UNITED STATES                         EPA/600/8-Si/i31
ENVIRONMENTAL PROTECTION               JUNE 1988
AGENCY                               FINAL
RESEARCH  AND
DEVELOPMENT
EVALUATION OF THE POTENTIAL CARCINQGENICITY OF

ETHYLENE OXIDE

<75-ZI»8)





IN SUPPORT OF REPORTABLE OUAHTITY ADJUSTMENTS

PURSUANT TO CERCLA SECTION 102
PREPARED  FOR

OFFICE OF EMERGENCY AND REMEDIAL RESPONSE

OFFICE OF SOLID WASTE AND EMERGENCY RESPONSE
PREPARED BY
CARCINOGEN ASSESSMENT GROUP
OFFICE OF HEALTH AND
ENVIRONMENTAL  ASSESSMENT
WASHINGTON, E).C.  20460

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                                  DISCLAIMER
This document has been reviewed in accordance with U.S.  Environmental
Protection Agency policy and approved for publication.   Mention of trade names
or commercial products does not constitute endorsement or recommendation for
use,
                                      LI

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                                   PREFACE








This report summarizes and evaluates information on the potential



carcinogenicity of a substance designated as hazardous under Section 101 (14)



of the Comprehensive Environmental Response, Compensation and Liability Act of



1980 (CERCLA).  Pertinent epidemiologic and toxicologic data were obtained



through on-line searches and from hard-copy sources.  On-line searches were



extended as far back as the data bases would allow.  Retrieval of historical



data was accomplished through searches of hard-copy sources and bibliographies



of relevant publications.  Every attempt has been made to rely upon primary



publications as opposed to data summaries or abstracts contained in secondary



sources such as monographs, surveys, review articles, criteria documents, etc.



The on-line data bases that were searched included CHEMLINE  (National Library



of Medicine [NLM]),  RTECS  (NLM), Toxicology Data Bank  (NLM),  TOXLINE  (NLM),



CANCERLINE  (NLM),  and Chemical Abstracts (DIALOG Information Services),



Unpublished data were not used in this evaluation.







The Agency's Methodology for obtaining, evaluating, and ranking CERCLA



potential carcinogens is described in the Technical Background Document to



Support Rulemaking Pursuant to CERCLA Section 102, Volume 3,  April 26, 1988



(EPA/600/8-89/053).   This document revises the previous methodology document



of 1986 according to the public comments received on the March 16, 1987 Notice



of Proposed Rulemaking (52 FR 8140).  The Methodology for Adjusting reportable



quantities is described in the Technical Background Document to Support



Rulemaking Pursuant to CERCLA Section 102,  Volume 1, March,  1985, and is also



summarized in Volume 2, August, 1986, and Volume 3, December, 1986,  The EPA's



Office of Emergency and Remedial Response  (OERR) has considered this



evaluation in adjusting reportable quantities pursuant to CERCLA Section 102.



This report is consistent with the revised methodology.  It  draws largely  on



information supplied by the Syracuse Research Corporation in 1984 under  EPA



Contract No. 68-03-3112.   Due to the amount of time elapsed  between the



original work performed by Syracuse Research Corporation and the present
                                      iii

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effort to produce this document, Environmental Monitoring & Services, Inc.,



under EPA Contract No. 68-03-31S2, has been involved in an extensive review of



all the Syracuse documents.  In some cases, this review involved updating the



information provided but it was primarily a quality assurance effort.  The



present document is a result of thig effort.
                                       IV

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                                   ABSTRACT
Ethylene oxide is a probable human carcinogen, classified as weight-of-evidence
Group Bl under the EPA Guidelines for Carcinogen Risk Assessment (U.S. EPA,
1986a).  Evidence on potential carcinogenicity from animal studies is
"Sufficient," and the evidence from human studies is "Limited,"

The potency factor for ethylene oxide is estimated to be 1.34 (mg/kg/day)  ,
placing it in potency group 2 according to the CAG's methodology for evaluating
potential carcinogens (U.S. EPA, 1986b),

Combining the weight-of-evidence group  and the potency group, ethylene oxide
is assigned a "MEDIUM" hazard ranking for the purposes of RQ adjustment., (When
the weight-of-evidence is expressed as  a range, i.e., Bl, the hazard ranking
is based on the higher weight-of-evidence group).

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                           TABLE OF CONTENTS
                                                                   Page
1.0 WEIGHT OF EVIDENCE 	  .....   1-1
1.1 ANIMAL STUDIES 	  .......   1-1
1.2 HUMAN STUDIES	,	1-3
1.3 WEIGHT-OF-EVIDENCE ASSESSMENT	1-4

2.0 POTENCY. .		2-1

3.0 HAZARD RANKING	   3-1

4.0 REFERENCES	4-1

    APPENDIX: SUMMARY OF SIGNIFICANT HUMAN AND/OR ANIMAL STUDIES
                                TABLES
Table 2-1.  DERIVATION OF POTENCY FACTOR (F)	2-2 .P
                                      VI

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                             1.0 WEIGHT OF  EVIDENCE
1,1 ANIMAL STUDIES

Weekly subcutaneous injections of 0.1-1.0 mg ethylene oxide for 95 weeks
induced dose-related local sarcomas in female NMRI mice (Dunkelberg, 1979,
1981),  but the incidence of tumors at distant sites was not significantly
greater in the treated mice than in controls,  Walpole (1958) reported that
subcutaneous injections of ethylene oxide over a period of 94 days did not
induce local sarcomas in 12 rats (species not stated).  The maximum total dose
(MTD) was 1 g/kg and the animals were observed for their lifetimes, but the
dosing schedule was not specified. Thrice weekly dermal applications of
ethylene oxide for life (approximately 10 mg per application) did not cause
skin papillomas or carcinomas in Swiss-Millerton mice (Van Duuren et al.,
1965).

