Document ID: EPA-HQ-OPP-2003-0248-0009
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2003-11-26T05:00Z

Page
1
of
28
CREOSOTE:
EPIDEMIOLOGY
AND
INCIDENTS
Creosote
is
a
complex
chemical
mixture
of
organic
compounds.
Most
compounds
in
creosote
are
polyaromatic
hydrocarbons
(
PAHs).
An
extensive
body
of
literature
on
creosote
and
commonly
associated
substances
has
been
published.
The
purpose
of
this
chapter
is
to
review
the
evidence
of
health
effects
in
humans
resulting
from
exposure
to
creosote.
In
particular,
the
acute
and
chronic
toxicity,
teratogenic/
reproductive
effects,
and
carcinogenicity
are
discussed.
Two
approaches
are
used
in
this
section:

°
The
potential
acute
health
effects
of
creosote
in
humans,
reported
as
incident
reports
from
different
sources,
are
summarized.

°
A
literature
search
of
chronic
health
effects
associated
with
creosote
exposure,
including
results
of
epidemiological
studies,
are
summarized.

4.1
INCIDENT
REPORT
DATA
ASSOCIATED
WITH
HEALTH
EFFECTS
OF
CREOSOTE
EXPOSURE
There
are
many
incident
reports
of
health
effects
associated
with
acute
creosote
exposure.
The
following
databases
have
been
consulted
for
the
poisoning
incident
data
on
the
active
ingredient
creosote
(
PC
Code:
025002):

1.
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,
sometimes
with
enough
cases
and/
or
enough
documentation
risk
mitigation
measures
may
be
suggested.

2.
Poison
Control
Centers
­
as
the
result
of
a
data
purchase
by
EPA,
OPP
received
Poison
Control
Center
data
covering
the
years
1993
through
1996
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.
Page
2
of
28
3.
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.

4.
National
Pesticide
Telecommunications
Network
(
NPTN)
­
NPTN
is
a
toll­
free
information
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.

5.
Published
Incident
Reports
­
Some
incident
reports
associated
with
creosote
related
human
health
hazard
are
published
in
the
scientific
literature.

4.1.1
OPP's
Incident
Data
System
(
IDS)

Please
note
that
the
following
cases
from
the
IDS
do
not
have
documentation
confirming
exposure
or
health
effects.
Registrants
are
not
required
to
report
incidents
involving
exposure
to
previously
treated
wood,
only
direct
exposure
to
creosote
itself.
Therefore,
it
is
possible
that
serious
adverse
effects
involving
exposures
to
treated
wood
have
been
missed
by
this
review.
Legal
claims
of
severe
damage
to
eyes
and
skin
including
infections
requiring
amputation
have
been
reported
but
only
in
a
cursory
way
and
without
enough
documentation
to
be
included
in
this
review.

Incident#
2796­
100
An
incident
was
investigated
in
the
United
Kingdom
in
1994
or
1995
(
date
of
incident
unknown)
involving
creosote.
After
a
landlord
treated
a
residence
with
creosote
the
male
tenant
complained
of
headache,
stomach
ache,
and
respiratory
irritation.
No
further
information
is
available
on
the
disposition
of
this
case.

Incident
#
2796­
119
An
incident
was
investigated
in
the
United
Kingdom
in
1994.
After
creosoting
work
was
done
on
the
flat
below
theirs,
a
male
and
female
reported
tearing,
burning
throat,
nausea,
and
vomiting.
No
further
information
is
available
on
the
disposition
of
this
case.

Incident
#
8760­
1
In
1997
a
38
year
old
railroad
worker
alleged
inhalation
and
dermal
exposure
to
creosote.
The
timing
and
duration
of
exposure
are
not
reported.
A
legal
claim
has
been
filed
alleging
nodular
malignant
melanoma.
No
further
information
is
available
on
the
disposition
of
this
case.
Page
3
of
28
Incident
#
8760­
3
A
worker
at
a
creosote
plant
was
exposed
in
1994
while
testing
boring
treated
wood.
He
reportedly
developed
skin
rash
on
wrists
and
forearms
and
visited
a
dermatologist.

4.1.2
Poison
Control
Center
No
data
were
reported
in
the
Poison
Control
Center
database
covering
the
years
1993
through
1996.

4.1.3
California
Data
­
1982
through
1996
Detailed
descriptions
of
124
cases
submitted
to
the
California
Pesticide
Illness
Surveillance
Program
(
1982­
1996)
were
reviewed.
In
114
of
these
cases,
creosote
was
used
alone
and
was
judged
to
be
responsible
for
the
health
effects.
Only
cases
with
a
definite,
probable
or
possible
relationship
were
reviewed.
Creosote
ranked
88th
as
a
cause
of
systemic
poisoning
in
California
(
1982­
1994).
Table
4­
1
presents
the
number
of
cases
due
to
creosote
exposure
reported
by
year.
Table
4­
2
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.
Page
4
of
28
Table
4­
1:
Cases
Due
to
Creosote
Exposure
in
California
Reported
by
Type
of
Illness
and
Year,
1982­
1996
Year
Number
of
Cases
Handling
Creosote
Exposed
to
Treated
Wood
Unknown
Total
1982
10
4
5
19
1983
3
3
­
6
1984
14
3
­
17
1985
15
2
2
19
1986
3
1
­
4
1987
5
5
­
10
1988
3
5
­
8
1989
5
2
1
8
1990
2
3
1
6
1991
­
6
­
6
1992
1
4
­
5
1993
­
2
­
2
1994
1
­
­
1
1995
­
2
­
2
1996
­
1
­
1
Total
62
43
9
114
Page
5
of
28
Table
4­
2:
Number
of
Persons
Disabled
(
taking
time
off
work)
or
Hospitalized
for
Indicated
Number
of
Days
After
Creosote
Exposure
in
California,
1982­
1996.

Number
of
Persons
Disabled
Number
of
Persons
Hospitalized
One
day
9
­

Two
days
12
1
3­
5
days
7
­

6­
10
days
2
­

more
than
10
days
­
­

Unknown
6
­

Most
of
the
cases
that
could
definitely
be
attributed
to
creosote
(
80%
of
the
50
cases
categorized
as
definite)
involved
workers
who
handled
creosote
directly
but
did
not
have
proper
protection
for
eyes
or
skin.
A
significant
number
of
cases
have
resulted
when
workers
have
been
exposed
to
treated
wood,
usually
by
handling
or
sawing
the
wood.
Most
of
these
cases
experienced
chemical
burns
to
the
skin
or
eyes.
The
number
of
cases
due
to
handling
creosote
versus
the
number
due
to
handling
treated
wood
are
presented
in
Table
4­
3
below.

Table
4­
3:
Illnesses
by
Activity
Categories
for
Creosote
Exposure
in
California,
1982­
1996
Activity
Category
Number
of
Cases
Handling
Creosote
Exposed
to
Treated
Wood
Unknown
Total
Applicator
62
43
9
114
4.1.4
National
Pesticide
Telecommunications
Network
(
NPTN)

On
the
list
of
the
top
200
chemicals
for
which
NPTN
received
calls
from
1984­
1991
inclusively,
creosote
was
ranked
118th
with
26
incidents
in
humans
reported
and
no
incidents
in
animals.
Page
6
of
28
4.1.5
Incident
Reports
Associated
with
Acute
Toxic
Effects
of
Creosote
Published
in
Scientific
Literature.

Dean
et
al.
(
1992)
reported
on
a
white
ten
week
old
female,
who
weighed
6
kilograms,
and
experienced
cyanosis,
irritability,
metabolic
acidosis,
and
a
lethal
methehemoglobin
level
of
71.4%.
She
was
taken
to
the
hospital
and
remained
for
three
days.
Three
days
earlier,
the
child's
father
replaced
an
aluminum
stove
pipe
leading
from
the
wood­
burning
stove
to
the
chimney
and
installed
a
straight
section
of
the
stove
pipe.
Green
slab
pine
wood
was
continuously
burning
in
the
stove.
Pine
tar
fumes
emitted
from
the
stove
were
the
suspected
source
of
creosote
oils.
The
girl's
cradle
was
approximately
five
feet
from
the
stove.

Bowman
et
al.
(
1984)
reported
on
a
seventy
year
old
man
who
was
found
unconscious
with
a
cup
of
creosote
beside
him.
On
admission
to
the
hospital,
the
man's
respiratory
effort
was
weak
and
on
auscultation,
widespread
crackles
were
heard.
His
face
and
clothes
were
stained
with
vomit
and
creosote.
He
was
immediately
administered
endotracheal
intubation
and
artificial
ventilation.
He
experienced
anuria
and
died.
After
his
death,
a
liter
of
mostly
creosote
fluid
was
found
in
his
stomach.

Thompson
et
al.
(
1994)
reported
that
during
1989
to
1991,
250
children
(
124
boys
and
126
girls)
under
10
years
old
out
of
6,
478
cases
were
taken
to
accident
and
emergency
departments
in
the
United
Kingdom
for
suspected
pesticide
poisoning.
Seven
percent
of
these
cases
were
due
to
creosote.

The
following
excerpts
were
taken
directly
for
the
Hazardous
Substances
Data
Bank
(
HSDB).
HSDB
is
a
toxicology
data
file
on
the
National
Library
of
Medicine's
Toxicology
Data
Network
(
TOXNET).
Data
are
derived
from
"
a
core
set
of
books,
government
documents,
technical
reports
and
selected
primary
journal
literature.
HSDB
is
peer­
reviewed
by
the
Scientific
Review
Panel
(
SRP),
a
committee
of
experts
in
the
major
subject
areas
within
the
bank's
scope."

