Document ID: EPA-HQ-OPP-2006-0328-0009
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-04-26T04:00Z

Chlorine
Dioxide
Incident
Reports
Case
4023
Jonathan
Chen,
Ph.
D.
Office
of
Pesticide
Programs
Antimicrobials
Division
U.
S.
Environmental
Protection
Agency
1200
Pennsylvania
Avenue,
NW
Washington,
DC
20460
February
23,
2006
TABLE
OF
CONTENTS
0.0
INTRODUCTION................................................................................................................................................
3
1.0
INCIDENT
REPORT
DATA
ASSOCIATED
WITH
HEALTH
EFFECTS
...............................................
3
1.1
OPP
=

S
INCIDENT
DATA
SYSTEM
(
IDS)
..............................................................................................................
4
1.2
POISON
CONTROL
CENTER
(
1993
 
2003)........................................................................................................
4
1.3
CALIFORNIA
DATA
­
1982
THROUGH
2003........................................................................................................
5
1.4
NATIONAL
PESTICIDE
TELECOMMUNICATIONS
NETWORK
(
NPTN).................................................................
5
1.5
INCIDENT
REPORTS
/
EPIDEMIOLOGICAL
STUDIES
PUBLISHED
IN
SCIENTIFIC
LITERATURE.
...........................
5
1.5.1
Respiratory
Effects
........................................................................................................................................
5
1.5.2
Ocular
Effects................................................................................................................................................
7
1.5.3
Dermal
Effects...............................................................................................................................................
8
1.5.4
Oral
Effects....................................................................................................................................................
8
1.4.5
Other
Related
Effects
..................................................................................................................................
10
2.0
SUMMARY
AND
CONCLUSION..................................................................................................................
11
3.0
REFERENCE......................................................................................................................................................
18
Page
3
of
22
0.0
INTRODUCTION
The
chemical
chlorine
dioxide
(
ClO2)
is
used
as
a
biocide
in
bleaching
cellulose,
paper
and
pulp,
flour,
leather,
fats
and
oils,
textiles,
and
beeswax;
in
purification
of
water;
for
taste
and
odor
control
of
water;
in
cleaning
and
detanning
leather;
in
the
manufacturing
of
chloride
salts;
as
an
oxidizing
agent;
as
a
bactericide,
antiseptic
and
deodorizer
(
The
Merck
Index,
2001).
The
purpose
of
this
chapter
is
to
review
the
evidence
of
health
effects
in
humans
resulting
from
exposure
to
chlorine
dioxide.

Two
approaches
are
used
in
this
section:

1.
The
potential
health
effects
of
chlorine
dioxide
in
humans,
reported
as
incident
reports
from
different
sources,
are
summarized.

2.
A
literature
search
of
chronic
health
effects
associated
with
chlorine
dioxide
exposure,
including
results
of
epidemiological
studies,
is
summarized.

1.0
INCIDENT
REPORT
DATA
ASSOCIATED
WITH
HEALTH
EFFECTS
The
following
databases
have
been
consulted
for
the
poisoning
incident
data
OPP
Incident
Data
System
(
IDS)
­
The
Incident
Data
System
of
The
Office
of
Pesticide
Programs
(
OPP)
of
the
Environmental
Protection
Agency
(
EPA)
contains
reports
of
incidents
from
various
sources,
including
registrants,
other
federal
and
state
health
and
environmental
agencies,
and
individual
consumers,
submitted
to
OPP
since
1992.
Reports
submitted
to
the
Incident
Data
System
represent
anecdotal
reports
or
allegations
only,
unless
otherwise
stated.
Typically
no
conclusions
can
be
drawn
implicating
the
pesticide
as
a
cause
of
any
of
the
reported
health
effects.
Nevertheless,
with
enough
cases
and/
or
enough
documentation,
risk
mitigation
measures
may
be
suggested.

Poison
Control
Centers
­
as
a
result
of
a
data
purchase
by
EPA,
OPP
received
Poison
Control
Center
data
covering
the
years
1993
through
2003
for
all
pesticides.
Most
of
the
national
Poison
Control
Centers
(
PCCs)
participate
in
a
national
data
collection
system,
the
Toxic
Exposure
Surveillance
System,
which
obtains
data
from
about
65­
70
centers
at
hospitals
and
universities.
PCCs
provide
telephone
consultation
for
individuals
and
health
care
providers
on
suspected
poisonings,
involving
drugs,
household
products,
pesticides,
etc.

California
Department
of
Pesticide
Regulation
­
California
has
collected
uniform
data
on
suspected
pesticide
poisonings
since
1982.
Physicians
are
required,
by
statute,
to
report
to
their
local
health
officer
all
occurrences
of
illness
suspected
of
being
related
to
exposure
to
pesticides.
The
majority
of
the
incidents
involve
workers.
Information
on
exposure
(
worker
activity),
type
of
illness
(
systemic,
eye,
skin,
eye/
skin
and
respiratory),
likelihood
of
a
causal
relationship,
and
number
of
days
off
work
and
in
the
hospital
are
provided.

National
Pesticide
Telecommunications
Network
(
NPTN)
­
NPTN
is
a
toll­
free
information
Page
4
of
22
service
supported
by
OPP.
A
ranking
of
the
top
200
active
ingredients
for
which
telephone
calls
were
received
during
calendar
years
1984­
1991,
inclusive,
has
been
prepared.
The
total
number
of
calls
was
tabulated
for
the
categories
human
incidents,
animal
incidents,
calls
for
information,
and
others.

Published
Incident
Reports
­
Some
incident
reports
associated
with
chlorine
dioxide
related
human
health
hazards
are
published
in
the
scientific
literature.

1.1
OPP
=

s
Incident
Data
System
(
IDS)

Four
incidents
have
been
reported
that
are
associated
with
chlorine
dioxide
in
the
OPP
incident
data
system.
These
incidents
are
listed
below.

1)
In
October
1995,
fogging
was
done
in
the
air
vents
of
an
occupied
apartment
building
with
the
product
Envirocon.
A
woman
complained
that
she
had
a
headache
afterwards.