Reyniers et al. (1964) observed that tumors developed at various sites  (e.g.,
ovaries, lymphatic system, lungs) in 63 of 86 female germ-free Swiss-Webster
mice that were accidentally exposed to ethylene oxide- treated ground-corncob
bedding for their lifespan (maximal, 900 days). No tumors were reported in 83
female mice (100-600 days old) that were not exposed to treated bedding.  It
should be emphasized that this study was not designed to test the
carcinogenicity of ethylene oxide, and that  the causative agent was not
identified since chemical analysis of the bedding was not performed.

A chronic inhalation study was performed by  the Bushy Run Research Center
 (Snellings et  al., 1984). Fischer 344 rats were exposed to 100, 33 and  10 ppra
ethylene oxide vapor for 6 hours/day, 5 days/week for 24.5 months  (females) or
25 months  (males).  Two untreated air groups were exposed under similar
conditions.  Initially, 120 rats/sex/group were exposed, but interim sacrifices
were conducted at 6, 12, and  18 months  (10,  10 and 20 rats,  respectively).  At
 terminal sacrifice, histopathologic examinations were performed on
approximately  15 major organs and tissues of rats in the 100 ppm  and both
control groups, and on potential  target tissues, selected tissues, and  tissues
                                      1-1

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with gross lesions in the 10 and 33 ppm groups.  The results showed that there
was a dose-related increase in the incidence of mononuclear cell leukemia in
the female rats at terminal sacrifice (15/26, 14/48, 11/54 and 11/115 in the
100, 33, 10 ppm and combined controls, respectively).  In male rats,
statistically significant increases in subcutis fibroma at 100 ppm  (15/58 vs.
4/137 in combined controls) and pancreas islet cell adenoma at 100 ppm (10/59
vs. 10/129 in combined controls) were found. The exposure of both the male and
female rats was temporarily terminated during exposure weeks 65 and 66, due to
a Sialodacryoadenitis virus infection, but no evidence was presented that the
infection increased tumor incidence.

The chronic inhalation toxicity and carcinogenicity of ethylene oxide was
evaluated in a 2-year inhalation bioassay (Lynch et al., 1984).  Five groups of
male weanling Fischer 344 rats, 80 per group, were exposed at 0 ppm (paired
control; filtered air),  50 ppra, or 100 ppra  (7 hr/day, 5 days/week)  for 104
weeks, statistically significant increase in mortality was observed in all
groups of exposed rats compared to controls.  Statistically significant
associations between ethylene oxide exposure and an increased incidence of the
following rat neoplasms  were observed: peritoneal mesothelioma, and mixed cell
brain glioma.  A statistically significant  increase in mononuclear  cell
leukemias was seen at the low dose (50 ppm) but not at the high dose (100 ppm) .

In  the Carman et al.  (1985) study, groups of F344 rats of each sex were exposed
to  either ethylene oxide vapor  (concentrations of 100, 33 or 10 ppm) or to room
air for  6 hours daily, 5 days/week, for up  to  2 years. Three representative
sections of  the brain from  each rat were evaluated. Twenty-three primary brain
tumors were  found, two of which were  in control animals.  Increased numbers of
brain  tumors were seen in 100 ppm and 33 ppm ethylene oxide exposed male and
female  rats. Significant trend  analyses were found  for both males and  females,
indicating  that, under the  conditions of this  study, ethylene oxide exposure
above  10 ppm was  related to the development of these brain tumors.

The National Toxicology  Program conducted  toxicological  and carcinogenesis
studies  of  ethylene  oxide by  exposing groups of 50  B6C3F1 mice of each sex  to
air containing  0,  50 or  100 ppm ethylene oxide for  6 hours/ day, 5  days/week
                                      1-2

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for 102 weeks (NTP, 1986).  This study has been peer-reviewed and the data is
reproduced In Appendix A, and suraarized below.

In male B6C3F1 mice, alveolar/bronchial adenomas or carcinomas and harderian
gland cystadenomas were produced with a positive trend.  Both the life table
and the incidental tumor tests showed a significant difference between controls
and experimentals exposed at 100 ppra.  At 50 ppm, the above two tests were also
significant for harderian gland tumors but not for alveolar/bronchial adenomas
or carcinomas.

In female B6C3F1 mice, alveolar/bronchial adenomas or carcinomas and harderian
gland cystadenomas, malignant lyraphomas and uterine adenocarcinoraas occurred
with positive trends.  Both life table and incidental tumor tests showed a
significant difference between controls and experimentals exposed at 100 ppm
for lung tumors, harderian gland tumors and malignant lymphomas, but not for
uterine adenocarcinomas.

The NTP staff and peer review group concluded that there was "clear evidence of
carcinogenic activity for B6C3F1 mice" as indicated by dose-response increases
in the incidence of benign and malignant neoplasms of the lung and benign
neoplasms of the harderian gland in both male and female mice.  The NTP also
concluded that  "in female mice, ethylene oxide caused additional malignant
neoplasms of the uterus, mammary gland and hemopoietic system (lymphoma)," but
of these tumors, only lymphomas were significantly different from concurrent
controls.  The  incidence of lyraphoraas in these ethylene oxide exposed mice was
not significantly different from historical controls for this strain of mice
(NTP, 1986).

1.2 HUMAN STUDIES

Three studies conducted  in Sweden reported an increased risk of leukemia
following occupational exposure to ethylene oxide.  In the first study
(Hogstedt et al.,  1979a), which also showed increased  rates of gastric cancer,
a  small number  of  Swedish ethylene oxide production workers were also
                                       1-3

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concurrently exposed to chemicals other than ethylene oxide and the increased
rates cannot confidently be attributed to ethylene oxide alone.

