REVISED EXTERNAL REVIEW DRAFT
NOVEMBER 1978
AN ASSESSMENT OF
THE HEALTH EFFECTS
OF COKE OVEN EMISSIONS
GERMANE TO LOW-LEVEL
EXPOSURES
NOTICE
This document is a preliminary draft. It has been
released by EPA for public review and comment
and does not necessarily represent Agency policy.
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PREFACE
The Environmental Protection Agency has prepared three
documents concerning the health effects of coke oven emissions on
the general population:
1. A health effects assessment,
2. An environmental exposure assessment, and
3. A population risk assessment based on the data pre-
v
sented in the first two documents.
This report, the health effects document, will be used by
the Environmental Protection Agency's Office of Air and Waste
Management, and by the:Administrator, to determine the scientific
basis for possible actions regarding coke oven emissions under
the Clean Air Act. The report was prepared under the direction
of Criteria Development and Special Studies Division, Office of
Health and Ecological Effects, with participation by the follow-
ing Division personnel:
Dr. Alan Carlin
Dr. Roger Cortesi
Dr. Arthur Saz
Drafts of the three documents were reviewed by the Environ-
mental Protection Agency's Science Advisory Board Subcommittee on
Air Quality Criteria for Coke Oven Emissions in public session on
May 30-31, 1978. The members of this panel were:
Dr. James H. Sterner
College of Medicine
University of California, Irvine
Irvine, California
Dr. Shao-Lee Soo
Department of Mechanical Engineering
University of Illinois
Urbana, Illinois
111
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Dr. Morton Corn
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, Pennsylvania
Dr. Charles Mittman
City of Hope Medical Center
Duarte, California
Dr. Beverly Paigen
Rosewell Park Memorial Institute
Buffalo, New York
Dr. Sati Mazumdar
Department of Bio Statistics
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, Pennsylvania
Review copies of this document were also provided to other
government agencies and to industrial and public interest groups,
as the result of a notice that appeared in the Federal Register,
Vol. 43, No. 76, page 16546, April 19, 1978.
Comments and criticisms received at these meetings and in
response to the Federal Register notice have been reviewed and
incorporated in the document as deemed appropriate.
IV
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CONTENTS
Preface iii
Figures vi
Tables vi
Abbreviations viii
Acknowledgment ix
Summary x
1. Introduction 1
2. Composition, Particle Size, and Health Effects 3
3. Experimental Evidence of Toxicity: Carcinogenesis 13
Experiments with Animals 13
Metabolism of P.olycyclic Aromatic Hydrocarbons ,- 15
4. Epidemiological Studies of High-Level Exposure 18
Introduction 18
Historical Perspective 20
Recent Studies 25
5. Ambient Pollution and Respiratory Disease 39
6. Analysis of Health Effects 43
Introduction 43
Bioassay Results 45
Characterization Difficulties and Health Effects 46
Bases for Interpreting Mortality Data 53
Estimating Health Effects From Occupational
Mortality Data 55
Estimating Exposure 60
Nonmalignant Respiratory Disease 68
Morbidity Statistics 70
Appendices
A. Selected Bioassay Results 77
B. Source and Concentration Data 84
References 95
v
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FIGURES
Number
Dose-response relationship for tumor induction in
mice and BaP administered subcutaneously 44
Least-squares fits of BaP in benezene- and
cyclohexane-soluble fractions of'total particulate
matter 52
Dose-response data for cumulative exposure to CTPV's,
nonwhite and white coke oven workers 62
Observed versus expected deaths from lung cancer
among coke plant workers as a function of cumulative
exposures, 1951-1966 65
TABLES
Number Paqe
1 Partial List of Constituents of Coke Oven Emissions 4
2 Some Toxic Constituents of Coke Oven Emissions and
Some of Their Noncarcinogenic Toxic Properties 5
3 Particle Size Range and Biological Significance of
Coke Oven Emissions 11
4 Temperature Range of Carbonizing Chambers and Excess
of Lung Cancer Reported 19
5 Summary of Epidemiological and Clinical Evidence
of Carcinogenicity 22
6 Summary of Mortality Data in Gas Workers Observed
by Doll 28
7 Summary of Relative Risks of Death From Cancer Among
Coke Oven Workers 32
VI
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TABLES (continued)
Page
8 Summary of Epidemiological Studies of Long-Term
Mortality of Coke Plant Workers 33
9 Relative Risk for Lung Cancer as a Function of Daily
Tar Dosage From Cigarettes in Male Smokers With Ten
Years or More of Smoking 48
10 Partial List of Tumorigenic Agents and Other Toxic
Compounds in Coke Oven Emissions and in Cigarette
Smoke 49
11 Estimates of Average Annual Lung Cancer Mortality
Rates Per 100,000 Person-years of Exposure for
Selected U.S. Smoking Groups (1954-1962) and Steel-
worker Groups (1953-1961) 57
12 Relative Risks for Lung Cancer Among Coke Plant
Workers Based on Comparison With Steelworkers and
With Nonsmoking General Population 59
13 Estimated Cumulative Exposure to BaP and CTPV and
Corresponding Observed Mortality 64
14 Estimation of Equivalent Lifetime Dose for the
General Population 67
15 Observed Bronchitis Mortality 69
16 Correlations for Chronic Bronchitis Among Coke Oven
Workers 72
17 Chronic Bronchitis in the Coke Industry 75
VII
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ABBREVIATIONS
A Aza-arene
AHH Aryl hydrocarbon hydroxylase
BaP Benzo(a)pyrene
BeP Benzo(e)pyrene
BSF Benzene-soluble fraction
BSO Benzene-soluble organic
CTPV Coal tar pitch volatile
DBA Dibenzanthracene
DMBA Dimethylbenzanthracene
MCA Methylcholanthrene
PAH Polycyclic aromatic hydrocarbon
POM Polycyclic organic matter
RR Relative risk
SMR Standardized mortality ratio
TLV Threshold limit value
TPM Total particulate matter
yg microgram
ym micrometer
ng nanogram
Vlll
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ACKNOWLEDGMENT
This document was prepared by EPA's Office of Research and
Development with extensive help from a team of consultants led by
Jeanne M. Stellman, Ph.D. Major contributors are Geoffrey Kabat,
Ph.D., and Dietrich Hoffmann, Ph.D.
IX
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SUMMARY
1. Coke oven emissions consist of a complex mixture of sub-
stances that are etiologically implicated in increased mortality
from a variety of malignant and nonmalignant diseases among
various populations of workers exposed to them for varying
lengths of time. These risks include the following:
a. Elevated risk for cancer of all sites (relative risk
[RR] 1.62; p<0.01; Redmond, 1976).
b. Elevated risk for respiratory cancer (RR 15.7; p<0.01;
Redmond, 1976).
c. Elevated risk for kidney cancer (RR 5.0; p<0.01;
Redmond et al, 1976).
d. Elevated risk for gastrointestinal cancer: large
intestine and pancreas (RR 2.93; p<0.01 — intestine;
RR 4.55, p<0.01 — pancreas; Redmond et al, 1976).
e. Elevated risk for pharyngeal and buccal cancer (RR
3.87; p<0.01; Redmond et al, 1976).
f. Elevated risk for nonmalignant respiratory disease (at
least 2-fold excess; Redmond, 1976).
Among lightly exposed workers (nonoven workers in coke plants) an
increased risk for nonmalignant respiratory disease and cancer of
several sites was also observed.
2. Although workers exposed to the emissions develop malignant
and respiratory diseases at an elevated rate, they enjoy a
favorable overall mortality as a group, in comparison with the
general population, a common observation in the study of occupa-
tional medicine. Thus the general population, which includes the
young, the old, and the infirm, should be considered more sus-
ceptible than the work force, especially for development of
chronic bronchitis, since they are generally in poorer health.
x
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3. Coke oven emissions contain an array of identified carcin-
ogens, irritants, particulate matter, trace elements, and other
chemicals. The toxic effects observed in both humans and animals
are greater than the effects that can be attributable to any
individual component. This fact suggests an interplay of factors
such as cocarcinogenesis, tumor initiation, and tumor promotion
that are involved in exposure to "coke oven emissions" as a
whole. Thus the emissions as a whole should be considered the
toxic agents, and it is inappropriate simply to attribute toxic-
ity of the emissions to any particular component such as benzo-
(a)pyrene (BaP), although BaP may serve as a useful chemical tool
for approximating overall exposure.
4. Extrapolations and approximations derived from occupational
data afford the crude estimate that there is an exposure differ-
ence of about 3 orders of magnitude between lightly exposed
workers and people living in the vicinity of a coke plant, as
indexed by BaP concentrations (3.32 yg/m ; 2 ng/m ). Since these
lightly exposed workers show an elevated risk for cancer and
nonmalignant respiratory disease, it is prudent to assume that
levels up to one hundredth of those to which lightly exposed
workers are subjected could cause an increased risk to the gen-
eral population.
XI
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SECTION 1
INTRODUCTION
A substantial body of evidence, both direct and indirect/
indicates that coke oven emissions, a complex mixture of many
components, are carcinogenic and toxic. The carcinogenic poten-
tial of various fractions of coal-tar-pitch volatiles (CTPV's),
which are a major constituent of coke oven emissions, and of
benzo(a)pyrene (Bap), a carcinogenic constituent of the volatiles,
has been established by laboratory studies. Epidemiological [
findings among coke oven workers show that coke oven emissions
are carcinogenic to humans and also can lead to the development
of nonmalignant respiratory disease, such as chronic bronchitis
and emphysema. Chronic lung disease is a serious, irreversible
condition that is often debilitating and can be fatal.
The epidemiological evidence relating to other coal carbon-
ization processes, such as those involved in commercial gas
production, and to cigarette smoke is also relevant here because
of congruence between many of the constituents of coke oven
emissions and the constituents of gas works effluents, tobacco
smoke, and other sources of combusted organic matter (National
Academy of Sciences, 1972). All of these effluents contain
polycyclic organic matter (POM), as well as a wide variety of
other chemicals"^
Our evaluation in this study of the evidence relating to
health hazards of other combustion products confirms that the
array of toxic effects observed in cigarette smokers and gas-
industry workers is similar to the effects observed among coke
oven workers. In particular, the finding that cigarette smoke
and coke oven emissions contain very similar compounds capable of
inducing cancer in humans and animals is of significance and can
1
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be considered evidence of the carcinogenicity of coke oven emis-
sions. Additional indirect evidence comes from data that support
an association between urban air pollution and incidence of
chronic bronchitis and possibly of lung cancer (Goldsmith and
Friberg, 1977), since polluted urban air also contains, in addi-
tion to other materials, compounds found in cigarette smoke and
coke oven emissions.
It is important that the effects described throughout this
report be regarded as resulting from the complex mixture that
constitutes coke oven emissions and not from any particular
components such as BaP or the benzene-soluble fraction (BSF) of
total particulate matter, components that often serve as indica-
tors of the emissions. As we will show, there is extensive
evidence that the effects observed are greater than the sum of
effects that could be attributed to individual components.
Further, the mixture is not accurately definable by any partic-
ular component.
The purpose of this report is to use the different bodies of
available evidence in assessing the magnitude of the health
effects of coke oven emissions on the population at large.
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SECTION 2
COMPOSITION, PARTICLE SIZE, AND HEALTH EFFECTS
Coke oven emissions include all of the constituents of
bituminous coal released into the atmosphere during the process
of carbonization. Among these constituents are a number of
carcinogens; at least one, B-naphythylamine, is a proven human
carcinogen (Mancuso et al, 1967). Toxicity of coke oven emis-
sions also is manifest in respiratory irritation, cocarcino-
genesis, tumor promotion, and other toxic effects. Table 1 shows
a partial list of the constituents of coke oven effluents, and
Table 2 summarizes some noncarcinogenic toxic effects, such as
skin irritation and irritation of the upper respiratory tract.
Appendix B gives some of the levels of various constituents that
have been measured.
In addition to chemical composition, the form in which the
various constituents are released into the atmosphere (e.g.,
aerosols, gases) and the size and density of the particulate
matter with which they are associated determine their effects on
human health. Most of the particles emitted are in the respir-
able range, which means that they can penetrate into the lungs
past the normal respiratory defense mechanisms. Particles rang-
ing from 0.1 to 2 ym in diameter are the optimum size for such
penetration and hence are the most biologically significant.
After entering the respiratory tract, they are largely retained
in the trachea, bronchi, and alveoli. Particles larger than 2.0
ym are trapped by the mucous membranes and do not enter the
lungs. Particles smaller than 0.1 ym are retained in the tracheo-
bronchial tree, but elution does not occur. Particles smaller
than 0.04 ym do not come out of suspension in the inhaled air and
are exhaled (Falk and Kotin, 1961). In the atmosphere, polycyclic
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Table 1. PARTIAL LIST OF CONSTITUENTS
OF COKE OVEN EMISSIONS
POLYNUCLEAR AROMATIC HYDROCARBONS
Anthanthrene
Anthracene
Benzidene b
Benz (a) anthracene
Benzo (b) f luoranthene bb
Benzo (ghi) tluoranthene
Benzo (j) fluoranthene
Benzo (k) fluoranthene
Benzofluorene
Benzo (a) fluorene
Benzo (b) fluorene
Benzo (c) fluorene
Benzophenanthrene
Benzo (ghi) peryiene
Benzo (a) pyrene
Benzo (e) pyrene^
Benzoquinoline
Chrysene
Coronene ^
Oibenz (ah) anthracene
Dibenzo (ah) pyreneb
Dihydroanthracene
Dihydrobenzo (a) fluorene
Dihydrobenzo (b) fluorene
Dihydrobenzo (c) fluorene
Dihydrobenz (a) anthracene
Oihydrochrysene
Dihydrofluoranthene
Oihydrofluorene
Dihydromethylbenz (a)
anthracene
Oihydromethlybenzo
(k and b) fluoranthenes
Dihydromethylbenro
(a and e) pyrenes
Dihydromethylchrysene
POLYNUCLEAP AZA-HETEROCYLIC
COMPOUNDS*
Acridine b
Benz (c) acridine
Dibenz (a,h) acridine
Dibenz (a,j) acridine
AROMATIC AMINESb
8-Naphthylamine
o-Naphthylamine
OTHER AROMATIC COMPOUNDS
Benzene
Phenol0
Toluene
Xylened
Dihydromethyltriphenylene
Dihydrophenanthrene
Dihydropyrene
Dihydrotriphenylene
Dimethylbenzo (b) fluoranthene
Dimethylbenzo (k) fluoranthene
Dimethylbenzo (a) pyrene
DimethyIchrysene
Dimethyl tnphenylene
Ethylanthracene
Ethylphenanthrene
Fluoranthene
Fluorene
Indeno (1,2,3-cd) pyrene
Methylanthracene
Methylbenz (a) anthracene
Methylbenzo (a) pyrene
Methylbenzo (ghi) perylene
Methylchrysene
Me thyIfluoranthene
Methylfluorene
Methylphenanthrene
Methylpyrene
Methyltriphenylene
Octahydroanthracene
Octahydrofluoranthene
Octahydrophenanthrene
Octahydropyrene
Perylene
Phenanthrene
o-Phenylenepyrene
Pyrene
Triphenylene
TRACE ELEMENTS
Arsenic
Beryllium
Cadmium
Chronium
Cobalt
Iron
Lead
Nickel
Selenium
OTHER CASES
Ammonia
Carbon ditulfide
Carbon monoxide0
Hydrogen cyanide^
Hydrogen tulfide
Methane0 .
Nitric oxide0 _
Sulfur dioxide
Lao et al (1975), except as noted.
Kornreicli (1976).
Smith (1971) .
White (1975).
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Table 2. SOME TOXIC CONSTITUENTS OF COKE OVEN EMISSIONS AND
SOME OF THEIR NONCARCINOGENIC TOXIC PROPERTIES
Constituent
Suggested Threshold
Limit Value (TLV)
Potential
health effect
Acetone
Ammonia
Acridine
Anthracene
Arsenic
Benzene
1000 ppm ..