Death
from
large
doses
of
creosote
appears
to
be
due
largely
to
cardiovascular
collapse.
Fatalities
have
occurred
14
to
36
hr
after
the
ingestion
of
about
7
g
by
adults
or
1
to
2
g
by
children.
The
symptoms
of
systemic
illness
included
salivation,
vomiting,
respiratory
difficulties,
thready
pulse,
vertigo,
headache,
loss
of
pupillary
reflexes,
hypothermia,
cyanosis,
and
mild
convulsions.
The
repeated
absorption
of
therapeutic
doses
from
the
gastroenteric
tract
may
induce
signs
of
chronic
intoxication,
characterized
by
disturbances
of
vision
and
digestion
(
incr
peristalsis
&
excretion
of
bloody
feces).
In
isolated
cases
of
"
self­
medication,"
hypertension
&
also
general
cardiovascular
collapse
have
been
described.
[
Clayton,
G.
D.
and
F.
E.
Clayton
(
eds.).
Patty's
Industrial
Hygiene
and
Toxicology:
Volume
2A,
2B,
2C:
Toxicology.
3rd
ed.
New
York:
John
Wiley
Sons,
1981­
1982.
2603]
Page
7
of
28
Contact
of
creosote
with
the
skin
or
condensation
of
vapors
of
creosote
on
the
skin
or
mucous
membranes
may
induce
an
intense
burning
and
itching
with
local
erythema,
grayish
yellow
to
bronze
pigmentation,
papular
&
vesicular
eruptions,
and
gangrene
and
in
isolated
instances
cancer.
...
Heinz
bodies
have
been
noted
in
the
blood
of
a
patient
one
yr
after
his
exposure
to
creosote.
...
Similar
observations
following
percutaneous
absorption
of
this
preparation.
Eye
injuries
can
include
keratitis,
conjunctivitis,
and
abrasion
of
the
cornea.
...
Permanent
corneal
scars
result
in
about
one
third
of
such
cases.
Photosensitization
has
been
reported
...
and
severe
systemic
illness.
[
Clayton,
G.
D.
and
F.
E.
Clayton
(
eds.).
Patty's
Industrial
Hygiene
and
Toxicology:
Volume
2A,
2B,
2C:
Toxicology.
3rd
ed.
New
York:
John
Wiley
Sons,
1981­
1982.
2603]

Contact
of
liquid
creosote
with
the
eye
has
caused
painful
protracted
keratoconjunctivitis.
This
has
involved
loss
of
corneal
epithelium,
clouding
of
the
cornea,
miosis,
and
long
lasting
irritability
and
photophobia.
In
one
report
concerned
with
creosote,
two
patients
have
been
described,
one
examined
2
wk
and
the
other
2
months
after
working
with
this
material,
both
complaining
of
haziness
of
vision,
which
was
found
to
be
associated
with
numerous
gray
spots
of
varied
size
in
the
corneas,
plus
a
superficial
keratitis.
[
Grant,
W.
M.
Toxicology
of
the
Eye.
3rd
ed.
Springfield,
IL:
Charles
C.
Thomas
Publisher,
1986.
283]

Injuries
to
the
skin
or
eyes
have
occurred
mainly
among
men
engaged
in
dipping
or
in
"
pickling"
and
handling
"
sleepers,"
mine
timbers,
and
woods
for
floors
and
other
purposes.
...
Calls
attention
to
burns
induced
by
fine
particles
of
sawdust
from
creosote­
treated
lumber.
...
The
burns
were
reduced
to
a
minimum
on
rainy
days,
probably
because
of
the
decreased
dispersion
of
both
the
wood
particles
and
creosote.
[
Clayton,
G.
D.
and
F.
E.
Clayton
(
eds.).
Patty's
Industrial
Hygiene
and
Toxicology:
Volume
2A,
2B,
2C:
Toxicology.
3rd
ed.
New
York:
John
Wiley
Sons,
1981­
1982.
2601]

Epitheliomas
can
result
from
prolonged
exposure
to
creosote.
[
Kirk­
Othmer
Encyclopedia
of
Chemical
Technology.
3rd
ed.,
Volumes
1­
26.
New
York,
NY:
John
Wiley
and
Sons,
1978­
1984.,
p.
V22
592
(
1983)]

Vapor
causes
moderate
irritation
of
nose
and
throat.
Liquid
may
cause
...
reddening
and
itching
of
skin.
[
U.
S.
Coast
Guard,
Department
of
Transportation.
CHRIS
­
Hazardous
Chemical
Data.
Volume
II.
Washington,
D.
C.:
U.
S.
Government
Printing
Office,
1984­
5.]

Old
creosote
treated
lumber
...
retains
a
considerable
portion
of
the
oil
for
periods
up
to
25
or
30
years.
[
Clayton,
G.
D.
and
F.
E.
Clayton
(
eds.).
Patty's
Industrial
Hygiene
and
Toxicology:
Volume
2A,
2B,
2C:
Toxicology.
3rd
ed.
New
York:
John
Wiley
Sons,
1981­
1982.
2604]
Page
8
of
28
4.2
EPIDEMIOLOGIC
STUDIES
ASSOCIATED
WITH
HEALTH
EFFECTS
OF
CREOSOTE
IN
HUMANS
To
summarize
the
epidemiologic
studies
associated
with
creosote
exposure,
considerable
attention
was
given
to
presenting
the
information
collected
during
the
review
in
as
logical
a
format
as
possible.
Reviewed
papers
are
primarily
organized
according
to
the
type
of
epidemiologic
method
followed,
i.
e.,
case
series
involving
chronic
effects,
cross­
sectional,
casecontrol
and
cohort
studies.

1.
Case
Series
Involving
Chronic
Effects
In
addition
to
the
acute
incidence
report
summarized
in
Section
4.1,
some
chronic
health
effects
are
also
reported
after
exposure
to
creosote
and
related
compounds.
Because
of
the
long
latency
period
after
exposure,
the
cause­
effect
relationship
may
not
be
apparent.
These
reports
also
are
summarized
in
this
document.

2.
Cross­
sectional
Study
This
kind
of
study
usually
is
done
by
conducting
a
survey
on
a
group
of
people
or
a
community,
perhaps
stratified
by
age,
sex,
ethnicity,
working
environment
etc.,
but
at
one
point
in
time
or
over
a
short
time
interval.
Although
a
snapshot,
horizontal
surveys
of
prevalence
and
intensity
within
different
age
classes
of
a
community
can
nevertheless
provide
valuable
information
on
the
rate
at
which
individuals
acquire
exposure
to
a
source
of
risk
through
time,
provided
that
the
exposed
population
and
the
source
of
the
risks
have
remained
approximately
stable
for
a
period
of
time.
With
statistical
approaches,
potential
association
of
the
risk
factors
(
exposure)
and
disease
is
suggested.

3.
Cohort
Study
Cohorts
studies
evaluate
individuals
selected
on
the
basis
of
their
exposure
to
the
agent
under
study
and
monitored
for
development
of
disease.
Prospective
studies
monitor
individuals
who
initially
are
disease­
free
to
determine
if
they
develop
the
disease
over
time.

4.
Case­
Control
Study
In
case­
control
studies,
subjects
are
selected
on
the
basis
of
disease
status:
disease
cases
and
matched­
cases
of
disease­
free
individuals.
The
exposure
histories
of
the
two
groups
are
compared
to
determine
key
consistent
features.

Within
each
category
of
epidemiologic
study,
the
information
in
this
document
includes
(
1)
population
investigated,
(
2)
what
health
effects
and
other
effects
were
found,
and
(
3)
what
level
of
confidence
should
be
assigned
to
the
study
results.
Table
4­
4,
attached
at
the
end
of
this
section,
summarizes
the
results
of
the
studies
reviewed
for
this
document.
Page
9
of
28
4.2.1
Case
Series
Involving
Chronic
Effects
Associated
with
Health
Effects
of
Creosote
in
Humans
4.2.1.1
Garrett
(
1975)

In
a
letter­
to­
the­
editor,
Garrett
reported
two
patients
diagnosed
within
eighteen
months
with
multi­
focal
transitional
cell
carcinoma
of
the
bladder
with
muscle
invasion.
Both
men
were
determined
to
have
had
chronic
exposure
to
cresol
and
creosote,
but
no
details
of
the
exposures
were
provided.

Reports
of
this
kind
may
be
useful
when
combined
with
other
reports
and
studies.
Considered
alone,
no
conclusion
regarding
association
of
exposure
to
creosote
with
development
of
bladder
cancer
can
be
made.

4.2.2
Cross­
Sectional
Studies
Associated
with
Health
Effects
of
Creosote
in
Humans
4.2.2.1
Koppers
(
1979a)
The
Koppers
Company
sponsored
a
cross­
sectional
study
of
workers
at
four
wood
preservative
plants
in
Pennsylvania,
South
Carolina,
West
Virginia,
and
Kentucky
where
creosote
and
creosote/
coal
tar
were
the
predominant
treatments.
The
study
was
specifically
aimed
at
identifying
any
health
problems
known
to
be
related
to
exposure
to
these
major
process
materials.
An
array
of
medical
examinations
were
performed
on
257
participants
(
73%
of
351
total
workers).
The
ratios
of
men
to
women
participants
were
similar
among
all
four
plants.
However,
the
ratios
of
black
to
white
workers
differed
significantly
among
the
plants,
therefore
the
ratios
of
black
to
white
participants
differed
also.
The
battery
of
examinations
included
a
medical
questionnaire,
chemical
exposure
questionnaire,
chest
x­
ray,
pulmonary
function
test,
clinical
chemistry
analysis,
hematology
analysis,
urinalysis,
sputum
cytology
exam,
and
urine
cytology
exam.

