Environ. Sci. Technol.

2004, 38, 5577-5583

Aqueous Chlorination Kinetics of

Some Endocrine Disruptors
M A R I E D E B O R D E , * , S Y L V I E R A B O U A N ,
H E R V E G A L L A R D , A N D
BERNARD LEGUBE
Laboratoire de Chimie de lEau et de lEnvironnement,
UMR CNRS 6008, Ecole Superieure dIngenieurs de Poitiers 40, avenue du Recteur Pineau - 86022 Poitiers Cedex, France,
and Laboratoire de Chimie Analytique, Faculte de Medecine et
Pharmacie - 34, rue du Jardin des Plantes,
BP 199-86005 Poitiers Cedex, France

The aqueous chlorination kinetics of six endocrine

disruptors (EDs: 4-n-nonylphenol, -estradiol, estrone,
estriol, 17R-ethinylestradiol, progesterone) were studied
in the 3.50-12.00 pH range, at 20 ( 2 C, in the presence
of an excess of total chlorine. Under these conditions,
all molecules with a phenolic group in their structure were
rapidly oxidized by chlorine, whereas progesterone
remained unchanged. In the first step, apparent kinetic
rate constants were determined at various pH levels. Then
each elementary reaction kinetic rate constant, i.e., the
reaction of hypochlorous acid (HOCl) with ionized EDs and
neutral EDs and an acid-catalyzed reaction of HOCl with
neutral EDs, was calculated in the second step. The results
showed that chlorination exhibits a second-order reaction
rate. The rate constants for the acid-catalyzed reaction
ranged from 3.02 104 M-1 s-1 (for 4-n-nonylphenol) to 1.822.62 105 M-1 s-1 (for hormones). The rate constants
of HOCl reactions with ionized EDs were found to be equal
to 7.5 104 M-1 s-1 (for 4-n-nonylphenol) and between
3.52 and 4.15 105 M-1 s-1 (for hormones), while the rate
contants of HOCl with neutral EDs were much lower,
i.e., between 1.31 M-1 s-1 (for 4-n-nonylphenol) and 3.744.82 M-1 s-1 (for hormones). At pH 7, the apparent-secondorder rate constants were calculated to range from
12.6 to 131.1 M-1 s-1. For a total chlorine concentration
of 1 mg/L, the corresponding half-life times at pH 7 were
about 65 min for 4-n-nonylphenol and 6-8 min for hormones.

Introduction
An endocrine disruptor was defined as an exogeneous
substance that causes adverse health effects in an intact
organism, or its progeny, consequent to changes in endocrine
function (1, 2). Numerous compounds have been reported
to have these effects (2). Among them, (i) hormones naturally
secreted by humans and animals, (ii) synthetic hormones
mainly used for contraception or management of menstrual
and menopausal disorders, and (iii) various chemical products (pesticides, phthalate plasticizers, alkylphenols, bisphenol A) are found in the environment as a result of industrial,
agricultural, and sewage runoff. In wastewater treatment,
natural and synthetic endocrine disruptors are subjected to
* Corresponding author phone: 335 49 45 44 74; fax: 335 49 45
37 68; e-mail: marie.deborde@etu.univ-poitiers.fr.
Faculte
de Medecine et Pharmacie.
Laboratoire de Chimie de lEau et de lEnvironnement.
10.1021/es040006e CCC: $27.50
Published on Web 09/22/2004

