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OCR for page 415
that BaP is not a good surrogate for PAHs in mixtures from different
sources, although more information is available on its effects than those
of other PAHs. However, a person who lives where the air contains BaP at
10 ng/m3 and who breathes 15 In of air per day would breathe in
roughly the same amount of BaP as he would from smoking five old-style
cigarettes (as discussed by Hoffmann et al. ). It is therefore not
unreasonable to assume that this degree of pollution, whicl' was very
common only 20 yr ago, may cause a s ignificant amount of lung cancer.
Studying the problem directly proves difficult, because one must he
especially careful to ensure that an observed effect is not attributable
to differences in smoking habits between high- and low-pollution areas.
The lung-cancer incidence is affected not only by the number of cigarettes
smoked, but by the tar content of the cigarettes, by how far down the
cigarette is smoked, and by smokers' ages at starting to smoke and at
stopping (if ever); all these aspects of smoking habits have to be
considered. It is impossible to allow for all these factors accurately,
so extrapolating from an extreme situation, in which small smoking-habit
differences can be ignored, is likely to be the best method of estimating
general air-pollution effects. Men employed in some occupations are
exposed intermittent ly to BaP in air at up to 16,000 ng/m ,1 and they
provide an opportunity to study lung-cancer effects in an extreme
situation.
OCCUPATIONAL EXPOSURE
-
Many epidemiologic studies of lung cancer have involved occupa-
tional exposure to PAH-containing mixtures.2633~ They showed that
exposure to high concentrations of PAH-containing mixtures increases the
risk of lung cancer.
Assuming that the exposed and nonexposed workers have the same
smoking habits and that their observed lung-cancer incidence rates are
r and rn, respectively, we can express the lung-cancer burden from
the exposure either as a ratio, R = re/rn, or as a difference,
D = re ~ rn. For general risk-assessment purposes, we can express -
these on the basis of per-unit exposure by divid ing R or D by the
"expo sure dose . "
Both R and D are valid measures of the risk to the occupational group
as a group, but they implicitly make very different assumptions about the
risks to individual members of the group with different smoking habits.
The relative-risk index, R. implicitly assumes that the risk of lung
cancer is increased in proportion to the individual's "underlying" risk--a
nonsmoker's risk is multiplied by R. and a 2-packs/d smoker's risk is also
multiplied by R. The additional risk of the 2-packs/d smoker is thus an
order of magnitude greater than the additional risk of the nonsmoker and
double the risk of a 1-pack/d smoker. This multiplicative (sometimes
referred to as synergistic) phenomenon appears to hold for lung cancer
caused "Jointly" by asbestos exposure and cigarette-smoking.23
C-S
OCR for page 416
The additional-risk index, D, implicitly assumes that the amount of
increased risk of lung cancer is independent of other lung-cancer risk--a
nonsmoker's risk is increased by the same absolute amount as a 2-packs/d
smoker's risk.
None of the occupational studies of exposure to PAH-containing
mixtures and lung cancer was conducted in such a way as to provide data to
help in distinguishing between the possible models (i.e., multiplicative,
additive, or somet'ning intermediate). Studies comparing urban and rural
lung-cancer rates (or rates in "heavily polluted" and "lightly polluted"
areas) in persons with different smoking habits do provide relevant data,
but the studies generally have few deaths and go not clearly identify the
correct model. Data from the study of Stocks3 (Table C-2) and from the
study of Hitosugil6 (Table C-3) illustrate the point. In both studies,
the data from the smokers are in good agreement with an additive model for
the effect of "air pollution," and these data provide no evidence for a
multiplicative model. The data from nonsmokers, however, confuse the
picture. In Stocks's study, the effect of air pollution is smaller in the
nonsmokers; in Hitosugi's study, there is no effect in nonsmokers. The
problem may simply result from basing the rates on such small numbers of
deaths in nonsmokers or from misclassifying the smoking habits of a few
persons who died of lung cancer. Because the additive model provides such
a good fit to the data on smokers, we have assumed this model in our
discussion of lung-cancer risk from occupational exposure to PAH-contain
· @
long mixtures.
To use occupational studies for risk-assessment purposes, we must
assume that, as far as lung cancer is concerned, occupational exposures
can be expressed as cigarette equivalents, i.e., that the form of
Equations 1 through 4 will hold for the excess lung cancer from such
exposure. We saw when discussing lung cancer and cigarette-smoking that
dose and duration of exposure are critical in determining lung-cancer
risk. The occupational studies must, at a minimum, provide a quanti-
tative estimate of the dose and duration of exposure to PAH-containing
mixtures. With this information and comparative information on the
smoking habits of the exposed and nonexposed workers, we can estimate the
absolute risk from such exposure. Unfortunately, only one occupational
study with high exposure to a PAH-containing mixture supplied even this
minimal information.l°
UNITED KINGDOM GASWORKERS
. .