No
exposure
parameter
was
evaluated
in
the
health
assessment
other
than
length
of
service.
With
the
exception
of
a
greater
than
expected
number
of
pustular
eruptions
of
the
skin,
all
other
tests
revealed
only
infrequent
and
borderline
abnormal
findings.
There
was
no
evidence
of
cancer
at
any
site
associated
with
work
at
these
plants.

Due
to
the
broad
nature
and
limited
depth
of
this
study,
only
gross
negative
health
effects
could
be
observed.
Since
no
exposure
assessment
for
creosote
was
performed,
no
association
between
observed
health
conditions
and
creosote
exposure
was
possible.
Within
these
limitations,
no
evidence
of
detrimental
health
effects
from
working
with
creosote
was
seen.
Page
10
of
28
4.2.2.2
Koppers
(
1979b,
c
and
1980a,
b,
c)

Cross­
sectional
studies
were
conducted
at
five
coal
tar
processing
plants
to
assess
the
health
status
of
the
work
forces
and
thereby
identify
possible
adverse
health
problems
associated
with
exposure
to
coal
tar
and
its
derivatives.
The
studies
were
conducted
by
contracted
researchers
as
part
of
a
continuing
health
and
safety
program
sponsored
by
the
parent
organization.
The
five
plants
studied
were
located
in
California,
West
Virginia,
Alabama,
Ohio,
and
Illinois;
all
five
provided
potential
exposure
to
many
industrial
products,
including
creosote,
resulting
from
distillation
of
coal
tar.
From
a
toxicological
evaluation
of
coal
tar
products,
an
appropriate
medical
examination
protocol
was
designed
to
measure
a
number
of
health
parameters
that
should
reveal
toxic
effects
from
the
target
coal
tar
products.
Included
among
the
procedures
were
collection
of
medical
and
work
history,
chest
x­
ray,
pulmonary
function
test,
clinical
chemistry
analysis,
blood
and
urological
analysis,
and
sputum
cytology
examination.

The
study
populations
included
men
and
women,
white
and
black,
but
participation
was
voluntary
resulting
in
an
overall
participation
rate
of
42%.
Length
of
employment
ranged
between
less
than
one
year
to
50
years,
but
a
majority
of
the
workers
who
participated
in
the
study
worked
10
years
or
less.
No
assessment
of
personal
exposure
to
specific
substances
was
performed.
The
sole
exposure
parameter,
which
was
collected
through
the
work
history
questionnaire,
was
the
number
of
years
of
potential
exposure
to
coal
tar
and
its
derivatives.

Among
the
results
from
the
broad
medical
examination,
a
number
of
excesses
and
atypical
findings
were
observed,
although
few
could
be
directly
associated
with
working
at
the
coal
tar
plants.
Restrictive
respiratory
deficits
were
found
in
the
populations
at
all
of
the
study
sites
and
considerable
excesses
were
seen
at
three
sites.
A
few
individuals
at
four
of
the
five
plants
also
were
observed
with
obstructive
respiratory
deficits.
Increases
in
gamma
glutamyl
transpeptidase
(
GGTP)
and
lactic
dehydrogenase
(
LDH)
levels
were
found
in
a
few
individuals
at
two
plants.
Results
from
hematological
examinations
showed
atypical
cells
or
abnormal
cell
counts
in
a
few
workers
at
all
five
plants.
Of
particular
interest
were
the
increased
eosinophil
counts
observed
in
13%
of
the
workers
at
one
plant.
The
only
notable
result
from
the
urine
analyses
was
the
observation
of
excess
RBCs
(
eight
workers)
and
WBCs
(
11
workers)
in
10%
of
the
participants
from
one
plant.
The
prevalence
of
folliculitis
was
greater
than
expected
at
three
of
the
plants,
with
one
of
the
plants
having
an
incidence
significantly
increased
(
11
out
of
105
workers
examined).
At
one
plant,
no
folliculitis
was
seen,
but
tar
warts
which
are
known
to
be
associated
with
exposure
to
coal
tar,
were
in
excess.
In
general,
few
atypical
cells
were
found
during
examinations
of
sputum.
One
exception
was
the
increased
C­
reactive
protein
observed
in
five
workers
at
the
same
plant
at
which
the
excess
blood
cells
in
urine
and
the
greatest
excess
in
folliculitis
occurred.
No
cancer
at
any
site
was
discovered
during
the
broad
medical
examination
program.

This
group
of
studies
showed
evidence
of
increased
prevalence
of
folliculitis
and
tar
warts
consistent
with
prolonged
exposure
to
coal
tar
products.
The
only
chronic
health
effect
observed
was
an
excess
of
restrictive
respiratory
deficit.
No
excess
cancer
occurrence
was
reported.
The
usefulness
of
results
of
this
study
are
weakened
by
the
lack
of
specificity
to
creosote
exposure,
by
Page
11
of
28
only
42%
participation
of
eligible
workers,
and
the
lack
of
individual
exposure
assessment
to
coal
tar
products.

4.2.2.3
NIOSH
(
1981)

Following
a
request
from
a
carpenters'
union,
NIOSH
conducted
an
evaluation
of
exposure
among
six
dock
builders
engaged
in
driving
creosote­
preserved
logs
into
a
river
bottom.
Health
surveys
also
were
administered
for
five
of
the
six
dock
builders.

Breathing
zone
and
area
air
concentration
measurements
collected
for
the
cyclohexane­
extractable
fraction
of
the
coal
tar
pitch
volatiles
ranged
from
below
the
detectable
limit
to
0.06
mg/
m3.
However,
because
of
atypical
weather
conditions
on
the
day
of
sampling
and
because
the
pile
driver
was
in
operation
for
less
than
one
hour,
the
industrial
hygiene
results
were
not
representative
of
normal
working
conditions.

A
medical
questionnaire
was
administered
to
five
of
the
six
workers.
The
questionnaire
covered
work
conditions
and
work
history,
past
exposures,
current
health
problems,
medical
history,
the
use
of
personal
protection
and
personal
hygiene.
Questions
on
health
problems
focused
on
skin,
respiratory,
gastrointestinal,
and
central
nervous
system
problems.
The
five
participating
workers
were
also
given
skin
examinations.
The
pile
drivers
were
between
24
and
61
years
of
age
(
average
age
44.6
years),
and
all
had
worked
at
the
current
site
for
at
least
five
months.
All
of
the
participants
had
been
employed
as
pile
drivers
for
an
average
of
16.6
years
of
which
an
average
of
8.3
years
had
involved
pile­
driving
creosote­
preserved
piles.
A
number
of
health
problems
were
reported
by
the
workers,
including
eye
irritation,
nausea,
lightheadedness,
and
swelling
of
the
face,
eyes,
and
hands.
Skin
problems
reported
by
the
workers
included
irritation,
rashes,
erythema,
burning,
dryness,
desquamation,
itching,
and
cracking.
On
hot
days,
symptoms
were
reported
to
be
worse,
and
in
addition,
the
workers
experienced
tearing
and
burning
eyes,
red
eyes,
swollen
or
puffy
eyes,
and
photophobia.
Four
of
the
five
workers
responding
to
the
questionnaire
reported
that
their
visual
acuity
had
gradually
worsened.

Skin
examinations
of
the
workers
revealed
erythema
on
the
face,
neck
and
hands,
dry
skin
with
desquamation
in
sun
exposed
areas,
black
comedones,
plugged
hair
follicles
on
hands
and
forearms,
and
mild
folliculitis
on
the
forearms.

The
symptoms
reported
by
the
dock
building
workers
and
the
observations
made
during
skin
examinations
were
consistent
with
phototoxic
skin
reactions.
The
folliculitis
was
consistent
with
prolonged
and
direct
contact
with
creosote.
No
chronic
health
effects,
including
cancers,
were
reported
or
observed,
and
because
of
the
small
number
of
workers
examined,
encountering
these
diseases
would
not
be
expected.
Page
12
of
28
4.2.2.4
EPA
(
1981a)

A
broad
health
evaluation
was
performed
in
1981
on
59
workers
(
total
of
79
workers
eligible)
at
a
wood
preservative
treatment
plant
in
Ohio.
The
workers
(
51
males,
eight
females)
were
aged
between
20
and
69
years,
with
only
a
slightly
higher
frequency
of
workers
aged
between
55
and
59
years.
Creosote
had
been
used
at
the
plant
since
the
1920s,
but
had
been
discontinued
in
1979.
A
large
battery
of
tests
including
chest
x­
rays,
pulmonary
function
tests,
clinical
chemistry
analyses,
hematology
and
urology
analyses,
and
sputum
and
urine
cytology
were
used
to
assess
effects
on
organs
and
body
systems
known
to
be
at
risk
from
exposure
to
chemicals
used
in
the
plant.
No
industrial
hygiene
monitoring
data
were
available,
and
no
exposure
assessments
for
individual
participants
were
made.

Fifteen
workers
were
observed
with
restrictive
or
obstructive
respiratory
deficits.
One
participant
had
elevated
serum
enzyme
levels
indicative
of
liver
disease.
Two
workers
had
proteinuria
and
one
other
had
evidence
of
urinary
tract
inflammation.
Thirteen
workers
were
found
to
have
elevated
serum
triglycerides,
but
only
one
with
levels
above
400mg/
100ml.