2400 mg/m
25 ppm ,
18 mg/m
0.25 mg/m
10 pom ,
30 mg/m
At 300 ppm — Slight irritation
500 ppm -- Still tolerated
1000 ppm — Chronic irritation of
respiratory tract,
dizziness
1 ppm — Odor detectable
20 ppm — Discomfort in uninured
workers, complaints
100 ppm — Irritation of respiratory
tract and conjuctivae
Powerful irritant:
Photosensitizer
Causes dermatitis
eyes
Irritant: eyes, skin,
respiratory tract
Photosensitizer
Contact dermatitis and
sensitization
Conjuctivitis
Ulceration and perforation
of nasal septum
Narcotic effects
Severe exposures cause
bone marrow and blood
changes
Myelotoxic
(continued)
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Table 2 (continued)
Constituent
Suggested Threshold
Limit Value (TLV)
Potential
health effect
Beryllium
Cadmium dust
Chromium
Cobalt
Formaldehyde
Hydrogen cyanide
(continued)
0.002 mg/m
0.05 mg/m
0.5 mg/m
0.01 mg/m3
2 ppm
10 ppm
25 ppm — Exposure for 12 years;
very little intoxication
reported
60 ppm — Blood changes reported
100-200 ppm — Deaths reported
Dermatitis, tracheobron-
. chitis
100 uq/m — pneumonitis
Distinctive, nonhypertropic
emphysema, with or without
damage to renal tubes;
anemia, eosinophilia,
anosmia, chronic rhinitus,
yellow ring on teeth,- bone
. changes
2-15 mg/m — Anosmia, proteinuria (low
molecular weight) pulmonary
emphysema, yellow ring on
teeth,eosinophilia, anemia
Dermatitis (salt)
Pulmonary involvement, chronic
3 interstitial pneumonitis
1-2 mg/m — Serious and occasionally fatal
results, hypersensitivity,
allerqic dermatitis
Irritant: eyes, respiratory
tract, sfcin
1-2 ppm — Itching eyes, dry and sore
throat, disturbed sleep,
unusual thirst on awakening
6 ppm — Eye irritation
20-40 ppm — Slight intoxication, variety
of neurological symptoms
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Table 2 (continued)
Constituent
Suggested Threshold
Limit Value (TLV)
Potential
health effect
Hydrogen sulfide
10 ppm
(15 mg/m )
500-1000 ppm —
50-500 ppm
250-600 ppm
5-100 ppm
Lead
0.15 mg/m
Nickel
Pyridine
1 mg/m
5 ppm
0.83-2.46 ml —
Acts primarily as systematic
poison causing unconscious-
ness and death through
respiratory paralysis
Acts primarily as a respira-
atory irritant
Prolonged exposure may lead to
pulmonary edema and bronchial
pneumonia
Associated with eye irrita-
tion
Nerve function disorders, in-
ability to sleep, fatigue,
constipation
Long-term exposure: anemia,
colic, neuritis, headaches,
loss of appetite, weakness,
double vision
Organic lead: mental distur-
bances, inability to sleep,
general anxiety, delerium -
acute
Increase in incidence of
nasal, sinus, and lung cancer
in workers in nickel
refineries
Was toxic in human therapy
with one death from liver
and kidney damage; central
nervous system affected;
stimulates bone marrow to
production of blood plate-
lets
Vapor - irritating to mucous
surfaces
(continued)
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Table 2 (continued)
Constituent
Suggested Threshold
Limit Value (TLV)
Potential
health effect
Selenium
0.2 mg/m~
15-330 ppm — Nausea, headache, insomnia
and nervousness, low back or
abdominal discomfort
Intense irritation of eyes,
nose, and throat, headache
Severe exposure: bronchial
spasms, asphyxiation, chills,
fever, bronchitis
0.007-0.05 mg/m —
0.2-0.4 mg/m3 —
oo
Sulfur dioxide
Toluene
5 ppm
13 mg/m
100 ppm ,
375 mg/m
Headache, tracheobronchitis ,
conjunctivitis
Garlic odor of breath, skin
rashes, indigestion, metallic
taste
Irritation of the mucous
membranes, coughing, eye
irritation, increased
pulmonary flow resistance;
adverse symptoms appear at
levels between 5 and 10 ppm.
100-1100 ppm — Enlargement of liver,
macrocytosis, moderate
decrease in erythrocyte
count and absolute lympho-
cystosis
200 ppm — Headache, nausea, lassitude
200-500 ppm — Impairment of coordination,
momentary loss of memory,
anorexia
500-1500 ppm — Palpitation, extreme weakness,
pronounced loss of coordi-
nation and impairment of
reaction time; red cell
decrease in 2 cases, aplastic
anemia (possible benzene
impurity)
(continued)
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Table 2 (continued)
Constituent
Suggested Threshold
Limit Value (TLV)
Potential
health effect
Xylene
0.1 mg/m~
200 ppm — Slight but definite changes in
muscular coordination; 7 hours
exposure to 200 ppm cause pro-
longation of reaction time,
decreases in pulse and systolic
blood pressure.
Acute oral and skin
irritation, sensitization,
gastrointestinal irritant.
Sources: Stellman et al (1973).
American Conference of Governmental Industrial Hyqienists (1976) .
Patty (1958).
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aromatic hydrocarbons (PAH's) are primarily found absorbed on
particulate matter, hence the presence of respirable particulate
matter increases the likelihood that PAH's will penetrate into
the lungs. Table 3 gives the range of particle sizes found in
coke oven emissions.
The trapped particles in the mucus that are not exhaled and
that also do not enter the lung are either swallowed or spit out.
Morgan (1975) hypothesizes that in asbestos exposure it is the
swallowing of asbestos-containing mucus that leads to the in-
creased incidence of neoplasia of the digestive organs. Elution
of PAH's from swallowed particle-contaminated mucus may also
explain the diverse sites of cancer associated with exposure to
coke oven emissions.
Elution of the PAH's requires a sufficient period of contact
between the soot particles and the respiratory epithelium. The
larger the particle (provided that it is respirable), the more
readily elution into the lungs takes place. PAH's that are
adsorbed onto particles smaller than 0.1 ym are not readily
eluted (Falk and Kotin, 1961). Furthermore, mucociliary defense
clearance mechanisms that normally may limit the entrance of
respirable materials are hampered by some chemical and physical
agents present in coke oven emissions.
In addition to evidence of the carcinogenic properties of
substances like PAH's and aza-arenes, various substances in coke
oven emissions are known to produce noncarcinogenic toxic effects,
such as nonmalignant respiratory disease, which is discussed
later. Many of the major toxic constituents of coke oven emis-
sions (Table 2) are irritants and cilia-toxic agents; some are
thought to be cocarcinogens. Sulfur dioxide and sulfuric acid
mist are known to cause irritation of the respiratory tract,
interfere with mucous clearance mechanisms, and produce broncho-
constriction, as reflected by increased airway resistance.
Sulfur dioxide is readily converted into the more powerful irri-
tant, sulfuric acid, in the presence of humidity and particulate
10
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Table 3. PARTICLE SIZE RANGE AND BIOLOGICAL
SIGNIFICANCE OF COKE OVEN EMISSIONS
Size3
0.1-1 ,.m (tarry
droplets)
1 um and up (dust)
1.5 urn
1.8 um
2.9 um
1 um-1.27 mm
5 um-1.27 mm
Site
Retort house
Retort house
Topside coke oven
Topside coke oven
Topside coke oven
Coke plant
Coke plant
Process
General atmosphere
(shift change)
During coking
Charging
Quenching
Reference
Lawther (1965)
Lawther (1965)
W
White, L.D. , et al
White, L.D. , et al&
White, L.D. , et alb
Fullerton, R.W. (1967)
Masek, V. (1970, 1971)
Biological
significance
Particles in the
0.1-2.0 uro range
are respirable
and largely re-
tained in the
trachea, bronchi.
and alveoli;
particles >2.0 pm
are trapped in the
mucous membranes;
particles <0.1 um
are retained but
elution does not
take place; par-
ticles <0.04 um are
exhaled (Falk and
Kotin, 1961)
For respirable particles, the rate of elution of PAH increases with the size of the particle to which the PAH is adsorbed.
No date.
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matter (Amdur, 1969). Hydrogen cyanide is also strongly cilia-
toxic and mucus-flow-inhibiting. Most toxicological research on
these noncarcinogenic constituents of coke oven emissions has
been concerned with exposure to the individual substances alone.
We can only guess at the combined toxic potential of the several
components as they occur in coke oven emissions.
12
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SECTION 3
EXPERIMENTAL EVIDENCE OF TOXICITY: CARCINOGENESIS
EXPERIMENTS WITH ANIMALS
Over the past few decades, both in vivo and in vitro
studies have helped establish the carcinogenicity of particular
PAH's. With regard to the potential carcinogenic hazard to
humans of PAH's in coke oven effluents, the most pertinent data
stem from experiments with animals involving cutaneous applica-
tion, intratracheal instillation, and inhalation exposure. These
methods of administration most resemble the routes by which
humans may be exposed to PAH's, and the studies also have helped
elucidate the role of synergism among different pollutants in the
production of cancers.
Cutaneous application on mouse skin is an important bioassay
method used as a model system for studying histological changes
associated with precarcinogenic and carcinogenic stages. Carcin-
ogenic activity on mouse skin has been demonstrated for various
tars, soots, oils, urban air pollutants, gasoline and diesel
engine exhaust "tars," the particulate matter of tobacco main-
stream and sidestream smoke, and several other combustion prod-
ucts (Hoffman and Wynder, 1976; Karbe and Park, 1974; Kipling,
1976; Hoffmann and Wynder, 1977). Studies of fractions of
environmental inhalants have demonstrated that the major type of
carcinogen in organic air particulates is the PAH, and that aza-
arenes contribute carcinogenic activity to a lesser degree (NAS,
1972).
Laskin et al (1970) showed the importance of synergism
between two of the most common pollutants in air, SO,, and BaP,
in respiratory carcinogenesis. When rats were exposed to the
irritant SO- alone, they developed hyperplastic and metaplastic
13
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aberrations. But when S02 exposure was combined with BaP expo-
sure (by inhalation), the rats developed squamous cell carcinomas
of the bronchus. It has been postulated that SO- synergism slows
ciliary action and therefore increases BaP retention and/or
causes chronic injury; following injury, the resultant regenerat-
ing cells may be more susceptible to the BaP (Scala, 1975).
Synergism has also been demonstrated between carcinogenic
chemicals and particulate matter (for example, carbon and iron
oxide). In a study by Saffiotti et al (1968), all of the ham-
sters that were administered a 50:50 mix of BaP and iron oxide
developed tumors of the respiratory tract, whereas none of the
hamsters given iron oxide or BaP alone developed any lung tumors.
The tumors induced in the hamsters were comparable with those
found in humans, both in histological type (squamous cell and
anaplastic carcinoma were most frequent) and in location in the
respiratory tract (largely from the epithelium of the major
bronchi or their primary divisions). A sequence of tumor devel-
opment from hyperplasia to squamous cell metaplasia was observed.
Montesano et al (1970) performed experiments of a similar
type, also with Syrian hamsters, using intratracheal instillation
of BaP and iron oxide. In a dose-response study, four groups of
hamsters were given weekly administrations of different doses of
a BaP/iron oxide mixture. The groups received 2.0, 1.0, 0.5, and
0.25 mg of BaP, each with an equal amount of iron oxide. The
results showed a definite, positive correlation of dose level and
tumor incidence. Also,'the greater the dose level, the earlier
the tumors appeared. Other studies indicated that a given total
quantity of BaP/iron oxide mixture administered in fractions by
frequent instillations would produce tumors earlier than a single
administration of the total dose. Again, the morphology and
topography of these experimentally induced tumors were markedly
similar to those in humans.
Crocker et al (1970) have demonstrated that intratracheal
instillation of a BaP/iron oxide mixture can induce respiratory
tract tumors in a primate, Galago crassicaudatus. Black ink
14
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powder has been used as the carrier for carcinogens in intratra-
cheal instillation studies. L. M. Shabad (1962) induced bron-
chogenic carcinomas in rats using dimethylbenzanthracene (DMBA)
on black ink powder.
Other animal studies, particularly those involving mouse
skin, have suggested a two-stage mechanism for tumor induction,
in which PAH's act as tumor initiators and phenols, aliphatic
hydrocarbons, 3- and 4-ring PAH's, and dihydroxybenzenes act as
tumor promoters (Van Duuren, 1969). As in cocarcinogenesis, the
initiation-promotion model is based on the combined action of
different compounds to produce an effect that no single compound
would produce by itself. The indication in laboratory experi-
ments that different components of coke oven emissions interact
synergistically lends support to the view that the toxic poten-
tial of the complex mixture—coke oven emissions cannot be related
to the potential of a single compound.
METABOLISM OF POLYCYCLIC AROMATIC HYDROCARBONS
In recent years much research has been conducted to clarify
the metabolism of carcinogenic PAH's. Maximum systemic excretion
of BaP and its metabolites is via the liver and biliary system
(Heidelberger and Jones, 1948; Kotin et al, 1959). There is a
maximum excretion rate into the bile in rats suggestive of
numerous storage sites. Adipose tissues, the central nervous
system, and the sebaceous glands have been identified as storage
sites (Chalmers and Peacock, 1936; Peacock, 1936).
It is the metabolic pathways of PAH's that are of interest.
Brookes and Lawley (1964) reported that there is no binding of a
PAH to any cellular constituents immediately after application of
PAH's to the skin, but rather that the maximum amount of binding
occurs only after an interval of 24 to 48 hours. This finding
strongly suggests that metabolic activation is a prerequisite for
macromolecular binding of PAH's. Gelboin (1969) found that
binding of BaP to DNA in vitro depended upon the presence of rat
liver microsomes, since without the microsomes no binding would
15
-------
occur. It is hypothesized that the aryl hydrocarbon hydroxylase
(AHH) system in the microsome fraction of rat liver cells can
"activate" the PAH's (Gelboin and Wiebel, 1971).
Elucidation of metabolic pathways is thus essential, since
the parent polycyclic hydrocarbons are largely chemically inert.
Current studies are working out in detail the biochemical conver-
sion of BaP to its carcinogenic metabolite(s) (e.g., Levin et al,
1977), which are thought to result from activation by the micro-
somal monoxygenase system (Miller and Miller, 1974; Jerina and
Daly, 1974; Sims and Grover, 1974; Gelboin et al, 1972). The
recent evidence suggests that reactive arene oxide intermediates,
particularly 7,8 diol-9, 10-epoxide, are powerful carcinogens
(Moore et al, 1977) and binding of such intermediates to nucleic
acids has been demonstrated (Kinoshita and Gelboin, 1978). There
is also evidence that a BaP derivative formed during the enzyme-
catalyzed hydrolysis of glucuronide binds to DNA, so that other
metabolic intermediates may be possibly carcinogenic as well
(Kinoshita and Gelboin, 1978).
Further evidence of the carcinogenic potential of various
PAH's is available by use of in vitro techniques, including organ
cell culture and microbiological procedures. Berwald and Sachs
(1963, 1965) first applied BaP and 3-methylcholanthrene (MCA) to
cultured hamster-embryo cells to obtain "transformed" or tumor
cells. These cells grew randomly and continuously in criss-
crossed, piled-up colonies; the random growth pattern was genet-
ically transmitted. Subcutaneous inoculation of these cells into
hamsters resulted in tumor formation (Berwald and Sachs, 1965).
Subsequently, by means of quantitative cloning techniques,
investigators found a direct relationship between the known
carcinogenic potency of a hydrocarbon and the number of clones
transformed (NAS, 1972). The ability of known chemical carcin-
ogens to transform cells in culture was confirmed by DiPaolo et
al (1969a).
A favored hypothesis for the development of neoplasms is
that they arise as a consequence of somatic mutations. It has
16
-------
been demonstrated that many mutagens are carcinogens and vice
versa. Therefore, a rapid, inexpensive procedure, useful for
screening potential carcinogens and also for determining carcin-
ogenicity of metabolites of the parent substance would be useful,
Microbiological tests that confirm the mutagenicity of various
compounds, including PAH's, have been reported.
The recently developed Ames test utilizes different strains
of bacterium, Salmonella typhimurium, to detect back-mutations
caused by a particular agent. All of these strains have defects
in the histidine operon such that they cannot grow in a histi-
dine-free environment. The theory behind the test is that a
mutagen will cause a shift "back" to the wild type, a type that
can grow in a histidine-free medium. The test measures the
number of reversions to growth that arise when the strains are
exposed to suspected mutagenic agents and placed in a histidine-
free medium (Ames et al, 1975). Several studies have found that
epoxides of known polycyclic carcinogens such as benz(a)anthra-
cene, dibenz(a,h)anthracene, and 7-methylbenz(a)anthracene were
mutagenic, but that the parent hydrocarbons were not mutagenic.
(Levin et al, 1976; Levin et al, 1976a; and Thakker et al, 1977).
17
-------
SECTION 4
EPIDEMIOLOGICAL STUDIES OF HIGH-LEVEL EXPOSURE
INTRODUCTION
In attempting to assess the health effects of high-level
exposure to coal-tar pitch volatiles, investigators have done
epidemiological studies involving coke oven workers as well as
workers employed in the production of gas for household use
('town-gas') and for industrial use (generator gas).* The inclu-
sion of mortality data relating to these different processes is
warranted by the earlier-mentioned similarity of the chemical
processes and effluents involved in coal gasification and in
coking. The relative proportions of the various constituents in
the different processes vary with the temperature of carboniza-
tion and with the type of coal used. Epidemiological evidence of
greater increases in disease rates among workers exposed to the
higher-temperature processes suggests that the higher the tem-
perature of carbonization, the higher the proportion of toxic
compounds released (see Table 4).
Exposure data on retort house gas workers and coke oven
workers show that the concentrations of pollutants are of the
same order of magnitude. Lawther et al (1965) measured the
concentrations of BaP and other PAH's (BeP; 1,12 benzperylene;
coronene) in gas works retort houses. The representative mean
concentrations of BaP in tarry fumes escaping from the retorts
for long-period samples (collected with a continuous sampler over
periods of 2 to 4 weeks) averaged 3 yg/m . The maximum was in
*
Coke-plant data come mainly from the United States, Russia, and
Czechoslovakia; coal gasification plant data come from Europe
and Japan.