2004 American Chemical Society

a variety of treatment processes but are only partially

removed. In a sewage treatment plant, Baronti et al. (3)
documented an average removal efficiency for some estrogens of between 61% (for estrone) and 95% (for estriol). Many
compounds are thus ultimately released into effluents and
surface waters (4). Recently, the presence of endocrine
disruptors in natural waters was clearly demonstrated (2, 5),
i.e., concentrations have been detected in the nanogram/L
range for hormones (6-8) and in the microgram/L range for
chemical products (9, 10). The lowest reported concentrations
of endocrine disruptors required to induce intersex are 10
ng/L for estradiol or estrone, 0.1 ng/L for ethinylestradiol
(11), and 50 g/L for nonylphenol (12). Therefore, in some
cases, surface water concentrations of these disruptors can
be near or equal to the lowest concentrations which were
found to induce reproductive disturbances in male fish in
controlled laboratory studies, so they might disrupt reproduction in wildlife.
Surface water is often used as a source of drinking water.
Little is currently known about the ultimate fate of endocrine
disruptors, particularly in the disinfection steps. However,
the authors of some recent studies on the effects of
chlorination and ozonation on some endocrine disruptors
considered that degradation is possible by such oxidation
processes (13-16). In their studies on oxidation of pharmaceuticals during ozonation, Huber et al. (13) reported that
17R-ethinylestradiol was rapidly removed by ozone with a
second-order rate constant of 3 106 M-1 s-1 at pH 7 and
20 C. On the basis of chemical characteristics, they also
estimated that, at pH 7 and 20 C, the following compounds
(with their corresponding second-order rate constants) would
likely be removed: estradiol (106 M-1 s-1), 4-nonylphenol
(1-10 106 M-1 s-1), bisphenol A (1-10 106 M-1 s-1), and
testosterone (105 M-1 s-1). Few kinetic studies concerning
chlorination have been conducted. However, Hu et al. (1416) studied products of aqueous chlorination of several
endocrine disruptors. In these studies, rapid elimination of
bisphenol A, 4-nonylphenol, and 17-estradiol was reported
at pH 7.5 and in the presence of 1.30 to 1.46 mg/L of
chlorine: 80% removal of bisphenol A, 84% of 4-nonylphenol,
and 100% of 17-estradiol were achieved after 10 min reaction
time. They also noted the production of numerous biologically active byproducts. The results of these studies, in
addition to the well-known reactivity of phenolic compounds
with chlorine (17, 18), suggest that other endocrine disruptors
could also be degraded in this way.
This study was designed to assess the potential of
chlorination for the oxidation of six endocrine disruptors.
These compounds, reported in Table 1, were chosen because
they are commonly found in the environment. They include
compounds from the 3 endocrine disruptor groups described
earlier, i.e. chemical products (4-n-nonylphenol (NP)), natural
estrogens and progestogens (-estradiol (E2), estrone (E1),
estriol (E3), and progesterone (P)), and synthetic hormones
(17R-ethinylestradiol (EE2)). Chemically, natural and synthetic hormones have a common cyclopentan-o-perhydrophenanthrene ring (6). All endocrine disruptors studied,
except progesterone, have a phenolic ring. The major aim of
this study was to determine, for each compound, the rate
constant of each elementary reaction in order to calculate
the apparent rate constant at a given pH. In the first part, the
chlorination kinetics were assessed in pure aqueous solution,
between pH 3.50 and 12.00 and at 20 ( 2 C. The reaction
rate order and apparent rate constants of chlorination were
determined for each molecule. In the second part, the rate
constants of each elementary reaction were determined on
VOL. 38, NO. 21, 2004 / ENVIRONMENTAL SCIENCE & TECHNOLOGY

5577

TABLE 1. Selected Endocrine Disruptors

the basis of the pH dependence of the rate constants and the

speciation of chlorine and endocrine disruptors.

Experimental Section
Standards and Reagents. All endocrine disruptors (NP, E2,
E1, E3, EE2, P) were supplied by Aldrich (purity g 97%).
Sodium hypochlorite solution was purchased from VWR
International and was controlled to ensure equimolar
concentrations of hypochlorite (ClO-) and chloride (Cl-) ions,
with 14.0% (m/V) of active chlorine.
All other reagents (Na2S2O3, NaOH, H2SO4, phosphate,
etc.) were analytical grade or better and used without further
purification. Solvents were HPLC grade. Ultrapurified water
(18 M cm) was obtained from Milli RO-Milli Q Millipore
system.
Analytical Methods. Each ED was analyzed by highperformance liquid chromatography (HPLC) using an automatic Waters 717 plus autosampler injector and a Waters
600E pump. Isocratic reversed-phase chromatography was
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ENVIRONMENTAL SCIENCE & TECHNOLOGY / VOL. 38, NO. 21, 2004

optimized for each ED using a C18 packed column (Hichrom

spherisorb S50DS2, C.I.L. Cluzeau, 5 m, 4.6 mm i.d., 25 cm
long). A water-methanol mixture (55-90% of methanol,
according to the studied ED) was used as the mobile phase,
with a flow-rate of 0.8 mL/min. The compounds were
detected either with a Waters 484 Tunable absorbance
detector set at 217 nm for E1 or 250 nm for P or a Waters 474
scanning fluorescence detector with an excitation wavelength of ex ) 217 nm and emission wavelength of em ) 300
nm for EE2, E2, E1 and ex ) 222 nm and em ) 307 nm for
NP.
Commercial solution and 19 mM stock solution of chlorine
were standardized by iodometry (19). In kinetic experiments,
chlorine was analyzed by the N, N-diethyl-p-phenylenediamine (DPD) colorimetric method (20).
pH was measured with a Tacussel LPH330T pH-meter
equipped with a Radiometer Analytical combined electrode
and previously calibrated with standard pH 4, 7, and 10
buffers.