In the second study (Hogstedt et al., 1979b),  three cases of leukemia occurred
in a small group (230) of Swedish workers who were exposed to fugitive ethylene
oxide emissions that originated from sterilized hospital equipment.  The
exposure to ethylene oxide in this study (20 ± 10 ppm) was fairly well
characterized. In 1984, Hogstedt et al. reported the first follow-up on their
original studies reported in 1979.  In this report, the reported cases of
leukemia increased from three cases to five cases. These were in women who had
been exposed to from two to 70 ppra ethylene oxide  (8 hr/day, time-weighted
average calculated to be 20 + 10 ppm).

Hogstedt et al. (1986) reported eight cases of leukemia and six cases of
stomach cancer in workers exposed to ethylene oxide as compared to 0.8 and 0.65
cases expected as indicated in a similar industrial cohort. This study was a
follow-up on their investigations reported previously in 1979 and  1984.

In another mortality study  (Morgan et al. , 1981),  no significant excess of
deaths from leukemia or other malignant neoplasms  was reported in  a group of
767 males who were potentially exposed to ethylene oxide for 5 to  18 years at a
U.S. production facility.  Although  the size of the cohort was small and the
workers appeared to have only minimal exposure (<10 ppm), exposure was
associated with increased incidences of pancreatic cancer and Hodgkin's disease
(U.S. EPA, 1985).

1.3  WEIGHT-OF-EVIDENCE ASSESSMENT

There are sufficient data to indicate that ethylene oxide is a carcinogen in
rats and mice when administered via  inhalation. Weekly subcutaneous injections
of ethylene oxide for  95 weeks produced a dose-related increase in the
incidence of  local tumors in mice.   The results of an inadequately reported
subcutaneous  injection study with rats were negative, and the  results of a
lifetime skin application bioassay with mice were  also negative.   An increased
incidence of  tumors was observed  in  a group of mice  that were  accidentally
                                      1-4

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exposed.   to   ethylene  oxide-treated   bedding,   but  the   exposure   was  not
characterized   and  this   observation  does  not   allow   an   evaluation  of
careinogenieity.

In  a.  two-year   inhalation study,   a  dose-related  increased  incidence  of
mononuclear cell  leukemia was  found  in female rats.   Significantly increased
incidences of  subcutis fibromas and  pancreatic  adenomas were  found  in males.
Gliomas were also significantly increased in both males and  females.
Thus  in  B6C3F1  mice,  there  was  clear evidence of carcinogenic  activity  as
indicated  by  a  dose-related   increased  incidence   of  benign and  malignant
neoplasms of the  lung as well as  benign neoplasms  of the  harderian gland. The
incidences were significantly elevated above control animals in both sexes.

The evidence indicating a carcinogenic effect in humans  due to ethylene oxide
exposure  is  limited because human exposure  has been  difficult to quantitate.
Three  studies  of  human populations  exposed occupationally to  ethylene oxide
have  shown  increased  rates  of stomach  cancer and leukemia, but  the exposure
associated with  these  increases  in cancer  has  been difficult  to quantitate,
making human  potency  estimates  tenuous.   The results  of  a  fourth  mortality
study  did not  report  increased  leukemia  or  sto r.ach cancer,   but significant
increases in pancreatic cancer and Hodgkin's disease were noted.

The  findings  of  leukemia  in rats  exposed  to ethylene   oxide  via  chronic
inhalation,  however, were  consistent with  the  epidemiologic data.   Thus, using
the  EPA  Guidelines  for   Carcinogen  Risk  Assessment  (U.S. EPA,  1986a)  for
evaluating the  overall weight  of evidence  to humans,  ethylene oxide  is most
appropriately  classified  as  a  Group  Bl  chemical.  The  appendix  contains
summaries of the significant human and/or animal studies cited in this review.
                                      1-5

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                                  2.0  POTENCY
The  potency   factor  (F)  for   ethylene   oxide  is  estimated   to   be  1.34
(mg/kg/day)-1,  placing it in potency group  2  under the CAG's 2-1 contains data
from the  selected  study  used to  derive  the potency  factor (F)  for ethylene
oxide.
                                      2-1

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                 Table 2-1.  Derivation of Potency Factor(F)
                                Agent:  Ethylene oxide
 REFERENCE:

 EXPOSURE ROUTE:

 SPECIES:

 STRAIN:

 SEX:

 VEHICLE OR PHYSICAL STATE:

 BODY WEIGHT:

 DURATION OF TREATMENT:

 DURATION OF STUDY:

 LIFESPAN OF ANIHAL:

 TARGET ORGAN(S):

 TUMOR TYPE:

 EXPERIMENTAL DOSES/EXPOSURE:8

 TRANSFORMED DOSES:b
   (mg/kg/day)

 TUMOR INCIDENCE:6

 ANIMAL POTENCY:
   (mg/kg/day)

HUMAN POTENCY :f
   (mg/kg/day)
              •1
NTP, 1986

inhalation

mice

B6C3F1
M

inhalation

0.035 kg

730 days (6 hrs/day, 5 days/week)

730 days

730 days

lung

adenomas and carcinomas

100 ppm             50 ppm

39.90               19.95
26/50d

0.106


1.34
19/50e
0 ppm

0


11/50
  Exposure was via inhalation for 6 hours/day,  5  days/week,  for  approximately  2  years.
b To derive the transformed dose from the experimental  dose  data:  experimental dose  (ppm)  x  0.041  x M.U. of ethylene oxide (44.05 g/mol) x 0.0432
  mg/day (rat's breathing rate)/ 0.035 kg (animal  weight)  x  5  (treatment  days/week)/?  (days/week)  x 6 (treatment hours/day)/24 (hours/day).
c Total  tumor count ratios based on number of  rats alive  at  24 months.
  One animal  developed both an adenoma and a  carcinoma.
e Two animals developed both an adenoma and a  carcinoma.
' Human  potency = animal  potency x (70 kg/0.035 kg)^'