18
-------
Table 4. TEMPERATURE RANGE OF CARBONIZING CHAMBERS
AND EXCESS OF LUNG CANCER REPORTED
Carbonizing
chamber
Temperature
range, °C
Reported excess
of lung
cancer among workers,
Vertical retorts
Horizontal retorts
Coke ovens
Japanese gas generators
400-500
900-1100
1200-1400
> 1500
27 (Doll, 1965)
83 (Doll, 1965)
255 (Lloyd, 1971)
800 (Lloyd, 1971)
-------
the same range as the levels to which coke oven workers are
exposed. In samples obtained with personal monitors the average
BaP concentration was 2.6 yg/m , which is approximately equiva-
lent to 0.26 mg/m of the benzene-soluble fraction of total
particulate matter [taking BaP as 1% of the benzene-soluble
organics (BSO), as calculated by Schulte et al, 1975] and is
comparable to the threshold limit value (TLV). All particles in
the gas retort houses were respirable (within the range of 0.1 to
1.0 ym).
A major difference between the coking process and the coal
gasification process appears to be the relative absence of S02 in
the latter (0.35 ppm) (Lawther et al, 1965). Absence of S02
would lead one to expect that rates of lung cancer among gas
workers would be lower than those among coke oven workers, since
SO- is believed to have a synergistic effect on carcinogenesis,
as demonstrated experimentally (Laskin et al, 1970). A similar
synergistic relationship with SO- has been hypothesized for
arsenic exposure (Lee and Fraumeni, 1969). Another difference is
that more workers labor on or near the top side of coke ovens and
hence are heavily exposed to the effluents, whereas only the top
man in a horizontal retort house has the highest exposure. The
effluent mixture itself varies with temperature of carbonization,
the higher temperatures apparently leading to a more carcinogenic
mixture. Comparison of the lower relative mortality of gas
retort workers reported by Doll (1952, 1965, 1972) with data in
an ongoing long-term study (e.g., Lloyd, 1971) of the mortality
of steelworkers and coke oven workers seems to bear out these
hypotheses.
HISTORICAL PERSPECTIVE
Epidemiological studies in different countries have demon-
strated that workers exposed to the products of the combustion
and distillation of bituminous coal experience an increased
incidence of cancer of several sites (lung, pancreas, kidney,
20
-------
bladder, skin). These studies are discussed below, and the
overall results are summarized in Table 5.
The earliest association of skin cancer with occupations
involving exposure to coal-combustion products was that of
Percivall Pott, who in 1775 observed the high incidence of scrotal
i
cancer among chimney sweeps exposed to soot. His observation has
now become a classic reference of occupational medicine for
cancer and for discussions of coal tar products. In the early
20th century several studies established the association (Sladden,
1928; Bridge and Henry, 1928; E.L. Kennaway, 1925). In a later
series of reports, Henry, Kennaway, and Kennaway (1931) and
Kennaway and Kennaway (1936, 1947) found an increased rate of
bladder and lung cancer in occupations involving exposure to coal
gas, tar, pitch, and soot. In their study of cancer of the
bladder and prostate, Henry, Kennaway, and Kennaway (1931) found
that workers in 8 out of 10 occupations involving exposure to
coal products showed an increased risk of bladder cancer as
compared with the general English male population. For 5 out of
10 occupations the risk was 1-1/2 to 4 times greater. Among 46
occupations examined, the three occupations with the highest risk
of bladder cancer were patent-fuel workers, gas works engine and
crane drivers, and tar-distiller workers. In a later retrospective
study of the incidence of cancer of the lung and larynx in
England and Wales from 1921 to 1932, Kennaway and Kennaway (1936)
noted an excess lung cancer mortality among British gas workers
and other coal carbonization and by-product workers. In this and
a follow-up study (1947) covering the period 1921 to 1938,
Kennaway and Kennaway noted an excess of lung cancer deaths among
gas producermen, chimney sweeps, and certain categories of
gasworks employees. Data on "gas stokers and coke oven charges"
showed an approximately 3-fold excess. Doll (1952) comments that
these findings are "suggestive of a special occupational risk,"
but are not conclusive "because the numbers of men engaged in the
various occupations had to be deduced from the evidence provided
by the censuses of 1921 and 1931 and were not known with any
21
-------
Table 5. SUMMARY OF EPIDEMIOLOGICAL AND CLINICAL EVIDENCE OF CARCINOGENICITY
Investigator
Kuroda and
Kawahata
Kawai,
Amamoto, and
Harada
Henry,
Kennaway , and
Kennaway
Kennaway and
Kennaway
Kennaway and
Kennaway
Doll
Doll
Date of
study
1936
1967
1931
1936
1947
1952
1965
Type of
study
Historical
prospective
Historical
prospective
Historical
prospective
Historical
prospective
Historical
prospective
Historical
prospective
8-year pro-
spective
Site
Lung
Lung
Bladder
Lung
Lung
Lung
Lung
Bladder
Results
(12 lung cancer deaths out
of a total of 15 deaths
for all cancers) . Relative
risks cannot be calculated
but there is suggestion of
26-fold excess over general
population (Lloyd, 1971)
33 times the rate for other
steelworkers
1-1/2 to 4-fold increased
risk relative to general
population
3-fold excess for "gas
stokers and coke oven
chargers"
81% excess of lung cancer
deaths
Those with heavy exposure
showed 69% excess relative
to those with minimal
exposure (by-products
workers)
Those with heavy exposure
showed 4- fold excess
relative to those with
minimal exposure
Characterization of exposure
Producer gas workers
Workers in producer gas works
Workers in 5 out of 10 occupa-
tions involving exposure to
coal products
British producer gas workers;
chimney sweeps and several
categories of gas-works
employees
Former gas retort workers
(pensioners)
Gas-worker mortality was
greatest for those with
greatest exposure (retort
house workers)
tvj
NJ
(continued)
-------
Table 5 (continued)
1
Irv/est igator
Doll
Reid and
Buck
Bruuagaard
Lloyd, Luridin.
Redmond, and
Geiser
Lloyd
Date of
study
1972
1956
1959
1970
1971
1
Type of
study
4-year
follow-up
of 8-year
prospective
Retrospec-
tive study
of deaths
among coke
plant workers
during 1949-54
Retrospec-
tive study
of deaths
among em-
ployed and
retired gas-
workers over
a 15-year
period
Prospective
study of
mortality
among steel-
workers by
work-area.
Detailed prospec-
tive study of
workers in steel-
workers cohort
Site
Lung
Lung
Lung
Bladder
Lung
Lung
Results
Heavily exposed workers
showed highly significant
excess; by-products
workers showed no excess
No excess in number of
cancer deaths among coke
plant workers as a whole
nor of lung cancer for
oven workers
6.4-fold increase over
general population
5 deaths that appeared
to be a significant
excess
Coke plant workers had
2-fold excess relative
to rate among steelworkers
Coke- oven workers showed
2-1/2-fold excess over
steelworkers population;
top-side workers had 5-fold
excess; workers with 5 or
more years full-time top-
side work had 10-fold excess;
nonoven workers may have
excess risk of digestive
cancer
Characterization of exposure
Coke plant workers
All deaths occurred among gas-
workers with at least 5 years
experience; most had more than
10 years
Coke plant workers
Coke plant workers
(continued)
-------
Table 5 (continued)
Invest iqator
Redmond ,
Ciocco, Lloyd,
and Push
Redmond et al
Redmond
Date of
study
1972
1976
1976
Type of
study
Follow-up to
above
Follow-up to
previous
studies
extended to
1970
Follow-up to
previous
studies
Site
Lung
Kidney
Prostate
Lung
Intestine
Pancreas
Kidney
Lung
Pancreas
Intestine
Buccal and
pharyngeal
Results
Coke oven workers had 1.34
excess risk relative to
nonoven workers
Coke oven workers had a
7.49 excess risk over
nonoven workers
Coke oven workers had
1.64 excess risk over
nonoven workers
15.72 excess for full-
time top-side oven
workers
2.37 excess for non-
oven workers
4.29 excess for non-
oven workers
5 excess for all coke
plant workers;
3.31 excess for oven
workers
4.95 excess for nonoven
workers
2.93 excess for nonoven
workers
3.87 excess for nonoven
workers
Characterization of exposure
Coke plant workers
-------
certainty after the latter date."
Another important report was a study by Kuroda and Kawahata
(1936) demonstrating a high incidence of lung cancer among
Japanese gas generator workers. Although lung cancer was a
relatively rare form of cancer in Japan during the 1930's,
accounting for 3.1 percent of all cancer, this study showed that
lung cancer accounted for 80 percent of all cancer (12 out of
15 cases) among the gas generator work force who were exposed to
extremely high quantities of material similar to coke oven
emissions.
RECENT STUDIES
In another study of 504 deaths among former gas workers at a
Japanese steel plant, Kawai et al (1967) found 6 deaths from lung
cancer in contrast with the expected number, 0.180, for other
workers at the same plant with no gas-generator work experience;
this value is 33 times the expected rate. Age-standardized
mortality from lung cancer in the control group was close to that
of the general male population. The large excess of lung cancer
deaths among the gas workers could not be attributed to smoking.
The authors note that the excess of lung cancer mortality oc-
curred only in the age group of 45 to 54 years. Data for those
in this group with 10 to 19 years of gas-generator work experi-
ence showed a marked increase in lung cancer risk, whereas data
for those under 45 years of age with the same work experience (10
to 19 years) showed no significantly excessive mortality. The
implications of this finding are discussed in Section 7.
Bruusgaard (1959) studied 125 deaths among former gas works
employees in Norway, all of whom had at least 5 years work exper-
ience and most of whom had more than 10 years. The number of
respiratory cancers was higher than expected (12, or 9.6% of the
total number of deaths, against 1.5% in males for the country as
a whole). The proportion of lung cancers to cancers of all sites
among the gas workers (29.2%) was also significantly higher than
25
-------
that in the general population, 9.2 percent. In addition, there
were five deaths from cancer of the bladder—12 percent of all
cancers. Although Bruusgaard gives no exposure data and occupa-
tional histories for most cases are incomplete, he notes that
workers with a history of employment in the retort houses had an
especially high incidence of respiratory cancer.
Reid and Buck conducted a mortality study in 1956 among 800
coke plant workers randomly selected from a total of 8000 em-
ployed over the years 1949-54, inclusive. The study did not show
an elevated cancer risk when death rates for all causes and for
cancer were compared with age-specific rates prevailing in the
period 1950-54 among workers in a large unspecified industrial
organization. The cause of death was ascertained either by
reference to the union's funeral fund records, which were re-
quired to be supported by a copy of the death certificate, or by
a special search at the General Register Office. The coke plant
workers were categorized by occupation: coke oven workers, those
handling by-products, and maintenance workers (further grouped as
laborers, workers, and foremen). No total excess in the number
of cancer deaths was found among the coke plant workers as a
whole, and there was a "complete lack" of any excess of respir-
atory cancer for men working on the ovens. When occupational
history was taken into account, no excessive cancer risk was
found for by-product workers and only a small excess was found
for men who had at some time worked at the oven.
This study was criticized by Lloyd (1971), who pointed out
that Reid and Buck may have underestimated the number of lung
cancer deaths since the records included only men dying while
still "on the books" during the period 1949-54. Lloyd also
states that "the population at risk and the distribution by age
and area of prior employment was based on an estimate of figures
which excluded retirees and those who had left employment."
Although employment history is inadequate and follow-up is incom-
plete, reanalysis of Reid and Buck's data shows that the only
occupational group with an excess for all cancer as cause of
26
-------
death was the oven-worker group. A higher death rate of the top-
side workers probably would be diluted in this study, since Reid
and Buck's definition of oven workers includes both top-side and
side-oven workers.
In an effort to further quantify the Kennaway and Kennaway
data suggesting a correlation between occupational exposure and
cancer mortality, Doll (1952) studied the mortality among male
pensioners (over age 60) of a large London gas works company for
a 10-year period (1939-1948) and compared the data with mortality
data for the population of Greater London. Table 6A, which
summarizes the results of this study, shows that retired gas
workers had a statistically significant excess of lung cancer
deaths as compared with the number of deaths expected at the
London rates. In this study, data on men who retired early were
included when the men reached age 60 so as not to bias the in-
vestigation by the exclusion of a particularly unhealthy group
who retired early because of health reasons. Age-standardized
mortality ratios were calculated by use of mortality rates for
England and Wales, which were weighted to approximate higher
rates in Greater London. The causes of death recorded by the
company had been copied from death certificates. The pensioners'
mortality from all causes was close to the expected (840 deaths
against 856 expected), but the mortality from cancer was in
excess of the expected (156 against 123.5; p<0.01). Cancer of
the lung accounted for the greatest excess (25 against 10.4;
p<0.001), which constitutes a significant increase in mortality.
To assess differences in risk among different jobs within
the gas works, Doll categorized the pensioners as those employed
outside the works and those involved directly in the production
of gas or in handling of the waste products, representing a low-
and a high-exposure group, respectively. Excess lung cancer
among the high-exposure group was significant (17 observed versus
8.6 expected; 0.01
-------
Table 6. SUMMARY OF MORTALITY DATA IN GAS WORKERS OBSERVED BY DOLL
A. Causes of death of pensioners from 1939 to 1948 compared with the experience of Londoners
N>
00
Cause of death
Cancer and other tumors
Cancer of stomach and
duodenum
Cancer of lungs and pleura
All causes
Expected
deaths at
England
and Wales
rates
123.5
25.0
10.4
831.5
London
weights'3
1. 10
0.93
1.33
1.03
No. of deaths
Expected at
London rates
135.9
23.3
13.8
856.4
Observed
156
32
25
840
Test of
signi f icance
of difference
between
observed and
expected ,
value of P°
<0.01
a Table 6A adapted from Doll (1952); 6B adapted from Doll (1972).
Since adequate mortality data for Greater London were not available, Doll initially used mortality
data for England and Wales to calculate the expected number of deaths. He then applied a weighting
factor to bring the values into conformity with the numbers that would be expected for residents
of Greater London.
c The values for P are probabilities with which as great or greater differences between the observed
and expected deaths might occur by chance. Values of greater than 0.05 are not recorded.
(continued)
-------
Table 6 (continued)
B. Standardized annual death rate per 1000 men: all four original boards grouped together, and England and Wales
(number of deaths in parentheses)
Cause of death
Cancer of lung
Cancer of bladder
Cancer of skin
and scrotum
Other cancer
Bronchitis
All causes
1 Sept. 1953
to 31 Aug. 1961
Class Aa
3.39 (55)
0.28 (4)
0.07 (1)
2.11 (36)
3.53 (51)
19.68 (304)
Class C^
1.16 (5)
0.00 (0)
0.00 (0)
2.41 (9)
2.10 (9)
15.00 (61)
E
and
W
2.05
0.17
0.02
2.57
1.61
18.66
1 Sept. 1961
to 31 Aug. 1965
Class A
4.08 (44)
0.42 (6)
0.19 (2)
3.02 (34)
2.42 (26)
21.69 (243)
Class Ci
1.78 (6)
0.29 (1)
0.00 (0)
2.37 (8)
3.12 (9)
14.50 (46)
E
and
W
2.24
0. 17
0.02
2.51
1.64
18.69
1 Sept. 1953
to 31 Aug. 1965
Class A
3.82 (99)
0.40 (10)
0.12 (3)
2.70 (70)
2.98 (77)
21.21 (547)
Class Cj
1.59 (11)
0.13 (1)
0.00 (0)
2.39 (17)
2.57 (18)
14.91 (107)
E
and
W
2. 13
0. 17
0.02
2.55
1.63
18.67
Significance of differ-
ence between observed
(Class A) and expected
value of P
<0.001
0.03; 0.02
<0.001
NJ
Standard population—total number of man-years at risk for both occupational classes and all four boards, 1953-65. The one
untraced man in Class A is counted as alive at the end of the study.
a Class A = heavy exposure, i.e., coal carbonizing process workers.
Class C. = exposure only to by-products, i.e., process and maintenance workers in chemical and by-products plant.
-------
those involved in the gasification process or included those
handling by-products. Evaluation of relative mortality rates was
further complicated because those listed as employed in other
sections of the plant may have been employed in the gas works at
an earlier time.
In a separate study, Doll (1965) carried out an 8-year
prospective analysis of mortality from different causes among
several occupational groups of gas workers and retirees covering
the years 1953-61. Table 6B, which summarizes the results of
this study and of a follow-up study, by Doll (1972), shows that
heavily exposed gas workers had statistically significant excesses
in mortality from lung cancer compared with the numbers of
deaths expected on the basis of the rates for England and Wales.
This study (1965) also noted an excess in mortality from bron-
chitis. The study included 11,499 men between 40 and 65 years of
age at the start of the study with 5 or more years in the gas
works plant. Observed gas worker mortality rates were compared
with those expected in populations of England and Wales and
regional metropolitan areas.
Information on the cause of death was obtained from death
certificates. The workers were grouped into three classes
y
according to their exposure: heavy exposure (A); intermittent
exposure (B); minimal exposure, or exposure only to by-products
(C). Again, elevated mortality was attributed to respiratory
system disease, specifically, cancer of the lung and bronchitis.