FIGURE 1. Pseudo-first-order kinetic plot of estriol chlorination at 20 ( 2 C, [HOCl]T ) 37.3 ( 0.4 M and three pH levels. Symbols represent
measured data, and the straight line is the linear regression. (Insert: estriol chlorination at pH 5.94 ( 0.02, 20 ( 2 C, and various [HOCl]T).
Kinetic Experiments. All experiments were performed in
a batch reactor thermostated at 20 ( 2 C, under pseudofirst-order kinetics conditions ([HOCl]T . 10 [ED]T). Tested
aqueous solutions (800 mL) were buffered using phosphate
salts (10 mM) for a 6-9 pH range. For pH < 6 and pH > 9,
pH values were preadjusted with H2SO4 and NaOH, respectively. The initial ED concentration was 1 M. At least 35 M
of total chlorine was added. Chlorine variations were less
than 5% under these conditions. The chlorine concentration
was thus assumed to be constant during the kinetic experiments.
Kinetic runs were initiated by injecting, under rapid
mixing, an aliquot of a 19 mM chlorine solution. At constant
time intervals, 3 mL of solution was withdrawn with a glass
syringe and added to 4 mL HPLC vials containing 100 L of
sodium thiosulfate solution (100 g L-1) to quench the residual
chlorine and stop the oxidation reaction. Samples were then
analyzed using HPLC to determine the remaining ED
concentration. When the EDs disappeared, the kinetic
experiments were pursued until at least 50% ED consumption
was achieved.

Results and Discussion

Reaction Rate Order and Apparent Rate Constants of
Chlorination. Among the studied EDs, only progesterone
did not react with chlorine under our experimental conditions
(i.e. 1 M ED with 35 M or 190 M total chlorine for 30 min,
at pH 3.80, 6.90, 7.00, and 8.25). For the other molecules, the
chlorination experiments exhibited a pseudo-first-order
dependence on the ED concentration, as demonstrated by
the linear time-course plot of Ln([ED]T.t/[ED]T.0). Figure 1
presents an example of the pseudo-first-order kinetic plot of
estriol chlorination at pH 3.50, 9.61, 10.53 and with a total
chlorine concentration of 37.3 ( 0.4 M. These plots were
linear (r2 > 0.99) for > 85% reactions. The correlation
coefficients were always superior to 0.96 for all reaction
compounds. Therefore, EDs disappeared at a pseudo-firstorder rate with respect to the total ED concentration

d[ED]T
) kobs[ED]T
v)dt

(1)

with kobs ) pseudo-first-order kinetic constant.

The reaction order relative to chlorine was then examined
for each ED by varying the chlorine concentration and
monitoring the disappearance of EDs. The insert in Figure

1 presents the case of estriol at pH 5.94 ( 0.02, for a total

chlorine range of 38.1-96.6 M. This figure illustrates that
the pseudo-first-order kinetic constant was proportional to
the total chlorine concentration (r2 > 0.99). Similar results
were obtained for the other EDs (r2 > 0.93). Therefore, the
chlorination kinetics of NP, E3, E2, EE2, E1 is a second-order
reaction, first-order relative to the free active chlorine
concentration ([HOCl]T) and to the total ED concentration
([ED]T)

v)-

d[ED]T
) kapp[HOCl]T[ED]T
dt

(2)

with

kapp ) kobs/[HOCl]T, second-order kinetic constant (3)

The kapp values were determined for about 20 pH values
for each ED.
pH Dependence Profile and Rate Constants of Elementary Reactions. Figure 2 presents the pH profile of the
apparent second-order rate constants for NP, EE2, and E1.
This figure also gives the standard deviations for each rate
constant. Similar profiles are obtained for E3 and E2. The
results show that the second-order apparent rate constant
was minimal at around pH 5 and maximal between pH 8 and
10, irrespective of the compound considered. Early kinetic
studies of chlorination of phenols (17) and resorcinols (18)
showed similar pH dependence profiles for second-order
apparent rate constants, thus strongly suggesting that the
phenolic ring in the estrogenic structure would control the
reactivity of chlorine. Based on these earlier works, the pH
profiles could be explained by taking the ionized (ED-) and
neutral (ED) species of EDs (reaction 4) into account