In a prospective study, Doll et al.6'L0 followed a cohort of
carbonization workers in British gasworks for up to 12 yr. Carboni-
zation workers were exposed to BaP at an estimated average air concen-
tration of 3, 000 ng/m3 during an 8-h shift20 and experienced a 142%
increase in lung-cancer mortality, compared with their nonexposed
workmates (Table C-4~. Although the smoking habits of only some 10t of
the cohort were ascertained by Doll and his colleagues,6 the exposed and
C-6
OCR for page 417
nonexposed workers appear to have had very similar smoking habits, with ^'
average current consumption of approximately 10 cigarettes/d. It is
reasonable, therefore, to assign the excess lung cancer in the exposed
group to their working conditions, specifically to the air to which they
were exposed.
The current age of a smoker and his age at,starting to smoke are both
important in determining his risk of lung cancer. Likewise, both current
age and age at starting as a carbonization worker are important in deter-
mining such a worker's lung-cancer risk. From the papers of Doll et
al.,6310 one may estimate the average age of the workers at the middle
year of the study to be approximately 58 yr and the average length of time
exposed to be approximately 23 yr. However, this does not necessarily
imply that their average age at starting such employment was 35 (58 - 23),
because "the men regularly change from one type of work to another."l°
If the men started working at age 20, their average worktime BaP
exposure would be
3,000~23/~58 - 20) ~= 1,816 ng/m3.
To express this in constant-exposure terms, we may proceed as follows:
Total BaP-carbonization
breathed per year = (1,816~9.6~5~('~9) ng
= 4.27 ma.
That is, 9.6 = m3 of air breathed at work in a working day--8 h at 20
L/min; 5 = working days in a week; and 49 = working weeks in a year. The
total air breathed in a year is
(15.91~7~49) + (12.48~7~3) = 5,719 m3.
That is, 15.91 = [~17.28~5) + (12.48~2~/7 = average m3 breathed per
day during a working week, 12.48 = m3 breathed per day during a
nonworking day; 17. 98 = m breathed per day during a working day--all
these values calculated with assumptions of 20 L/min at work for 8 h, 6
t/min asleep for 8 5, and 10 L/min otherwise. If the gasworkers' exposure
is expressed in constant-exposure terms, as though the men breathed such
air throughout the day every day, the average BaP-carbonization pollution
to which they were exposed is
4.27 mg/5,719 m3 = 747 ng/m3.
This led to a 1427 increase in the rate of lung cancer over "background,
an estimate roughly 90% of which was caused by the meets smoking habits.
If we assume that the relation between duration of exposure and lung
cancer risk is the same for gasworks exposure as it is for cigarette-
smoking and that the men started work and started to smoke regularly at
roughly the same age, we may write (in lung-cancer terms)
C-7
OCR for page 418
10 U.K. cigarettes/d = 0.9
and BaP-carbonization at 747 ng/m3 = 1.42.
Those two equations permit us to express BaP-carbonization in terms of
U.K. cigarettes as
BaP-carbonization at 47.3 ng/m3 = 1 U.K. cigarette.
Calculation of the effect of other ages at starting carbonization-
work exposure requires more elaborate computation, and the above esti-
mate appears to be the best that can be made with the limited data
available.30
Note that reasonable changes in the estimate of the proportion of the
background lung-cancer rate that was caused by cigarette-smoking have only
minor effects on this estimated equivalence. For example, if a figure of
80Z, rather than 90t, is assumed, the equivalence is BaP-carbonization at
42.1 ng/m3 = 1 U.K. cigarette.
We assumed in the above calculations that the gasworker breathed 9.6
m3 [(8)(60)(20) L/min] of air at work each working day. The "average"
adult breathes roughly half this amount at work. If we assume further
that gasworkers and the average 3an breathe similarly at other tines, then
the average man breathes 4~543 m of air per year' or 79% (4~543/5,719)
as much air as a gasworker. The above equivalent of 47.3 must therefore
be divided by this figure to make the exposure applicable to "average"
man. Our best estimate is thus finally 59.5, i.e., BaP-carbonization at
59.5 ng/m3 = 1 U.K. cigarette. We estimate from Equation 3 that the
lifetime lung-cancer risk associated with exposure to BaP-carbonization at
1 ng/m3 would be 43/100,000.
UNITED STATES COKE WORKERS
Lloyd and his colleagues21, 32 found in cohort studies of U. S .
steelworkers that coke-oven workers experienced a substantial excess risk
of lung cancer. These workers, like the British gasworkers, are exposed
to the products of coal carbonization. Compared with nonoven workers at
the same plants, the coke-oven workers as a group had 2.8 times the
lung-cancer mortality rate; and coke-oven workers who had more than 5 yr
of "topside" exposure had 6.9 times the lung-cancer mortality rate. No
data were given on the smoking habits of these workers or of nonexposed
workers, on length of employment, on age, or on average BaP exposure.
However, Jackson et al. found average BaP concentrations on the
battery roof of a coke-manufacturing plant of 6, 700 ng/m . If this is
taken as the BaP exposure of the topside workers, these estimates of
lung-cancer risk are remarkably compatible with those from the study of
British carbonization workers.