The lung cancer mortality rate was 69 percent higher for Class A
than for Class C. A 4-fold higher rate of bladder cancer was
also observed in Class A as compared with Class C. The increase
in bladder cancer verged on significance (p=0.06) according to
Doll, who concluded that the mortality of gas workers varied
significantly with the type of work and that mortality was
highest among workers with greatest exposure to the products of
coal carbonization. A report on an additional 4 years of obser-
vation of the cohort (Doll, 1972) provided follow-up information
on 2449 coal-carbonizing process workers and 579 maintenance
30
-------
workers on mortality rates gathered at annual intervals from 1961
to 1965. Additional employees of four other gas boards were also
followed over periods of 7 to 8 years.
Heavily exposed workers (Class A) experienced a highly
significant elevated mortality from lung cancer (p<0.001) and
bronchitis (p<0.001). Data on by-product workers (Class C) show
no excessive mortality and over the 12-year period provide no
substantial evidence of increased occupational risk for this
group. The additional 4 years of data in this study support the
earlier association between exposure to the products of coal
carbonization and increased lung cancer and also a risk of blad-
der cancer (p=0.06). However, the increased mortality from
bronchitis, noted earlier, was no longer apparent.
An important series of reports on the mortality of coke oven
workers is the extensive, ongoing study of steelworkers conducted
by Lloyd, Redmond, and their colleagues at the University of
Pittsburgh. These reports, the results of which are summarized
in Tables 7 and 8, indicated increased relative risks for certain
cancers among coke oven and nonoven coke plant workers. In the
course of their study of mortality among nearly 60,000 steelworkers,
these investigators began to concentrate on coke oven workers as
a subgroup within the steelworker population apparently because
of the observed elevated mortality of that subgroup from respiratory
and other cancers. This work has confirmed and extended the
well-established findings that workers exposed to the coal-
carbonization process experience a markedly increased cancer
risk. The successive phases of this study also show increased
cancer response rates with increased exposure and dose. The
results of these studies and available cumulative exposure data
are discussed in detail below, along with potential health
effects at lower-level exposures, which were approximated within
the constraints of the data.
The coke plant workers studied by Lloyd were employed in by-
product coke plants. In contrast to the older beehive coke oven,
31
-------
Table 7. SUMMARY OF RELATIVE RISKS OF DEATH FROM
CANCER AMONG COKE OVEN WORKERS3
Length of employment
(1953-1970), yr
Work area
Total coke oven
Coke oven
Oven top-side full-time
Oven top-side part-time
Oven side only
Nonoven
No one coke plant area
Distribution
of workers
5 +
1860
993
150
290
553
836
31
10+
1194
574
72
245
257
578
42
15 +
790
325
29
159
137
392
73
Deaths and RR's of death from
malignant neoplasms
5+
Obs.
166
101
35
26
40
65
0
RR
1.47b
1.66b
3.70b
1.59b
1.17
1.28
d
10 +
Obs.
136
85
22
31
32
48
3
RR
1.50b
1.95b
5.12b
1.85b
1.46
1.10
d
15 +
Obs.
108
63
12
32
19
39
6
RR
1.62b
2.40b
7.63b
2.73b
1.51
1.13
1.34
Deaths and RR's of death from
respiratory cancer
5+
Obs.
54
25
12
17
RR
3.02b
9.19b
2.29b
1.79C
10+
Obs.
44
16
16
12
RR
3.42b
11.79b
3.07b
1.99b
15+
Obs.
33
8
18
7
RR
4.14b
15.72b
4.72b
2.00
10
K>
All malignant neoplasms of digestive system
Large intestine
Pancreas
Other
Deaths and RR's of death from
cancer of digestive system among non-
oven workers
5+
Obs.
28
11
8
9
RR
1.58C
2.31C
3.67b
0.83
10 +
Obs.
23
10
7
6
RR
1.53
2.52b
3.75b
0.65
15 +
Obs.
19
8
6
5
RR
1.53
2.37C
4.29b
0.65
Adapted from Redmond (1976).
P<0.01.
P<0.05.
Less than five deaths.
-------
Table 8. SUMMARY OF EPIDEMIOLOGICAL STUDIES OF LONG-TERM
MORTALITY OF COKE PLANT WORKERS
Year
1970
1971
1972
1975
1976
1976
Author
Lloyd, Lundin,
Redmond, Geiser
Lloyd
Redmond,
Ciocco, Lloyd,
Rush
Hazumdar ,
Redmond,
Sollecito,
Sussman
Redmond,
Strobino,
Cypess
Redmond
Title
Long-Term Mortality Study of
Steelworkers IV. Mortality
by Work Area
Long-Term Mortality Study of
Steelworkers V. Respiratory
Cancer in Coke Plant Workers
Long-Term Mortality Study of
Steelworkers VI. Mortality
from Malignant Neoplasm
Among Coke Oven Workers
An Epidemiological Study of
Exposure to Coal Tar Pitch
Volatiles Among Coke Oven
Workers
Cancer Experience Among Coke
By-Products Workers
Epidemiological Studies of
Cancer Mortality in Coke
Plant Workers
Study population
and years of
observation
SMRs of workers
by area - coke
plant; white, non-
white
Oven and nonoven
workers employed
in 1953-1961 and
prior years
Any worker with
coke oven exper-
ience, 1951-1955
(expanded to also
include 10 plants
not in Allegheny
County - 12 plant
study)
Coke oven workers
from 12 plants.
1951-1966, 1953-
1966 (see above)
Oven and nonoven
workers, 1953-1966
Oven and nonoven
workers, 1953-1970
Comparison group
Total steelworker population.
(58,828 men) , 1953-1961
Total steelworker population.
(58,828 men) 1953-1961
1) All Steelworkers including nonoven
coke plant workers employed from
1951-1955 in 10 plants
2) Steelworkers including nonoven
coke plant workers employed in
1953 in two Allegheny County plants
Steelworkers including nonoven coke
plant workers from 12 plants, 1951-
1966 and 1953-1977 (see above)
All Steelworkers with no coke
plant exposure, 1953-1966
All Steelworkers with no coke
plant exposure, 1953-1970
U)
U)
Standard Mortality Ratios.
-------
which released the volatile matter (by-products) into the atmos-
phere, the by-product oven recovers most of the tar, oil, and
chemicals from the volatiles. Exposure to effluents from by-
product coke ovens is due to the escape of volatiles during
charging, quenching, and discharging and to their escape through
improperly sealed openings.
In these studies the workers were classified by work area
within the plant in terms of function and exposure to effluents,
a task made difficult by the variety and vagueness of job titles
used in occupational histories by different companies and changes
in titles over long periods of time. The by-product coke plant
was therefore analyzed in terms of three distinct areas: 1) the
coal-handling area, 2) the coke oven area, and 3) the by-products
plant for recovery of gas and chemical products (areas 1 and 3
are nonoven workers). Since earlier work (e.g., Doll, 1972;
Kennaway and Kennaway, 1936, 1947) had shown no apparent in-
creased cancer risk for men involved in work similar to that
performed in areas 1 and 3, some of the initial study groups
included only those workers employed in area 2.
In this long-term study, Lloyd (1971) examined the mortality
records of the workers in relation to length of employment and
work area within the coke plant and compared the cause-specific
mortality of coke plant workers as a whole with the mortality of
the total steelworker population. Thus he eliminated the diffi-
culty of comparing nonworkers with supposedly healthier workers.
The cohort for the study included all men employed in two of the
three Allegheny County steel plants operating coke plants during
1953. Coke plant workers were categorized as oven workers and
nonoven workers. In this phase of the study, the excess mortal-
ity from respiratory cancer among all coke plant workers employed
in 1953 could be accounted for by the excess mortality of workers
employed on the coke oven itself (20 observed, 7.5 expected).
The excess mortality of coke oven workers was further demon-
strated when men employed at the ovens before 1953 were included
34
-------
in the coke oven worker category. This inclusion added 84 deaths
and increased the mortality rate by 84 percent. Deaths among men
employed in 1953 accounted for 13 of the 33 deaths observed from
respiratory neoplasms, more than twice the expected number. In
total, the current plus the former coke oven workers experienced
a 2-1/2-fold excess mortality from respiratory cancer.
Although the initial study also showed a difference between
white and nonwhite workers, this difference resulted from too few
white workers and disappeared later when more white workers were
added to the study. Further, a significant excess of cancers of
the digestive system was observed in nonoven workers employed in
1953 and prior years (17 vs. 9.7 expected; significant at the 5%
level). Cancer of the pancreas and large intestine showed the
greatest excess.
The results of this first study showed the importance of
analyzing mortality by job classification, indicative of relative
exposures, and by length of exposure. Deaths among full-time
top-side workers accounted for all of the excess mortality of
coke oven workers from all causes and almost all of the mortality
from lung cancer. Deaths from lung cancer among full-time top-
side workers were 7 times the expected rate (19 vs. 2.6; signif-
icant at the 1% level). Lloyd comments that because the popula-
tion was followed for only 9 years, his estimates of lung cancer
mortality may be conservative owing to the long period of latency
in occupational lung cancers (15 to 25 years), a comment borne
out by the continuing studies.
Elevated rates in mortality of coke oven workers from all
causes of death were associated with length of employment.
Excess mortality among men employed at the ovens less than 5
years was slight, whereas among those employed more than 5 years
the overall mortality was 17 percent higher than expected and the
lung cancer death rate was 3-1/2 times that expected. These
findings can be interpreted as preliminary evidence for a dose-
response relationship between respiratory cancer and exposure to
35
-------
coke oven emissions. Total mortality of men employed 5 or more
years at full-time top-side jobs was twice the expected value (35
vs. 17; significant at the 1% level). Almost all of this in-
crease was due to a 10-fold risk of lung cancer for full-time
top-side workers (15 vs. 1.5; significant at the 1% level).
Redmond et al (1972), in a follow-up of earlier reports in
the series, examined the mortality records of cohorts of ccke
oven workers in an expanded study at 12 steel plants. In addi-
tion, the data from the earlier study (1971) of two Allegheny
County plants were updated from 1961 to 1966 and were compared
with data from 10 other plants for the same period. The cohorts
at the 10 additional plants included all men who had worked at
the oven at any time in the 5-year period 1951 through 1955.
(The criterion for inclusion in the prior Allegheny County study
was employment in one of the two coke plants during 1953.)
The findings of Redmond et al indicate that both the level
and duration of .exposure to coke oven emissions are correlated
with mortality from various types of cancer. The additivity of
time and dose was further substantiated. Analysis of mortality
by cause shows significantly elevated mortality of coke oven
workers from malignant neoplasms (RR 1.34; p<0.01), from malig-
nant neoplasms associated primarily with respiratory cancer (RR
2.85; p<0.01), from kidney cancer (RR 7.49; p<0.01), and from
prostate cancer (RR 1.64; not significant).
Initial analysis showed a discrepancy between the risks of
white and nonwhite coke oven workers until data on relative
exposure by race were analyzed. The data showed that 41.5 per-
cent of the nonwhites and 29.8 percent of the whites had been
employed at the coke ovens for 5 or more years at the time of
entry to the study. Only 2.2 percent of the whites had been
employed full-time top-side and 11.2 percent were employed part-
time top-side; in contrast, 27.3 percent of the nonwhites were
employed full-time top-side. Since top-side work entails the
heaviest exposure to coke oven emissions, the exposure of
36
-------
nonwhite workers clearly is disproportionately heavy relative to
that of white workers.
The study showed that men employed at full-time top-side
jobs for 5 years or more have a relative risk of lung cancer of
6.87 (p<0.01) as against risks of 3.22 (p<0.01) for men with 5
years of mixed top-side and side-oven experience and 2.10 (p<0.05)
for men with 5 or more years side-oven experience. These data
indicate a definite gradient in response based on both type and
duration of exposure. When relative exposures and responses are
accounted for, the racial differences are lost.
Overall, the study confirmed the Lloyd findings of a 2-1/2-
fold excess of mortality from respiratory cancers. A new finding
of Redmond's was a significant excess of kidney cancer among coke
oven workers (RR 7.49; p<0.01).
Redmond concludes that the 6.87 (p<0.01) relative risk'for
malignant neoplasms of the respiratory system for men employed
full-time top-side and the 1.70 relative risk (not significant)
for men employed less than 5 years suggest a dose-response rela-
tionship, which Mazumdar et al (1975) further substantiates by
calculating cumulative exposures of the cohort to CTPV's. (These
data are analyzed later.) Redmond's work also confirms the need
to allow an adequate induction period in study design, since
workers with less than 5 years of experience at time of entry
could have accumulated only 20 years of total exposure at most.
Table 7 summarizes additional data (1967 to 1970) analyzed
by Redmond (1976). These data from the Allegheny County steel
plants demonstrated a consistent increase in the level of risk of
malignant neoplasms with increased exposure for each of the coke
oven groups. Further, the risk of side-oven workers for lung
cancer, which had not been statistically significant in the
earlier studies, reached significance (RR 1.79; p<0.05). Al-
though no dose-response relationship was apparent, the relative
risk for cancer of the pancreas and the relative risks for
respiratory diseases other than cancer increased markedly with
37
-------
length of exposure. Estimates of exposure levels for this set of
studies are discussed later.
The latest study by Redmond et al (1976) again confirmed
elevated risks for coke oven workers for lung cancer (44 deaths
vs. 24.5 expected; p<0.01) and genitourinary cancer, relative
risk 1.82 (p<0.05), due primarily to a 5-fold increase in kidney
cancer. Data on nonoven workers continue to demonstrate excess
kidney cancer, and the most recent studies in the Lloyd series
show that incidences of buccal and pharyngeal malignancies are
highly significant.
Redmond's study also presents evidence that the observed
elevated incidence of intestinal and pancreatic cancer is not
attributable to the country of origin of the workers, an impor-
tant consideration because studies of migrants have established
differences in risk among those populations. The overall conclu-
sion of the paper is that "these observations indicate the need
to consider nonoven coke plant workers as well as oven workers
when evaluating cancer hazards in the plant." The health impli-
cations of these data are discussed in Section 6.
38
-------
SECTION 5
AMBIENT POLLUTION AND RESPIRATORY DISEASE
The effects of exposure to-coke oven emissions among the
general population are not well understood. There are no defin-
itive epidemiological studies of low-level exposure of popula-
tions near coke plants to coke oven emissions. A recent paper
(Graff and Lyon, 1977) reports findings near a large coke oven in
a northern Utah county. A statistically significant excess of
lung cancer cases (as compared with controls) was found among
residents living 4.8, 6.4, and 8 kilometers from the coke oven
but not at points nearer (1.6 and 3.2 kilometers) and farther (16
and 24 kilometers) from the oven. Only an abstract of this paper
is available, and without more- information the results are
difficult to interpret.
Most of the pollutants that make up coke oven emissions are
present in urban air but in different proportions from those
found in the vicinity of coke ovens. Some studies on urban air
pollution have found that the lung cancer death rate in urban
areas is roughly twice that in rural areas (NAS, 1972), and
several studies have shown a correlation between the "urban
factor" and BaP concentrations (Carnow and Meier, 1973; Pike et
al, 1975). However, because of the confounding effect of cigar-
ette smoking as the dominant cause of lung cancer and because of
the limitations of benzo(a)pyrene as an indicator of the carcin-
ogenic potential of air pollution, it has not been possible to
demonstrate conclusively that part of the urban excess of lung
cancer cases is due to general air pollution.
Nevertheless, researchers in a recent conference, after
weighing the available evidence, concluded that:
39
-------
"Combustion products of fossil fuels in ambient air, proba-
bly acting together with cigarette smoke, have been respon-
sible for cases of lung cancer in large urban areas, the
numbers produced being of the order of 5-10 cases per
100,000 males per year. The actual rate will vary from
place to place and from time to time, depending on local
conditions over the previous few decades." (Environ. Health
Perspectives, 1978).
It has been noted that the occurrence of cancer of certain
other sites besides the lung is higher in urban than in rural
areas. Using mortality data from Erie County (which includes
Buffalo) for the years 1959 to 1961, Winkelstein and Kantor
(1969a, 1969b) found positive associations between suspended
particulate air pollution and stomach cancer and between sus-
pended particulate air pollution and prostrate cancer. Associa-
tions obtained in correlation studies of this kind, as the
authors point out, must be interpreted cautiously in view of the
small numbers of cases involved and the "...many possible ways in
which unknown factors might be influencing the distribution."
Information concerning occupation, smoking, and residence history
was not taken into account in these studies. The authors note,
however, that their findings of associations of stomach and
prostate cancer with suspended particulate agree with similar
findings of Hagstrom et al (1967) based on the Nashville Air
Pollution Study. Coke ovens appear to be a major source of air
pollution in Erie County.
In contrast to the inconclusiveness of the data linking air
pollution and lung cancer, there is substantial evidence that air
pollution contributes to the increased incidence of both morbid-
ity and mortality from nonmalignant lung disease [much of this
evidence is cited in a recent review of air pollution and health
by Goldsmith and Friberg (1977)]. For example, the College of
General Practitioners (1961) in Great Britain has published data
showing a 2- to 4-fold increase in the incidence of chronic
bronchitis in urban over rural areas, a difference not completely
accounted for by the 2- to 3-fold increase in incidence of
chronic bronchitis attributed to smoking.