ED / ED- + H+ KaED

(4)

[ED]T ) [ED] + [ED-]

(5)

with

and, the different species of chlorine (reactions 6 and 7):

Cl2 + H2O / HOCl + Cl- + H+

HOCl / ClO- + H+

KCl2

(6)

KaCl

VOL. 38, NO. 21, 2004 / ENVIRONMENTAL SCIENCE & TECHNOLOGY

(7)
9

5579

FIGURE 2. pH-dependence of the apparent-second-order rate constants of nonylphenol, ethinylestradiol, and estrone chlorination at 20
( 2 C. Symbols represent measured data and lines represent the model calculations.
Under our experimental conditions, the sodium hypochlorite solution used was controlled to ensure that it was
equimolar in hypochlorite and chloride. Based on reported
equilibrium constant values for the hydrolysis of Cl2 (reaction
6) (21) and for [Cl-] ) [HOCl]T ) 3.5 10-5 M, the maximum
Cl2 concentration was calculated to be very low at pH 3.5 (ca.
1 10-9 M). Further experiments showed that kapp increased
linearly when the chloride concentration increased (results
not presented), which could be explained by the reactivity
of Cl2 with phenolic compounds. The results also showed
that at low chloride concentrations (35 M) kapp levels were
not significantly different from kapp levels extrapolated for
[Cl-] ) 0. Consequently, Cl2 species was considered to be
negligible in our conditions, so only ClO- and HOCl species
were taken into consideration (reaction 7). The concentration
of free active chlorine ([HOCl]T) was as follows:

[HOCl]T ) [HOCl] + [ClO-]

(8)

The lower reactivity of EDs with chlorine at pH 5 could

be explained by the slow reaction between HOCl and neutral
ED species. However, the increase at more acidic values (pH
< 4) could be explained by the catalytic effect of protons on
the reaction between HOCl and neutral ED species (reactions
9 and 10).

ED + H2OCl+ f byproducts

k1

(12)

with

k1 ) k1/K1

(13)

Moreover, in the 5-10 pH range, the increased reactivity

could be explained by the reaction between HOCl and ionized
ED species (reaction 14).

ED- + HOCl f byproducts

k3

(14)

The maxima in the rate constant profiles might be

explained if HOCl is the only active oxidant and the ClOreactivity is negligible.
Considering that chlorination involves reactions 9, 10,
and 14, the ED chlorination kinetics can be expressed as
follows:

v)-

d[ED]T
) [HOCl](k1[ED][H+] + k2[ED] + k3[ED-])
dt
(15)

Replacing [HOCl], [ED], and [ED-] by their expressions as

ratios of [HOCl]T or [ED]T, the rate of EDs disappearance is

d[ED]T
)
dt
+
(k1RED[H ] + k2RED + k3R ED-)RCl[HOCl]T[ED]T (16)

v)ED + HOCl + H+ f byproducts

ED + HOCl f byproducts

k2

k1

(9)
(10)

Following Rebenne et al. (18) who studied the chlorination

of resorcinols, an alternative pathway involving H2OCl+
species could be proposed to explain reaction 9. If this
mechanism applies in the case of EDs, reactions 11 and 12
would explain the increase in kapp at pH < 4

HOCl + H+ / H2OCl+ K1
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ENVIRONMENTAL SCIENCE & TECHNOLOGY / VOL. 38, NO. 21, 2004

with RCl ) hypochlorous acid fraction of total chlorine, with

RED ) neutral ED fraction, and with RED- ) ionized ED
fraction.
Combining eqs 2 and 16, kapp is a function of pH

kapp )

k1[H+]3 + k2[H+]2 + k3[H+]KaED

[H+]2 + [H+]KaED + [H+]KaCl + KaClKaED

(17)

The intrinsic constants k1, k2, and k3 were calculated by

TABLE 2. Second-Order Rate Constants Calculated for the ED Chlorination Mechanism (20 ( 2 C, 3.5-12.0 pH Range)
compounds

k1 (() (M-1 s-1)

k1 (() (M-2 s-1)

k2 (() (M-1 s-1)

k3 (() (M-1 s-1)

4-n-nonylphenol
17R-ethinylestradiol
-estradiol
estrone
estriol

3.02 (0.34) 107

2.04 (0.16) 108
2.24 (0.17) 108
2.62 (0.18) 108
1.82 (0.15) 108

3.02 (0.34) 104

2.04 (0.16) 105
2.24 (0.17) 105
2.62 (0.18) 105
1.82 (0.15) 105

1.31 (0.13)
4.33 (0.53)
3.78 (0.42)
3.74 (0.57)
4.82 (0.50)

