cancer in particular (Liddell 1973b). There was a wide disparity
between the SMR of miners employed at the face (49) and the SMR of
those working on the surface (82). This disparity can be explained in
that surface miners may smoke while at work, but underground
miners cannot, and that the less healthy miners tend to move away
from coal face work and to be employed in easier jobs on the surface.

Ortmeyer and colleagues (1973; Lainhart et al. 1969) studied the
death rate of Pennsylvania coal miners who had been awarded
compensation for occupationally related respiratory disability. The
overall SMR was the same as that of white men in Pennsylvania.
Excess death rates were found in subjects with a reduced ventilatory
capacity, in particular when the FEV,/FVC was below 50 percent,
and in ex-miners with stage B and C complicated CWP. "Disabled"
miners with simple CWP had a normal SMR. Later, Ortmeyer and
colleagues (1974) studied a group of randomly selected Appalachian
miners and ex-miners. They showed that the overall life expectancy
for miners and ex-miners combined was the same as that for the
general U.S. population and for the States from which the cohort
originated. The effects on mortality of the years worked under-
ground, cigarette smoking, and airways obstruction were investi-
gated. Ex-miners had a slightly but significantly increased death
rate. Simple CWP had no effect on life expectancy; however,
complicated CWP was associated with decreased longevity. Although
both cigarette smoking and airways obstruction were associated with
an increased SMR, the number of years of work underground had no
discernible effect.

About the same time these reports were published, Cochrane
(1973) described his findings from a 20-year followup of the male
population of the Rhondda Fach in Wales. Survival rates for miners
and ex-miners were independent of the radiographic presence of
simple CWP or category A complicated pneumoconiosis. Further
studies of the same cohort from the Rhondda Fach showed a normal
life expectancy in those with simple CWP and category A complicat-
ed CWP (Cochrane et al. 1979). The death rate for bronchitis and
other respiratory diseases was elevated. The smoking habits of this
population were not examined.

A 20-year followup of a population sample from Derbyshire
(Cochrane and Moore 19801, aged 25 to 34, included four groups of
workers whose work was categorized as nondusty, pure coal mining,
pure foundry, or other and mixed. There were no significant
differences in the SMRs of the dust-exposed group of miners,
compared with the non-dust-exposed group of miners; however, only
20 deaths were recorded in the study.

Rockette (19771, in a NIOSH-supported study, investigated the
mortality rates among coal miners covered by the United Mine
Workers of America (UMW) Health and Retirement Fund. Unfortu-

301


nately, unlike the studies of Ortmeyer and colleagues (1973,1974), in
this investigation the population was not randomly chosen and
smoking histories were not available. A 10 percent sample of miners
eligible for benefits in January 1959 was randomly selected from the
original 550,000. Doubt exists whether miners covered by the UMW
Health and Retirement Fund are necessarily representative of U.S.
coal miners as a whole. The SMR for all causes was 101.6 and for all
cancer, 97.7. The SMRs for asthma, emphysema, and tuberculosis
were significantly elevated at 174, 144, and 145, respectively. The
SMR for lung cancer was minimally but significantly elevated at
112; however, a disproportionate number of miners from southwest-
ern West Virginia were subsequently shown to have been included in
the cohort. The death rate for lung cancer in this part of the United
States is significantly higher than the rate for the United States as a
whole and for other parts of West Virginia. In the absence of
smoking histories, little can be made of such a small increment in
mortality. Deaths due to accidents were high (SMR 144). The SMR
for bronchitis was 89.7, but, as previously mentioned, the SMR for
emphysema was elevated. There was a significantly increased death
rate for stomach cancer, but the SMR for pneumoconiosis could not
be determined because of difficulties with death certification and
classification.

A lengthy report of coal miners' morbidity in relation to x-ray
category, lung function, and exposure to airborne dust (Miller et al.
1981) described the findings for 31,611 British miners who were
surveyed at 24 pits from 1953 to 1958. Again, the coal miners had a
lower mortality than British men in general. Although this was
attributed to the healthy worker effect, no supporting evidence for
this conclusion was given. Miners with PMF had an increased death
rate. Mortality from bronchitis was associated with increased dust
exposure, but it is apparent that with increased dust exposure, there
would also be an increased cumulative exposure to cigarette smoke.
Appropriate data whereby the two effects could be separated were
not available, since cumulative cigarette smoking history or, indeed,
a smoking history of any kind was not available. Deaths from lung
cancer were not increased.