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                              3.0  HAZARD RANKING
Based on the weight-of-evidence Group Bl for ethylene oxide, and the potency
factor (F) of 1,34 (mg/kg/day)"^-, ethylene oxide receives a hazard ranking of
"MEDIUM."
                                       3-1

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                                4.0  REFERENCES
Dunkelberg, H.,  1979.  On the Oncogenic Activity of Ethylene Oxide and
Propylene Oxide in Mice.  Br. J. Cancer,  39(4); 588-589,

Dunkelberg, H. ,  1981.  Carcinogenic Activity of Ethylene Oxide and Its Reaction
Products 2-Chloroethanol, 2-Bromoethanol, Ethylene Glycol, and Diethylene
Glycol.  I. Carcinogenicity of Ethylene Oxide in Comparison with 1,2-Propylene
Oxide After Subcutaneous Administration in Mice. Zentrabl, Bakteriol.,
Mikrobiol.  Hyg.  174(5): 383-404.

Carman, R.H., W.M. Snellings, and R.R. Maronpot, 1985.  Brain Tumors in F344
Rats Associated with Chronic Inhalation Exposure to Ethylene Oxide,
Neurotoxicology 6(1): 117-138.

Hogstedt, C,, D. Rohlen, B.S. Berndtsson, 0. Axelson and L. Ehrenberg, 1979a.
A Cohort Study of Mortality and Cancer Incidence in Ethylene Oxide Production
Workers.  Br. J. Ind. Med.  36(4): 276-280.

Hogstedt, C., N. Malmgrist and B. Wadraan, 1979b.  Leukemia in Workers Exposed
to Ethylene Oxide.  J. Araer. Med. Assoc.  241(11): 1132-1133.

Hogstedt, C., L. Aringer, A. Gustavsson, 1984,  Ethylene Oxide and Cancer:
Review of the Literature and Follow-up of 2 Studies.  Arb. Halsa 49:1-32.

Hogstedt, G., L. Aringer, A. Gustavsson, 1986.  Epidemiologic Support for
Ethylene Oxide as a Cancer-causing Agent.  J. Am. Med. Assoc. 255:1575-1578.

Lynch, D.W., T.R. Lewis, W.J. Moorman, J.R. Burg, D.H. Groth, A. Khan, L,J.
Ackerman, and B.Y. Cockrell, 1984.  Carcinogenic and Toxicologic Effects of
Inhaled Ethylene Oxide and Propylene Oxide in F344 Rats. Toxicol.  Appl.
Pharraacol.  76:  69-84.
                                      4-1

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Morgan, R.W.,  K.W. Claxton, B.J. Divine, S.D. Kaplan and V,B, Harris, 1981,
Mortality Among Ethylene Oxide Workers.  J. Occup, Med.  23(11): 767-770.

National Toxicology Program (NTP),  1986 (Final Draft).  Toxicology and
Carcinogenesis Studies of Ethylene Oxide in B6C3F1 Mice.  NTP TR 326. National
Institute of Health, Research Triangle Park, NC.

Reyniers, V.,  M. Sachsteder and L,  Ashburn, 1964.  Multiple Tumors in Female
Germ-Free Inbred Albino Mice Exposed to Bedding Treated with Ethylene Oxide.
J. Natl. Cancer Inst.  32; 1045-1057.

Inhalation Study of the Carcinogenic Potential of Ethylene Oxide in Fischer 344
Rats, Toxicology and Applied Pharmacology 75: 105-117.

U.S. EPA (Environmental Protection Agency), 1985.  Health Assessment Document
for Ethylene Oxide, Final Report.  EPA/600/8-84/009F, Office of Health and
Environmental Assessment, Washington, D.C., June, 1985.  NTIS PB86-102597.

U.S. EPA (Environmental Protection Agency), 1986a.  Guidelines for Carcinogen
Risk Assessment, 51 FR 33992-34003, September 24, 1986.

U.S. EPA (Environmental Protection Agency), 1986b.  Methodology for Evaluating
Potential Careinogenieity in Support of Reportable Quantity Adjustments
Pursuant to CERCLA Section 102, OHEA-C-073, December 1986.   Available from
CERCLA Docket 102RQ-273C.  The public document for RQ rulemaking is located in
room M2427, U.S. Environmental Protection Agency, 401 M Street, SW, Washington,
DC 20460.  It is available for inspection Monday through Friday excluding
Federal holidays, between the hours of 9:00 a.m. and 4:00 p.m.

U.S. EPA (Environmental Protection Agency), 1988.  Technical Background
Document to Support Rulemaking Pursuant to CERCLA Section 102, Volume 3, Draft,
Appendix A, April 26, 1988.

Van Duuren, B., L, Orris and N. Nelson, 1965.  Carcinogenicity of Epoxides,
Lactones, and Peroxy Compounds.  II.  J. Natl. Cancer Inst. 35: 707-717.
                                      4-2

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Walpole, A., 1958.  Carcinogenic Action of Alkylating Agents.   Ann NY Acad.
Sci,  68: 750-761.
                                      4-3

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                     APPENDIX
SUMMARY OF SIGNIFICANT HUMAN AND/OR ANIMAL STUDIES

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                                                                 Table A.   Animal
                                                              Agent:   Ethylene Oxide
                                                        Reference:   Dunkelberg,  1979;  1981
Exposure Species/
Route Strain Sex
subcu- mice/NMRI F
taneous


subcu- mice/NMRI F
taneous


subcu- mice/NMRI F
taneous

subcu- mice/NMRI F
taneous


Dose
or
Exposure
1 .0 mg/in-
jection/wk


0.3 mg/in-
jection/wk


0.1 mg/in-
jection/wk

0.0 mg/in-
jection/wk


Duration Duration Purity Vehicle or
of of of Physical
Treatment Study Compound State
95 weeks 91 weeks NRb tricapry-
lin


