary disinfectant in
the stream treated with gaseous CIO,. NH2C1 was produced by the
addition of Cl2 followed by ammonia (NHj) in the treatment process.
Sample Collection and Analyses
Water samples for each study were collected at the end of each
treatment stream (#1, 3, 5 and 6) as well as prior to the use of a
secondary disinfectant (#2 and 4) in order to evaluate the effects
of C102 alone on mutagenicity (Figures 5-7). Total organic carbon
(TOC) and total organic halide (TOX) concentrations were determined
for each sample. The water samples were concentrated by adsorption
on XAD resins for mutagenicity testing as described in the methods.
The columns contained 65 ml of each resin, XAD-8 over XAD-2. The
flow rate was 200 ml/min. Water samples of 125L were concentrated,
except in the August study, when only 50L of each water sample were
concentrated. Each column was eluted with 3 bed volumes of ethyl
acetate. The 8000-fold concentrates were assayed for mutagenicity
as previously described using Salmonella strains TA100, TA98 and
TA102, without metabolic activation.
Results and Discussion
Mutagenic activity was detected in all of the water samples,
including a low level in the non-disinfected samples. The highest
level of activity was observed in strain TA100 for all of the
samples in each of the three studies. (Figure 8 and Table 2)
These observations are consistent with the results from the
Jefferson Parish pilot study previously discussed.
814

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In the April study, the levels of mutagenic activity observed
for samples treated with liquid or gaseous CI02 alone were essenti-
ally the same. The samples in which liquid or gaseous CIO, was
followed by FeCl2 reduction and chlorination also showed similar
levels of mutagenic activity. These data indicate that the method
of C102 application did not affect the levels of mutagenicity
observed.
In the June study, the reducing agent was omitted from the
liquid C102 treatment train, however, the two samples treated with
ClOj followed by chlorination still had similar levels of mutagenic
activity. This suggests that the use of FeCl? did not have a
significant effect on the level of mutagenic activity observed.
In each of the three studies, water samples collected after
treatment with CI02 only, prior to addition of the secondary disin-
fectant, showed lower levels of mutagenic activity than those
samples collected following treatment with a secondary disinfec-
tant, either Cl2 or NH2C1. This indicates that the majority of the
mutagenic activity was produced by the secondary disinfectant.
This observation is more likely related to the individual disinfec-
tants used rather than the point at which they were added in the
treatment train. This is based on the results of a previous study
in which river water was treated with either CI2, NH,C1 or C102.(1"
In this study, the relative mutagenic potencies of the disinfected
water samples were, in order of decreasing activity: Cl,> NH,C1>
C102.
In all three studies, the levels of mutagenic activity present
in samples treated with liquid or gaseous CIO, followed by Cl2 were
essentially the same as samples treated with cl2 alone, talcing into
account the variability in the concentration and assay procedures.
Consequently, the results indicate that the treatment processes
used in this study, CIO, pre-disinfection followed by FeCl, reduc-
tion, had little effect on the levels of mutagenicity observed.
The substitution of NH2C1 for Cl2 as the secondary disinfectant
following gaseous CIO^ in the August study did, however, appear
beneficial. In strain TA100, the level of mutagenicity in the
sample treated with NH,C1 was reduced by more than 50% compared to
the levels present in the August samples treated with CIO, and CI,
or CI, alone. Similar results were observed in strains TA98 and
TA102.
The concentrations of TOX present in the Evansville water
samples showed a pattern similar to that of the mutagenicity data
(Table 3). In each of the studies, those samples treated with C102
alone had low levels of TOX, approximately equal to those of the
non-disinfected samples. Samples treated with CIO, followed by Cl2
had TOX concentrations similar to samples treated with Cl2 alone.
The substitution of NH,C1 for Cl2 as the secondary disinfectant in
the August study resulted in a much lower level of TOX compared to
samples in which Cl2 was used. The concentrations of TOC, by con-
trast, were similar for all of the water samples collected within
a given study. The data thus shows that the pattern observed for
815