Higgins and colleagues (19811, in a followup study of a group of
miners from Richwood and Mullens, West Virginia, were unable to
show any significant difference in the mortality of miners and ex-
miners as compared with nonminers. The death rates from respira-
tory diseases were appreciably higher in coal miners; however, there
are doubts as to the accuracy of the cause of death on the death
certificates because compensation was often awarded to ex-miners'
families solely on the basis of a death certificate that mentioned
respiratory disease (Comptroller General 1980, 1982). Another
problem encountered was that some miners had moved away from

302


the district and could not be traced. In many instances, their status
proved impossible to determine. A clear-cut effect of smoking on
mortality was evident in nonminers, but was less evident in miners
and ex-miners. Here again the advent of black lung compensation
may have been an incentive for disability applicants to underesti-
mate their smoking habits.

The publication of the Registrar General's Decennial Supplement
(1970-1972) on occupational mortality (1978) indicated that mortali-
ty rates for coal miners were somewhat increased for both under-
ground and surface workers. The SMR for most respiratory diseases
other than lung cancer showed a mild to moderate increase.

Jacobsen (1976,1977) concluded that coal miners as a group have a
normal SMR. He also indicated that there was no excess death rate
from bronchitis and emphysema among coal miners, nor was there
an increase in mortality from these conditions with increasing time
worked in dusty occupations. Among men with no pneumoconiosis,
there was a clear and significant mortality gradient with increases
in estimates of cumulative exposures to airborne dust. However, the
decision to study the SMR of selected subgroups of miners whose
cigarette smoking habits were unknown, and in whom other possible
confounding factors may have been present, detracts from his
conclusions. The demonstration that the presence of bronchitis in
coal miners is associated with increased mortality and morbidity is
of little special significance for coal miners because the same
situation applies to the general population. The increased mortality
and morbidity are for the most part attributable to cigarette
smoking in the general population, and only if it were possible to
show an increased death rate in nonsmoking bronchitic coal miners
would this observation be convincing evidence that the presence of
bronchitis of itself portends premature disability and death.

In conclusion, the majority of recent mortality studies have shown
that coal miners have a normal life expectancy. Although there is an
increased SMR in miners with PMF, the overall prevalence of PMF
in working miners is so low that any effect it has on the SMR is more
than counterbalanced by decreased death rates from lung cancer and
heart disease. Although in certain studies, death rates from bronchi-
tis and emphysema have been found to be elevated, this has not been
a consistent finding; in other studies, especially those in which it has
been possible to quantitate the effects of cigarette smoking, no
increased death rates have been demonstrable. There is little or no
evidence that the inhalation of coal mine dust contributes to excess
morbidity or mortality in regard to lung conditions other than PMF,
such as emphysema, asthma, tuberculosis, or pneumonia. By way of
contrast, cigarette smoking has repeatedly been shown to have a
clear and easily demonstrable effect on the death rate of both miners
and nonminers. There is some recent suggestion that cigarette

303


smoking prevalence increased in British coal miners between 1965
and 1975, possibly related to their increased standard of living, but it
is too early for any discernible changes in cigarette consumption to
be reflected in mortality and morbidity statistics.

Lung Function in Coal Miners

Although there is no substantial clinical effect of an increasing
category of simple CWP on the ventilatory capacity of coal miners,
most studies in which coal miners have been compared with a
suitable reference population of nonminers have demonstrated a
significant decrement in the ventilatory capacity of the miners
(Higgins 1972). Regardless of radiographic evidence of simple CWP,
FEV, of coal miners--or any other suitable index of ventilator-y
capacity-is generally reduced in comparison with FEV, of nonmin-
ers. This suggests that decrements in FEV, and simple CWP are both
related to dust exposure, but the two measures represent separate
biologic responses in the lung to the inhalation of coal dust.

Higgins studied three populations in the United Kingdom, all of
which contained a significant proportion of miners and ex-miners,
along with a comparable reference population. The areas chosen
were Leigh, the Rhondda Fach, and Stavely (Higgins 1960; Cochrane
et al. 1961). The reduction in the ventilatory capacity of miners that
was observed could not be explained on the basis of cigarette
smoking; indeed, coal miners at that time generally smoked less
than nonminers. Since then, several other studies have found similar
results and the data have been reviewed by Higgins (1972). Possible
explanations for the observation that coal miners have a lower
ventilatory capacity and that this finding is unrelated to radiograph-
ic findings are. that (1) coal dust can produce or exacerbate
emphysema or airway narrowing and that these changes occur
independent of the changes that result in an abnormal radiograph,
or (2) the lower ventilatory capacity in miners results from either
industrial selection or differential migration. Thus, were the more
healthy miners to leave their employment and move to other parts of
the country to seek new jobs, those who remain would be less healthy
and almost certainly have lower lung function. Although the second
hypothesis is a consideration, especially during hard times when
unemployment in the coal mines is high, recent studies have shown
that it is the weaker and the less muscular man who is more likely to
leave the coal mine within the first few months of his employment
(McLintock 1971). Thus, the first hypothesis seems much more
probable and requires further consideration.