2)
In
September
1995,
a
failure
in
the
chlorine
dioxide
reservoir
sensor
caused
a
temporary
overload
of
chlorine
into
the
fish
thawing
line
in
the
processing
building
of
Bumble
Bee
Seafood.
Sixty­
six
employees
were
evacuated
and
three
of
those
employees
went
to
the
doctor
when
they
experienced
symptoms
of
headache,
nasal
congestion,
eye
irritation,
nausea
and
dizziness.
All
three
employees
were
back
at
work
the
following
day.

3)
In
July
2000,
a
power
outage
caused
the
chlorine
system
at
a
Smuckers
plant
to
surge.
The
exhaust
system
was
also
not
operational.
The
combination
caused
a
strong
odor
of
chlorine.
Five
workers
on
the
strawberry
processing
line
complained
of
the
smell
and
experienced
itchy
watery
eyes,
runny
nose,
sore
throat
and
headache.
A
total
of
six
workers
saw
physicians.

4)
In
May
1999,
equipment
operators
standing
near
a
bottle
cooler
complained
of
fumes
and
said
the
fumes
were
giving
them
headaches
and
sore
throats.
The
water
in
the
bottle
cooler
had
been
treated
with
Akta
Chlor
25
which
contains
chlorine
dioxide
as
the
active
ingredient.

For
comparison,
these
incidents
are
summarized
in
Table
1.
Inhalation
exposure
is
the
primary
route
of
exposure.
Irritation
type
reactions
and
headache
are
the
primary
concerns
that
have
been
reported.

1.2
Poison
Control
Center
­
1993
through
2003
There
are
no
chlorine
dioxide
specific
incidents
that
have
been
reported.
Page
5
of
22
1.3
California
Data
­
1982
through
2003
There
are
20
incidents
that
have
been
reported
in
the
California
Pesticide
Surveillance
Program
Database
(
1982­
2003)
as
possibly
or
probably
chlorine
dioxide
related
(
summarized
in
Table
2).
Eleven
of
these
reported
incidences
are
not
agriculturally
related.
Lightheadedness,
headache,
nausea,
coughing,
throat
irritation,
sinus
tightness,
difficulty
breathing
and
chest
tightness
are
the
common
symptoms
reported
in
these
incidents.
Table
3
presents
the
types
of
illnesses
reported
by
year.
Table
4
gives
the
total
number
of
workers
that
took
time
off
work
as
a
result
of
their
illness
and
how
many
were
hospitalized
and
for
how
long.

1.4
National
Pesticide
Telecommunications
Network
(
NPTN)

There
is
no
incident
reported
in
the
NPTN
database
related
to
chlorine
dioxide.

1.5
Incident
Reports
/
Epidemiological
Studies
Published
in
Scientific
Literature.

Both
chlorine
and
chlorine
dioxide
dissolve
in
water,
then
hydrolyze
to
produce
hypochlorous
acid
and
hypochlorite
ion.
These
breakdown
products
tend
to
react
in
a
swimming
pool
with
the
organic
content,
temperature
and
pH
to
produce
predominant
breakdown
by­
products
which
were
identified
in
WHO
(
2000)
as
trihalomethanes
(
e.
g.,
chloroform),
chloramines,
haloacetic
acids,
haloacetonitriles,
haloketones,
chloropicrin,
and
chloral
hydrate.
When
it
is
in
an
aqueous
media,
it
is
difficult
to
separate
incidents
associated
with
chlorine
dioxide
from
incidents
associated
with
chlorine,
chlorite
and
hypochlorite
ions.
Therefore,
some
of
the
incidents
associated
with
all
the
related
chemicals
will
also
be
discussed.

1.5.1
Respiratory
Effects
The
most
common
symptoms
reported
for
cases
of
inhalation
exposure
were
respiratory
irritation/
burning,
irritation
to
mouth/
throat/
nose,
coughing/
choking,
shortness
of
breath,
dizziness,
flu­
like
symptoms,
and
headache.
A
chlorine
dioxide
concentration
of
5
ppm
was
definitely
irritating.
Concentrations
averaging
between
trace
and
0.25
ppm
were
associated
with
minor
respiratory
ailments.
A
concentration
of
19
ppm
can
cause
death
(
ACDIH,
2001).

A
woman
gardener
49
years
of
age
suffered
inhalation
intoxication
from
chlorine
dioxide
while
bleaching
dried
flowers.
Preparation
of
the
bleaching
solutions
was
associated
with
a
sharp
pungent
smell,
coughing,
pharyngeal
irritation
and
headache.
Seven
hours
later
increasing
cough
and
dyspnea
led
to
hospitalization.
Clinical
findings
were
tachypnea,
tachycardia,
and
rales
of
auscultation;
clinical
chemistry
revealed
marked
leucocytosis.
Chest
X­
ray
did
not
yield
any
abnormal
findings.
Initially
the
vital
capacity
and
forced
expiratory
volume
in
1
sec
markedly
reduced
and
the
resistance
correspondingly
enhanced.
Blood
gas
analysis
showed
hypoxemia
despite
alveolar
hyperventilation.
Administration
of
corticosteroids
resulted
in
significant
alleviation
of
complaints
and
in
improved
lung
function
with
stabilization
in
a
highly
normal
range,
as
Page
6
of
22
confirmed
by
follow­
up
examination
two
years
later.
The
chlorine
dioxide
intoxication
had
been
due
to
pH
level
reduction
resulting
from
an
incorrect
proportioning
and
handling
of
the
individual
bleaching
agent
components
when
preparing
the
solution
(
Exner­
Freisfeld
et
al.,
1986
cited
in
HSDB).