The British carbonization workers had a relative risk of lung cancer
of 2.42 at a BaP exposure of 3,000 ng/m3, so we may write
C-8
OCR for page 419
Nonexposed British lung-cancer rate = 1.0,
Carbonization workers' rate = 2.42,
Increment per 1,000 ng/m3 of
BaP-carbonizat ion exposure = ~ 2 .42 - 1.0~/3 = 0.47.
At the time of these surveys, the age-adjusted U.S. national lung-cancer
mortality rate was just half the British rate.l2~37 Taking into account
this fac t and the relative risk of 6.9 for the U. S . topside workers, we
may wri te
Nonexposed U. S. lung-cancer rate = 0. 5,
Topside workers' rate = 0.5 x 6.9 = 3.45,
Increment per 1, 000 ng/m3 of
BaP-carbonization exposure = (3.45 - 0.5~/6.7 = 0.44.
The experience of coke-oven workers in the U. S . steel industry is
thus in very close agreement with the British data on gasworkers in
BaP-exposure terms.
LONDON DIESEL-BUS GARAC.F WnRKF.RR
the lung-cancer incidence among diesel-bus garage workers employed by
the London Jr~s~rt Authority (LTA) has been examined for the period
1950-1974. 1 , ,~ These men were exposed to more diesel emission than
other LTA employees, but they showed no greater risk of lung cancer than
the other employees.
No detailed information on the garage workers' duration of exposure
to diesel fumes has been published, but the concentration of smoke was
measured inside and outside selected garage s.2, 1 Waller41 concluded
that "the indications are that the overall exposure of garage workers to
benzota] pyrene during their working 1 Eves would not differ much from those
of the general population." The BaP exposure of the U.K. gasworkers
discussed above was some 100 times background and was associated with a
14Z; increase in lung-cancer rates. It is therefore hardly surprising
that the very small increase over background pollution in a diesel garage
(certainly less than a twofold increase) did not produce an
epidemiologically measurable effect. Other possible biases in comparing
the LTA workers in dif ferent job categories were discussed at length by
Harris.15 The study must be considered noninformative, rather than
negative; we have discussed it here because it was used as an important
data source in recent NRC reportsl5~25 on the impact of particulate
emission from diesel-powered light-duty vehicles.
OTHER OCCUPATIONALLY EXPOSED GROUPS
. .
Results of other studies of groups of workers exposed to PAH-
containing mixtures were reviewed recently. 25, 34 None of these studies
provided evidence of very high exposure; most provided no measure of
C-9
OCR for page 420
actual length or intensity of exposure to PAH-containing mixtures or
comparative cigarette-smoking habits. Their results are not useful for
purposes of quantitative risk assessment.
GENERAL AIR-POLLUTION EXPOSURE
Studies of the effects of exposure to general air pollution have been
reviewed in numerous reports.439~26334 These reviews have found that
lung-cancer rates (as well as rates of cancer at almost all other sites)
are higher in urban (i.e., "polluted") than in rural areas (Santodonato et
al.,34 Table 6-47~. Interpretation of the increased rates is invariably
confounded however, by lack of information on the possible contribution
of occupation-induced lung cancer, the possibility of greater accuracy of
death certification in urban areas, and, most critically, the lack of
detailed information on smoking history.
The confounding by occupationally induced lung cancer and more
accurate death certification in urban areas is unlikely to be the
explanation of most of the urban excess. The confounding by lack of
smoking-history information is likely to be the most important.9 We
have seen (Figure C-1) that the lung-cancer risk among cigarette-smokers
depends strongly on age at starting to smoke, and this holds true even
into old age. For valid comparison of lung-cancer rates between urban and
rural areas, which allows for smoking-habit differences, it is therefore
necessary to know, at a minimum, not only the current smoking habits in
the areas being compared, but also the past smoking habits in these
areas . In most countries, cigarette-smoking became popular much later in
rural than in urban areas; this itself ensures (even allowing for current
smoking habits) that lung-cancer rates will be higher in urban than in
rural areas of such countries.
The above arguments make urban-rural comparisons a very weak basis
for evaluating the effect of general air pollution on lung-cancer rates.
Moreover, most urban-rural comparisons are of no use for quanti-
tative risk-assessment purposes, because they include no estimate of PAH
concentrations in the air in the di [ferent areas.
LIVERPOOL-NORTH WALES COMPARISON
The urban-rural comparison study undertaken by Stocks38 covering
the years 1952-1954 in Liverpool (urban) and parts of North Wales (rural)
is perhaps unique, in that he not only measured air pollution, but also
addressed the issue of long-term smoking habits. The air pollution in the
two areas was measured in terms of average BaP concentration over a 2-yr
period starting in October 1954: the average BaP concentration in the air
was 6.7 ng/m3 in the rural area and 59.2 ng/m3 in the urban area.
Stocks addressed the issue of long-term smoking habits by showing that, in
men aged 50-59 at the time of the survey in 1953-1955, the urban-rural
contrast in smoking habits did not differ from that of 20 yr earlier.
C-10
Representative terms from entire chapter:
smoking habits