This
study
identified
no
occupationally
related
disease
and
showed
little
evidence
of
chronic
effects
from
working
for
long
periods
in
a
wood
preservative
treatment
plant.
The
small
size
of
the
study
cohort
and
the
lack
of
assessment
of
individual
exposures,
including
the
absence
of
data
on
number
of
years
employed,
seriously
limited
the
possibility
of
observing
negative
health
effects.

4.2.2.5
EPA
(
1986)

A
cross­
sectional
study
was
conducted
on
113
of
the
total
140
workers
at
a
lumber
preservative
treatment
plant.
Thirty­
nine
of
the
participants
worked
less
than
one
year,
40
had
worked
between
one
and
10
years,
and
34
had
worked
between
11
and
35
years.
The
plant
had
used
creosote,
creosote/
tar
solution,
Wolman
salt
(
CCA),
and
pentachlorophenol
(
PCP)
for
many
years
since
1946
as
wood
preservatives.
A
fire
retardant,
NCX,
also
was
used
since
1978.
The
study
focused
on
creosote
and
PCP
since
these
were
considered
the
chemicals
of
concern.

Health
effects
from
working
at
the
wood
treatment
plant
were
evaluated
by
a
battery
of
tests
including
chest
x­
ray,
pulmonary
function
test,
clinical
chemistry
analysis,
hematology
and
urology
analyses,
and
sputum
and
urine
cytology
studies.
Detailed
medical
and
work
history
questionnaires
were
administered,
however,
no
individual
exposure
assessment
was
conducted.
Air
concentrations
for
coal­
tar
pitch
volatiles
were
available
from
a
single
industrial
hygiene
survey
conducted
in
1978.

No
evidence
of
skin
cancer,
bladder
cancer,
or
lung
cancer
were
seen
in
the
study
population.
Pustular
eruptions
likely
related
to
exposures
at
the
plant
were
observed
in
a
greater
than
expected
number
of
workers.
A
number
of
workers
had
restrictive
or
obstructive
pulmonary
deficits,
and
two
workers
showed
evidence
of
liver
disease.
There
was
no
evidence
of
kidney
disease
or
blood
disease.
Page
13
of
28
This
study
showed
little
evidence
of
chronic
effects
from
working
for
long
periods
in
a
wood
preservative
treatment
plant.
The
small
size
of
the
study
cohort
and
the
lack
of
assessment
of
individual
exposures
limited
the
possibility
of
observing
negative
health
effects.

4.2.3
Cohort
Studies
Associated
with
Health
Effects
of
Creosote
in
Humans
4.2.3.1
EPA,
(
1981b
and
1982)

An
in­
depth
study
of
mortality
in
4048
males
who
worked
at
eight
Koppers
coal
tar
plants
was
conducted
by
Tabershaw
Occupational
Medicine
Associates
and
reported
by
Koppers
in
1981.
The
plants
were
located
in
Illinois,
West
Virginia,
California,
New
Jersey
(
two
plants),
Texas,
Alabama,
and
Ohio;
and
all
plants
except
for
one
of
the
New
Jersey
plants
distilled
crude
coal
tar.
Creosote
was
among
the
distillation
by­
products
resulting
from
the
plants'
operations
.
The
cohort
was
initially
defined
as
all
males
who
worked
at
least
10
days
between
1946
and
1977.
Persons
who
worked
in
strictly
clerical
or
secretarial
positions
were
excluded,
as
were
women
because
of
their
small
number.

The
cohort
consisted
of
2,150
workers
(
53.1%)
known
to
be
white,
1,104
workers
(
27.3%)
known
to
be
black,
and
794
workers
(
19.6%)
whose
race
was
unknown.
Demographic
information
including
date
of
hire,
date
of
termination,
and
complete
work
history
was
collected
from
plant
personnel
files.
Vital
status
follow­
up
information
was
collected
by
using
plant
records,
SSA,
motor
vehicle
bureaus,
and
finally
local
phone
directories.
The
total
cohort
provided
64,600
person­
years
of
observation
with
9,917
person­
years
attributed
to
workers
whose
race
was
unknown.
Of
the
total
cohort,
703
(
17.4%)
were
identified
as
deceased,
and
the
vital
status
of
359
(
8.9%)
remained
unknown.

During
the
analysis
of
the
1981
study,
it
was
recognized
that
the
lack
of
race
information
for
almost
20%
of
the
cohort
presented
a
serious
weakness
in
the
study
and
imposed
considerable
difficulties
with
the
interpretation
and
validity
of
results.
This
was
further
complicated
by
the
fact
that
163
of
the
workers
classified
as
"
race
unknown"
also
had
unknown
vital
status.
Because
of
this
weakness,
a
re­
analysis
of
data
for
only
those
workers
whose
race
was
verified
was
performed
in
1982,
therefore,
the
results
from
the
1981
study
are
not
presented
here.
The
redefined
cohort
excluded
the
794
workers
with
unknown
race.
The
number
of
person­
years
of
follow­
up
was
36,635
for
the
white
workers
and
18,047
for
the
black
workers.
Within
the
cohort,
701
deaths
had
occurred
by
the
close
of
the
study
(
12/
31/
77),
and
death
certificates
were
retrieved
for
632
workers
(
359
white,
273
black).

The
second
analysis
looked
at
cause­
specific
deaths
for
six
subgroups
of
the
total
population
of
workers
with
known
race.
These
groups
were
(
1)
all
white
workers,
(
2)
white
workers
employed
for
less
than
six
months,
(
2)
white
workers
employed
for
six
months
or
more,
(
4)
all
black
workers,
(
5)
black
workers
employed
for
less
than
six
months,
(
6)
black
workers
employed
for
six
months
or
more.
Page
14
of
28
For
the
entire
population
of
white
workers,
the
standard
mortality
ratio
(
SMR)
for
all
causes
was
109.
However,
the
SMR
for
deaths
from
all
cancers
was
considerably
elevated
(
SMR=
126)
largely
due
to
the
significant
excess
in
cancers
of
the
lung
(
SMR=
160,
p=
0.05).
Excesses
also
were
observed
for
cancers
of
the
stomach,
large
intestine,
rectum,
bladder,
and
kidney,
however,
none
of
the
SMRs
were
statistically
significant.
When
only
white
workers
employed
for
less
than
six
months
were
considered,
a
large
excess
in
total
mortality
was
observed
(
SMR=
137,
p=
0.01),
and
the
SMR
for
deaths
from
all
cancers
was
125,
though
not
significant.
The
increases
in
overall
mortality
were
due
largely
to
significant
excesses
in
deaths
from
cirrhosis
of
the
liver
(
SMR=
340,
p=
0.01),
accidents
(
SMR=
238,
p=
0.01),
and
cancer
of
the
stomach
(
four
observed,
0.74
expected,
SMR=
540,
p=
0.05).
When
only
white
workers
employed
for
six
months
or
more
were
considered,
the
only
significant
excesses
observed
were
for
cancer
of
the
respiratory
system
(
SMR=
182,
p=
0.01),
largely
due
to
an
excess
of
lung
cancer
(
SMR=
180,
p=
0.01).
Deaths
from
all
other
cause­
specific
cancers
were
within
expected
numbers.

For
the
combined
population
of
black
workers,
a
number
of
statistically
significant
excesses
(
p=
0.05)
were
found,
including
deaths
from
all
causes
(
SMR=
113),
all
cancers
(
SMR=
138),
cancer
of
the
rectum
(
SMR=
439),
and
lung
cancer
(
SMR=
173).
The
number
of
deaths
from
accidents,
poisoning,
and
violence
were
also
highly
elevated
(
SMR=
186,
p=
0.01).
When
only
black
workers
employed
for
less
than
six
months
were
considered,
large
excesses
were
seen
for
total
mortality
(
SMR=
154,
p=
0.01),
for
deaths
from
all
cancers
(
SMR=
171,
p=
0.05),
and
for
accidents
(
SMR=
241,
p=
0.01).
The
SMR
for
cancer
of
the
respiratory
system
was
significantly
increased
(
226,
p=
0.05),
influenced
greatly
by
the
SMR
for
lung
cancer
(
SMR=
243,
p=
0.01).
The
SMR
for
cancer
of
the
esophagus
was
also
greatly
increased
(
326),
though
it
was
based
on
only
three
deaths
with
0.92
expected.
When
only
black
workers
employed
for
more
than
six
months
or
more
were
considered,
the
SMR
for
all
causes
of
death
was
90,
and
the
only
significant
excess
observed
was
for
bladder
cancer
(
SMR=
531,
p=
0.05)
based
on
three
deaths.
Nonsignificant
excesses
also
were
observed
for
deaths
from
all
cancers
and
several
specific
diseases,
including
cancers
of
the
digestive
system
and
skin,
diseases
of
the
hematopoietic
system,
and
accidents.
None
of
the
excesses
were
statistically
significant
and
were
based
on
small
numbers
of
deaths.
Overall,
mortality
in
the
group
of
black
workers
employed
six
months
were
higher
than
in
the
black
workers
employed
less
than
six
months.