95 weeks 91 weeks NRb tricapry-
I in


95 weeks 91 weeks NR tricapry-
lin

NA 91 weeks NA tricapry
I in

QUALITY OF EVIDENCE
Target
Organ
inject i on
site (inter-
scapular)

injection
site (inter-
scapular)

injection
site (inter-
scapular)
injection
site (inter-
scapular)

Tumor Type
total tumors
sarcoma6
lymphoma
granuloma
total tumors
sarcoma0
lymphoma
basal cell carcinoma
total tumors
sarcoma0
lymphoma
total tumors
sarcoma6
lymphoma

Tumor
Incidence
(P value)
15/100
11/100
2/100
2/100
12/100
8/100
2/100
2/100
7/100
5/100
2/100
5/100
4/100
1/100

Strengths of Study:

Weaknesses of Study:

Overall Adequacy:

Comments:
Multiple dose levels of the compound were administered over  a significant portion of the lifespan.

A non-natural route of administration was employed.

Limited.

The number of tumors at distant sites was not  significantly  greater  in  treated mice compared with vehicle controls.
  Preliminary results up to 91st week of treatment.
  Purity not reported,  but impurities checked for by IR, GC,  and Fluoresence methods.
c Predominately fibrosarcomas.
NA * Not applicable;  NR - Not reported

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      Table A.  Animal





    Agent: Ethylene Oxide





Reference: Lynch et al.(  1984
Dose Duration Duration Purity Vehicle or
Exposure Species/ or of of of Physical Target
Route Strain Sex Exposure Treatment Study Compound State Organ
inhal- rats/ M 100 ppm 104 weeks 104 weeks 99. 7X filtered adrenal
ation Fischer pure air
344
brain
body
cavity
pancreas
pituitary
spleen
inhal- rats/ H 50 ppm 104 weeks 104 weeks 99.7% filtered adrenal
ation Fischer pure air
344
brain glioma (mixed
body
cavity
pancreas
pituitary
spleen
Tumor Type
pheochromocytoma
glioma (mixed cell)
peritoneal
mesothel iomas
islet cell
adenoma
adenoma
mononuclear
cell leukemia
pheochromocytoma
cell)
peritoneal
mesothel iomas
islet cell
adenoma
adenoma
mononuclear
cell leukemia
Tumor
Incidence
(P value)
13/78
(MS)
5/79
(P<0.05)
21/79
(P<0.01)
15/73
(MS)
21/67
(P<0.05)
30/76
(MS)
14/77
(MS)
2/77
(NS)
9/79
(NS)
16/73
(MS)
20/66
(P<0.05)
38/79
(P<0.05)

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                                                                 Table A.  Animal





                                                               Agent:  Ethylene Oxide





                                                      Reference:  Lynch  et  al., 1984   (Page 2)
Dose
Exposure Species/ or
Route Strain Sex Exposure
inhal- rats/ H 0 ppm
ation Fischer
344





Duration Duration Purity Vehicle or
of of of Physical Target
Treatment Study Compound State Organ
104 weeks 104 weeks 99.7% filtered adrenal
pure air
brain
body
cavi ty
pancreas
pi tui tary
spleen
QUALITY OF EVIDENCE
Tumor Type
pheochromocytoma
gl ioma (mixed cell)
peri toneal
mesothel iomas
islet eel I
adenoma
adenoma
mononuc lear
cell leukemia

Tumor
Incidence
(P value)
8/78
0/76
3/78
23/77
44/73
24/77

Strengths of Study:





Weaknesses of Study:





Overall Adequacy:





Comments:
2-year study duration





Only one species and strain used





Adequate





Other response data was given,  but is not recorded in this table.

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          Table A.   Animal





       Agent:   Ethylene Oxide





Reference:   NTP,  1986-Draft (Page 1)
Dose
Exposure Species/ or
Route Strain Sex Exposure
inhal- mice/ H 0 ppm
at ion B6C3F1




inhal- mice/ H 50 ppm
at ion B6C3F1




inhal- mice/ M 100 ppm
at ion B6C3F1




Duration Duration Purity Vehicle or
of of of Physical Target
Treatment Study Compound State Organ
102 weeks 104 weeks >99X air lung
pure

lung


102 weeks 104 weeks >99X air lung
pure

lung


102 weeks 104 weeks >99X air lung
pure

lung


Tumor Type
alveolar/
bronchiolar
adenoma
alveolar/
bronchiolar
carcinoma
alveolar/
bronchiolar
adenoma
alveolar/
bronchiolar
carcinoma
alveolar/
bronchiolar
adenoma
alveolar/
bronchiolar
carcinoma
Tumor
Incidence
(P value)
5/10


6/50


11/50
(P=0.095)

10/50
(P*0.230)

11/50
(P=0.127)

16/50
(P=0.019)


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          Table A.   Animal





       Agent:   Ethylene Oxide





Reference:   NTP,  1986-Draft  (Page  2)
Dose
Exposure Species/ or
Route Strain Sex Exposure
inhal- mice/ F 0 ppm
ation B6C3F1






inhal- mice/ F 50 ppm
ation B6C3F1






inhal- mice/ F 100 ppm
ation B6C3F1






Duration Duration Purity Vehicle or
of of of Physical Target
Treatment Study Compound State Organ
102 weeks 104 weeks >99X air lung
pure

lung


lymph
gland
102 weeks 104 weeks >99X air lung
pure

lung


lymph
gland
102 weeks 104 weeks >99X air lung
pure

lung


lymph
gland
Tumor Type
alveolar/
bronchiolar
adenoma
alveolar/
bronchiolar
carcinoma
mal ignant
lymphoma
alveolar/
bronchiolar
adenoma
alveolar/
bronchiolar
carcinoma
malignant
lymphoma
alveolar/
bronchiolar
adenoma
alveolar/
bronchiolar
carcinoma
mal i gnant
lymphoma
Tumor
Incidence
(P value)
2/49