Potts
(
1996)
reported
that
the
general
symptoms
of
complaints
from
most
swimmers
treated
with
chlorinated
disinfectants
are
upper
and
lower
respiratory
tract
symptoms
such
as
coughing,
chest
tightness,
wheezing
and
dyspnea.
They
stated
that
other
symptoms
may
include
headaches,
nausea,
lethargy,
soar
throat,
and
irritation
of
the
eyes,
nose
and
throat.
Other
complaints
have
been
diagnosed
to
include
mild
bronchial
irritation
of
the
swimmer's
airways
(
Rycroft
and
Penny,
1983).
Mustchin
and
Pickering
(
1979)
found
that
many
competitive
swimmers
experienced
coughing,
soar
throat,
and
chest
tightness.
In
one
incident
three
children
were
diagnosed
with
reversible
airway
obstruction.
Zwick
et
al.
(
1990)
have
reported
that
competitive
swimmers
had
a
higher
prevalence
of
allergies
and
subclinical
sensitization
to
aeroallergens,
altered
cellular
immunity,
and
non­
specific
bronchial
hyper
responsiveness.

Potts
(
1996)
also
reported
the
results
of
a
comprehensive
survey
of
738
competitive
swimmers
conducted
previously
(
Potts,
1994)
which
indicated
that
bronchitis
(
24.9%),
hay
fever
(
16.9%),
asthma
(
13.4%)
and
pneumonia
(
10.2%)
were
experienced
most
frequently
among
swimmers.
Survey
participants
(
73.8%)
reported
smelling
a
strong
chemical
odor
in
the
swimming
pool.
The
symptoms
the
swimmers
associated
with
the
odor
included
coughing
(
40.9%),
breathing
difficulty
(
36.4%),
sore
eyes
(
26.3%),
sneezing
(
25.2%),
sore
throat
(
22.9%),
headaches
(
22%),
chest
congestion
(
21.3%),
chest
tightness
(
21.0%)
wheezing
(
20.9%)
and
nausea
(
11.7%).

Helenius
et
al.
(
1998),
Drobnic
et
al.
(
1995),
Rothery
(
1991),
and
Rycroft
and
Penny
(
1983)
reported
increased
bronchial
responsiveness
in
elite
swimmers
and
also
reported
that
long­
term
and
repeated
exposure
to
chlorine
compounds
in
swimming
pools
during
training
and
competition
may
contribute
to
the
increased
occurrence
of
asthma,
bronchial
hyperresponsiveness
and
airway
inflammation
in
swimmers.

Trichloramine
levels
were
measured
in
the
atmosphere
of
indoor
swimming
pools
and
the
results
indicated
that
life
guards
are
at
risk
of
developing
irritant
eyes,
nasal
and
throat
symptoms
(
WHO,
2000).
A
relationship
between
bronchial
hyperresponsiveness
and
exposure
initially
had
not
been
found,
however,
WHO
(
2000)
did
not
rule
out
the
possibility
that
lifeguards
may
be
at
risk
of
developing
transient
bronchial
hyperresponsiveness.

Small
and
Murray
(
1987)
presented
the
results
of
a
controlled
trial
of
ten
swimmers
which
studied
the
acute
effects
on
nasal
mucosa
as
a
result
of
swimming
in
a
chlorinated
pool.
The
results
are
reported
to
indicate
that
sodium
hypochlorinated
water
in
concentrations
of
three
parts
per
million
does
not
have
any
short­
term
effect
on
nasal
mucosa,
despite
prolonged
immersion.
Morgan
and
Shenoi
(
1989)
reported
that
swimming
in
chlorinated
water
does
not
affect
eustachian
tube
function.
Page
7
of
22
1.5.2
Ocular
Effects
From
the
cited
literature,
it
appears
that
chloramines
in
the
chlorinated
pool
water
may
cause
ocular
effects
manifested
by
symptoms
such
as
red,
watery
eyes.
Chloramine
causes
irritation
of
the
conjunctiva
and
effects
the
mucous
membranes
of
the
eye
causing
eye
irritation
(
conjunctival
chemosis,
hypermia,
corneal
epithelial
erosions,
and
edema)
and
possibly
temporary
vision
problems.
One
study
(
Rylander
et
al.,
1973)
indicated
that
the
difference
in
concentration
of
free
chlorine
and
pH
may
cause
increasing
levels
of
eye
irritation.
Below
is
a
summary
of
the
literature
for
ocular
hazards.

Chloramines
are
known
to
cause
irritation
of
the
conjunctiva
and
effects
on
mucous
membranes
of
the
nasopharynx.
Haag
and
Gieser
(
1983)
reported
the
results
of
their
study
which
found
that
68%
of
subjects
saw
rainbows
and/
or
halos
around
lights
after
swimming
in
a
chlorinated
pool.
A
large
percentage
(
94%)
of
subjects
had
corneal
epithelial
erosions
in
a
punctate
or
a
linear
pattern
demonstrated
by
fluorescein
staining
on
slit­
lamp
examination.
Visual
acuity
was
not
decreased
in
any
of
the
subjects.
Increasing
the
chlorine
concentration
from
0.05
to
0.5
ppm
produced
a
slight
increase
in
eye
irritation.

Chiswell
and
Wildsoet
(
1989)
reported
that
chloramines
may
be
responsible
for
eye
irritation
such
as
conjunctival
chemosis
and
hyperemia,
along
with
corneal
epithelial
erosions
and/
or
edema.
The
symptoms
may
include
blurred
vision,
halo
effects,
photophobia
and
sore
or
burning
eyes.
In
another
study,
Chiswell
and
Wildsoet
(
1986)
reported
that
superficial
punctate
keratitis
may
be
caused
by
exposure
to
chlorinated
swimming
pool
water.
They
noted
that
pool
water
toxicity,
pH
and
a
variety
of
chlorine
species
(
e.
g.,
hypochlorite,
chloramines)
may
impact
such
reactions.
They
also
noted
that
a
gaseous
form
of
chloramines
collect
above
pool
water
in
sufficient
concentration
to
cause
eye
irritation.
Verhulst
and
Crotty
(
1971)
also
noted
eye
irritation
from
swimming
in
disinfected
pools
as
a
frequent
occurrence.

Rylander
et
al.
(
1973)
found
slight
eye
irritation
in
certain
subjects
when
water
was
applied
containing
1.0
mg
Cl2/
L.
At
2.0
mg
CL2/
L,
the
irritation
was
found
to
be
greater.
Variations
of
pH
between
seven
and
nine
showed
no
significant
influence.
Different
individuals
showed
different
sensitivities
to
irritations
of
the
eye.
Eye
irritation
was
decreased
when
the
time
spent
in
the
pool
was
less
than
30
minutes.