7.5 (0.27) 104

3.52 (0.10) 105
3.64 (0.11) 105
4.15 (0.17) 105
3.56 (0.12) 105

FIGURE 3. Linear correlation between the log(k3) and molecule pKa for phenolic compounds monitored: (b) in this study, (O) by Gallard
and Von Gunten (17).
multiple regression of the experimental kapp data. Values of
k1, k2, and k3 were obtained for the lowest quadratic mean
deviation, defined as ((kapp exp - kapp theo)2/(kapp exp)2), where
kapp exp and kapp theo represent the experimental and theoretical
apparent second-order rate constants, respectively. The
chlorine acidity constant used for the calculation was pKaCl
) 7.54 (22). ED pKa values were derived from the literature
and are reported in Table 1. For E2 and E1, the pKa values
were estimated according to Perrin (25) from the analogy of
their structure with EE2 and E3.
Figure 2 represents the experimental and the modeled
pH profiles for NP, EE2, and E1. Similar correlations were
obtained for E3 and E2. A good correlation between the
experimental and modeled values was obtained. In the case
of 4-n-nonylphenol, the theoretical curve seems to be slightly
shifted toward the right as compared to the experimental
values at pH > 7. For these pH values, the total reaction was
mainly controlled by the reaction between HOCl and the
ionized ED. This shift could thus be explained by uncertainty
concerning the pKa value which would underestimate the
ionized ED concentration. The best fit could be obtained for
a pKa value of 10.4, whereas a value of 10.7 was given by
Maguire and used in this study (23) and the theoretical value
of 10.25 was calculated by Lipnick et al. (26).
Table 2 shows, for each studied compound, the values of
k1 (HOCl-acid-catalyzed reaction), k2 (HOCl reaction with
ED), and k3 (HOCl reaction with ED-) as well as the k1 value
(H2OCl+ reaction with ED) from eq 13 with K1 ) 10-3,
according to Rebenne et al. (18). As expected from their
molecular structure, the 4 hormones that have a phenolic
ring showed similar rate constants. The rate constants of
chlorine with dissociated forms range from 3.52 105 to 4.15
105 M-1 s-1, which is about 10-fold higher than the
corresponding rate constants of phenol (17) and 4-nnonylphenol. Therefore the chemical structure of these
hormones molecules seems to enhance the chlorine reactiv-

ity. This suggested that there could be a similar reactivity for

some other hormones that have a phenolic ring (e.g. equilin,
equilenin, diethylstibestrol, etc.).
As for other phenolic compounds (17, 18), the reactivity
of chlorine with neutral ED species was 104 to 105 times weaker
than with the ionized form. Attenuation of the electron-donor
character of the hydroxyl group, i.e., change of the O- group
in OH, thus decreases the reaction rates. For pH values
between 4 and 6, ED chlorination is mainly controlled by the
reaction between HOCl and undissociated species. At higher
pH, the reaction between HOCl and the dissociated species
is prevalent.
For aromatic compounds, the substituent effect on the
second-order rate constants with oxidants can be illustrated
by linear free energy relationships using the Hammett-type
correlation for example. Good correlations were also obtained
for phenol chlorination using pKa values (17, 18). Figure 3
shows that in the case of NP, the plot of k3 vs pKa was in line
with the correlation obtained with data from Gallard and
Von Gunten (17) for phenolate species substituted in the
ortho and para positions. Even though the 3 estrogens have
a phenolic ring, they did not fit with the above correlation
because they also have a much more complex structure
(steroid moiety) than phenols, which probably affects the
overall charge density and thus the reactivity with chlorine.
To assess the effect of chlorine disinfection on EDs in
drinking water treatment conditions, the half-life times of
each compound were calculated for 3 chlorine concentrations
(0.1, 0.5, and 1 mg/L) at pH 7. Table 3 gives the apparent
second-order rate constant values and the corresponding
half-life times for each studied ED at these chlorine concentrations. These results show that chlorination of drinking
water prompted rapid elimination of the studied estrogens
at a chlorine concentration of 1 mg/L (t1/2 ) 6-8 min). The
reaction with nonylphenol was much slower, with a half-life
time of 65 min at a 1 mg/L chlorine concentration.
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5581