0/49


9/49

4/48

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                                                                 Table A.   Animal





                                                              Agent:   Ethylene Oxide





                                                       Reference:   NTP,  1986-Oraft  (Page  3)
Dose
Exposure Species/ or
Route Strain Sex Exposure
inhala- mice/ F 50 ppm
ation B6C3F1




100 ppm






Duration Duration Purity Vehicle or
of of of Physical Target
Treatment Study Compound State Organ Tumor Type
102 weeks 10A weeks >99% air uterus uterine
pure adenocarci noma
mammary mammary gland
gland adenocarcinoma or
adenosquamous
carcinoma
uterus uterine
adenocarcinoma
mammary mammary gland
gland adenocarcinoma or
adenosquamous
carcinoma
QUALITY OF EVIDENCE
Tumor
Incidence
(P value)
1/A7
(P=0.383)
8/A8
(P=0.012)


5/A9
(P=0.051)
6/A9
(P=0.087)



Strengths of Study:





Weaknesses of Study:





Overall Adequacy:





Comments:
Used two sexes; 2-year study duration; statistical  information given.





Only one species and strain of animal  used.





Adequate





Authors report benign neoplasms of the Harderian gland (not  included  in  this  table).

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        Table A.  Animal





     Agent:  Ethylene Oxide





Reference:   Snelling et  al.,  1981
Dose Duration Duration Purity Vehicle or
Exposure Species/ or of of of Physical Target
Route Strain Sex Exposure* Treatment Study Compound State Organ Tumor Type
inhal- rat/F344 H 100 ppm 98 weeks 100 weeks NR vapor subcutis fibroma
at ion
pancreas adenoma
pituitary adenoma
peritoneum mesothel ioma
spleen leukemia
Tumor
lncidencec
(P value)
10/28e
(P<0.001)
15/78e
(P<0.001)
5/30
(NS)
11/80
(P<0.05)
12/29
(NS)
11/80
(P<0.05)
4/30
(NS)
21/80
(P<0.001)
8/30
(NS)
25/80
(NS)

-------
            Table A.  Animal





Reference:   Snelling et  al.,  1981  (cont.)
Dose Duration Duration Purity Vehicle or
Exposure Species/ or of of of Physical Target
Route Strain Sex Exposure8 Treatment" Study Compound State Organ Tumor Type
inhal- rat/F344 H 33 ppm 98 weeks 100 weeks NR vapor subcutis fibroma
ation
pancreas adenoma
pituitary adenoma
peritoneum mesothel ioma
spleen leukemia
inhal- rat/F344 H 10 ppm 98 weeks 100 weeks NR vapor subcutis fibroma
at ion
pancreas adenoma
pituitary adenoma
peritoneum mesothelioma
spleen leukemia
Tumor
Incidence0
(P value)
1/34e
(NS)
3/75e
(NS)
V2f
1/43f
13/39
(NS)
16/79
(NS)
4/39
(NS)
6/80
(P<0.05)
10/39
(NS)
23/80
(NS)
8/48e
(P<0.01)
10/776
(P<0.001)
2/30
2/32f
15/51
(NS)
26/79
(NS)
2/51
(NS)
3/80
(NS)
9/51
(NS)
21/80
(NS)

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            Table A.  Animal





Reference:  SnelUng et  al.,  1981  (cont.)
Dose
Exposure Species/ or
Route Strain Sex Exposure8
inhal- rat/F34A H 0 ppm
at ion








inhal- rat/F3A4 F 100 ppm
at ion


33 ppm



10 ppm



0 ppm"

Duration Duration Purity Vehicle or
of of of Physical Target
Treatment Study Compound State Organ Tumor Type
NA 100 weeks NA NA subcutis fibroma

pancreas adenoma

pituitary adenoma

peritoneum mesothelioma

spleen leukemia

96 weeks 98 weeks NR vapor spleen leukemiad



96 weeks 98 weeks NR vapor spleen leukemiad



96 weeks 98 weeks NR vapor spleen leukemiad



NA 98 weeks NA NA spleen leukemiad

Tumor
Incidence0
(P value)
3/91
4/154
7/97
7/160
19/97
43/157
2/97
3/160
13/97
38/160
15/26
(P<0.001)
27/80
(P<0.001)
K/48
(P<0.01)
24/80
(P<0.01)
11/54
(P<0.05)
H/80
(NS) .
11/115
22/156

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                                                                Table A.  Animal

                                                    Reference:   Smelling et  al.,  1981  (cont.)

Exposure
Route

Species/
Strain Sex
Dose
or
Exposure8
Duration
of
Treatment
Duration
of
Study
Purity
of
Compound
Vehicle or
Physical
State

Target
Organ Tumor Type
Tumor
Incidence0
(P value)
                                                               QUALITY  OF  EVIDENCE

Strengths of Study:    Multiple exposure levels  were  administered  by  a  natural  route over  a  significant portion of the lifespan.

Weaknesses of Study:   All rats became infected  with  sialodacryoadenitis virus  during the  15th  exposure month.