Hery
et
al.
(
1995)
reported
that
chloramines,
and
specifically
nitrogen
trichloride,
are
the
likely
irritants
(
ie.
eye,
lung
and
throat)
and
lachrymators
in
the
atmosphere
of
indoor
swimming
pools.
Good
correlations
were
found
for
chloramine
concentrations
and
irritation
levels.
The
first
complaints
from
participants
in
the
study
were
registered
at
0.5
mg/
m­
3
of
nitrogen
trichloride.
At
0.7
mg/
m­
3
of
nitrogen
trichloride,
all
participants
complained
of
irritation.

Momas
et
al.
(
1993)
maintain
the
health
effects
for
subjects
attending
a
well­
kept
school
swimming
pool,
maintained
according
to
French
public
health
regulations.
The
authors
found
that
bathers
experienced
fatigue
and
eye
irritation
significantly
more
often
(
p
<
0.001)
than
non­
bathers.
The
eyes
were
red
(
38%
of
bathers)
and/
or
watery
(
16%)
after
swimming,
but
this
resolved
Page
8
of
22
spontaneously
within
24
hours.
Bathing
behavior
(
bath
duration,
head
immersion,
wearing
swimming
goggles)
did
not
affect
these
incident
rates
noticeably.
There
were
no
differences
between
bathers
and
non­
bathers
with
regard
to
other
symptoms,
especially
otolaryngological
ones.

1.5.3
Dermal
Effects
Dermal
effects
indicated
in
the
cited
literature
include
contact
urticartia,
a
short
burning
sensation
in
the
tip
of
the
penis,
and
generalized
rash.
One
author
(
Fisher,
1987)
indicated
however
that
irritant
dermatitis
is
uncommon
and
allergic
reactions
are
rare.
Below
is
a
summary
of
the
literature
for
dermal
hazards.

Fisher
(
1987)
noted
that
irritant
dermatitis
is
uncommon
and
allergic
reactions
are
extremely
rare
from
chlorine.
He
reports
that
some
men
experience
a
burning
sensation
in
the
tip
of
their
penis
for
a
short
time
after
swimming
in
chlorinated
pools.
During
urination,
this
sensation
is
reported
to
be
augmented.
Dermatitis
does
not
accompany
these
symptoms.
One
patient
is
reported
to
have
acquired
contact
urticaria
whenever
he
swam
in
a
pool
disinfected
with
sodium
hypochlorite.
The
authors
concluded
that
swimming
pool
water
may
result
in
contact
urticaria.

Neering
(
1977)
reported
that
a
healthy
34­
year­
old
adult
experienced
intermittent
urticaria
after
swimming
in
a
pool
disinfected
with
NaOCl.
This
reaction
was
further
confirmed
with
patch
tests.
The
authors
recommended
that
contact
urticaria
from
chlorinated
swimming
pool
water
should
be
borne
in
mind
in
patients
suspected
of
aquagenic
urticaria.

Ng
and
Goh
(
1989)
reported
that
swimming
in
chlorinated
water
caused
a
generalized
rash
which
lasted
for
one
week
in
a
47­
year­
old
man.
The
individual
was
also
found
to
have
allergic
contact
dermatitis
from
flavine
and
from
sodium
hypochlorite.

Leung
(
1985)
reported
that
a
3­
year­
old
girl
developed
erythema
multiforme
following
swimming
in
an
outdoor
chlorinated
pool.
The
erythematous
rash
occurred
all
over
her
body,
face,
and
extremities.
Generalized
erythematous
maculopapular
eruption
was
noted
after
five
days.
The
rash
subsided
within
two
weeks.
The
author
cited
other
works
that
report
chlorine
may
cause
corneal
epithelial
erosions
and
bronchial
irritation.

Sasseville
et
al.
(
1999)
reported
a
case
of
diffuse
dermatitis
in
an
individual
that
swam
in
heavily
chlorinated
public
pools
and
of
hand
dermatitis
upon
exposure
to
sodium
hypochlorite
bleach.

Valsecchi
et
al.
(
1985)
reported
an
incidence
of
a
pool
worker
that
experienced
a
6­
month
period
of
eczema
affecting
his
feet
and
legs
as
a
result
of
using
Tego
(
dodecylic
aminoethyl
glycine
hydrochloride)
(
0.1%
and
1%
in
water)
for
disinfecting
the
pool
and
baths.

1.5.4
Oral
Effects
Page
9
of
22
An
investigation
took
place
of
workers
exposed
for
5
years
to
chlorine
dioxide
in
a
sulfite­
cellulose
plant.
Chlorine
in
small
amounts
was
also
present,
as
was
sulfur
dioxide.
Symptoms
and
signs
of
irritation
of
the
eyes
and
respiratory
tract
leading
to
slight
bronchitis
were
found
in
a
majority
(
7
of
12)
of
the
workers.
Some
workers
showed
irritation
of
GI
tract
but
no
cerebral
effects
(
ACGIH,
2001
Cited
in
HSDB).

Two
adults
ingested
250
mL
of
chlorine
dioxide
in
water
containing
concentration
of
40
mg/
L.
Within
5
min
of
ingestion,
sudden
headache,
nausea,
abdominal
discomfort,
and
light­
headedness
were
observed.
The
reported
effects
disappeared
within
5
min
(
NRC,
1981).

Escartin
et
al.
(
2000)
reported
an
increased
prevalence
of
dental
stains
in
competitive
swimmers.
They
proposed
that
dental
stains
in
swimmers
are
caused
by
the
chemical
used
to
disinfect
the
pool
water.
These
disinfectants
denature
the
saliva
proteins
which
are
deposited
as
a
film
on
the
surface
of
the
tooth.
Escartin
et
al.
(
2000)
also
proposed
that
the
mixture
of
water
with
oral
fluids
produces
inorganic
substances
which
may
be
deposited
together
with
the
denaturized
proteins
on
the
teeth
and
that
more
than
6
hours
of
training
per
week
increased
the
risks
of
dental
stains.