40
-------
Buck and Brown (1964) found high correlations of particulate
matter and sulfur dioxide with bronchitis mortality, and Toyama
(1964) found significant correlations between bronchitis and
dustfall in 21 Tokyo districts where age-standardized mortality
rates reflected increased levels of exposure. Nose (1960) re-
ported a strong association of bronchitis and pneumonia with
dustfall in Ube, Japan. Carnow et al (1970) correlated sulfur
dioxide concentrations with increased chronic bronchitis. Spicer
et al (1962) observed that respiratory symptoms in patients with
chronic bronchitis were associated with SO2 levels measured 38
hours previously. This finding was substantiated by McCarroll
et al (1967), who reported intervals of 24 hours and 48 hours
between the occurrence of sulfur dioxide and particulate pollu-
tion and symptoms of respiratory ailment.
Winkelstein et al (1967), using mortality data from Buffalo
and Erie counties for the years 1959 to 1961, found a positive
association between air pollution, as indexed by suspended par-
ticulate, and chronic respiratory disease.
A number of acute air pollution episodes, described by
Goldsmith and Friberg (1977), have demonstrated that an extreme
deterioration in air quality can have a serious effect on human
health. Most of these episodes occurred when stagnant polluted
air was trapped over a city for several days during a temperature
inversion. The numbers of deaths and hospital admissions due to
respiratory complications rose dramatically during these episodes,
the greatest number of cases occurring among older persons.
During the worst recorded episode (in London in 1952), the total
excess of deaths was between 3500 and 4000, with bronchitis,
bronchopneumonia, and heart disease as the main causes of death.
The only common factor revealed by autopsy was irritation of
their respiratory tract (Ministry of Health; London, England,
1954) . In the London episode, as in other episodes, the levels
of sulfur dioxide and particulate matter were exceedingly high.
Both general air pollution studies and the effects of- acute
air pollution episodes suggest that bronchitis is related to air
41
-------
pollution, but the parameters of a possible dose-response rela-
tionship are not well defined.
42
-------
SECTION 6
ANALYSIS OF HEALTH EFFECTS
INTRODUCTION
Assessment of the health effects attributable to the array
of toxic pollutants in coke oven emissions must be based on
quantitative and qualitative judgments. Qualitatively, it is
clear that coke oven emissions represent a serious carcinogenic
risk to human beings. Extensive epidemiological evidence shows
that workers exposed to relatively high levels of coke oven
emissions develop cancer, especially cancer of the respiratory
tract, at rates significantly higher than those reported for
other workers and for the general population.
The epidemiological evidence is confirmed by equally power-
ful results of experimental bioassays, which show that BaP is
carcinogenic in all species tested by all routes of administra-
tion (see Table Al for examples). Further, other components of
the emissions also induce cancer in test animals, and combina-
tions of the components are even more effective in experimental
induction of cancer (Hoffmann and Wynder, 1976; Laskin et al,
1970). Dose-response relations are observed in these assays. An
example of the dose-response data is given in Figure 1.
Investigations of the binding of various PAH metabolites to
DNA have yielded additional evidence of potential human health
hazards (Gelboin, 1969; Sims et al, 1974; Huberman et al, 1976).
These findings have been supplemented by positive Ames tests
indicating the mutagenicity of various PAH's as noted in Table
A2. This microbiological assay system is in many instances
correlated with carcinogenicity.
The data describing human experience, tests with animals,
and in vitro experiments constitute one body of evidence.
43
-------
95
90f
*«
• 80
o 70
£ 60
o 50-
5 40
2c 30
S 20
^ 10
? 5
3.3 10 30 90
DOSE, yg
270
iSource: Pott et al, 1977]
Figure 1. Dose-response relationship for tumor induction
in mice and BaP administered subcutaneously.
44
-------
Further, it is known that the particulate size distribution
associated with coke oven emissions is optimum for penetration
and absorption into the human respiratory system, and that the
composition of the particulate matter [hematite, (Saffiotti, et
al, 1968); carbon, (Boren, 1964; and others)] optimizes such
absorption. Considered together, these facts lead to the conclu-
sion that coke oven emissions present a definite health hazard to
persons exposed to industrial concentrations.
Despite the strength of the evidence, difficulties arise in
attempts to quantify the level of risk and to extrapolate it to
the population at large, who are exposed to much lower levels of
the pollutants. Part of the difficulties are experimental, part
theoretical, and a large part philosophical. The problems are
addressed systematically in the following analysis.
BIOASSAY RESULTS
Although extensive experimental evidence shows that many of
the components of coke oven emissions are carcinogenic, experi-
mental carcinogenesis does not purport to establish that a given
factor contributes to cancer in man. At present, such proof can
be based only on epidemiological data. The laboratory studies do
allow us to identify the chemical and physical nature of tumori-
genic agents, to explore their biological action and to devise
means of reducing their concentrations in or eliminating them
from our environment.
In the past 25 years considerable progress has been made in
developing organ-specific bioassay techniques, in understanding
damage to host defenses against toxic agents, and in exploring
the metabolic activation of environmental carcinogens (Hoffmann
and Wynder, 1976). Laboratory studies support the concept that
in only a few cases is a single factor responsible for an in-
creased risk of developing a specific type of cancer and that
cancer attributable to environmental factors often is induced by
the combined effects of several agents (Van Duuren et al, 1969).
Model studies have helped to explain the combined effects of
45
-------
occupational factors, smoking, and urban pollution in induction
of cancer of the lung (Hoffmann and Wynder, 1976).
Experimental data are not adequate, however, to allow
determination of a safe dose for any chemical carcinogen, below
which there will be no tumorigenic response in humans. Bioassays
can be used to evaluate the carcinogenic potential of various
environmental agents by means of observed dose-response relation-
ships.
An abundance of in vivo and in vitro experimental evidence
confirms the carcinogenicity of various PAH's and elucidates the
roles of other PAH's, irritating substances, a variety of sol-
vents, and other factors in promoting and initiating tumors and
in cocarcinogenesis. These findings are discussed in Section 3
and are detailed in Table Al. It is important to note that in
these studies all animal species tested developed tumors in many
sites by all routes of administration.
CHARACTERIZATION DIFFICULTIES AND HEALTH EFFECTS
In addition to the widely recognized problems inherent in
extrapolating among species and in applying results of experi-
ments with animals to humans, the multiple and varied constitu-
ents of coke oven emissions further complicate the assessment of
health effects.
Most investigators of the carcinogenic effects of air
pollutants use BaP as an index of the level of carcinogens. Many
inaccuracies are inherent in a BaP index. Sawicki (1967) notes
that urban pollution from various sources is characterized by
different proportions of polycyclic arenes, some carcinogenic and
some not. However, some PAH's thought to be noncarcinogenic
alone may, in combinations with other factors such as ultraviolet
light, induce tumors. Thus, Sawicki suggests that the nature of
the mixture determines its carcinogenicity for humans. This
suggestion has been verified in laboratory experiments (Van
Duuren et al, 1969; Laskin et al, 1970).
46
-------
The problem of an accurate index need not be considered if
we treat "coke oven emissions" as a whole and do not apply an
exposure index, such as the concentration of BaP or the sum of
the concentrations of several PAH's in extrapolating health :
effects. Because the extensive epidemiological evidence de-
scribes adverse health effects experienced by an industrial work
force exposed to "coke oven emissions" (i.e., the total, complex
mixture, often characterized as the benzene-soluble fraction of
the total particulate matter), we need not delineate, for the
human experience, the effects of the constituents acting sepa-
rately or in various combinations with each other. IT IS, THERE-
FORE, ESSENTIAL THAT THE ASSESSMENT OF HEALTH EFFECTS PRESENTED
HERE BE APPLIED TO "COKE OVEN EMISSIONS" AS AN ENTITY AND NOT TO
ANY PARTICULAR COMPONENT, SUCH AS BaP.
Other biological evidence supports the position that coke
oven emissions must be considered as a whole in evaluation of
health effects. For example, the association between lung cancer
and cigarette smoking confirms the interaction of various factors
in a complex mixture, since the carcinogenicity of cigarette
smoke cannot be explained by the identified carcinogens alone
(Hoffmann and Wynder, 1976).
The similarity of the constituents of tobacco smoke and
those of coke oven effluents further supports the plausibility of
a dose-response relationship for coke oven emissions, since there
is such a relationship for cigarette smoke (Table 9). The pres-
ence of irritants, toxicity promoters, and cocarcinogens must
play an important role in the carcinogenicity of coke oven emis-
sions as it does in cigarette smoke since, as Table 10 shows,
similar agents are present in both mixtures.
The temperature of carbonization in cigarette smoking is
about 860°C, whereas in coal carbonization the temperatures range
from 1200° to 1400°C. As noted earlier, the proportion of toxic
compounds produced by carbonization increases with an increase in
temperature, and there is a corresponding increase in the incidence
of disease, as shown in Table 4. The greater concentration of
47
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Table 9. RELATIVE RISK FOR LUNG CANCER AS A FUNCTION
OF DAILY TAR DOSAGE FROM CIGARETTES IN MALE
SMOKERS WITH TEN YEARS OR MORE OF SMOKING3
Tar dosage,
ing
Up to 340
341 - 480
481 - 630
631 - 1000
1001 and up
Nonsmokers
No. of
cigarettes/day
up to 20
20 - 29
29 - 37
37 - 59
59 and up
No. cases of
lung cancer
54
71
102
159
109
8
No. controls
247
231
216
270
197
509
Relative
riskd
13.9
19.6
30.0
37.5
35.2
a Source: S. Stellman, in preparation.
b Average daily tar intake for the past 10 years.
c For example, a cigarette that contains 17 mg tar.
d Relative risk is defined as the incidence of disease in the exposed group
divided by the incidence of disease in the nonexposed group, as estimated
by the odds ratio.
48
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Table 10. PARTIAL LIST OF TUMORIGENIC AGENTS AND OTHER TOXIC COMPOUNDS IN
COKE OVEN EMISSIONS AND IN CIGARETTE SMOKE
Toxic aqent
Range of concentration in coke oven emissions
Concentrat ion
in smoke of
one cigarette
Carcinogens
Diraethylnitroso compounds
N-nitroso compounds (6 compounds)
Hydrazine
Vinyl chloride
6-naphthylamine
PAH (tumor initiators)
Benzo (a) pyrene (+++)C
Benz (a) anthracene (+)
Benzo (b) fluoranthene (++)
Benzo (j) fluoranthene (+•+)
Benzo (e) pyrene
Benzo (h) fluoranthene
5-Methylchrysene (+++)
Dibenz (a,h) anthracene (++)
Dibenzo (a,h) pyrene {++)
(continued)
present but not quantified
present but not quantified
present but not quantified
present but not quantified
3b
2 ng/m
0.21-15 gg/m3 (coke plant)d
17 gg/m^ (ambient air)e
12.9 ug/m3 (coke plant)ec
13.1 ug/m^ (ambient air)
5.04 ug/m
1.78 ug/n
present but not quantified
present but not quantified
present but not quantified
present but not quantified
present but not quantified
Carcinogenic
subset
identified by
Schulte et al
as comprising
2* of BSD
fraction
5-180 ng
2-200 ng
24-43 ng
10-40 ng
22 ng
10-50 ng
40-70 ng
30 ng
60 ng
5-40 ng
0.6 ng
40 ng
present but not
quantified
-------
Table 10 (continued)
Toxic agent
Range of concentration in coke oven emissions
Concentration
in smoke of
one cigarette
Ul
O
Dibenz (a,]) acridine (++)
Indeno (1,2,3-cd) pyrene (+)
Chrysene (+)
Methylchrysenes (+)
Methylfluoranthenes (+)
Tumor promoters
Formaldehyde
Volatile phenols
Cilia toxic agents
Hydrogen cyanide
FormaIdehyde
Acrolein
Acetaldehyde
Cocarcinogens
Cathechol
1-Methylindoles
9-MethyIcarbaroles
present but not quantified
present but not quantified
present but not quantified
present but not quantified
present but not quantified
0.311 mg/m
0.14 mg/m (coke oven charging)6
2000-4000 mg/m (in coke oven gas);e
0.4 mg/m3'(top-side)6
0.311 mg/m
0.55 mg/m
present but not quantified
present but not quantified
present but not quantified
present but not quantified
3-10 ng
4 ng
40-60 ng
18 ng
50 ng
20-90 ug
150-500 ug
100-700 ug
20-90 ug
45-140 ug
18-1440 ^g
200-500 jg
1000 ng
140 ng
a Wynder and Hoffmann, Tobacco and Tobacco Smoke, Seminars in Oncology, Vol. 3, No. 1 (March 1976).
b Doll (1972).
Indications of carcinogenicity refer to NAS (1972).
Sawicki (1976) .
White, L., Doctoral Dissertation (1975).
-------
toxic substances may explain why the observed incidence of lung
cancer among coke oven workers is equivalent to a risk 3 times
that of a person who smokes two packs of cigarettes per day. The
cancer rate among coke oven workers appears to be due not just to
the carcinogens but also to irritants and particulate matter.
This fact is in accord with evidence of synergism between irritants
and carcinogens in animal studies (Laskin et al, 1970; Saffiotti
et al, 1968; Boren, 1964) and with epidemiological evidence.
Despite the need to consider coke oven emissions as an
entity, some of the discussion and the experimental results are,
of course, based on exposures to BaP. This is inevitable because
most scientific work relating to air pollution relies on BaP as
an indicator substance, although, in fact, most environmental
assays of coke oven emissions have dealt with the benzene-soluble
fraction of total particulate matter (CTPV). To facilitate the
interpretation of epidemiological evidence, we sometimes "trans-
late" CTPV values into the corresponding BaP concentration units.
The use of BaP units is a method of converting the available data
on coke oven emissions, usually given as CTPV, into the same
units given in most data on urban exposures, although the ratio
of constituents varies with the source.
The conversion of CTPV data to BaP units is not a trivial or
obvious procedure. As Sawicki (1967) notes, there is a "tremen-
dous range" in concentrations of airborne particulates, benzene-
soluble organics (BSO), and BaP in various urban air samples.
Figure 2a shows that a good correlation between BaP and the
benzene-soluble fraction of CTPV can be obtained (Smith, 1971).
As shown in Figure 2b, the correlation between cyclohexane ex-
tracts and BaP is not as good, particularly at low concentrations
(Smith, 1971). For purposes of this discussion, the concentra-
tion of BaP is taken as 1 percent of the total organic fraction.
This approximation probably involves at most a 2-fold,error and
is commonly applied by others (Schulte et al, 1975).
51
-------
25
20
r = 0.8415
15
10
o.
-------
The validity of extrapolation and comparison of exposure
levels among various studies is limited even further by the
sampling method. A 2- to 4-fold margin of error is probable in
comparison of values obtained by high-volume air samples with
those obtained with a personal monitoring pump, as demonstrated
by Schulte et al (1975). Other sources (White, 1975) believe
that the error may be even greater. Combinations of these
errors, if they are acting in the same direction, may lead to as
much as 4- to 8-fold overestimate or underestimate of exposure to
BaP. Since, however, we are here dealing with differences of 3
to 5 orders of magnitude in exposures of the general population
and occupational exposures to BaP (based on urban exposure levels
due to coke oven emissions as determined by Stanford Research
Institute, 1977), a 4- to 8-fold range of error can be tolerated,
although it is certainly not desirable.
BASES FOR INTERPRETING MORTALITY DATA
Overall and cancer mortality rates of the general population
are not readily applicable in evaluating the effects on the
general population of exposure to coke oven emissions. First, if
an increased rate of lung cancer among the general population
results from exposure to coke oven emissions, such an increase
may be masked by the very large increase in lung cancer due to
cigarette smoking. Although coke oven emissions contain similar
and possibly more potent carcinogenic agents, the levels of
pollution from coke oven emissions in the general population,
away from the plant, are very much lower than those of cigarette
smoke. As Wynder and Hoffmann (1972) calculate, "heavily pol-
luted air" contains a maximum of 100,000 particles per cubic
centimeter of air as compared with 5 billion particles per cubic.
centimeter in tobacco smoke, a difference of 4-1/2 orders of
magnitude. When the relative amounts of air breathed in are
taken into account, a difference of about 2 orders of magnitude
remains.
53
-------
The long period of induction for lung cancer, usually 15 to
30 years, increases the difficulties of correlating urban air
pollutants with lung carcinogenesis because of such factors as
urban mobility and the inadequacies of both air quality data and
mortality data. For these reasons, it is useful to examine the
results of human high-level (occupational) exposures in estimat-
ing the health effects of exposure to coke oven emissions for the
general population.
It is important to note that the overall mortality experience
of coke oven workers is better than that of the general population,
either urban or rural, in most epidemiological studies. This is
typical of an industrial work force and has come to be called the
"healthy worker effect." If a person is strong and healthy
enough to be an industrial worker, that person is part of a group
that on the average must be stronger and healthier than nonworkers
and hence experiences a more favorable mortality rate. Therefore,
because it is in direct contrast to an otherwise favorable mor-
tality rate, the unfavorable mortality rate for specific causes
of death such as all cancer, respiratory cancer, bladder cancer,
kidney cancer, and bronchitis among coke oven workers as compared
to others is of special interest. In general, caution must be
exercised against "underinterpreting" data and incompletely
evaluating the magnitude of the risk. As is shown in Table 7, as
the period of observation increased, the relative risk or relative
mortality also increased. Further, as noted by Mazumdar et al
(1975), the current period of observation, on the average 20
years, is not long enough to allow full assessment of magnitude
of risk.