This
study
provided
a
large
amount
of
mortality
data
on
a
reasonably
large
occupational
cohort.
Moderately
convincing
evidence
is
presented
that
employment
at
the
eight
coal
tar
distillation
plants
may
result
in
increased
risk
of
death
from
a
range
of
malignancies.
The
study
appeared
to
be
well
planned
and
executed,
though
the
validity
of
the
findings
is
limited
by
a
number
of
shortcomings.
These
include
the
lack
of
race
information
on
a
large
fraction
of
the
cohort,
the
small
number
of
deaths
observed
for
many
of
the
diseases
reported
in
excess,
and
the
very
crude
measure
of
exposure
based
only
on
employment
at
one
or
more
of
the
plants.
Page
15
of
28
4.2.3.2
Steineck
et
al.
(
1989)

Steineck,
et
al.
employed
a
complex
job­
exposure
matrix
to
estimate
exposure
for
calculating
relative
risk
for
development
of
renal
pelvic
cancer
(
RPC)
or
bladder
cancer
(
BC)
in
a
Swedish
population.
The
cohort
was
defined
as
all
males
born
in
Sweden,
aged
20­
64
in
1960,
who
reported
themselves
employed.
Cases
of
renal
RPC
or
BC
occurring
during
the
19­
year
study
period
were
identified
through
the
National
Swedish
Cancer
Registry.

The
job­
exposure
matrix
used
to
determine
exposed
and
unexposed
subpopulations
was
based
on
self­
reported
job­
related
information
collected
in
1960
for
census
purposes.
Based
on
this
information,
subjects
were
classified
into
292
occupational
titles
and
308
industrial
categories,
yielding
292
X
308
possible
work
tasks.
Potential
exposure
to
50
single
agents
or
groups
of
substances
were
assigned
for
each
possible
work
task
defined
by
the
matrix.
Among
the
potential
exposures
selected
for
evaluation
were
most
of
those
cited
in
the
literature
as
potential
risk
factors
for
the
two
cancers
of
interest,
and
creosote.

Relative
risks
were
calculated
after
adjusting
for
age
in
1960
(
six
categories).
For
some
calculations,
adjustments
also
were
made
for
marital
status,
socioeconomic
group,
and
urbanization
of
residence.
Among
the
total
study
population
of
1,905,660
persons,
556,
429
were
judged
to
be
exposed
to
at
least
one
of
the
selected
substances.
During
the
19
years
of
observations
within
the
study,
there
were
714
cases
of
RPC
with
542
cases
occurring
among
the
unexposed
subjects.
There
were
10,123
cases
of
BC
with
7,432
cases
occurring
within
the
unexposed
group.
For
individuals
categorized
as
exposed
to
creosote,
the
relative
risk
for
BC
was
1.4
(
95%
CI
0.7­
2.6)
compared
to
cohort
members
not
assigned
any
exposure.
It
is
notable
that
all
of
the
BC
cases
categorized
as
exposed
were
leather
tanners
who
were
also
assigned
a
number
of
other
exposures.
When
adjustments
for
applied
for
age,
marital
status,
socioeconomic
group,
and
degree
of
urbanization,
the
relative
risk
for
BC
remained
between
1.25
and
1.30.

This
study
provides
very
limited
evidence
of
association
between
exposure
to
creosote
and
occurrence
of
bladder
cancer.
Weaknesses
include
exposure
assessment
based
solely
on
selfreported
occupational
information
from
a
single
census
observation,
lack
of
control
for
multiple
exposures,
and
no
consideration
for
nonoccupational
exposures.

4.2.3.3
Karlehagen
et
al.
(
1992)

Karlehagen,
et
al.
studied
cancer
incidence
among
922
men
exposed
to
creosote
at
13
wood
impregnating
plants
in
Sweden
and
Norway.
Most
participants
worked
as
impregnators
while
36
men
repaired
or
maintained
railroad
cars
used
to
transport
creosote.
Study
participants
were
employed
at
least
one
year
between
1950
and
1975,
and
follow­
up
was
1958­
1985
for
the
workers
in
Sweden
and
1953­
1987
for
the
workers
in
Norway.
Cancers
were
identified
through
national
cancer
registries
in
both
countries.
Cancer
registration
is
compulsory
in
both
countries,
and
quality
and
completeness
of
the
registries
was
considered
to
be
good.
Page
16
of
28
No
individual
exposure
measurements
were
available
for
participants,
however,
levels
of
naphthalene
and
benzo(
a)
pyrene
(
major
constituents
of
creosote)
at
several
of
the
plants
had
been
determined
to
be
0.1­
11
mg/
m3
and
0.03
µ
g/
m3,
respectively.
Levels
for
both
constituents
were
well
below
accepted
exposure
limits.
Consequently,
exposure
assessment
for
study
participants
was
based
on
minimum
length
of
employment
at
plants
known
to
use
creosote
regularly.
Information
on
the
type
of
work
performed
at
each
plant
was
collected
through
use
of
a
questionnaire
completed
by
plant
personnel,
but
not
by
participants.
No
differences
in
exposure
conditions
among
the
13
plants
were
observed.

The
total
incidence
of
cancer
was
lower
than
expected
with
129
cases
observed
and
137
cases
expected.
Some
differences
were
seen
between
the
Swedish
and
Norway
subgroups
but
the
differences
were
small.
Increased
risks
were
observed
for
lip
cancer
(
SIR=
2.50,
P=
0.05),
nonmelanoma
skin
cancer
(
SIR=
2.37,
P=
0.02),
and
malignant
lymphoma
(
SIR=
1.9,
P=
0.06).
When
a
latency
period
of
20
years
since
first
exposure
was
applied,
the
SIRs
for
lip
cancer,
nonmelanoma
skin
cancer,
and
malignant
melanoma
were
3.7,
2.0,
and
2.2
respectively.
Only
the
SIR
for
lip
cancer
(
five
cases
observed,
1.34
cases
expected)
was
statistically
significant.
No
increase
in
the
incidence
of
lung
cancer
was
observed
in
this
population,
with
or
without
consideration
for
time
since
first
exposure.

This
study
presents
reasonable
evidence
that
exposure
to
creosote,
as
measured
by
employment
at
creosote
plants,
is
likely
associated
with
development
of
nonmelanoma
skin
cancer.
Increased
risks
of
lip
cancer
and
malignant
melanoma
(
Norway
subgroup
only),
and
malignant
lymphoma
were
also
observed
in
the
study
population,
but
the
risks
were
not
statistically
significant.
Because
the
workers
in
the
study
worked
outdoors
part
of
the
time,
the
validity
of
the
associations
observed,
particularly
for
lip
cancer,
nonmelanoma
skin
cancer,
and
malignant
melanoma,
may
be
weakened.

4.2.4
Case
Control
Studies
Associated
with
Health
Effects
of
Creosote
in
Humans
4.2.4.1
Flodin
et
al.
(
1987)

Risk
factors
for
development
of
multiple
myeloma
(
MM)
were
investigated
in
a
study
of
131
cases
and
431
controls
in
Sweden.
The
cases
were
identified
from
records
at
six
hospitals
in
southeast
Sweden
and
were
required
to
be
less
than
81
years
of
age,
of
Swedish
ethnicity,
resident
in
the
catchment
areas
of
the
hospitals
at
the
time
of
diagnosis,
and
capable
of
responding
to
a
questionnaire.
The
131
cases
represented
approximately
one
third
of
the
total
number
of
MM
cases
occurring
in
the
area
as
reported
to
the
cancer
registry.
The
discrepancy
between
total
number
of
cases
and
the
number
of
cases
identified
from
the
six
hospitals
was
attributed
to
simple
administrative
record
keeping
and
was
judged
to
not
impose
any
bias
on
the
study
findings.
Controls
were
randomly
selected
from
population
registries
for
the
same
catchment
areas
from
which
the
cases
were
drawn.
Differences
in
average
age
and
distributions
of
gender
were
found
between
cases
and
controls.
The
average
age
for
cases
was
64
years
and
for
controls,
58
years.
Within
the
131
cases,
57
percent
were
males;
within
431
controls,
46
percent
were
males.
Page
17
of
28
Assessment
of
exposure
was
through
a
nine­
page
questionnaire
consisting
of
17
major
questions
of
which
10
related
to
occupational
exposures.
Some
of
the
occupational
questions
also
asked
further
questions
regarding
details
of
exposures.
Reported
exposures
lasting
less
than
one
year
and
all
reported
exposures
within
five
years
prior
to
diagnosis
were
ignored
in
the
analyses.

Crude
rate
ratios
were
significantly
increased
for
occupational
exposure
to
creosote
(
RR=
6.0,
95%
CI
2.00­
18.2),
fresh
wood,
engine
exhaust,
farming,
and
bricklaying.
When
the
cases
and
controls
were
stratified
into
four
age
groups,
the
elevated
risk
ratios
remained
for
creosote,
fresh
wood,
and
engine
exhaust.
The
increased
risks
associated
with
creosote,
engine
exhaust,
and
fresh
wood
also
remained
significant
when
analyses
controlled
for
confounding
effects
of
other
determinants.

This
study
provides
moderate
evidence
that
exposure
to
creosote,
as
measured
by
self­
reporting
via
mailed
questionnaire,
may
be
linked
to
development
of
MM.
The
association
is
less
convincing
because
the
numbers
of
cases
and
controls
reporting
exposure
to
creosote
were
quite
small.
Also,
the
study
suffers
the
same
limits
as
other
studies
using
similar
assessment
methods.

4.2.4.2
Persson
et
al.
(
1989)

A
case­
control
study
was
conducted
in
Sweden
by
Persson,
et
al.
to
investigate
associations
between
exposure
to
creosote
and
subsequent
development
of
Hodgkin
disease
(
HD)
or
non­
Hodgkin's
lymphoma
(
NHL).
Cases
were
160
patients
(
101
men,
59
women)
with
HD
or
NHL
identified
through
the
registry
at
Orebro
Medical
Centre
Hospital
and
diagnosed
between
1964
and
1986.
The
cases
remained
alive
at
least
through
the
data
collection
period
in
1986
and
were
required
to
be
at
least
20
years
of
age
at
diagnosis,
born
in
Sweden,
living
in
the
area
of
the
hospital
at
time
of
diagnosis,
less
than
80
years
of
age
at
time
of
data
collection,
and
mentally
capable
of
responding
to
the
study
questionnaire.
The
275
controls
(
157
men,
118
women)
were
a
subset
of
a
larger
set
of
controls,
previously
used
in
earlier
studies,
randomly
drawn
from
general
population
registries
in
catchment
areas
of
several
hospitals.
For
the
current
study,
only
individuals
in
the
catchment
area
from
which
the
patients
were
drawn
were
used
as
controls.
The
controls
were
required
to
meet
the
applicable
inclusion
criteria
used
for
patients.