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TOX and mutagenicity is not just a function of the amount of
organic matter present, but is related to the treatment processes
used.
SUMMARY
The results of the Jefferson Parish study presented here
showed that treatment with NH.Cl resulted in a lower level of
mutagenic activity than that produced by chlorination.
Additionally, disinfection with 0, prior to treatment with either
CI, or NH2C1 resulted in a lower level of mutagenicity than when
either disinfectant was used alone. In the Evansville study, pre-
disinfection with C102 followed by reduction with FeClj appeared to
have little effect on the levels of mutagenicity observed. Most of
the mutagenic activity was apparently produced by the secondary
disinfectant. As in the Jefferson Parish study, the use of Cl2 as
the secondary disinfectant produced a higher level of mutagenic
activity than was produced by chloramination.
In the absence of sufficient human epidemiological and/or
animal data, information from genotoxicity tests can assist in
determining those drinking water treatment processes which pose the
least concern for adverse human health effects. However, the
minimization or elimination of mutagenicity is, of course, only one
of numerous criteria to be considered in the overall evaluation of
drinking water processes. In attempting to minimize the potential
risks associated with the use of disinfectants and the subsequent
formation of disinfection by-products, one must not lose sight of
the necessity of maintaining drinking water that is microbio-
logical ly safe as well.
Acknowledgements
The authors wish to acknowledge Robert Miller, Paul Ringhand,
John Glass, Sr. and David Cmehil, who were responsible for sample
collection and concentration. The authors thank Wayne Koffskey,
chief chemist, Jefferson Parish Department of Public Utilities,
Jefferson Parish, LA. and Mark Griese, manager, water quality and
research, Evansville Water and Sewer Utility, Evansville, IN. for
their assistance. The authors also thank Carolyn Smallwood for her
reivew of the paper and Steve Waltrip, Jeanette Daley, Sandra
Dryer, and Maura Lilly for their assistance in the preparation of
the paper.
This paper has been reviewed in accordance with the U.S.
Environmental Protection Agency's peer and administrative review
policies and approved for presentation and publication. Mention of
trade names or commercial products does not constitute endorsement
or recommendation for use by the USEPA.
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1.	Murphy, P.A. and G.F. Craun (1990) A review of recent epidem-
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water disinfection and cancer, in: R.L. Jolley et al.
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pp. 361-372.
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von Borstel and D.T. Williams (1988) Evaluation of
alternative drinking water treatment processes at pilot-
scale by means of mutagenicity testing, AWWA Research
Foundation, Denver, CO.
4.	Noot, D.K., W.B. Anderson, S.A. Daignault, D.T. Williams and
P.M. Huck (1989) Evaluating treatment processes with the
Ames mutagenicity assay, Jour. AWWA, 81:9:87.
5.	Hollstein, M., J. HcCann, F.A. Angelosanto and W.W. Nichols
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Brown, V.F. Simmon, V.Dunkel, J. HcCann, K. Mortelmans,
M. Prival, T.K. Rao and V. Ray (1986) The Salmonella
tvohimurium/mammalian microsomal assay: A report of the
U.S. Environmental Protection Agency Gene-Tox program,
Hut. Res., 168:69.
7.	Maron, D.M. and B.N. Ames (1983) Revised methods for the
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8.	Tennant, R.W., B.H. Margolin, M.D. Shelby, E. Zeiger, J.K.
Haseman, J. Spalding, W. Caspary, M. Resnick, S.
Stasiewicz, B. Anderson and R. Minor (1987) Prediction of
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toxicity assays, Science, 236:933.
9.	Lucas, S.V. (1984) GC/MS analysis of organics in drinking
water concentrates and advanced waste treatment
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11.	Wilcox, P., F. van Hoof and M. van der Gaag (1986) Isolation
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A. Leonard and M. Kirsch-Volders (Eds.) Proceedings of
XVIth Annual Meeting of the European Environmental
Mutagen Society, Brussels, Belgium, pp 92-103.
817