With these caveats in mind, we must attempt to establish
that the elevated mortality rates of coke oven workers can be
attributed to their exposure to coke oven emissions. In his
analysis of long-term mortality among steelworkers, Lloyd (1971)
develops criteria for interpreting excessive mortality as a
consequence of environmental exposures as opposed to excessive
mortality that can be associated with selection for health; that
54
-------
is, the criteria should differentiate between a true causative
agent in a work area and the movement of people into and out of a
work area because of health considerations. Lloyd states that if
the excess mortality is limited to a single organ system or a
single cause, then one would tend to suspect a causative factor
in the workplace environment. (The converse is not necessarily
true. If excess death from many causes is observed, one cannot
rule out the environment as a cause.)
A second Lloyd criterion that can be useful in differentiat-
ing effects due to occupational exposures from effects associated
with selection for health is that within certain work areas
excessive mortality is unaffected by race, nativity, and residence.
When the Lloyd criteria are applied to the subgroup of
steelworkers who are employed at the coke ovens, it is observed
that, contrary to general mortality of steelworkers, the reason-
ing he applied implicates environmental factors as the cause of
disease among coke oven workers. Since diseases of one system,
the respiratory system, and one disease in particular, lung
cancer, are the most prominent causes of excessive mortality
among coke oven workers, the first criterion is fulfilled. The
second criterion is also fulfilled, since the mortality from
cancer and respiratory disease crosses bounds of race, nativity,
and residence among coke oven workers. Lloyd, of course, drew
the same conclusions, and he and others have been investigating
the experience of workers exposed to coke oven emissions.
ESTIMATING HEALTH EFFECTS FROM OCCUPATIONAL MORTALITY DATA
In assessing the health risk of coke plant workers and its
meaning for the general population, one must make several approx-
imations and assumptions. The problem of assembling a comparison
group for epidemiological investigations, especially those
involving occupational exposures, is always a great one, and the
long-term mortality study of steelworkers studies is no exception.
As Table 8 shows, the series of reports devoted to the mortality
of coke plant workers is based on the use of several different
55
-------
comparison groups. In several studies the oven and nonoven
workers were compared with the entire steelworker population,
then steelworkers with no direct oven work experience but with
nonoven work experience in the coke plant, and finally, with
steelworkers with no coke plant exposure. A further difference
in these studies is that some reports include all workers em-
ployed in 1953, and others include workers employed in 1951-1955
(Redmond et al, 1972). Because the studies involve different
comparison groups as controls and because the basic study popula-
tion is not constant, it is difficult to compare the relative
risks cited in different reports of the series.
In gauging the effects of coke oven emissions on coke plant
workers, it is instructive to compare the lung cancer death rate
of steelworkers having no coke plant experience with that of the
nonsmoking general population. In Redmond's (1976) calculation
of the risk for lung cancer among coke oven workers, the popula-
tion of steelworkers with no coke plant exposure served as the
control population. This population has a mortality rate (127
per 100,000) greater than that of a person in the 45-54 year age
bracket who smokes two packs of cigarettes per day (95 per
100,000) and comparable to that of moderate and heavy smokers in
higher age brackets. In all age brackets the mortality of steel-
workers from lung cancer is 15- to 100-fold greater than that of
nonsmokers. Table 11 shows the age-specific mortality from lung
cancer of steelworkers per 100,000 person-years of exposure and
the mortality rates of cigarette smokers and nonsmokers. The
data show that the excess mortality of the coke oven workers from
lung cancer cannot be attributed solely to cigarette smoking.
The relative risk of lung cancer among coke oven workers can
be recomputed using the nonsmoking general population as a con-
trol. This is done by drawing on statistics comparing the lung
c incer death rate of two-pack-per-day smokers and of'the nonsmok-
ing general population. Such an approximation will overestimate
the risk in the higher age brackets where the steelworkers mor-
tality is less than that of a two-pack-per-day smoker, and will
56
-------
Table 11. ESTIMATES OF AVERAGE ANNUAL LUNG CANCER MORTALITY RATES '
PER 100,000 PERSON-YEARS OF EXPOSURE FOR SELECTED U.S. SMOKING GROUPS (1954-1962)
AND STEELWORKER GROUPS (1953-1961)a
U.S. smokers
Steelworkers
b
Never smoked or occasional only
b
Current cigarette smokers - total
b
Current cigarette smokers, 1-9/day
b
Current cigarette smokers, over 39/day
Steelworkers
Coke oven, never top- side
Coke oven, top- side
Age, years
35-44
S
<45
12
9
141
45-54
42
95
1
45-54
127
230
819
55-64
10
138
53
316
I55
162
313
1356
65-74
3C
281
132
606
cn
* From National Institute for Occupational Safety and Health, 1973.
b Kahn (1966).
-------
underestimate the risk in the lower age brackets, where the
steelworker lung cancer mortality is greater than that of a two-
pack-per-day smoker.
The conversion (Table 12) of Redmond's relative risks to
relative risks taking the nonsmoking general population as a
control is calculated by use of the following algorithm:
Derived death rate coke death rate 2 pack/
relative risk _ oven workers day smokers
nonsmoker ~ death rate x death rate
steelworkers nonsmokers
. (the death rate * (death rate
w 2 pack/day smokers) steelworkers)
Since the mortality rate of steelworkers shown in Table 11 is
approximately that of the two-pack-per-day smokers, a conversion
factor for a comparison of steelworkers and nonsmokers is derived
from data compiled by Hammond (1966), calculating age-specific
mortality rates of smokers with respect to nonsmokers. This
relationship, of course, is not rigorously true, but the error is
certainly not inordinately great and the formula may yield an
underestimate, since the steelworker mortality is greater that
that of smokers, at least in the 45-54 age bracket. The mortal-
ity ratio for smokers over 40 years of age is used. This is
equivalent to a relative risk for lung cancer of 16.6 for smokers
relative to nonsmokers. Multiplying the data presented by
Redmond et al, 1976, by this factor gives the data in Table 12.
It is clear that since mortality due to lung cancer is
considerably higher in the steelworker population than in the
nonsmoking general population, use of the steelworker population
as a standard for evaluating coke plant workers, as is done in
this study, yields an underestimate of the potential effects of
coke oven emissions on the general population. Although some of
the elevated risk can be attributed to cigarette smoking, this
does not affect the argument because, whatever its cause, the
mortality rate still exceeds that of the nonsmoking general
58
-------
Table 12. RELATIVE RISKS FOR LUNG CANCER AMONG COKE PLANT
WORKERS BASED ON COMPARISON WITH STEELWORKERS AND WITH
NONSMOKING GENERAL POPULATION3
Coke plant workers
Coke oven workers
Nonoven workers
Relative risks
Steelworker
comparison
1.93
3.19
0.95
Derived nonsmoker
nonsteelworker
comparison
32.0
53.0
15.8
Data from Redmond (1976); Redmond, Strobino, Cypess (1976);
Hammond (1966).
Relative risks shown in the right-hand column were derived from
relative risks given in Redmond, Strobino, and Cypess (1976),
and from established data for two-pack-per-day smokers in
comparison with the lung cancer death rate for the nonsmoking
general population using the following algorithm:
Derived relative risk nonsmoker =
death rate coke plant workers death rate 2 pack/day smoker
death rate steelworkers death rate nonsmokers
and where death rate steelworkers = death rate 2 pack/day smoker
(NIOSH, 1973).
Thus, the values in the right-hand column were obtained by
multiplying the values in the middle column by 16.6.
59
-------
population. When the elevated mortality rate of steelworkers is
taken into account, the relative risks for nonoven workers and
all coke plant workers for death from lung cancer grow to 15.8
and 3'2.0, respectively. Of course, some of the excess cancer
observed among the coke oven workers is also attributable to
smoking, and thus the mortality risks shown in the table cannot
be attributed solely to exposure to coke oven emissions. However,
cigarette smoking cannot solely account for observed elevated
cancer incidence, expecially since no documented evidence is
available that indicates that coke oven workers smoke to any
greater extent than the steelworkers in the control population.
Thus the true value of the relative risk for lung cancer must lie
between the values presented here, which are as high as a 53-fold
relative risk, and those in Redmond et al (1976), which are at
least a 16-fold relative risk.
ESTIMATING EXPOSURE
Once revised mortality estimates are calculated it is, of
course, essential to estimate corresponding exposures to etio-
logical agents, in this case coke oven emissions. One approach
was applied to the gas production workers studied by Doll (1952,
1965, 1972) and was carried out by Pike et al (1975).
"The carbonization workers were exposed to an estimated 2000
ng/m^ BaP for about 22 percent of the year (assuming a 40
hour working week, 2 weeks paid leave, 1 week sick leave);
very roughly, the men were exposed to the equivalent of 440
(2000 x 0.22) ng/m^ BaP general air pollution. This expo-
sure caused an extra 160/10^ lung cancer cases, so that we
may estimate, assuming a proportional effect, that each
ng/m3 BaP causes 0.4/105 (160/10^ T 440) extra lung cancer
cases per year. A city with 50 ng/m^ BaP air pollution
might therefore have an extra 18/10^ lung cancer cases per
year. These numbers are not negligible, although they are
small when compared, say, to smoking a pack of cigarettes
every day.
This estimate of a small, but not negligible, general air
pollution effect on lung cancer agrees with most other
epidemiologic evidence on the subject."
60
-------
Another approach can be derived from studies of steelworkers
by Lloyd, Redmond, and their colleagues, who observed a dose-
response relationship among the cohort of coke oven workers.
(Table 7 summarizes some of the findings.) In an evaluation of
the cumulative exposure to CTPV's in the cohorts of these studies,
Mazumdar et al (1975) derived exposure histories from occupational
records and air quality measurements conducted by the Pennsylvania
Department of Health and thus quantified the dose. The results
obtained for nonwhite coke oven workers are taken from Mazumdar .
and are presented in Figure 3.
The cumulative exposures were calculated from an algorithm
combining length of time spent in various jobs with average
levels of CTPV's. The death rate was calculated by the direct
method of age adjustment using the nonwhite coke oven workers as
a control population. The second value on the x-axis represents
an estimate of the equivalent of BaP exposure of the cohort
calculated for the purposes of this study and is not part of the
original publication. The BaP values are taken as 1 percent of
the CTPV's, which gives an estimate well within an order of
magnitude of error.
It is interesting to contrast the results in Figure 3a with
those in Figure 3b, the plot of cumulative exposure versus death
rate for the white coke oven workers, in which a dose response
relationship was not originally apparent. According to Mazumdar
et al the failure to observe such a relationship "may be due to
the small numbers of white workers in the high exposure categor-
ies." In neither: case, however, can one carry out a simple
extrapolation from the death rate in the figure to the death rate
of the general population because of the constraints of the age-
adjustment method used, in which the nonwhite coke oven worker
population served as the control.
It is possible to carry out a very approximate extrapolation
of the death rate observed in the coke oven worker population to
the death rate expected for the general population. The statis-
tics for nonwhite workers are used here because it is among the
61
-------
200
Oi
to
UJ
I 100
*» 10
o
o
oc
TOTAL MORTALITY
CANCER
(ALL SITES
LUNG CANCER
200 400 600 800 1000 CTPV
2.0 4.0 6.0 8.0 10.0 BaP
CUMULATIVE EXPOSURE, mg/m3-months
O£.
UJ
200
100'
OC
Ul
O.
U-
O
UJ
CQ
10
TOTAL MORTALITY
CANCER (ALL SITES)
LUNG CANCER
200 400 600 800 1000 CTPV
2.0 4.0 6.0 8.0 10.0 BaP
CUMULATIVE EXPOSURE, mg/m3-months
a. Nonwhite workers, ane-adjusted,
b. White workers, age-adjusted,
1951-1966.
Figure 3. Dose-response data for cumulative exposure to CTPV's, nonwhite and white
coke oven workers. [CTPV values from Mazumdar et al, 1975.
BaP values = 1% CTPV per Schulte et al, 1975.]
-------
nonwhites that the dose-response relationship was observed. The
age stratum 45 to 54 years at time of entry into the study is
selected because men in the age range of 45 to 70 would be the
most likely to be developing cancer and other diseases over the
course of this study. An expected death rate is derived from the
U.S. Vital Statistics, using 1960 data on age-specific, cause-
specific rates for deaths of nonwhite males from all causes, all
malignant neoplasms (140-205), and all respiratory cancer (160-
164). The rates for ages 45 to 54 and 55 to 64 are each applied
to the number of workers at risk in each exposure category, as •<
calculated by Mazumdar et al (1975). The resulting expected
numbers of deaths are averaged as follows:
(rate factor x (rate factor x
No. of number at risk number at risk
expected = 45-54 years) + 55-64 years)
deaths 2
The rate factor is the annual rate multiplied by 14.5, which is
an approximation of the number of years of observation, which
ranged from 13 to 16 years, depending on when the worker entered
the study. The factor is divided by 1000 to allow comparison
with the Mazumdar rate, which is given as deaths per thousand.
No corrections are made for adjusting the number at risk to take
into account those who had already died, which results in only a
very small underestimate of the true number. The results of this
calculation, given in Table 13, represent the range of observed
and expected deaths for each of the exposure categories. Figure
4 also compares observed and expected deaths.
It should again be noted that as in other calculations,
overall mortality of the coke oven workers is more favorable than
that of the general population, and respiratory cancers again
account for a relatively large proportion of the total cancer
mortality. Although the ratio of observed/expected overall
mortality in this calculation is highly approximate, it can serve
as the basis of a crude measure of the estimated increase in
63
-------
Table 13. ESTIMATED CUMULATIVE EXPOSURE TO BaP AND
CTPV AND CORRESPONDING OBSERVED MORTALITY3
/mg/m -months CTPV x 10~2)
Cumulative exposure
\ ng/m •
month BaP
\
Nonwhite coke oven
workers
Number at risk,
age 45-64
Overall mortality
Number of deaths
observed
Death rate/1000
Estimated expected
deaths0
Observed/estimated
expected
Cancer, all sites
Number of deaths
observed
Death rate/1000
Estimated expected
deaths0
Observed/estimated
expected
Lung cancer
Number of deaths
observed
Death rate/1000
Estimated expected
deaths0
Observed/estimated
expected
<1.99
54
14
259.2
18.4
0. 761
3
55.6
3.07
0.977
1
18.5
0.497
2.01
2.00-4.99
151
48
317.9
51.5
0.932
11
72.9
8.57
1.28
3
19.9
1.39
2.16
5.00-6.99
108
30
277.8
36.9
0.813
10
92.6
6.13
1.63
5
46.3
0.993
5.03
7.00+
155
45
290.3
52.9
0.851
19
122.6
8.80
2.16
8
51.6
1.43
5.59
Total
nonwhite oven
workers
468
137
292.7
159.6
0.858
43
91.9
26.6
1.62
17
36. 3
4.30
3.95
a Age-adjusted, age-specific death rates for overall mortality, cancer of all
sites, and lung cancer, based on mortality observed from 1951-1966 for nonwhite
coke plant workers, by estimated cumulative exposure to BaP and CTPV, and age
of entry into study. Expected rates are derived from average of U.S. age-
specific mortality by cause for nonwhite males aged 45-54 and 55-64 with
approximated average of exposure time of 14.5 years. Adapted from Mazumdar
(1975).
Derived from mg/m of coal tar pitch volatiles.
c Estimated from average cause and age-specific U.S. mortality rate, I960, for
age brackets 45-54, 55-64 over estimated average exposure of 14.5 years.
64
-------
Ul
ID
16
14
£ 12
LU
O
fe 10
QC
UJ
i *
z
6
4
2
- 1 1 Expected deaths calculated from average of U.S.
' — 'vital Statistics for ages 45-54 and 55-64.
- f"j Calculated for 14.5 years, the midpoint value.
-
-
-
-
-
F^l
l:: :Jl 1
n
n
m;
n
^
:-::;:
-•
-
-
-
-
-
-
-
199
200-499
500-600
700+
TOTAL
NONOVEN
o WORKERS
CUMULATIVE EXPOSURE TO COAL TAR PITCH VOLATILES, mg/m -months
Figure 4. Observed versus expected deaths from lung cancer among coke plant
workers as a function of cumulative exposures, 1951-1966.
-------
mortality rate of the general population if they were exposed to
lifetime dosages similar to those of coke oven workers.
Each of the columns in Table 13 represents a cumulative
exposure in mg/m -months for members of the work force, as
calculated by Mazumdar. For estimation purposes we can calculate
equivalent exposures for the general population. By setting
arbitrary durations of exposure, say 60 months, the ambient
levels needed to achieve a particular cumulative exposure are
obtained simply by dividing the exposure by the duration. In
this way one can determine the ambient concentration that, over a
period of time (e.g., 5 years, 60 months), would give a total
exposure equivalent to that experienced by the various segments
of the cohort in the Mazumdar study.