Information
for
assessment
of
exposures
was
collected
through
a
nine
page
questionnaire
mailed
to
each
case
and
control.
Of
17
main
questions,
10
questions
addressed
occupational
exposures
with
some
of
the
occupational
questions
having
additional
subquestions
asking
for
details.
Questions
also
were
asked
about
exposures
during
leisure
activities.
Exposures
reported
for
periods
of
less
than
one
year
were
not
considered.
A
latency
period
between
exposure
and
development
of
disease
was
imposed
by
considering
only
exposures
within
five
to
45
years
prior
to
diagnosis
for
the
cases.
For
the
controls,
exposures
were
only
considered
if
they
occurred
five
to
45
years
before
the
point
in
time
of
selection.

Age
ranges
for
cases
and
controls
were
similar;
20­
73
for
HD,
22­
79
for
NHL,
and
20­
77
for
controls.
Crude
odds
ratios
(
ORs)
for
both
HD
and
NHL
were
increased
for
exposure
to
wood
Page
18
of
28
preservatives
and
for
exposure
to
creosote
specifically
(
OR
10.5
for
HD,
OR
13.6
for
NHL).
Although
the
numbers
of
cases
and
controls
exposed
to
creosote
were
small,
logistic
analyses
were
performed
to
control
for
age
at
time
of
case
diagnosis,
gender,
and
two
exposure
determinants,
i.
e.,
farming
and
exposure
to
fresh
wood.
For
HD,
the
logistic
OR
for
occupational
exposure
to
creosote
was
still
elevated
(
OR
10.7,
CI
90%
1.1­
103).
For
NHL,
the
logistic
OR
was
9.4
(
CI
90%
1.2­
69).

Assuming
the
instrument
for
exposure
assessment
and
the
methodology
for
administration
was
not
biased,
this
study
provides
good
evidence
that
exposure
to
creosote
is
a
risk
factor
for
development
of
both
HD
and
HNL.
The
study
is
somewhat
weakened
by
the
small
of
number
of
persons
reporting
creosote
exposure.

4.2.4.3
Feingold
et
al.
(
1992)

Feingold,
et
al.
studied
associations
between
parental
exposures
and
cancers
in
children
born
subsequent
to
the
exposures.
The
252
incident
cases,
identified
from
a
Colorado
cancer
registry,
were
in
children
0­
14
years
of
age,
diagnosed
between
1976
and1983.
The
cases
were
compared
with
222
controls
selected
by
random
digit
dialing
in
the
same
geographical
area
as
the
cases
and
matched
on
age
(+/­
three
years),
gender,
and
telephone
exchange
area.

Assessment
of
parental
exposure
was
based
on
job
history
information
(
including
job
title,
industry,
and
employment
dates)
collected
by
personal
interview.
A
job­
exposure
matrix,
derived
from
past
industrial
hygiene
surveys
and
knowledge
of
industrial
processes,
was
used
to
assign
exposures
to
individuals
on
the
basis
of
job
title
and
industry
of
employment.
All
jobs
held
for
six
months
or
longer
by
mothers
and
fathers
during
the
year
prior
to
birth
of
the
child
were
linked
to
all
chemicals
assigned
to
the
job.
Analyses
were
then
performed
to
determine
associations
between
cancer
incidence
and
parental
exposure
to
a
large
number
of
substances.

Creosote
was
not
identified
as
an
exposure
for
any
of
the
mothers
of
cases
or
controls.
An
adjusted
odds
ratio
of
2.5
(
CI
=
0.8­
8.1)
was
found
for
association
of
fathers'
exposure
to
creosote
during
the
year
prior
to
birth
of
children
with
any
type
of
cancer
in
the
offspring.
When
associations
between
fathers'
exposure
to
creosote
and
the
incidence
of
specific
cancers
in
children
born
subsequently
were
investigated,
an
odds
ratio
of
3.7
(
CI
=
0.8­
16.6)
was
observed
for
childhood
brain
cancer.
Fathers
assigned
exposure
to
creosote
were
chiefly
in
the
construction
industry
or
were
farmers.

The
major
limitation
of
this
study
is
the
imprecision
of
the
exposure
assessment.
Exposures
to
individuals
with
the
same
job
titles
and
working
in
the
same
industries
vary
widely.
Therefore,
assignments
of
exposures
to
specific
chemicals,
such
as
creosote,
based
entirely
on
job
titles
and
industries
may
be
invalid
for
some
individuals.
Also,
the
credibility
of
occupation
information
collected
from
mothers
for
fathers
is
likely
to
be
only
60­
80%.
However,
exposure
misclassification
resulting
from
the
lack
of
individual
exposure
data,
or
due
to
the
necessary
use
of
information
from
surrogates,
is
likely
to
be
equal
among
parents
of
cases
and
controls
and
therefore,
should
be
nondifferential.
Page
19
of
28
4.2.4.4
Persson
et
al.
(
1993)

A
case­
control
study
was
conducted
in
Sweden
by
Persson,
et
al.
among
124
patients
with
HD
or
NHL
to
reexamine
earlier
findings
of
associations
between
exposure
to
creosote
and
HD
and
NHL.
Cases
diagnosed
between
1975
and
1984
were
identified
through
a
regional
cancer
registry
located
at
a
university
hospital
serving
a
three
county
area.
Only
men
were
included
in
the
study,
and
were
required
to
be
at
least
20
year
of
age,
born
in
Sweden,
living
in
the
area
of
the
hospital
at
time
of
diagnosis,
less
than
80
years
of
age
at
time
of
data
collection
and
mentally
capable
of
responding
to
the
study
questionnaire.
The
204
controls
were
randomly
drawn
from
general
population
registries
for
the
catchment
area
of
the
university
hospital
from
which
the
patients
were
drawn.
The
controls
were
required
to
meet
the
applicable
inclusion
criteria
used
for
patients.

Information
for
assessment
of
exposures
was
collected
through
a
nine
page
questionnaire
mailed
to
each
case
and
control.
Of
17
main
questions,
10
addressed
occupational
exposures
with
some
of
the
occupational
questions
having
additional
subquestions.
Exposures
of
less
than
one
year
were
not
considered,
and
only
exposures
five
to
45
years
prior
to
diagnosis
were
considered
pertinent
for
the
cases.
For
the
controls,
the
window
of
time
during
which
exposures
were
considered
had
been
determined
based
on
the
time
of
diagnosis
of
the
patients
in
earlier
studies.

None
of
the
cases,
and
only
four
controls
reported
exposure
to
creosote.
Assuming
a
null
hypothesis
for
association
of
creosote
with
HD
or
NHL,
the
number
of
cases
expected
to
report
creosote
exposure
would
be
2.4
based
on
the
number
of
controls
reporting
creosote
exposure
and
the
ratio
of
cases
to
controls.
This
study
shows
no
evidence
of
an
association
of
creosote
exposure
with
these
diseases.

4.2.4.5
Tynes
et
al.
(
1994)

A
nested
case­
control
study
was
conducted
to
assess
the
presence
of
an
association
between
exposure
to
electromagnetic
fields
existing
at
Norwegian
railways
and
occurrence
of
brain
tumors
or
leukemia
in
railway
workers.
Limited
information
on
exposure
to
creosote
was
collected
for
analysis
as
a
confounder.

The
cohort
from
which
the
cases
were
selected
included
13,030
male
railroad
workers
employed
in
1957
on
either
electric
or
non­
electric
railways
and
included
line
workers,
outdoor
station
workers,
and
electrical
workers.
The
cases
identified
from
the
Norway
Cancer
Registry
to
which
all
new
cancer
cases
are
reported
included
men
diagnosed
with
brain
tumors
or
leukemia
during
the
follow­
up
period
between
1958
and
1990.
Four
or
five
controls
were
selected
for
each
case
matched
on
year
of
birth.
Controls
were
required
to
survive
to
the
age
at
which
the
matching
case
was
diagnosed.
Information
on
whether
the
participants
ever
smoked
was
collected
through
telephone
interviews.
Page
20
of
28
Assessment
of
exposures
to
electromagnetic
fields
for
the
cases
and
controls
was
based
on
job
titles,
work
histories,
and
job
descriptions.
Exposures
to
other
potential
hazards,
including
creosote,
were
estimated
and
analyzed
as
confounders.
An
exposure
matrix
was
constructed
using
categories
of
exposure
frequency
(
0=
never,
1=
monthly,
2=
weekly,
3=
daily)
and
years
of
employment
as
factors.

No
association
of
brain
tumors
or
leukemia
with
estimated
exposure
to
creosote
was
observed
in
this
study.
As
is
true
in
many
similar
studies,
assessment
of
exposures
was
based
on
qualitative
information
relevant
to
jobs
and
departments,
and
therefore
is
not
precise,
or
accurate
for
any
particular
individual.