Overall Adequacy:      Adequate

a Exposures were 6 hours/day,  5 days/week.
  Exposures were temporarily terminated during weeks  64  and  65  to  permit recovery  from sialodacryoadenitis virus infection.
c Pooled control data given.  Incidence of  tumors  In  rats  at final  sacrifice  listed  first. Combined incidence of tumors in rats
  at final sacrifice and rats  dying  spontaneously  or  euthanized when  moribund listed second.
  Hononuclear cell leukemia
e Examined only if gross lesions were  present (except  flank  region  which was  routinely examined microscopically).
  Data from the 33 and 10 ppm  groups were not statistically  analyzed  because  tissues wsere not  examined from all rats (e.g.,
  only gross lesions were examined).
9 Two untreated air groups were exposed.

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                                                                 Table  A.   Animal





                                                              Agent:  Ethylene  Oxide





                                                         Reference:  Snelling  et  al.,  1984
Dose
Exposure Species/ or
Route Strain Sex Exposure
inhal- rats/ F 100 ppm
ation F344
33 ppm
10 ppm
0 ppm
Duration
of
Treatment
730 days
730 days
730 days
730 days
Duration
of
Study
730 days
730 days
730 days
730 days
Purity Vehicle or
of Physical
Compound State
99. 9X air
99. 9X air
99. 9X air
99. 9X air
Target
Organ
hematopoetic/
brain
hematopoetic/
brain
hematopoetic/
brain
hematopoetic/
brain
Tumor Type
leukemia/
gliomas
leukemia/
gliomas
leukemia/
gl iomas
leukemia/
gliomas
Tumor
Incidence
(P value)
32/73
27/72
15/71
23/186
QUALITY OF EVIDENCE
Strengths of Study:





Weaknesses of Study:





Overall Adequacy:





Comments:
Both male and female rats were used.  Two control groups were used.





Only the results which the author considereJ significant were reported.





Sufficient





Dosage was 6 hrs/day,  5 days/wk.

-------
                                                                 Table A.   Animal

                                                              Agent:   Ethylene  Oxide

                                                       Reference:  Van Duuren et al., 1965
Exposure Species/
Route Strain
dermal mice/
Swiss
Hi llerton
dermal mice/
Swiss
Hi llerton

Strengths of Study:
Weaknesses of Study:
Overall Adequacy:
Dose Duration Duration Purity Vehicle or
or of of of Physical Target
Sex Exposure Treatment Study Compound State Organ Tumor Type
F approx. 10 mg/ life life 99. 7X acetone skin papilloma
application carcinoma
thrice weekly*
F 0 mg/appli- NA life MA acetone skin papilloma
cation (vehicle carcinoma
control)
QUALITY OF EVIDENCE
The compound was administered over the lifespan and all gross tumors were con firmed microscopically.
Aqueous solutions are not typical for dermal exposure. All organs were not examined.
Adequate
Tumor
Incidence
(P value)
0/30
0/30
0/60
0/60




a Approximately 0.1 ml of a 10X solution/application.
b Median survival times in the treated and control rats were 493 and 447 days,  respectively.
NA * Not applicable

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         Table B.   Humans



      Agent:  Ethylene Oxide



Reference:  Hogstedt et al., 1979a
Exposure
Route
inhal-
ation




inhal-
ation




inhal •
at ion



inhal •
ation




inhal •
ation


inhal •
ation


Size of
Exposed
Populat ion
89 (1324
person
years)



NR (372
person
years)



86 (1211
person
years)


NR (736
person
years)



66 (955
person
years)

NR (603
person
years)

Size of
Control Level of Duration of
Population Sex Exposure8 Exposure
Swedish M fulltlme >.! yr exposure,
population exposure >.10 yrs latency




Swedish H fulltlme >.10 yr exposure,
population exposure >.20 yrs latency




Swedish M Intermit- >,1 yr exposure,
population tent expo- >.10 yrs latency
sure


Swedish H intermit- >.! yr e>P-osure,
population tent expo- >20 yrs latency
sure



Swedish H unexposed >,1 yr exposure,
population £10 yrs latency


Swedish H unexposed >.10 yr exposure,
population >20 yrs latency


Target
Organ
total tumors

stomach

hematopoiet ic

total tumors

stomach

hematopoiet ic

total tumors

stomach
hematopoiet ic

total tumors

stomach

hematopoiet ic

total tumors

stomach
hematopoiet ic
total tumors

stomach
hematopoiet ic
Number of
Tumor Tumors
Type Observed
NR

NR

leukemia

NR

NR

leukemia

NR

NR
leukemia

NR

NR

leukemia

NR

NR
leukemia
NR

NR
1 eukemia
9

3

2

5

1

1

3

1
1

3

1

1

1

0
0
1

0
0
Number of
Tumors
Expected15
3.4

0.4

0.14

1.1

0.13

0.04

3.4

0.4
0.13

2.6

0.3

0.1

2.0

NA
NA
1.6

NA
NA
Relative
Risk
(P value)
2.7
(P<0.01)
7.5
(P<0.01)
14.3
(P<0.01)
4.5
(P<0.01)
7.7
(NS)
25
(P<0.05)
0.9
(NS)
(NS)
7.7
(NS)
1.2
(NS)
3.3
(NS)
10
(NS)
0.5
(MS)
NA
NA
0.6
(NS)
NA
NA

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                                                                 Table  B.   Humans

                                                        Reference:   Hogstedt  et  al.,  1979a

Exposure
Route
Size of
Exposed
Population
Size of
Control
Population Sex

Level of
Exposure8

Duration of
Exposure

Target
Organ

Tumor
Type
Number of
Tumors
Observed
Number of
Tumors
Expected15
Relative
Risk
(P value)
                                                               QUALITY OF EVIDENCE
Strengths of Study:    Adequately controlled mortality study.
Weaknesses of Study:
Overall Adequacy:
Comments:
Subjects were exposed to a variety of  other  chemicals,  some that are documented animal carcinogens (see
Footnote a). Exposure durations and concerntrat ions were uncertain.  Group sizes were small in the subco-
hort with HO years employment and 20  years  induction-latency.