Lifetime cumulative exposure , , . , . . . , ,
— 7-r ••—-3—5 r~-— = Ambient concentration level
Hypothesized duration
For example:
mg/m 'months „,„/ 3
months = m9/m
(The CTPV values are converted to BaP concentrations by multiply-
ing by 1 percent, as previously.)
Performing this calculation for the time periods of 5 years
(60 months) to 50 years (600 months) yields the levels given in
Table 14. These levels range from a low of 3.32 yg/m BaP to a
high of 116.7 yg/m . Each column represents the concentration
necessary for the given time period in the left hand column to
yield lifetime dose equivalent to that experienced by coke oven
workers. These equivalent exposure values can be compared with
the exposures of the general population to BaP and coke oven
emissions when assessing the risk to the general population.
Although it is difficult to extrapolate an exact expected
rate, the following should be kept in mind. First, the cancer
rates observed in the studies discussed here represent the mini-
num increase in rate because the period of observation has been
only 14 to 16 years and Mazumdar's "...data indicate that the
66
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Table 14. ESTIMATION OF EQUIVALENT LIFETIME DOSE FOR
THE GENERAL POPULATION3
Lifetime
exposure,
(ug BaP-months)
m3 x 10
ug BaP/m x 10 -months
fl.99
2.00-4.99
(calc. as 3)
5.00-6.99
(calc. as 6)
7.10
Duration,
months
Calculated concentration leading to lifetime dose,
ug/m3
60
120
180
240
300
360
420
480
540
600
33.2
16.6
11.1
8.29
6.63
5.53
4.74
4.15
3.69
3.32
58.3
29.2
19.4
14.6
11.7
9.72
8.33
7.29
6.48
5.83
100
50
33.3
25.0
20.0
16.7
14.3
12.5
11.1
10
116.7
58.3
38.9
29.2
23.3
19.4
16.6
14.6
13.0
11.7
Values calculated represent the ambient air levels required
to achieve the lifetime dose listed for the hypothetical
time periods shown in the first column.
67
-------
time between first exposure to coal tar pitch volatiles and death
from lung cancer varies from 10 to 40 years, with an average of
25 years." Second, the exposure values are inaccurate because of
the sampling and analysis problems discussed earlier. If the
combination of insufficient observation time and sampling error
together act toward underestimation, the actual increased risk of
the exposed population may be much greater than the calculations
show.
Comparison of the ambient data calculated by the Stanford
Research Institute (SRI) with the calculated ambient data in
Table 14 shows that a value of 2 ng/m BaP, a median concentra-
tion given by SRI, which is within about 3 orders of magnitude of
the lowest level in Table 14, results in at least a doubling of
the lung cancer rate. For reasons stated earlier, this rate is
assuredly an underestimate.
NONMALIGNANT RESPIRATORY DISEASE
Several mortality studies have shown that workers at coke
plants are at an increased risk of dying from chronic bronchitis.
Unlike the risks from respiratory malignancy, the risk appears to
be about the same for coke oven workers and for nonoven workers
employed at the coke plant. The data, summarized in Table 15C,
show that the risk of coke plant workers is significant and is
greater than 2-fold relative to the rate of mortality from
chronic bronchitis in the steelworker population.
Doll (1965, 1972) has observed a similar excess mortality
from chronic bronchitis among gas retort workers. In these
studies the risk again extended to men with heavy and light
exposures to the effluent from the retorts. These data, tabu-
lated in Table 15B, indicate the same magnitude of risk as that
observed in the studies of Lloyd, Redmond, and their colleagues.
Mortality rates for nonmalignant respiratory disease con-
stitute an incomplete assessment of any potential correlation
between occupational exposure to coke oven emissions and chronic
bronchitis and emphysema. This is so because, unlike lung cancer,
68
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Table 15. OBSERVED BRONCHITIS MORTALITY
A. Standardized annual death rate per 1000 men for bronchitis; all gas
boards grouped together and England and Wales, 1953-61.a
Occupational class
A
2.89
B
1.34
Cl
1.94
C2
1.19
C
1.28
All classes
1.62
England and
Wales
1.36
Class A = heavy exposure in carbonizing plants; Class B =
intermittent exposure to conditions in other gas-croducing
plants; Class Cj = exposure only to by-products, i.e., process
and maintenance workers in chemical and by-products plant.
Class C2 = minimal or no exposure, i.e., all other employees;
Class C = C, + C,.
B. Numbers of deaths from bronchitis in each occupational class and
numbers expected from the experience of all gasworkers, allowing for
age and employing board.3
Occupational class
A
Observed
49
Expected
28.54
B
Observed
40
Expected
47.33
C
Observed
52
Expected
65.13
Probability
of trend
arising due
to chance
<0.001
C. Observed deaths and relative risks of death from nonmalignant
respiratory diseases, 1953-1970, for coke plant workers by work
area and length of employment through 1953.b
Work area
Total coke plant
Coke oven
Nonoven
No one coke
plant area
Years employed throu?
5+
Obs.
34
20
14
0
RR
1.47C
1.47
1.45
e
10+
Obs.
31
17
14
0
RR
1.82d
1.92C
1.75
e
h 1953
15+
Obs.
25
12
13
0
RR
2.01d
2.20C
2.07C
e
Adapted from Doll (1965).
From Redmond (1976).
p <.05.
Less than 5 deaths.
69
-------
from which mortality is extremely high, other chronic lung
disease is not necessarily fatal. A better measure of the
effects of coke oven emissions in producing nonmalignant respir-
atory disease is a combination of increased incidence of both
morbidity and mortality. An increase in incidence of both
morbidity and mortality has been observed in several investiga-
tions of the chronic bronchitis rate of coke plant workers.
Adequate morbidity data for nonmalignant respiratory disease
are difficult to obtain. Whereas lung cancer has been readily
diagnosed for at least the last 30 years, some cases of chronic
bronchitis very probably remain undiagnosed (Ferris, 1973).
Also, chronic bronchitis is not a reportable disease. For this
reason, observations of bronchitis and other nonmalignant respir-
atory disease therefore usually entail monitoring and medical
surveys of working populations, from which retirees are most
oEten excluded.
In light of the combination of the relatively low rate of
fatality from nonmalignant respiratory disease, the competitive
risk from other diseases associated with coke oven exposure, and
the difficulties of estimating incidence, the true incidence of
such nonmalignant respiratory disease must be greater than the
sum of the morbidity and mortality data presented here. Coke
plant workers are both healthier than the general population and
younger than the population at greatest risk for chronic bron-
chitis, among whom are the elderly. The very young are also
highly susceptible to bronchitis. The increased mortality among
coke plant workers from this disease therefore indicates that
coke oven emissions pose a powerful hazard to the respiratory
systems of exposed workers.
MORBIDITY STATISTICS
A consideration in assessment of risk for bronchitis among
coke plant workers is that these workers have been "selected" for
tolerance to sulfur dioxide mixed with particulates, both con-
stituents of coke oven emissions. It has been estimated that 10
70
-------
to 20 percent of healthy young adults show susceptibility to
industrial levels of S02 (Burton et al, 1969) and are unable to
work at jobs involving exposure. This means that the workers who
are included in epidemiological studies are those who can toler-
ate industrial levels of S0~ and can be considered to be less
sensitive to, or able to adapt to, these levels, as noted by
Amdur (1969). If this relatively "S02 resistant" portion of the
work force is showing an increased rate of bronchitis, it is
prudent to assume that lower levels will produce similar effects
on the general population, which includes those who are at ele-
vated risk for bronchitis by virtue of age, preexisting condi-
tions, or other factors.
Mittman et al (1974) in a survey of the incidence of chronic
bronchitis among 246 coke plant workers, found that 33 percent of
the workers complained of symptoms and 17 percent were classified
as having varying degrees of chronic bronchitis, defined by
standard criteria for sputum production and dyspnea. The authors
conclude that consumption of cigarettes by the entire group was
related to the severity of symptoms, and they emphasize the need
for more data on the influence of smoking and on genetic suscep-
tibility as factors in occupational disease. Despite the authors'
emphasis on genetics and smoking, careful examination of their
data reveals that exposure to coke oven emissions (that is, the
index of job exposure) is the most significant correlate for the
occurrence of pulmonary disease.
The analysis of Mittman et al is summarized in Table 16.
Three groups of workers were tested for symptoms of chronic
bronchitis and smoking, work exposure history, and genetic sus-
ceptibility (as determined by serum trypsin inhibitory character-
istics [STIC] and Pi phenotypes). Simple correlation coeffi-
cients were calculated. The worker groups were (1) all 246 coke
oven workers in the study; (2) 81 men with symptoms and 20 men
chosen at random; and (3) 42 men with diagnosed chronic bronchitis,
Even though the authors' conclusion that the incidence of chronic
71
-------
Table 16. CORRELATIONS FOR CHRONIC BRONCHITIS AMONG COKE OVEN WORKERS
-j
to
Smoking history
Total cigarettes
(Pack years)
Family history
(o=none, l=yes)
Work experience
Duration (yr on
oven)
Type of job
(index)
Duration X
index of oven
jobs
Duration X
index of all
jobs
Antitrypsin
studies
STICC (units)
Pi phenotypes
Group I
overall group
(246 coke oven workers)
r
0.28
0.28
0.09
-0.05
0.1
0.02
r2b
7.8
7.8
0.08
-0.3
0.1
0.04
P
0.01
0.01
NS
NS
NS
NS
Group II
81 men with symptoms
20 men chosen at random
r
0.2
0.3
0.19
-0.02
0.19
0.21
0.05
0.04
r2b
4.0
9.0
3.6
-4
3.6
4.4
2.5
0.4
P
BS
0.01
0.05
NS
BS
0.05
NS
NS
Group III
42 men with diagnosed
chronic bronchitis
r
0.07
0.18
0.52
0.02
0.52
0.49
0.20
-0.15
r2b
0.5
3.2
27
4
27
24
4.0
2.3
P
NS
NS
0.01
NS
0.01
0.01
NS
NS
Taken and adapted from Mittman, C., Pedersen, E., Barbels, T., and Lewis, H. Prediction
and Potential Prevention of Industrial Bronchitis: An Epidemiologic Study of a Group of
Coke Oven Workers. Amer. J. of Med. 57:192-199, (1974).
Percentage of cases explained.
Serum trypsin inhibitory characteristics.
NS-= Not significant. BS = Barely significant (probability of change significance just
exceeds 5%).
-------
bronchitis of the entire group tested is not significantly corre-
lated to job exposure is valid, it is important that the calcu-
lated index of total job exposure was the only statistically
significant measure among the third group tested, those with
chronic bronchitis. Furthermore, the index for total job expo-
sure is the correlate that explains the largest percentage of
variability shown in the study; about 25 percent of the bronchi-
tis was explained by total job exposure. It should also be noted
that in this group cigarette smoking was not a statistically
significant variable, accounting for only about 0.5 percent of
the disease.
Among the second group of workers cigarette smoking and work
experience were of comparable statistical significance and
explained the same small percentage of variability in the data.
The apparent inconsistency of the results may stem from the
inclusion in the overall group of many workers with only a few
years of heavy exposure to substances that cause chronic bron-
chitis. This would dilute the incidence of disease and decrease
the possiblity of observing an effect of working conditions on
pulmonary disease. This effect of duration of exposure is con-
sistent with the results of other studies. The reports of Lloyd
and others (Table 15) indicated that chronic bronchitis mortality
increased by 33 percent after 10 years of additional follow-up
and also reached statistical significance. Unfortunately,
because Mittman et al (1974) do not present data on the distri-
bution of workers according to exposure or to years of work, this
hypothesis cannot be independently confirmed or denied.
Walker et al (1971), in a study of bronchitis among British
coke plant workers, observed that of 112 men who had worked for 1
year or more in the vicinity of the oven, 18.8 percent (26) had
bronchitis, defined by productive phlegm, as compared with 11.3
percent (27 out of 212) of the other coke plant workers. The
authors found a strong correlation between prevalence of bron-
chitis and cigarette smoking, and they suggest that smoking, a
combination of smoking and exposure to coke oven emissions, and
73
-------
previous employment in dusty industry (e.g., coal mining) all
have an important effect on the incidence of bronchitis. "Oven-
men" in this study were defined as workers who had spent 1 year
or more in the environment of the coke ovens. The effect of
long-term exposure to coke oven emissions on the incidence of
bronchitis is difficult to determine because the study gives no
data on the length of exposures of the oven men and nonoven men.
The work of Lloyd, Redmond, Doll, and others indicates that
both oven workers and nonoven workers are at risk for nonmalig-
nant respiratory disease. It may be that those suffering the
greatest risk are cigarette smokers. However, when the data
presented by Walker are examined for the incidence of chronic
bronchitis among nonsmokers, ex-smokers, pipe smokers, and light
smokers (1 to 10 cigarettes per day), analysis shows that this
mixed group having less exposure to cigarette smoke also exper-
iences a significant incidence of chronic bronchitis, about 13.7
percent, as shown in Table 17. The table also shows the observed
relationship between age and bronchitis incidence. The incidence
of bronchitis among relatively young men should be noted.
Walker et al (1971) conclude that some adverse effects
apparently are due to a combination of smoking and history of
earlier exposure to a dusty environment, and that inclusion of
workers with only 1 year of exposure in the study population may
produce an underestimate. Thus, the report can be taken as
further evidence of a risk of bronchitis among workers exposed to
coke oven emissions and as evidence of the complexity of inter-
actions of such various etiologic agents as smoking, job exposure,
and previous history.
Since the elevated risk in all the studies discussed here
appears to be coke-plant-wide, it is not unreasonable to extrap-
olate the health effects for the general population from the
effects observed for those in the study group with the lowest
exposure to the emissions, the nonoven workers at the coke plants.
This means that workers exposed to the constellation of factors
that make up coke oven emissions (e.g., particulate matter,
74
-------
Table 17. CHRONIC BRONCHITIS IN THE COKE INDUSTRY*
A. Incidence and smoking habits
Nonsmokers, ex-smokers (all workers)
Nonsmokers, ex-smokers (all
workers over 25 yr old)
Light smokers (1-10 cigarettes/day)
Pipe smokers
Total
No. of men
242
224
150
52
444
Bronchitis
No.
16
16
40
5
61
%
6.6
7.1
26.7
9.6
13.7
B. Incidence and age
Age, yr
No bronchitis
Bronchitis
Total
15-24
No.
51
2
53
%
96.2
3.8
100.0
25-34
No,
119
17
214
%
87.5
12.5
100.9
.35-44
No.
184
30
214
%
86.0
14.0
100.0
45-54
No.
206
57
263
%
78.3
21.7
100.0
55-64
No.
152
63
214
%
70.7
29.3
100.0
All ages
No.
712
169
881
%
80.8
19.2
100.0
* Adapted from: Walker et al (1971).
75
-------
sulfur dioxide, PAH) at levels well below those that are normally
associated with "exposure" suffer a significantly increased risk
of developing nonmalignant respiratory disease, an irreversible,
debilitating condition. Levels of BaP measured at the periphery
of coke plants have been as low as 150 ng/m (Jackson et al,
1974), a value that is within one to two orders of magnitude of
general population exposure levels presented by SRI.
76
-------
APPENDIX A
SELECTED BIOASSAY RESULTS
77
-------
00
Table Al. IN VIVO BIOASSAYS FOR CARCINOGENICITY OF PAH'S AND OTHER POLLUTANTS
Animal
Agent
Complete carcinogenicity
I
Cutaneous application
Nice
BaP
Urban pollutants
2 U.S. cities
Subcutaneous injection
Mice
BaP, MCA, DBA
Urban pollutants
7 U.S. cities
Dose
0.001-0.5%
Total org. sample 12.5%
Neutral portion
N-l 5.25-12.0%
N-2(PAH) 0.48-0.9%
N-3 20.8-22.5%
Acidic portion
1.6-3.7%
0.001-1 mg
Total org. sample
4 mg/month
Neutral portion
N-l 0.5 mg/month
N-2(PAH) as in 4 mg
sample once a month
N-3 0.1 mg/month
Tumor bearing
animals
Reference
Dose response study
30 - 87
0
70 - 95
0
Dose response study
0-15
0-2
0-10
0-18
Wynder et al, 1957
Hoffmann and
Wynder, 1977
Bryan and Shimkin,
1943
Hueper et al, 1938
N-l, N-2, N-3 refer to different fractions.
(continued)
-------
Table Al (continued)
Animal I Agent
Subcutaneous injection (contin
Mice
Infant
mice
Urban pollutant*
Texas city near
petroleum plant
MCA, DBA, DMBA
Pollutants
New York City
Dose
ued)
Total org. sample
1965 - 68 1.0-10 mg
1969 2.5-10 mg
4.5 - 10 pg/g
Total org . sample
10-40 mg M
F
Neutral fraction
10-40 mg M
F
N-l
10-40 mg M
F
N-2 (PAH)
10-40 mg M
F
N-3
10-40 mg M
F
Basic fraction
10-40 mg M
F
Acidic fraction
10-40 mg M
F
Insoluble portion
10-40 mg M
F
Solvent alone
M
F
% Tumor bearing
animals
0-7
12 - 61
Induction of lymphomas.
lung adenomas,
hepatomas
28.2
12.5
19.1
20.8
11.9
31.8
22.4
40.7
22.0 - 32.7
24.4 - 35.4
46.4
43.5
6.5
0
15.5
17.2
16.1
8.6
Reference
Rigdon and Neal, 1971
Delia Porta and
Terracini, 1969
Asahina et al , 1972
(continued)
-------
Table Al (continued)
Animal
Agent
Dose
Tumor bearing
animals
Reference
Intratracheal instillation
Syrian
oo
o
BaP (on Fe2O3>
BaP (on
210
(on
BaP +.