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12.	Ringhand, H.P., J.R. Meier, F.C. Kopfler, K.M. Schenck, W.H.
Kaylor and D.E. Mitchell (1987) Importance of sample pH
on recovery of mutagenicity from drinking water by XAD
resins, Environ. Sci. Technol., 21:4:382.
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97:267.
14.	Standard Methods for the Examination of Water and
Wastewater, 17th ed.; American Public Health Association,
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15.	Glaze, W.H. (1987) Drinking-water treatment with ozone,
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16.	Cheh, A.M., J. Skochdopole, P. Koski and L. Cole (1980)
Nonvolatile mutagens in drinking water: Production by
chlorination and destruction by sulfite, Science 207:90.
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Seasonal variation of mutagenic activity in drinking
water, Bull. Environ. Contam. Toxicol., 26:188.
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J.R. Meier, H.P. Ringhand, M. Robinson and B.C. Castro
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Gaag (1985) The influence of water treatment processes on
the formation of organic halogens and mutagenic activity
by post chlorination, in: R.L. Jolley et al. (Eds.),
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23.	Griese, M.H., K. Hauser, M. Berkemeier, arid G. Gordon (1991)
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drinking water, Jour. AWWA, 84:11:69.
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Table 1
Mutagenicity of Water Samples Disinfected by Alternative Methods
at Jefferson Parish Pilot Plant (Sept., 1989)
Revertants per Liter Equivalent
TA100	TA98	1A97	TA102
Treatment
-S9
+S9
-S9
+S9
-S9
+S9
-S9
+S9
Non-Disinfected
138 ± 19
86 ± 10
29 ± 3
33 ± 6
120 ± 13
NS
NS
NS
CI,
4104 ± 170
22S8 ± 111
623 * 34
249 ± 19
2239 ± 96
1321 ± 85
2230 ± 201
NS
Nil,CI
1384 ± 36
71$ ± 49
248 ± 19
102 ±7
1112 x 24
501 ± 27
NS
NS
O. + CI,
2121 ± 67
849 ± 54
187 ± 14
88 ± 14
1281 ± 119
578 ± 33
939 ± 97
NS
O, + NH,CI
947 ± 34
317 ± 12
80 ± 6
43 ± 6
580 ± 23
232 t 10
NS
NS
NS: Not significant
S9; Metabolic activation

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Table 2
Direct Acting Mutagenicity of Evsnsville Water Samples
Following Alternative Treatments
Reveruots per Liter Equivalent
Treatment
April 1992
TA98
Non-dianfcc
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Table 3
Total Organic Carbon (TOC) and Total Organic Halide (TOX)
Concentrations of Evansville Water Samples
Following Alternative Treatments
Treatment April 1992 TOC (mg/L)	TOX (mg/L)
——=====saa=^sg^gggggaqBsg==SBa=M^=ag:^PKasaamss=sasaagBsae=	, ¦
Noo-disinfected	13	0.02
Liquid CIO.	1.6	0.05
Liquid aOj + FeCl, + Cl| + DM	1.5	0.11
Gaseous CIO,	13	0.05
Gaseous CIO, + FeCl, + CI, + DM	1.3	0.10
q,	is	o.ii
Treatment	June 1992
———	1 "	.I———-	¦ II » ——		 ¦ ¦ —-r-—--—--—-mm——
Non-disinfected	1.8	0.01
Liquid CIO.	1.7	0.03
Liquid CIO, + Cls + DM	1.7	0.20
Gaseous CIO,	1.6	0.05
Gaseous CIO. + FeCl, + CI, + DM	1.4	0.19
Clj	1.7	0.23
Treatment	August 1992
Non-disinfected	2.0	0.05
Liquid CIO.	10	0,03
Liquid CIO, + CI, + DM	2.1	0,19
Gaseous CIO,	2.0	0.05
Gaseous CIO, + FeCl, + CI, + NH, + DM	1.9	0.05
CI,	2.0	0.19
DM: Dual media (anthracite and sand)
822
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Figure 1. Scheme for the Concentration of
Water Samples for Mutagenicity Testing
Water sample
In-line
static mixer
Effluent