Rose
and
Carey
(
1995)
also
reported
that
prolonged
exposure
to
pool
water
can
cause
stains
to
develop
on
swimmers'
teeth.
ADAHF
scientists
have
labeled
brown
dental
deposits
that
form
on
the
teeth
of
swimmers
as
"
swimmers'
calculus."
Dental
calculus
is
made
up
of
organic
and
inorganic
components.
The
relatively
small
organic
components
of
calculus
(
15
to
25%)
consist
of
plaque
bacteria
and
bacterial
remnants,
as
well
as
components
from
saliva
and
gingival
fluid.
The
larger
inorganic
components
consist
of
calcium
phosphates,
magnesium
fluoride
and
carbonate.
Dental
calculus
rarely
forms
in
children
younger
than
nine
years
of
age.
The
authors
reported
that
in
a
survey,
approximately
58%
of
competitive
swimmers
between
6
and
18
years
had
swimmers
calculus.

Centerwall
et
al.
(
1986)
reported
that
erosion
of
dental
enamel
among
competitive
swimmers
at
a
gas­
chlorinated
swimming
pool
is
due
to
prolonged
exposure
to
pool
water
at
low
pH
(
i.
e.
acidic).
In
another
study,
Prindle
(
1983)
reported
that
a
pool
with
a
pH
of
2.7
(
i.
e.
an
acid
concentration
approximately
100,000
times
that
recommended
for
swimming
pools)
resulted
in
general
enamel
erosion
in
13%
of
the
subjects.
Tooth
enamel
did
not
decalcify
in
acidic
solutions
unless
the
pH
was
below
6.0.
Gabai
et
al.
(
1988)
conducted
a
study
investigating
the
effect
of
swimming
pool
water
pH
levels
on
the
dissolution
of
powdered
human
tooth
enamel
and
tooth
surface
morphology
and
concurred
that
frequent
exposure
to
acidic
swimming
pool
water
may
lead
to
possible
tooth
erosion.

Detweiler
and
Barelli
(
1995)
reported
that
chlorinated
swimming
pool
water
may
be
linked
to
triggering
the
recurrent
herpes
simplex
virus
1
(
HSV­
1).
The
authors
stated
that
the
action
of
the
chemical
or
chemicals
in
the
swimming
pool
water
on
the
oral
mucosa
or
tongue
may
be
responsible
for
the
virus
reactivation.
They
believed
that
chlorine
or
chlorine
in
combination
with
one
or
more
of
the
chemicals
frequently
added
to
swimming
pool
waters
(
e.
g.
bicarbonate
of
soda,
calcium
chloride,
soda
ash,
muratic
acid,
alum,
antioxidants
and
antifungal
products)
may
be
the
triggering
element
for
recurrent
oral
lingual
herpes
simplex
virus
1.
In
a
more
recent
report,
Detweiler
and
Barelli
(
1997)
reconfirmed
that
strenuous
forty­
five
to
fifty­
minute
swimming
sessions
in
Page
10
of
22
chlorinated
swimming
pools
will
cause
reactivation
of
oral­
lingual
HSV­
1.

1.4.5
Other
Related
Effects
Other
related
effects
of
chlorinated
pool
water
include
inhalation
of
chloroform.
At
high
doses,
chloroform
is
toxic
to
the
liver
and
kidneys
and
may
be
a
chronic
concern
for
sensitive
individuals
(
e.
g.
pregnant
women)
and
people
with
liver
and
kidney
problems.
Chlorine
gas
and
chlorine
dioxide
are
strong
irritants
and
may
be
of
particular
concern
with
accidental
exposure
to
chlorine
gas
leaks
in
chlorination
systems.
At
least
one
author
concluded
that
chlorinated
water
may
have
acted
as
the
oxidant
trigger
for
an
acute
hemolytic
crisis
in
a
7­
year­
old
boy
with
Down's
syndrome
and
G­
6­
PD
deficiency.
Below
is
a
summary
of
the
literature.

Aiking,
et
al.
(
1994)
reported
that
high
doses
of
chloroform
are
toxic
to
the
liver
and
kidneys.
Since
chloroform
and
other
chlorinated
compounds
are
volatile,
high
concentrations
are
found
immediately
above
the
water
surface.
Since
inhalation
is
the
main
route
of
exposure,
particularly
high
exposures
are
experienced
by
those
who
swim
for
a
long
time
under
high
physical
strain.
They
believed
that
people
who
swim
in
chlorinated
swimming
pools
for
many
years
at
a
stretch
may
be
at
risk
and
that
swimming
in
chlorinated
swimming
pools
at
an
early
stage
of
development
may
also
have
undesirable
consequences
later
in
life.

Ong
and
Kearney
(
1994)
reported
that
swimming
in
an
indoor
pool
that
used
ozone
and
very
high
concentrations
of
sodium
hypochlorite
precipitated
a
hemolytic
crisis
in
a
7­
year­
old
boy
with
Down's
syndrome
and
G­
6­
PD
deficiency.
The
authors
concluded
that
the
chlorinated
water
had
acted
as
the
oxidant
trigger
for
the
acute
hemolytic
crisis.

A
study
was
carried
out
in
9
Italian
towns
between
October
1999
and
September
2000
that
aimed
to
evaluate
the
association,
if
any,
between
chlorite
and
chlorate
in
drinking
water
and
both
preterm
delivery
and
babies
that
are
small
for
their
gestational
age
at
term.
While
controlling
for
numerous
possible
confounding
factors,
the
study
showed
that
there
is
an
association
between
babies
that
are
small
for
their
gestational
age
at
term
and
chlorite
in
drinking
water
when
the
chlorite
levels
are
greater
than
200
µ
g/
L
and
there
is
high
exposure
from
both
ingestion
and
inhalation
(
from
daily
showering
and
bathing).
However,
as
the
authors
point
out,
this
association
may
be
due
to
a
different
disinfection
byproduct
produced
by
chlorine
dioxide
or
to
a
not
yet
identified
confounding
factor.
There
was
no
correlation
between
preterm
delivery
and
exposure
to
chlorite
or
chlorate
in
drinking
water
(
Aggazzotti
et
al.
2003).