210p0 +
(on F62O3)
BaP +
210Po +
(on Fe2<>3)
Inhalation studies
Rats
Dose response study M
F
IS x 0.3 mg
60 rads
12 rads
15 x 0.3 mg
60 rads
15 x 0.3 mg
12 rads
10 ppm SO2 (6 hr/day) +
10 mg/m3 BaP + 3.5 ppm
S02 (1 hr/day)
10 mg/ra^ BaP + 3.5 ppm
(1 hr/day)
10 ppm SO2 (6 hr/day)
0-60 trachea
0-80 bronchi tumors
7.6 lung tumors
12.2 lung tumors
10.8 lung tumors
34.2 lung tumors
10.8 lung tumors
5 rats out of 21,
bronchogenic
carcinoma
2 rats out of 21,
bronchogenic
carcinomas
no tumors
Saffiotti et al,
1972
McGandy et al,
1974
Laskin et al,
1970
(continued)
-------
Table Al (continued)
Animal
Incomplete c
Agent
ircinogenicity
1
Tumor initiation
Mice (skin)
(Promoter
2.5%
Croton
oil)
BaP
PAH fractions
from urban
pollutants
from 80,000
m3 air (2
U.S. cities)
Tumor promotion
Mice (skin)
(Initiator
300 vq
DMBA)
Urban pollu-
tants
2 U.S. cities
Dose
50; 100; 200 ug
11 samples
containing
34 - 130 gg
BaP
Neutral portion
N-l 5.25-12.0%
N-3 2.8-5.2%
Acidic portion
1.6-3.7%
DMBA (control)
% Tumor bearing
animals
0.6; 1.2; 2.3
Tumors per mouse
0.2 - 3.6
Tumors per mouse
30 - 50
30 - 80
10 - 60
7
Reference
Hoffmann and
Wynder, 1977
00
-------
Table A2. IN VITRO BIOASSAYS OF EXTRACTS OF AIRBORNE PARTICULATE
Bacterial strain
Salmonella typhimunum
TA 100
TA 100
TA 100
TA 100
TA 98
TA 98
TA 98
TA 98
Liver enzyme
none
S-9 (Aroclor 1254)
none
S-9 (Aroclor 1254)
none
S-9 (Aroclor 1254)
none
S-9 (Aroclor 1254)
Test material3
Air particulate extract
Buffalo
Air particulate extract
Buffalo
Berkeley airduct
particulate extract
Berkeley airduct
particulate extract
Buffalo air particulate
extract
Buffalo air particulate
extract
Berkeley airduct
particulate extract
Berkeley airduct
particulate extract
Relative.
activity
1
9
8
4
1
5
9
5
Reference
Talcott and
Wei, 1977
-
CO
ro
Air particulate extracts (400 pg) prepared from filters with acetone and rendered for assay
as 10 mg residue/ml dimethyl sulfoxide.
Relative activity based on net revertants/plate with 400 ug extract. Buffalo sample without
activation rated 1 in each strain.
(continued)
-------
Table A2 (continued)
Bacterial strain
TA 1537
TA 1537
TA 1537
TA 1537
Liver enzyme
none
S-9 (Aroclor 1254)
none
S-9 (Aroclor 1254)
Test material3
Buffalo air particulate
extract
Buffalo air particulate
extract
Berkeley airduct
particulate extracts
Berkeley airduct
particulate extracts
Relative
activity13
1
5
6
5
Reference
00
to
a Air particulate extracts (400 pg) prepared from filters with acetone and rendered for assay
as 10 mg residue/ml dimethyl sulfoxide.
Relative activity based on net revertants/plate with 400 gg extract. Buffalo sample without
activation rated 1 in each strain.
-------
APPENDIX B
SOURCE AND CONCENTRATION DATA
84
-------
Table Bl. PAH CONCENTRATIONS IN COKE OVEN EMISSIONS
oo
Ul
Compound
Octahydrophenanthrene
Octahydroanthracene
Dihydrof luorene
Dihydrof luorene
Benzidene
Fluorene
Dihydrophenanthrene
Dihydroanthracene
2-Me thy If luorene
1 -Me thy If luorene
9-Me thy If luorene
Me thy If luorene
Benzoquinoline
Acridine
Phenanthrene
Anthracene
Fluorene carbonitnle
Methylphenanthrene
Nethylanthracene
Ethylphenanthrene
Ethylanthracene
Octahydrof luoranthene and
octahydro-pyrene
Dihydrof luoranthene
Dihydropyrene
Fluoranthene
Dihydrobenzo(a) f luorene
Dihvdrobenzo(b) f luorene and
dihydrobenzo(c) f luorene
Pyrene
Benzo(a) f luorene
Benzo(b) f luorene
Benzo(c) f luorene
Sample No. la
Peak
No.
1
la
2
2a
3
4,4a
4b,5
6
7
a
9
10
11
12,12
13
14
15
16
17
IB
19
20
21
22
23
24
25
26
27
28
29
Concentration,
ug/g of sample
31.85
29.89
30.31
18.76
106.73
271.52
586.98
168.88
98.71
73.46
44.32
87.84
77.74
> 85.98
2,828.54
942.85
180.29
1,023.41
1,692.26
1,578.60
1,096.71
280.42
115.07
575.06
••>. 979. 74
75*1.41
213.53
4,627.33
971.18
109.45
627.02
Sample No. 2
Peak
No.
1
2
2a
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
2J
24
25
26
27
28
Concentration,
ug/g of sample
8.77
13.62
6.72
20.86
79.55
21.92
9.06
24.35
11.81
10.77
8.34
32.44
163.53
46.44
16.76
44 .67
85.30
58.04
49.19
11.06
73.57
36.65
269.74
^4.03
28.77
206.35
87.42 \
16.70 j
38.96
Sample No. 3°
Peak
No.
1
la
2
3
4
5
5a
6
7
8
9
11
lla
lib
12
13
14
15
16
17
18
19
20
21
22
23
Concentration,
ug/g of sample
29.98
15.68
58.15
19.29
316.49
101.68
8.87 ")
44.01 J
6.71
31.41
74.98
458.80
305.89
32.55
130.22
258.93
202.97
249.86
64.36
64.87
52.29
451.95
99.07
472.09
62.97
290.03
Sample No. 4
Peak
No.
2
2a
2b
2c
2d
3
4
5
6
6a
7
8
9
9a
9b
10
11
12
13
13a
13b
14
15
16
17
17a
17b
17c
Concentration,
ug/g of sample
70.31
18.26
23.20
20.81
15.37
325.83
232.54
40.28
102.83
10.38
79.77
172.79
636.98
500.36
11.47
283.92
573.25
197.39
1,473.68
44.53
31.86
404.25
1,097.82
46.38
1,446.64
37.21
22.6}
98.47
(continued)
-------
Table Bl (continued)
Compound
Me thy If luoranthene
Methyl f luoranthene
Hethylpyrene
Hethylpyrene
Benzo (c) phenanthrene
Benzo(qhi) f luoranthene
Dihydrobenz (a) anthracene.
dihydrochrysene and
dinydrotnphenylene
Benz (a) anthracene
Chrysene and triphenylene
Dihydromethylbenz (a)anthracene
dihydromethylchrysene and
dihydrome thy 1 triphenylene
Hethylbenz (a) anthracene
Nethyltriphenylene
He thy 1 Chrysene
Dihydromethylbenzo(k and b)
f luoranthenes and
dihydrome thy Ibenzo
(• and elpyrenes
Dime thy Ibenz (a) anthracene
dimethyltriphenylene and
dinethylchrysene
Benzol}) f luoranthene
Benzo (k) f luoranthene and
benzo(b) f luoranthene
Hethylbenzo(k) f luoranthene
•nd methylbenzo(b)
f luoranthene
Benzo (e) pyre ne
Benzo(a) pyrene
Perylene
He thy Ibenzo (a I pyrene
Dtwethy Ibenzo(k) f luoranthene
and dimethy Ibenzo (b)
f luoranthene
Dlaethylbenio (a) pyrene
Sample No. 1*
Peak
No.
30
31
32
31
34
35
36
37
3B
39
40
41
42
43
Concentration,
ug/9 of sample
1,817.37
390.94
1,016.76
856.91
220.45
677. J5
383.03
2,740.45
4,202.02
841.67
159.33
463.99
1,151.61
434.38
44,44a 246.35
45
46
47
48
48a
49
50
51
52
176.92
3.930.34
735.95
103.86
2,630.92
702.12
330.85
116.74
82.68
Sample No. 2
Peak
No.
29
30
31
32
33
34
34a
35
36
37
38
39
40
40a
41
42
43
44
45
46
47
Concentration,
ug/g of sample
124.73
21.87
31.12
106.34
82.70
164.25
54.75
105.15"?
119. 04J
93.30
22.36
40.81
107.59
8.63
46.73
18.66
155.03
33.05
122.15
22.07
5.88
Sample No. 3C
Peak
No.
24
25
26
27
28
29
29a
30
30a
31
32
33
34.
35
36
37
38
39
40
41
42
43
44
45
46
Concentration,
ug/g of sample
126.03
179.04
97.80
233.37
1,510. 34
201.74
101.78
5.509.43
247.80
1,015.70
371.97
193.68
185.08
174.71
62.25
30.16
80.04
2,170.92
430.05
2,007.75
616.85
344. 12
73.13
70.18
Sample No. 4
Peak
No.
18
18a
19
20
21
21a
22
23
2 3d
24
25
26
26a
27
28
29
30
31
32
33
34
Concentrat ion,
ug/g of sample
101.56
34.83
120.66
175.42
2.156.14
151.88
271.38
2.673.65
86.35
1,669.72
369.10
448.19
137.26
160. 89
451.70
285. 34
2,556.98
492.13
2.29T1 .33
698.44
247.96
CD
(continued)
-------
Table Bl (continued)
Compound
Dlbensanthracene
o-Pheny lenepyrene
Bcnzo(thi)perylene and
•nthanthrene
Hethyldibenzanthracene
He thy Ibenzo ( thi ) pery lene
Coronene
Dlbenzopyrene
Sample No. 1*
Peak
No.
S3
54
55
56
57
58
59
Concentration.
ug/g of sample
123.66
101.54
72.35
89.04
36.79
864.55
693.21
Sample No. 2b
Peak
No.
Concent rat ion,
ug/g of sample
Sample No. 3C
Peak
No.
47
51
52
Concentration,
ug/g of sample
84.52
833.30
587.05
Sample No. 4
Peak
No.
35
36
Concentration,
ug/g of sample
766.58
493.27
CO
-J
* Glass fiber filter No. 1: total weight of material collected. 12.59 nig; total volume of solvent extract.
1 ml; injected sample size, 10 pi.
Glass fiber filter No. 2: total weight of material collected, 39.67 mg; total volume of solvent extract,
1.0 ml; injected sample size 10 ul.
C Sliver membrane filter No. 1: total weight of material collected, 5.75 mg; total volume of solvent extract,
0.6 ml; injected sample size, 6 ul-
Silver membrane filter No. 2: total weight of material collected, 1.96 mg; total volume of solvent extract.
1.0 ml; injected sample size, 10 ul.
Source: Lao et al (1975).
-------
Table B2. MINOR CONSTITUENTS OF COKE OVEN GAS
Substance
Concentration,
mg/m3
Country
HCN
NO
Dust
Benzo(a)pyrene
Benzene
Toluene
Xylene
2,000-4,000
1,300-3,000
120
0.8-4.9
22
16-24
3.5-4.5
1,800-36,000
334 ave
158-515
190-630
35,800
23,900
21,400
3,000
1,520
500
Czechoslovakia
USSR
West Germany
USSR
USSR
USSR
USSR
West Germany
USSR
USSR
USSR
USSR
USSR
West Germany
USSR
West Germany
USSR
Source: White et al.
88
-------
Table B3. ESTIMATED ATMOSPHERIC EMISSIONS FROM
COKE PLANTS IN POLAND AND CZECHOSLOVAKIA
Type of
emission
Dust
Tar
so2
CO
NH3
H2S
HCN
NO
Phenols
Benzene
Coke production
Emissions in
Poland (1966) ,
tons
16,039
8,565
40,385
5,457
1,702
1,794
166
351
13 million
Emissions in
Czechoslovakia (1968) ,
tons
9,900
13,000
3,030
950
990
99
990
1,660
4 million
Source: White et al.
89
-------
Table B4. COMPARISON OF SELECTED POLLUTANTS AT
TOP-SIDE WORKPLACES IN THE SOVIET UNION
(concentrations, mg/m^)
Pollutant
NH3
CO
Cyanides
Pyridine Bases
Phenols
Benzo (a)pyrene
Conventional charging
6.3-8
40-74
0.9-3.6
0.17
0.14
0.0718
Smokeless charging
3.5-4.4
6-18
0.3-0.4
0.02
0.07
0.0177
Table B5. CONTENT OF NOXIOUS POLLUTANTS IN THE WORKPLACE
ENVIRONMENT OF CZECHOSLOVAKIAN COKING PLANTS
(concentrations, mg/m^)
Compound
Benzene
CO
HCN
so2
Top-side
0.1-13.0
1.0-36
0.0-0.4
0.1-4.7
Side
0.0-0.2
0.0-0.5
0.0-0.1
0.0-0.2
Source: White et al,
90
-------
Table B6. CONCENTRATION OF PYRIDINE AND ITS HOMOLOGUES
AT WORKSITES IN CZECHOSLOVAKIA
(yg/m3)
Compound
Pyridine
2-Methylpyridine
3-Methylpyridine
4-Methylpyridine
2 , 5-Dimethylpyridine
2 , 6-Dimethylpyridine
Coal coke battery
155-1854
348-8256
73-402
47-289
47-107
48-903
Pitch coke battery
222-827
2100-4157
110-411
112-337
114-455
210-572
Table B7. SELECTED VAPOR CONCENTRATIONS IN THE COKE-OVEN
BATTERY ENVIRONMENT AT FIVE PLANTS IN THE UNITED STATES
(mg/m3)
Compound
Benzene
Toluene
Xylene
Naphthalene
Mean
9.5
0.6
0.3
0.7
Maximum
162.7
1.38
1.03
1.31
OSHA TLV
34.3
800
435
50
Source: White et al.
91
-------
Table B8. COMPARISON OF SELECTED PARTICULATE CONCENTRATIONS
Country
Concentration, ing/itf
Czechoslovakia
USSR
USSR
England
USA
Czechoslovakia
Czechoslovakia
Czechoslovakia
USA
USA
USA
England
England
Czechoslovakia
(continued)
Charging levels
(conventional)
(smokeless)
(conventional)
(smokeless)
(catwalk)
Top-side levels
(total particulate)
(respirable)
(total particulate)
(respirable)
(total particulate)
(respirable)
Battery side levels
(pusher)
(coke car)
1.13-113
173.3
15.4-38.9
143-851
1-57
374.3
39.1-84.2
8.3-17.35(13.3 ave)
1.9-40.8
1.1-78.8 (15.2 ave)
0.28-9.22 (3.34 ave)
2.6-6.9
0.35-84.2 (8.05 ave)
26.7-64
4.1-15.7
0.6-1.7
5.1-8.5
1.7-3.7
0.4-395
1-136
92
-------
Table B8 (continued)
Country
Concentration, ng/rrf
USSR
USA
USA
500 meters from battery
Cigarette smoke
Urban levels
1965
1.2-2.7
95,000
up to 1.254
(0.105 ave)
Source: White et al.
93
-------
Table B9. COMPARISON OF BENZO(a)PYRENE CONCENTRATIONS
MEASURED AT COKE OVEN BATTERIES AND AT OTHER SELECTED SITES
Country
Year
Concentration,
Top-side
Side
Soviet Union
Soviet Union
Japan
Norway
Czechoslovakia
Czechoslovakia
Czechoslovakia
Czechoslovakia
England
USA
USA
USA
USA
USA
USA
USA
Switzerland
USSR
England
England
USA
USA
1962
1968
1968
1959
1966
1967
1968
1974
1965
1974
1960
1974
1974
1968
1961
1961
1961
1966
1965
1965
1959
1966
1.27-27.4
0.05-7.38 (3.84)a
2-7.3
1.1-94.8
3.6-32.2
10.7-12.7
0.1-13.1
3-216
1.2-15.9 (6.5)
8.3-51
0-225.9
0.18-36.3 (5.78)
0.08-0.27 (0.17)
1.5-3.14
95
6.1
14-78
640
13.7-22
(0.02)
2330
(0.022)
(0.0185)
0.6-3.4
0.3-1.98 (1.0)
(9.55)
Contrast
Cigarette smoke
Auto exhaust
Roof tarring
Roof tarring
Aluminum Plant
Urban - London
Maximum found in
fumes emitted from
coke ovens
Birmingham
Birmingham
a Mean.
Source: White et al.
94
-------
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