4.2.4.6
Schildt
et
al.
(
1999)

Associations
between
a
number
of
occupational
exposures
including
creosote
with
oral
cancer
was
investigated
in
a
case­
control
study
in
Sweden.
The
population­
based
study
included
410
verified
cases
of
squamous
cell
oral
cancer
reported
to
a
four­
county
cancer
registry
during
1980­
1989
and
410
controls
drawn
from
a
national
population
registry.
Among
the
cases
(
175
alive,
235
deceased)
were
134
women
and
276
men.
A
control
was
matched
to
each
case
on
age,
gender,
and
county
of
residence.
For
deceased
cases,
deceased
controls
were
selected
from
the
the
National
Registry
for
Causes
of
Death.
In
addition
to
the
other
matching
criteria,
deceased
controls
also
were
matched
on
year
of
death.

Assessment
of
exposures
was
based
on
information
collected
through
mailed
questionnaires.
For
deceased
participants,
the
questionnaire
was
sent
to
the
next­
of­
kin
in
the
order
of
spouse,
child,
parent,
sibling,
or
other.
The
questionnaire
included
a
lifetime
work
history
and
other
questions
concerning
exposure
factors
of
interest
for
oral
cancer.
Exposures
associated
with
occupations
held
for
less
than
one
year
were
ignored.

Analysis
of
association
between
exposure
to
creosote
and
oral
cancer
showed
no
increased
risk
(
OR
=
0.5,
CI
=
0.1­
2.0).
The
reliability
of
this
result
is
weakened
by
the
method
of
exposure
assessment
and
by
the
small
numbers
of
individuals
exposed
(
three
cases
and
six
controls).
Page
21
of
28
4.3
SUMMARY
AND
CONCLUSIONS
OF
THE
HEALTH
EFFECTS
OF
CREOSOTE
IN
HUMANS
Creosote
and
creosote­
containing
substances
are
widely
used
in
industry
and
by
certain
subgroups
of
individuals,
resulting
in
a
large
population
of
persons
with
potential
exposure.
According
to
California
data,
the
majority
of
poisoning
incident
cases
occurred
as
a
result
of
handling
creosote
and
applying
it
to
wood
without
proper
protection
for
the
skin
and
eyes.
The
number
of
these
cases
has
dropped
quite
markedly
in
the
1990s.
Substantial
contact
with
treated
wood
appears
to
be
a
risk
factor
for
skin
and
eye
burns,
even
years
after
the
wood
was
treated.
Symptoms
experienced
were
burns
and
rashes
on
the
exposed
body
areas,
chemical
conjunctivitis,
headaches,
nausea,
and
eye
irritation.

While
a
number
of
human
health
studies
are
available
that
include
creosote
as
a
possible,
or
even
likely,
target
exposure,
few
studies
are
available
with
enough
information
for
a
rigorous
assessment
of
chronic
health
effects
attributable
to
creosote
specifically.
By
far,
the
most
common
limitation
of
studies
aimed
at
evaluating
effects
of
creosote
exposure
is
the
almost
total
absence
of
objective
exposure
measurements
for
the
study
participants.
For
most
of
the
studies,
assessment
of
exposure
is
based
on
information
about
past
occupational
activities
provided
by
the
participants
or
assigned
by
health
studies
professionals
such
as
industrial
hygienists
with
general
knowledge
of
occupations
and
materials.
In
almost
all
cases,
possible
exposure
to
other
materials,
either
separately
or
concomitantly,
cannot
be
excluded.
A
second
important
limitation
often
seen
in
studies
on
effects
of
creosote
is
the
lack
of
statistical
significance
calculated
for
many
of
the
apparent
associations
between
assigned
creosote
exposure
and
development
of
disease.

These
limitations
notwithstanding,
among
the
epidemiological
studies
on
effects
of
creosote
exposure,
increased
risks
for
development
of
a
number
of
diseases
have
been
observed.
Diseases
typically
found
to
be
in
excess
include
skin
cancer
and
nonmalignant
skin
disorders,
bladder
cancer,
lung
cancer
and
nonmalignant
respiratory
diseases.
Considering
the
information
presently
available,
conclusions
regarding
chronic
health
effects
from
exposure
to
creosote
alone
should
be
considered
tentative.
Page
22
of
28
Table
4­
4.
Health
studies
in
workers
and
non­
workers
exposed
to
creosote
Date
Journal
Author(
s)
Study
type
Population
Exposure
Pure/
Mixed
Effects
Location
Category
N
Health
Other
1975
Journal
of
Occupational
Medicine
Garrett
Case
series
CA
Patient
2
Pure
Two
patients
with
bladder
cancer
had
histories
of
chronic
exposure
to
cresol
and
creosote
1979a
Koppers
Company,
Inc.

Report
Tabershaw
Occupational
Medicine
Associates
Crosssectional
PA,

SC,
WV,

KY
Occup
257
Mixed
Excess
pustular
eruptions
of
skin.
Occasional
borderline
abnormalities.
No
evidence
of
cancer
associated
with
employment.

1979b
1979c
1980a
1980b
1980c
Koppers
Company,
Inc.

Report
Tabershaw
Occupational
Medicine
Associates
Crosssecional
CA,
WV,

AL,
OH,

IL
Occup
Mixed
Increased
prevalence
of
folliculitis
and
tar
warts
consistent
with
prolonged
exposure
to
coal
tar
products.

Excess
restrictive
respiratory
deficit.
No
excess
cancer.

1981
NIOSH
HHE
80­
238­

931
NIOSH
(
work
by
Baker
and
Fannick)
Crosssectional
NY
Occup
5
Pure
No
chronic
effects
reported
or
observed.
Acute
skin
problems
reported
or
observed
included
irritation,
desquamation,
itching,

cracking,
and
erythema.
On
hot
days,
burning,
swollen
or
puffy
eyes,
and
photophobia
were
reported.

1981
EPA­
OTS
86­
870001567
Tabershaw
Occupational
Medicine
Associates
Crosssectonal
OH
Occup
59
Mixed
No
evidence
of
disease
associated
with
past
exposure
to
creosote.
Table
4­
4.
Health
studies
in
workers
and
non­
workers
exposed
to
creosote
Date
Journal
Author(
s)
Study
type
Population
Exposure
Pure/
Mixed
Effects
Location
Category
N
Health
Other
Page
23
of
28
1986
EPA­
OTS
86­
870001566
Tabershaw
Occupational
Medicine
Associates
Crosssectional
SC
Occup
113
Mixed
No
evidence
of
skin,
bladder,
or
lung
cancer.
No
evidence
of
kidney
disease
or
blood
disease.

Liver
disease
observed
in
two
workers.
Greater
than
expected
pustular
eruptions.

1981
EPA­
OTS
86­

870001549
Tabershaw
Occupational
Medicine
Associates
Cohort
mortality
IL,
WV,

CA,
NJ,

TX,
AL,

OH
Occup
4,048
Mixed
SMRs
for
all
cancers
and
other
cause­
specific
cancers
increased.

1982
EPA­
OTS
86­

870001547
Tabershaw
Occupational
Medicine
Associates
Cohort
mortality
IL,
WV,

CA,
NJ,

TX,
Al,

OH
Occup
3,254
Mixed
SMRs
for
all
cancers
and
other
cause­
specific
cancers
increased.

1989
American
Journal
of
Industrial
Medicine
Steineck
et
al.
Cohort
Sweden
Occup
1,905,66
0
Mixed
Increased
relative
risk
for
bladder
cancer
in
population
assigned
exposure
to
creosote
based
on
self­
reported
occupation
in
1960.

1992
Scandinavian
Journal
of
Work
and
Environmental
Health
Karlehagen
et
al.
Cohort
incidence
Sweden
and
Norway
Occup
922
Pure
Increased
risks
for
lip
cancer,

nonmelanoma
skin
cancer,

malignant
melanoma,
and
malignant
lymphoma
observed
for
men
employed
at
creosote
plants.
Table
4­
4.
Health
studies
in
workers
and
non­
workers
exposed
to
creosote
Date
Journal
Author(
s)
Study
type
Population
Exposure
Pure/
Mixed
Effects
Location
Category
N
Health
Other
Page
24
of
28
1987
American
Journal
of
Industrial
Medicine
Flodin
et
al.
Case­
control
Sweden
Occup
131/
431
Mixed
Analysis
of
risk
factors
for
multiple
myeloma
showed
crude
ratios
increased
for
occupational
exposure
to
creosote,
engine
exhausts,
and
fresh
wood.

1989
British
Journal
of
Industrial
Medicine
Persson
et
al.
Case­
control
Sweden
Public
160/
275
Mixed
Crude
and
logistic
ORs
for
HD
and
NHL
increased
for
exposure
to
creosote
(
for
HD,
ORs
10.5
and
10.7,
for
NHL,
OR
13.6
and
9.4)

1992
Cancer
Causes
and
Control
Feingold
et
al.
Case­
control
CO
Public
252/
222
Mixed
Odds
ratios
for
association
of
total
childhood
cancer
and
childhood
brain
cancer
with
exposure
of
father
to
creosote
during
year
prior
to
child's
birth
=
2.5
(
ns)
and
3.7
(
ns).

1993
Cancer
Persson
et
al.
Case­
control
Sweden
Public
124/
204
Mixed
None
None
of
124
patients
and
four
of
204
controls
reported
exposure
to
creosote
1994
American
Journal
of
Epidemiology
Tynes
et
al.
Nested
casecontrol
Norway
Occup
92/
442
(
Cohort
13,030)
Mixed
No
association
between
brain
tumors
or
leukemia
and
exposure
to
creosote
observed.