Adequate

The observed increases cannot  be attributed  definitely  to ethylene oxide alone.
8 Ethylene oxide production workers who were exposed to estimated ethylene oxide levels of <25 mg/m  (with occasional
  exposures up to the odor threshold (1300 mg/m3)  during 1941-1947.   The workers were also exposed to ethylene chlorohydrin (approx. 5
  mg/m3), ethylene dichloride (approx.  100.05 mg/m3),  bis(2-chloroethyl) ether (approx. 0.05mg/m3} and ethylene (approx. 600 mg/m3); it is
  possible that up to 1000 times these concentrations  may have occurred momentarily.   Exposure time was estimated as a slightly
  more than 1 ho.ur/shift.  From 1950 to 1963,  exposure  to chemicals other than ethylene oxide decreased because of production
  changes, and exposure to ethylene oxide increased  (10-50 mg/m3  with  peaks above the odor threshold). Subsequnt years were
  characterized by a lower ethylene oxide exposure (approx.  1-10  1119/in   with higher peaks), but also by exposure to proplene oxide
  (10-25 mg/m3, occasionally 120-150 mg/m3).
  The expected number of deaths due to malignanoise  were calculated  from the cause-,  sex-, and age-specific Swedish national
  death rates from respective 5-year age categories.
NR « Not reported; NS = Not significant

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                                                                 Table  B.   Humans

                                                              Agent:  Ethylene Oxide

                                                        Reference:   Hogstedt  et  al.,  1979b

Exposure
Route
inhal-
ation
Size of
Exposed
Population
230
Size of
Control
Population Sex
U.S. M,F
population

Level of
Exposure8
20 + 10
ppm

Duration of
Exposure
Afl-yrs

Target
Organ
hematopoiet ic

Tumor
Type
leukemia
Number of
Tumors
Observed
3
Number of
Tumors
Expected15
0.2
Relative
Risk
(P value)
15 (NS)
                                                               QUALITY OF EVIDENCE

Strengths of Study:    Exposure concentrations and components were fairly well  characterized.

Weaknesses of Study:   The cohort was small,  and the duration of exposure was short.

Overall Adequacy:       Limited

Comments:              One of the subjects with leukemia had "some occasional contact"  with benzene in laboratory work.

8 Workers were employed in a small Swedish factory that  sterilized hospital  equipment.  Seven people (4 males, 3 females) were
  sterilizer operators, 70 (68 females,  2 males) were exposed via outgassing from treated boxes in a storage hole for 8
  hours/day, and 153 other workers (101  females, 52 males)  were eni^.oyed in  neighboring rooms.

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                                                                Table B.   Humans

                                                             Agent:  Ethylene Oxide

                                                         Reference:  Morgan et al., 1981

Exposure
Route
inhal-
ation





Size of Size of
Exposed Control Level of
Population Population Sex Exposure8
767 U.S. M <10 ppma
(13,969 population
person-
years)




Duration of Target
Exposure Organ
5-18 years All malignant
pancreas
bladder
brain/CHS
lymphatic

hematopoietic

Tumor
Type
neoplasms
cancer
cancer
cancer
Hodgkin's
disease
leukemia
Number of
Tumors
Observed
11
3
1
2
2

0
Number of
Tumors
Expected
15.24
0.80
0.31
0.70
0.35

0.70
Standard
Mortality
Ratiob
72 (NS)
375 (NS)
322 (NS)
285 (NS)
571 (NS)

0 (NS)
Strengths of Study:


Weaknesses of Study:



Overall  Adequacy:
                                        QUALITY OF EVIDENCE

The subjects were employed in a plant that is one of the largst and oldest producers of ethylene oxide in
the United States.

Cohort size was small,  and exposures were poorly characterized.  Additional  tests of significance
demonstrated a relationship between ethylene oxide and the incidence of  Hodgkins disease and
pancreatic cancer0.

Limited
a The subjects  had potential  exposures to ethylene  oxide  at  a  Texaco  Chemical  Company  plant  that  continuously produced
  ethylene  oxide.  A recent  (1977)  industrial  hygiene  survey  indicated time-weighted average  concentrations  "well  below"  the OSHA
  50 ppm limit;  detectable  concentrations were routinely  <10 ppm.
  Each of  these  standard mortality ratios (number of  tumors  observed/number of  tumors  expected  x  100)  has  a lower 95X confidence limit  under
  100 (i.e.,  not  significantly elevated).
0 EPA evaluation  of the  Morgan data,  June,  1985.

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                                                               Table  B.   Humans





                                                            Agent:  Ethylene  Oxide





                                                      Reference:  Hogstedt et al.,  1986
Exposure
Route
inhal-
ation


Strengths
Weaknesses
Size of
Exposed
Population
733
(total)


of Study:
of Study:
Overall Adequacy:
Comments:

Size of
Control Level of
Population Sex Exposure8
Swedish H,F 2-300 ppm
population


Duration of Target
Exposure Organ
19-48 yrs stomach,
hematopoietic,
lung

QUALITY OF EVIDENCE
Three groups of exposed workers in various locations all demonstrated
The cohort was relatively small, and
Limited
The author noted that one group had
used in the previous two studies.
exposures were not well defined.

Tumor
Type
adenocar-
cinoma,
leukemia,
adenocar-
cinoma

Number of
Tumors
Observed
4
2
5
1


Number of
Tumors
Expected6
0.3
0.5
0.6
0.16


Relative
Risk
(P value)
13
4
8
6


increased rates of cancer.
There were no

worker cohort

controls.



an exposure to almost pure ethylene oxide compared to the cohorts
Sterilization workers from hospitals combined with production workers.

-------