A
study
was
carried
out
to
investigate
the
possible
association
between
maternal
periconceptional
exposure
to
public
drinking
water
chlorination
byproducts
and
the
incidence
of
congenital
cardiac
defects
in
a
Swedish
county
between
January
1,
1982
and
December
31,
1996.
Information
in
Swedish
health
registers
was
linked
with
information
on
municipal
drinking
water
composition.
Individual
data
on
drinking
water
composition
was
obtained
for
58,669
women.
Among
the
infants
born
to
these
women,
753
had
a
cardiac
defect.
Chlorine
dioxide
use
in
disinfection
was
found
to
be
an
independent
risk
factor
for
cardiac
defect
and
so
was
increasing
trihalomethane
concentrations
(
THM
concentrations
higher
than
10
µ
g/
L
were
statistically
significantly
associated
with
cardiac
Page
11
of
22
defects).
The
study
concluded
that
the
individual
risk
for
cardiac
defect
caused
by
chlorine
dioxide
is
small,
but
because
a
large
population
is
exposed
to
public
drinking
water,
"
the
attributable
risk
for
cardiac
defects
may
not
be
negligible"
(
Cedergren
et
al.,
2002).

An
epidemiologic
study
of
198
persons
exposed
for
12
weeks
to
drinking
water
that
had
been
disinfected
with
chlorine
dioxide
was
conducted
in
a
rural
village.
A
control
group
of
118
nonexposed
persons
was
also
studied.
Chlorite
ions
in
the
water
averaged
5.28
ppm
during
the
study
period.
Based
on
water
consumption
information,
the
mean
chlorite
dose
received
was
10.3
mg/
day
and
the
range
0­
39.4
mg/
day.
Statistical
analysis
of
multiple
hematologic
and
serum
clinical
chemistry
measurements
failed
to
identify
any
significant
adverse
health
effects
related
to
exposure
(
Michael
et
al.,
1981).

A
study
of
the
blood
chemistry
parameters
of
20
renal
dialysis
patients
was
conducted
after
it
was
found
out
that
a
local
water
district
had
introduced
chlorine
dioxide
as
a
disinfectant
for
12
months
without
informing
the
renal
dialysis
clinic.
Renal
dialysis
patients
are
considered
to
be
more
sensitive
to
chemicals
in
tap
water
than
the
general
population
because
not
only
are
they
in
a
compromised
state
of
health,
but
while
the
average
population
consumes
1­
2
liters
of
tap
water
per
day,
about
100­
125
liters
of
tap
water
is
used
during
the
process
of
renal
dialysis.
However,
the
chlorination
products
measured
at
the
clinic
after
it
had
purified
the
water
used
in
the
preparation
of
the
dialysate
consisted
only
of
0.02­
0.08
mg/
L
chlorite.
No
evidence
of
chlorine
dioxide
induced
anemia
was
found
and
no
other
clinically
significant
effects
were
observed
(
Ames
and
Stratton,
1987).

2.0
SUMMARY
AND
CONCLUSION
There
are
incidents
associated
with
chlorine
dioxide
exposure
reported
in
both
the
OPP
Incident
Data
System
and
the
California
Department
of
Pesticide
Regulation
Database
(
1982­
2003).
Among
the
reported
incidents
in
these
databases,
inhalation
is
the
primary
route
of
exposure.
Irritation
is
the
primary
reported
symptom.

When
it
is
in
aqueous
media,
it
is
difficult
to
separate
incidents
associated
with
chlorine
dioxide
from
incidents
associated
with
chlorine,
chlorite
and
hypochlorite
ions.
Therefore,
some
of
the
incidents
associated
with
the
related
chemicals
are
also
discussed.
Inhalation,
dermal,
ocular,
oral,
and
other
health
concerns
are
reported.
Page
12
of
22
Table
1.
Incidents
Associated
with
Chlorine
Dioxide
­
OPP
Incident
Data
System
(
IDS)

Package
Information
Route
of
Exposure
Causality
Incident
Data
Package
ID
Incident
Number
Product
Name
Data
Incident
was
Reported
Dermal
Ocular
Ingestion
Inhalation
Unknown
Eye
Irritation/

Burning
Itching
Vomiting/

Nausea
Nasal
Congestion/

Runny
Nose
Sore
Throat
Headache
Dizziness
Unknown
Likely
Possible
Unlikely
I002913
1
Envirocon
12/
6/
95
x
x
x
I003377
16
Akta
Klor
9/
27/
95
x
x
x
x
x
x
x
I010817
1
Chlorine
Dioxide
10/
19/
00
x
x
x
x
x
x
x
I008802
2
Akta
Klor
25
5/
31/
99
x
x
x
x
Page
13
of
22
Table
2.
Case
Reports
Received
by
the
California
Pesticide
Illness
Surveillance
Program,
1982
 
2003
in
Which
Health
Effects
Were
Definitely,
Probably,
or
Possibly
Attributed
to
Exposure
to
Chlorine
Dioxide
Year
Case
Identified
Case
Number(
a)
Relationship(
b)
Days
Lost
from
Work
/
Days
Hospitalized
(
c)
Ag
/

Non­
Ag
(
d)
Medical
Description
(
e)
Narrative
Description
1990
848
Probable
4
/
0
Non­
Ag
SMELLED
CHLORINE
DEVELOPED
BREATHING
DIFICULTY,
HEADACHE,
COUGH,
DIZZINESS.

DIAGNOSED
BRONCHIAL
IRRITATION.
SAFETY
EQUIPMENT
NOT
REPORTED.
CHLORINE
DIOXIDE
DELIVERY
SYSTEM
DID
NOT
WORK
CORRECTLY
THAT
DAY.

1990
1478
Probable
0
/
0
Non­
Ag
WORKER
APPLYING
MATERIAL
FROM
SPRAY
BOTTLE
GOT
FUMES
IN
EYES
AND
LUNGS
CAUSING
BURNING.
SHE
ALSO
SUFFERED
FROM
COUGHING
AND
SHORTNESS
OF
BREATH.
SHE
WORE
ONLY
RUBBER
GLOVES
FOR
PROTECTION.