TABLE 3. Apparent-Second-Order Rate Constants and Half-Life

Times Calculated at pH 7, 20 C for Total Chlorine Doses
Ranging from 0.1 to 1 mg/L
t1/2 (min)

compounds

kapp
(M-1 s-1)

chlorine
concn
0.1 mg/L

chlorine
concn
0.5 mg/L

chlorine
concn
1 mg/L

4-n-nonylphenol
17R-ethinylestradiol
-estradiol
estrone
estriol

12.6
112.1
115.2
131.1
113.6

651
73.2
71.2
62.6
72.2

130
14.6
14.2
12.5
14.4

65.1
7.3
7.1
6.3
7.2

In the presence of ozone, and under the same conditions,

i.e., pH 7 at 20 C, the second-order rate constants estimated
for E2, EE2, and NP are about 106 M-1 s-1 (13), which is
significantly higher than for chlorine. For an ozone concentration of 0.4-1 mg/L, the half-life times are < 0.1 s.
Ozonation would therefore be much more efficient for
removing the selected EDs.
Even though high quantities of estrogens can be removed
by biological treatments (3), municipal wastewaters are
known to be an important source of endocrine disruptors in
the environment. Typical wastewater chlorination dosages
of 1 to 4 mg/L are used with a minimum contact time of 15
min. Assuming a theoretical constant chlorine concentration
of 2 mg/L and a minimum 15 min contact time, the calculated
estrogen removal efficiency is about 95% for a 7-8 pH range.
For NP under the same conditions, the removal efficiency is
only 27%, so a contact time of 140 min is necessary to achieve
95% removal efficiency. Chlorination of municipal wastewater
thus not only helps to further remove such compounds but
also participates in the discharge of chlorinated estrogens.
To assess the overall efficiency of oxidation treatments,
byproducts of parent EDs should be identified, and their
reactivity with oxidants and their biological activity should
be evaluated. The structure of chlorinated ED byproducts
and their reactivity with chlorine can be estimated from the
known reactivity of structurally related compounds. Considering the nonreactivity of progesterone and the pH profile
of rate constants of other phenolic-like EDs, the phenol
moiety is probably the chlorine reaction site. According to
Burttschell et al. (27), phenol chlorination proceeds by the
stepwise substitution of 2, 4, and 6 positions of the aromatic
ring. In this case, two primary byproducts could be expected
from the chlorination of the studied EDs: 2 monochloro-ED
and 2,6 dichloro-ED (where OH is in position 1). For NP and
E2, these two byproducts have been analyzed or suspected
(15, 16). For phenol, each chlorine substitution causes a
decrease of 1 order of magnitude for the elementary rate
constant of phenolate with chlorine (17). Moreover, chlorine
substitution makes the substituted phenol more acidic (i.e.
decrease in pKa values with increasing chlorine substitution).
The lower reactivity of chlorinated phenolates is thus
compensated by their higher concentration at pH 6-8. Then
the magnitudes of the apparent chlorination rates of phenols
in the neutral pH range are similar to those of chlorophenols
(28). If chlorinated ED byproducts have a similar behavior,
at neutral pH, chlorinated EDs would likely be degraded with
apparent rates similar to those of the parent EDs. For NP and
E2, mono and dichloro byproducts were monitored using
HPLC (15, 16). The results showed that these compounds
are effectively removed by chlorine but can remain for more
than 1-2 h in the presence of low residual chlorine
concentrations.
Finally, some recent studies showed that estrogenic
activity is usually reduced as a result of chlorination (15, 16,
29). However, chlorination of a solution of E2 (10-7 M, pH 7)
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ENVIRONMENTAL SCIENCE & TECHNOLOGY / VOL. 38, NO. 21, 2004

with 1.5 mg/L of chlorine for 10 min contact time did not
show a significant decrease in estrogenic activity (29). Under
these chlorination conditions, residual E2 was calculated to
be only 23% using the rate constants determined in our study.
As shown by Hu et al. (15), these results confirm that the
initial chlorinated byproducts of E2 exhibit estrogenic activity
similar to that of their parent compounds. Further chlorination led to more drastic transformation of the molecule (ring
opening), with a loss of estrogenic activity. Further identification, kinetic studies, and evaluation of the biological
activity of chlorinated byproducts are thus required to model
the fate of these compounds in the environment and assess
the health impact of drinking tap water.

Acknowledgments
The authors thank Prof. Marc Arnaudon, Mathematics
section, University of Poitiers, for helpful discussions and
advice for the statistical calculations.

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Received for review January 12, 2004. Revised manuscript

received July 26, 2004. Accepted August 2, 2004.
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