EPIDEMIOLOGY AND INCIDENTSINCIDENT REPORTS ASSOCIATED WITH

Creosote

PC Code: 025002

March 9, 2008

U.S. Environmental Protection Agency

Office of Pesticide Programs

Antimicrobials Division

TABLE OF CONTENTS

  TOC \o "1-3" \h \z \u    HYPERLINK \l "_Toc192841956"  0.0
INTRODUCTION	  PAGEREF _Toc192841956 \h  1  

  HYPERLINK \l "_Toc192841957"  1.0	INCIDENT REPORT DATA ASSOCIATED WITH
HEALTH EFFECTS OF CREOSOTE EXPOSURE	  PAGEREF _Toc192841957 \h  1  

  HYPERLINK \l "_Toc192841958"  1.1 	OPP’s Incident Data System (IDS)	
 PAGEREF _Toc192841958 \h  2  

  HYPERLINK \l "_Toc192841959"  1.2 	 Poison Control Center	  PAGEREF
_Toc192841959 \h  3  

  HYPERLINK \l "_Toc192841960"  1.3 	California Data - 1982 through 1996
  PAGEREF _Toc192841960 \h  3  

  HYPERLINK \l "_Toc192841961"  1.4 	National Pesticide
Telecommunications Network (NPTN)	  PAGEREF _Toc192841961 \h  6  

  HYPERLINK \l "_Toc192841962"  2.0 	EPIDEMIOLOGIC STUDIES ASSOCIATED
WITH  HEALTH EFFECTS OF CREOSOTE IN HUMANS	  PAGEREF _Toc192841962 \h  9
 

  HYPERLINK \l "_Toc192841963"  2.1 	Case Series Involving Chronic
Effects Associated with Health Effects of Creosote in Humans	  PAGEREF
_Toc192841963 \h  10  

  HYPERLINK \l "_Toc192841964"  2.2 	Cross-Sectional Studies Associated
with Health Effects of Creosote in Humans	  PAGEREF _Toc192841964 \h  10
 

  HYPERLINK \l "_Toc192841965"  2.3 	Cohort Studies Associated with
Health Effects of Creosote in Humans	  PAGEREF _Toc192841965 \h  14  

  HYPERLINK \l "_Toc192841966"  2.4 	Case Control Studies Associated
with Health Effects of Creosote in Humans	  PAGEREF _Toc192841966 \h  17
 

  HYPERLINK \l "_Toc192841967"  3.0 	SUMMARY AND CONCLUSIONS OF THE
HEALTH EFFECTS OF CREOSOTE IN HUMANS	  PAGEREF _Toc192841967 \h  22  

  HYPERLINK \l "_Toc192841968"  4.0	REFERENCES	  PAGEREF _Toc192841968
\h  26  

 

0.0	INTRODUCTION tc \l1 "0.0	INTRODUCTION 

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.

1.0	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):

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.

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.

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 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
creosote related human health hazard are published in the scientific
literature.

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.

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.

1.2 	 Poison Control Center

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

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 1 presents the number of
cases due to creosote exposure reported by year. Table 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.  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 3. 

Table 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



Table 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	

-



Table 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



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.

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. <NOINDEX>[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]

</NOINDEX>

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.
<NOINDEX>[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]

</NOINDEX>

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. <NOINDEX>[Grant, W.M. Toxicology
of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986.
283]</NOINDEX>

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.
<NOINDEX>[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]</NOINDEX>

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

</NOINDEX>

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

</NOINDEX>

Old creosote treated lumber ... retains a considerable portion of the
oil for periods up to 25 or 30 years. <NOINDEX>[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]</NOINDEX>

2.0 	EPIDEMIOLOGIC STUDIES ASSOCIATED WITH 4.2  TOXICITY ASSESSMENT OF
CARCINOGENIC EFFECTS tc \l2 "4.2  TOXICITY ASSESSMENT OF CARCINOGENIC
EFFECTS  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, case-control, and  cohort studies. 

Case Series Involving Chronic Effects

In addition to the acute incidence report summarized in Section 1.0,
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.

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.

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.

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.

2.1 	Case Series Involving Chronic Effects Associated with Health
Effects of Creosote in Humans

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.

2.2 	Cross-Sectional Studies Associated with Health Effects of Creosote
in Humans

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.

 

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 only 42% participation of
eligible workers, and the lack of individual exposure assessment to coal
tar products.

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.

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.

 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.

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.

2.3 	Cohort Studies Associated with Health Effects of Creosote in Humans

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.

For the entire population of white workers, the standard mortality r

atio (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.

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 self-reported occupational
information from a single census observation, lack of control for
multiple exposures, and no consideration for nonoccupational exposures.

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.

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 0.03μg/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.

2.4 	Case Control Studies Associated with Health Effects of Creosote in
Humans

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.

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.

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 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.

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.

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.

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.

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.

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).

3.0 	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.



Table 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	

Cross-sectional	

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	

Cross-secional	

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)	

Cross-sectional	

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	

Cross-sectonal	

OH	

Occup	

59	

Mixed	

No evidence of disease associated with past exposure to creosote.	





1986	

EPA-OTS 86-870001566	

Tabershaw Occupational Medicine Associates	

Cross-sectional	

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	

1,905,660	

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.	





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 case-control	

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	





4.0	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 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 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.

„

O

Û

	

	

&

'

(

)

-

.

b

c

d

~



€

‚

ƒ

„

…

†

¢

£

£

¤

¥

©

ª

õ

ö

÷

,

-

.

H

I

J

L

M

N

O

P

Q

m

n

n

o

p

t

u

¸

¹

º

Ô

Õ

Ö

Ø

Ù

Ú

Û

Ü

Ý

ù

ú

û

ü

j;

j¸

kdv

愀Ĥ摧撃R

|

愀Ĥ摧撃R

&

„@

„Àô^„@

y of non-Hodgkin’s lymphoma: Recent findings regarding an emerging
epidemic.  Annals of Oncology.  5(Suppl. 1):S19-S24.

 PAGE   

 PAGE   

 PAGE   1 

 PAGE   1 

	

`