NOV
ISSUED
FOR
USE
OF
AN
UNREGISTERED
PRODUCT
AND
FOR
NO
TRAINING
1990
2474
Probable
0
/
0
Non­
Ag
DISINFECTANT
USED
IN
A
MEAT
PACKING
FACILITY
OVER
A
PERIOD
OF
TIME
CAUSED
A
FEMALE
EMPLOYEE
TO
DEVELOP
SOB,
LIGHT
HEADEDNESS
AND
THROAT
IRRITATION
FROM
CONSTANT
EXPOSURE
DUE
TO
INHALATION.

EMPLOYEE
WEARING
PROPER
CLOTHING
AND
RUBBER
GLOVES.
DIAGNOSIS­
CHE
1991
2230
Possible
UN
/
0
Non­
Ag
MODERATE
CONJUNCTIVAL
HYPEREMIA
OF
BOTH
EYES.
WORKER
WAS
SORTING
TOMATOES
ON
A
SORTING
BELT.
WATER
FROM
THE
WATER
BATH
WAS
SPLASHING
ONTO
THE
SORTING
BELT
AND
SOME
SPLASHED
UP
INTO
HER
EYES.
SHE
IMMEDIATELY
FLUSHED
HER
EYES
OUT
AND
PUT
EYE
DROPS
IN
THEM.
SHE
THEN
SOUGHT
MEDICAL
ATTENTION.

1991
2574
Probable
0
/
0
Ag
BRONCHOSPASM.
MECHANICAL
PROBLEMS
CAUSED
BY
A
SORTING
FLUME
BACK­
UP,
ALLOWING
AN
EXCESSIVE
AMOUNT
OF
CHLORINE
DIOXIDE
TO
BE
INJECTED
INTO
THE
SYSTEM.
THREE
WORKERS
WERE
EXPOSED
TO
THE
CHLORINE
FUMES
AND
SOUGHT
MEDICAL
ATTENTION.
Page
14
of
22
1991
2575
Probable
0
/
0
Ag
PNEUMONITIS,

VOMITING,
COUGHING.
MECHANICAL
PROBLEMS
CAUSED
BY
A
SORTING
FLUME
BACK­
UP,
ALLOWING
AN
EXCESSIVE
AMOUNT
OF
CHLORINE
DIOXIDE
TO
BE
INJECTED
INTO
THE
SYSTEM.
THREE
WORKERS
WERE
EXPOSED
TO
THE
CHLORINE
FUMES
AND
SOUGHT
MEDICAL
ATTENTION.
Page
15
of
22
Table
2.
Case
Reports
Received
by
the
California
Pesticide
Illness
Surveillance
Program,
1982
 
2003
in
Which
Health
Effects
Were
Definitely,
Probably,
or
Possibly
Attributed
to
Exposure
to
Chlorine
Dioxide
(
Continued)

Year
Case
Identified
Case
Number
(
a)
Relationship
(
b)
Days
Lost
from
Work
/
Days
Hospitalized
(
c)
Ag
/
Non­
Ag
(
d)
Medical
Description
(
e)
Narrative
Description
1994
847
Possible
0
/
0
Ag
RESPIRATORY
IRRITATION,

COUGHING,

DIZZINESS,
SLIGHT
BACK
AND
CHEST
DISCOMFORT.
FOUR
WORKERS
NOTICED
AN
ODOR
WHILE
INSPECTING
ONIONS
ON
A
CONVEYOR
BELT
AND
BECAME
ILL.

THE
ONIONS
ARE
PRESSURE
WASHED
WITH
CHLORINATED
WATER
UNDER
A
SHIELDED
HOOD.
SEE
ALSO
94­
848
TO
850.

1994
848
Possible
0
/
0
Ag
THROAT
IRRITATION,

DRY
COUGH.
SEE
94­
847.

1994
849
Possible
0
/
0
Ag
COUGHING,
THROAT
IRRITATION,
NAUSEA.
SEE
94­
847.

1994
850
Possible
0
/
0
Ag
COUGHING,
MILD
RHINORRHEA,

NAUSEA.
SEE
94­
847.

1994
930
Possible
0
/
0
Non­
Ag
COUGHING,
THROAT
IRRITATION,
SHORTNESS
OF
BREATH,
WATERING
EYES.
WORKER
SUFFERED
RESPIRATORY
AND
EYE
PROBLEMS
WHILE
INSPECTING
ONIONS
ON
A
CONVEYOR
BELT.
THE
ONIONS
HAD
BEEN
WASHED
IN
A
CHLORINATED
SOLUTION.
SHE
SOUGHT
MEDICAL
ATTENTION
FOUR
DAYS
LATER.

1994
1030
Possible
0
/
0
Non­
Ag
BURNING
EYES,

COUGHING,
NAUSEA,

HEADACHE.
WORKER
WAS
INSPECTING
ONIONS
AND
WAS
EXPOSED
TO
FUMES
FROM
THE
CHLORINE
WASH.
Page
16
of
22
Table
2.
Case
Reports
Received
by
the
California
Pesticide
Illness
Surveillance
Program,
1982
 
2003
in
Which
Health
Effects
Were
Definitely,
Probably,
or
Possibly
Attributed
to
Exposure
to
Chlorine
Dioxide
(
Continued)

Year
Case
Identified
Case
Number
(
a)
Relationship
(
b)
Days
Lost
from
Work
/
Days
Hospitalized
(
c)
Ag
/
Non­
Ag
(
d)
Medical
Description
(
e)
Narrative
Description
1997
237
Probable
UN
/
0
Ag
CHEST
TIGHTNESS.
A
CHLORINE
DIOXIDE
PIPE
EXPLODED
IN
A
CARROT
PACKING
PLANT.
FIFTEEN
FEET
AWAY,
A
WORKER
CLEANING
A
TANK
SMELLED
CHLORINE
AND
JUMPED
FROM
THE
TANK.
THE
JUMP
INJURED
HIS
LEG
AND
BROKE
HIS
FOOT.
HE
ALSO
COMPLAINED
OF
TRANSITORY
CHEST
TIGHTNESS.