1999
Oncology
Reports
Schildt
et
al.
Case­
control
Sweden
Public
410/
410
Mixed
No
association
between
oral
cancer
and
exposure
to
creosote
observed
Page
25
of
28
Page
26
of
28
REFERENCES
Boffetta
P,
Jourenkova
N,
Gustavsson
P.
1997.
Cancer
risk
from
occupational
and
environmental
exposure
to
polycyclic
aromatic
hydrocarbons.
Cancer
Causes
and
Control.
8(
3):
444­
472.

Bowman
CE,
Muhleman
MF,
Walters
E.
1984.
A
fatal
case
of
creosote
poisoning.
Postgraduate
Medical
Journal
60:
499­
500.

Dean
BS,
Lopez
G,
Krenzelok
EP.
1992.
Environmentally­
induced
methemoglobinemia
in
an
infant.
Clinical
Toxicology
30:
127­
133.

Feingold
L,
Savitz
DA,
John
EM.
1992.
Use
of
a
job­
exposure
matrix
to
evaluate
parental
occupation
and
childhood
cancer.
Cancer
Causes
and
Control.
3(
2):
161­
169.

Flodin
U,
Fredriksson
M,
Persson
B.
1987.
Multiple
myeloma
and
engine
exhausts,
fresh
wood
and
creosote:
A
case­
referent
study.
American
Journal
of
Industrial
Medicine.
12(
5):
519­
529.

Garrett
JS.
1975.
Association
between
bladder
tumors
and
chronic
exposure
to
cresol
and
creosote.
Journal
of
Occupational
Medicine.
17(
8):
492.

Henry
SA.
1950.
Cutaneous
cancer
in
relation
to
occupation.
Annals
of
the
Royal
College
of
Surgeons
of
England.
7:
425­
454.

Henry
SA.
1946.
Cancer
of
the
scrotum
in
relation
to
occupation.
Humphrey
Milford
Oxford
University
Press,
New
York,
8­
105.

Hueper
WC.
1963.
Environmental
carcinogenesis
in
man
and
animals.
Annals
of
the
New
York
Academy
of
Sciences.
180(
3):
963­
1038.

International
Agency
for
Research
on
Cancer.
1987.
IARC
Monographs
on
the
evaluation
of
the
carcinogenic
risks
to
humans
­
Overall
evaluations
of
carcinogenicity:
An
updating
of
IARC
Monographs
Volumes
1­
42.
Supplement
7.
International
Agency
for
Research
on
Cancer,
Lyon,
France.

International
Agency
for
Research
on
Cancer.
1985.
Coal­
tars
and
derived
products.
In:
IARC
Monographs
on
the
evaluation
of
carcinogenic
risk
of
chemicals
to
humans.
Volume
35.
International
Agency
for
Research
on
Cancer,
Switzerland,
83­
159.

Karlehagen
S,
Andersen
A,
Ohlson
C­
G.
1992.
Cancer
incidence
among
creosote­
exposed
workers.
Scandinavian
Journal
of
Work
and
Environmental
Health.
18(
1):
26­
29.

Koppers
Company,
Inc.
1980a.
Cross­
sectional
health
study
of
workers
at
the
Woodward,
Alabama
coal
tar
plant
of
Koppers
Company,
Inc.
Conducted
by
Tabershaw
Occupational
Page
27
of
28
Medicine
Associates,
P.
A.,
Rockville,
MD.

Koppers
Company,
Inc.
1979c.
Cross­
sectional
health
study
of
workers
at
the
Youngstown,
Ohio
plant
of
Koppers
Company,
Inc.
Conducted
by
Tabershaw
Occupational
Medicine
Associates,
P.
A.,
Rockville,
MD.

Koppers
Company,
Inc.
1979a.
Cross­
sectional
health
study
of
workers
of
four
forest
products
plants
of
Koppers
Company,
Inc.
Volume
A.
Conducted
by
Tabershaw
Occupational
Medicine
Associates,
P.
A.,
Rockville,
MD.

Koppers
Company,
Inc.
1979b.
Cross­
sectional
health
study
of
workers
at
the
Follansbee,
West
Virginia
plant
of
Koppers
Company,
Inc.
Conducted
by
Tabershaw
Occupational
Medicine
Associates,
P.
A.,
Rockville,
MD.

Koppers
Company,
Inc.
1980b.
Cross­
sectional
health
study
of
workers
at
the
Fontana,
California
plant
of
Koppers
Company,
Inc.
Conducted
by
Tabershaw
Occupational
Medicine
Associates,
P.
A.,
Rockville,
MD.

Koppers
Company,
Inc.
1980c.
Cross­
sectional
health
study
of
workers
at
the
Chicago,
Illinois
plant
of
Koppers
Company,
Inc.
Conducted
by
Tabershaw
Occupational
Medicine
Associates,
P.
A.,
Rockville,
MD.

National
Institute
for
Occupational
Safety
and
Health.
1981.
Health
Hazard
Evaluation
Report.
HHE­
80­
238­
931.
New
York
Port
Authority,
Brooklyn,
New
York.
NTIS
PB83­
127365.

Persson
B,
Dahlander
A­
M,
Fredriksson
M,
Brage
HN,
Ohlson
C­
G,
Axelson
O.
1989.
Malignant
lymphomas
and
occupational
exposures.
British
Journal
of
Industrial
Medicine.
46(
8):
516­
520.

Persson
B,
Fredriksson
M,
Olsen
K,
Boeryd
B,
Axelson
O.
1993.
Some
occupational
exposures
as
risk
factors
for
malignant
lymphomas.
Cancer.
72(
5):
1773­
1778.

Research
Triangle
Institute.
1996.
Toxicological
profile
for
wood
creosote,
coal
tar
creosote,
coal
tar,
coal
tar
pitch,
and
coal
tar
pitch
volatiles.
(
Update).
Prepared
for
U.
S.
Department
of
Health
and
Human
Services
Agency
for
Toxic
Substances
and
Disease
Registry,
Atlanta,
GA.

Schildt
E­
B,
Eriksson
M,
Hardell
L,
Magnuson
A.
1999.
Occupational
exposures
as
risk
factors
for
oral
cancer
evaluated
in
a
Swedish
case­
control
study.
Oncology
Reports.
6(
2):
317­
320.

Steineck
G,
Plato
N,
Alfredsson
L,
Norell
SE.
1989.
Industry­
related
urothelial
carcinogens:
Application
of
a
job­
exposure
matrix
to
census
data.
American
Journal
of
Industrial
Medicine.
16(
2):
209­
224.

Steineck
G,
Plato
N,
Norell
SE,
Hogstedt
C.
1990.
Urothelial
cancer
and
some
industry­
related
Page
28
of
28
chemicals:
An
evaluation
of
the
epidemiologic
literature.
American
Journal
of
Industrial
Medicine.
17(
3):
371­
391.

Syracuse
Research
Corporation.
1985.
Monograph
on
human
exposure
to
chemicals
in
the
workplace:
Creosote.
Final
report.
Prepared
for
National
Cancer
Institute,
Bethesda,
MD.

Syracuse
Research
Corporation.
1988.
Evaluation
of
the
potential
carcinogenicity
of
creosote
(
8001­
58­
9).
Prepared
for
U.
S.
Environmental
Protection
Agency,
Washington,
DC.

Thompson
JP,
Casey
PB,
Vale
JA.
1994.
Suspected
paediatric
pesticide
poisoning
in
the
UK.
II.
Home
accident
surveillance
system
1989­
1991.
Human
&
Experimental
Toxicology
12:
534­
536.

Tynes
T,
Jynge
H,
Vistnes
AI.
1994.
Leukemia
and
brain
tumors
in
Norwegian
railway
workers,
a
nested
case­
control
study.
American
Journal
of
Epidemiology.
139(
7):
645­
653.

U.
S.
Environmental
Protection
Agency.
1981a.
Occupational
health
evaluation
of
the
Orrville,
Ohio
plant
of
Koppers
Company,
Inc.,
forest
products
group
(
final
report).
Conducted
by
Tabershaw
Occupational
Medicine
Associates,
P.
A.,
Rockville,
MD.
EPA­
OTS
U.
S.
Environmental
Protection
Agency.
1981b.
An
epidemiologic
study
of
mortality
among
workers
at
the
Koppers
coal
tar
plants.
Conducted
by
Tabershaw
Occupational
Medicine
Associates,
P.
A.,
Rockville,
MD.
EPA­
OTS/
86­
870001549.
NTIS/
OTS0515709.
/
86­
870001567.

U.
S.
Environmental
Protection
Agency.
1982.
Mortality
among
Koppers
workers
employed
at
eight
coal
tar
facilities
1946­
1977.
Conducted
by
Tabershaw
Occupational
Medicine
Associates,
P.
A.,
Rockville,
MD.
EPA­
OTS/
86­
870001547.
NTIS/
OTS0515707.

U.
S.
Environmental
Protection
Agency.
1986.
Cross­
sectional
health
study
of
workers
at
the
Florence,
South
Carolina
plant
of
Koppers
Company,
Inc.,
with
attachments.
EPA­
OTS/
86­
870001566.

U.
S.
Environmental
Protection
Agency.
1987.
Health
effects
assessment
for
creosote.
EPA­
600/
8­
88/
025).

Von
Burg
R,
Stout
T.
1992.
Toxicology
Update.
Creosote.
Journal
of
Applied
Toxicology.
12(
2):
153­
156.

Weisenburger
DD.
1994.
Epidemiology
of
non­
Hodgkin's
lymphoma:
Recent
findings
regarding
an
emerging
epidemic.
Annals
of
Oncology.
5(
Suppl.
1):
S19­
S24.