Add HCI to adjust pH to 2
Elute with ethyl acetate
1. Separate residual water
from ethyl acetate
"~ 2. Remove remaining water
by addition of Na2S04
Concentrate by
rotary evaporation
Exchange solvent to DMSO—~ +
E
8000X concentrate
Ames Salmonella assay
823
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Figure 2. Row Schematic of Jefferson Parish, LA Pilot Plant
Mississippi River Water
Clarlfier
Pressure Sand
Flters
Sand

Sand
PI
£L

Piter
CI,
Baffled

Baffled

Baffled
Drum

Drum

Drum
XAD
1
XAD
1
XAD
Column
Column
Column
-NHjCI
XAD
Column
3	*

CI
2 *"
NH2CI—*•

Contact

Contact

Contact
Chamber

Chamber

Chamber
Sand
Filter

Sand
Rlter
Baffled
Drum

Baffled
Drum
XAD
Column
824
-------
Figure 3. Direct Acting Mutagenicity in Strain TA100 of
Water Samples Disinfected by Alternative Methods
at Jefferson Parish Pilot Plant (Sept 1989)
1400-"
1200--
600 "
Non—disinfected
200- -
0.4
OB
0 .05 0.1
Liter Equivalents per Plate
825
-------
Figure 4. Direct Acting Mutagenicity in Strain TA100 of
Water Samples Disinfected by Alternative Methods
at Jefferson Parish Pilot Plant
jzl
non-
disinfected
it
CI,
¦ Sept 1989
~	March 1990
~	July 1990

O,
followed
by CI,
NH,CI
O,
followed
by NH,CI
826
-------
Figure 5. Flow Schematic of Evansvflle Pilot Plant
Apr! 1992
Raw WMBT
Lima
f>C | (RMHCMf A|«ltl
ChtmHtr, U>M
Fteeei4at>on Sacondar
ChamMr Sattling
i—Lima
		FtClf [AaMwcnf A|«ntl
XftaMwa U>H M*aU»a«t>
FlsceiJatian Sacondaf"
ChamBar Sattling
827
-------
Figure 6. Flow Schematic of Evansville Pilot Plant
June 1992
Raw Watar
CI Ot
Lima
(pH AdMtmant)
I—Lima
L — F«Clf [Radwclnf Agent)
^Contact
Chwnbara I** AdtuatmwK)
RoccuUtton Sacond«r
Chamber Stctiing
628
-------
Figure 7. Flow Schematic of Evansville
August 1992
Pilot Plant
Raw Water
cr"!
UqwM
PdiN
C«0(
¦hk
2 Sttga
Rapid Mi
(pH A«JuittMA(|
L ¦ ¦f+Of (R«tfvelnf Agant)
2 8ug«
Rapid Mx
CMabirt
Lfcn« U>H Adjustment]
629
-------
Figure 8. Direct Acting Mutagenicity in Strain TA1QQ of Evansville
Water Samples Following Alternative Treatments
I »
f
S
If
II*
¦ t
1
i
£ i<
April 18B2

« jst1

•
' ^
I

liquid
Liquid
G«t«ou«
GimmmjI
CiO,
chd,«.
CiO,
CiO,*

F«C4,»

F«Cl, ~

a,***

CJ»*0*
1 »"
s
a
ar
if
i hA
e
I
Jurw 1992

Han-	liquid
dillnlMIMl CIO,
Augutl 1992
Unuls
CIO,*
CI,.DM
r
il-
c
I.
Gnww CUmoui
CIO, CIO,*
F*Ci,«
CI, •OK
CI.
•a.
II	1
DM: dual
Non* Liquid Liquid Gamouk Qa««oua CI.
dtalnlocM CIO, CIO,* CIO, CIO,*
CI,-DM	F*a,*CI,
«NH,,OM
830
-------