1997
1040
Possible
4
/
0
Non­
Ag
RESPIRATORY
IRRITATION,

COUGHING,
EYE
IRRITATION.
CHLORINE
DIOXIDE
WAS
BEING
ADDED
TO
WATER
IN
A
TANK
WHILE
AN
EMPLOYEE
WAS
OPERATING
A
CANNING
MACHINE.
SHE
WAS
EXPOSED
TO
THE
FUMES
AND
DEVELOPED
SYMPTOMS.
SHE
SOUGHT
MEDICAL
ATTENTION
4
DAYS
LATER.

1997
1096
Probable
0
/
0
Non­
Ag
SORE
THROAT,

STOMACH
ACHE,
CONSTIPATION,

PAIN
AND
TIGHTNESS
IN
THE
CHEST,

COUGHING.
CHLORINE
DIOXIDE
WAS
BEING
USED
AS
A
SANITIZING
RINSE
ON
PACKING
PLANT
EQUIPMENT,

WHEN
A
POWER
LOSS
OCCURRED.
THIS
SHUT
OFF
A
VENTING
FAN
SO
THE
CHLORINE
DIOXIDE
VENTED
INTO
A
ROOM
OF
WORKERS.
SEE
97­
1103
AND
1104.

1997
1103
Probable
0
/
0
Non­
Ag
WHEEZING,
COUGHING.
SEE
97­
1096.
THREE
WORKERS
DEVELOPED
SYMPTOMS
AND
SOUGHT
MEDICAL
ATTENTION.

1997
1104
Probable
0
/
0
Non­
Ag
SORE
THROAT,

COUGHING,
EYE
IRRITATION,

NAUSEA.
SEE
97­
1096.

2001
354
Possible
0
/
0
Ag
COUGHING,
HEADACHE,

VOMITING.
TWO
PROCESSING
PLANT
EMPLOYEES
DEVELOPED
SYMPTOMS
WHILE
WORKING
ON
THE
STRAWBERRY
PROCESSING
LINE.
THIS
EMPLOYEE
SORTED
STRAWBERRIES
ON
A
CONVEYOR
BELT.
LAB
REPORTS
SHOWED
THE
WASH
WATER
CHLORINE
LEVELS
A
LITTLE
HIGH
5
TIMES
THAT
DAY.
SEE
2001­
355.
Page
17
of
22
Table
2.
Case
Reports
Received
by
the
California
Pesticide
Illness
Surveillance
Program,
1982
 
2003
in
Which
Health
Effects
Were
Definitely,
Probably,
or
Possibly
Attributed
to
Exposure
to
Chlorine
Dioxide
(
Continued)

Year
Case
Identified
Case
Number
(
a)
Relationship
(
b)
Days
Lost
from
Work
/
Days
Hospitalized
(
c)
Ag
/
Non­
Ag
(
d)
Medical
Description
(
e)
Narrative
Description
2001
355
Probable
0
/
0
Ag
COUGHING,
CHEST
PAIN,
SORE
THROAT,
HEADACHE.
SEE
2001­
354.
THIS
EMPLOYEE
DUMPED
CRATES
OF
STRAWBERRIES
INTO
THE
CHLORINATED
WASH
TANK
WATER.

2001
937
Possible
UN
/
0
Non­
Ag
SORE
THROAT,
DRY
AND
IRRITATED
NOSE,
COUGHING,

NAUSEA,
LIGHTHEADEDNESS.
A
MAILROOM
CLERK
DEVELOPED
SYMPTOMS
WHEN
A
TECHNICIAN
DISINFECTED
THE
VENTILATION
SYSTEM.
THE
NEXT
DAY,
SHE
REPORTED
HER
SYMPTOMS
TO
THE
SUPERVISOR
WHO
SENT
HER
FOR
A
MEDICAL
EVALUATION.
SHE
NO
LONGER
WORKS
AT
THE
COMPANY
AND
COULD
NOT
BE
LOCATED.

Note:

(
a)
Case
numbers
are
assigned
sequentially
from
1
each
year.

(
b)
A
relationship
of
`
Definite'
indicates
that
both
physical
and
medical
evidence
document
exposure
and
consequent
health
effects.

`
Probable'
relationship
indicates
that
limited
or
circumstantial
evidence
supports
a
relationship
to
pesticide
exposure.

`
Possible'
relationship
indicates
that
evidence
neither
supports
nor
contradicts
a
relationship
.

(
c)
Counts
full
days
only.
An
entry
of
`
Indefinite'
indicates
the
event
occurred,
but
the
time
period
is
not
known.
UN
=
unkown.

(
d)
The
abbreviation
'
Ag'
stands
for
'
Agricultural'
and
indicates
pesticide
use
intended
to
contribute
to
production
of
an
agricultural
commodity.
All
other
situations
are
designated
'
Non­
Ag'.

(
e)
The
medical
description
field
was
added
to
the
database
in
1991.
Page
18
of
22
Table
3:
Cases
Due
to
Chlorine
Dioxide
Exposure
in
California
Reported
by
Type
of
Illness
and
Year,
1982­
2003
Illness
Type
Year
Systemic
Mouth
Eye
Skin
Respiratory
Combinationa
Total
1990
­
­
­
­
3
­
3
1991
1
­
1
­
2
1
3
1994
2
­
­
­
4
2
4
1997
­
­
­
­
4
­
4
2001
1
1
2
2
­
1
5
Total
4
1
3
2
13
4
19
a
Category
includes
combined
effects
to
eye,
skin,
mouth
and
respiratory
systems.

Table
4:
Number
of
Persons
Disabled
(
taking
time
off
work)
or
Hospitalized
for
Indicated
Number
of
Days
after
Chlorine
Dioxide
Exposure
in
California,
1982­
2003.

Number
of
Persons
Disabled
Number
of
Persons
Hospitalized
One
day
­
­

Two
days
­
­

3­
5
days
2
­

Unknown
3
­
Page
19
of
22
3.0
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