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Emphysema, Exposure to Coal Dust, and Cigarette Smoking
The pathology associated with CWP, both simple and complicated,
has been well described, and it is generally accepted that simple
CWP has a relatively specific set of histological findings (College of
American Pathologists 1979). Initially, dust starts to accumulate
around the second division of respiratory bronchioles. As this occurs,
there may be a little reticulin or, exceptionally, some collagenous
fibrosis. Subsequently, the respiratory bronchiole dilates to form a
condition known as focal emphysema. Gough (1947) and Heppleston
(1947, 1954) suggested that this condition develops as a result of
weakening and atrophy of the smooth muscle in the bronchiolar
wall. The site at which focal emphysema develops is identical to that
of the centrilobular emphysema found in cigarette smokers. Some
researchers, however, believe that the focal emphysema of coal
workers seldom extends to involve the gas-exchanging regions of the
lung, namely, the respiratory bronchioles and alveoli (Heppleston
1972). Heppleston (1972) and Gough (1968), moreover, claimed to be
able to distinguish focal emphysema from centrilobular emphysema,
and suggested that the former is characterized by an absence of
bronchiolitis in the smaller airways. Not all researchers accept these
opinions (Cockcroft, Seal et al. 1982).
Dust exposure has long been associated with increasing severity of
focal emphysema. Gough (1968) wrote that in a young coal miner
with short exposure to dust, dying of accident or of nonpulmonary
disease, there is an accumulation of coal dust specifically related to
the terminal and respiratory bronchioles. The lungs can evidently
withstand this deposition without harm for some years. Emphysema
then develops, and in miners who have been exposed for 20 years,
some degree of dilatation of the proximal order of the respiratory
bronchiole is usual and may be marked. After 40 years of dust
exposure, the majority of miners will show focal dust emphysema
(FDE), although there is a surprising range in the quantity of dust
deposited, and in the degree of emphysema, in miners working under
similar conditions. FDE refers to dilatation of the respiratory
bronchioles and there can be no doubt, because of the time sequence,
that the dust deposition precedes the emphysema. Although Gough's
remarks imply that there is a direct relationship between dust
exposure and the development of focal emphysema, until recently
his views were not entirely accepted. In a similar context, there is a
clear-cut relationship between coal dust exposure and the develop-
ment and progression of simple CWP (Jacobsen 1980).
Ryder and colleagues (1970) reported the results of a survey in
which they correlated pathological, physiological, and radiological
findings from the lungs of 247 deceased South Wales miners and ex-
miners, most of whom had been diagnosed as suffering from coal
workers' pneumoconiosis during life. The researchers were particu-


iarly ;,oncerned with the relationship of emphysema to dust exposure
and TO the radiological findings present antemortem in these
subjects. A control series of autopsies was drawn from nonmining
nlen autopsied at the same hospital and matched for age `by decade.
Whole lung sections were made and emphysema was quantified with
standard techniques. Virtually all of the mining population had been
examined by the Pneumoconiosis Panel during life, and most were
receiving benefits. Post-mortem findings of emphysema were then
related to clinical findings, ventilatory capacity measurements, and
radiological findings. Emphysema was much more common among
the disabled coal miners than among the control population of
nonminers, but it is difficult to interpret this observation, as the
miners were largely selected from among those who had respiratory
disability and the control population was not selected in anv similar
way. They also found that miners with the punctate type of opacity
were more likely to have emphysema than those with nodular or
micronodular lesions. Lung function showed no correlation to
progressive x-ray changes for simple pneumoconiosis, but declined
with increasing severity of progressive massive fibrosis. The mean
emphysema score increased with increasing age in the control
population, but not in the miners. The absence of a relationship
between emphysema score and age in the miners may be secondary
to their having been selected (even at the younger ages) because they
presented with respiratory disability. The mean emphysema score
correlated well with antemortem measurements of FEV1, but was
not greater in those miners with categories B and C of progressive
massive fibrosis than in miners with lesser degrees of radiologic
change. The absence of smoking data in this population of disabled
miners and the poor correlation of emphysema score with radiologic
change makes it difficult to ascertain the relative contributions that
cigarette smoking and coal dust exposure may have made to the
emphysema found in this population.

A later publication on the same population of disabled miners
(Lyons et al. 1972) included some smoking data. Lung function
declined with increasing severity of radiologic progressive massive
fibrosis, but actually improved with increasing severity of radiologic
simple pneumoconiosis. This dichotomy of lung function and radio-
graph may be due to the selection of the autopsy population largely
from those who had been disabled from pneumoconiosis in life, as the
certification of disability may require more severe functional abnor-
malities in the absence of radiographic abnormalities than it would
in the presence of advanced simple pneumoconiosis on the radio-
graph. They again showed a correlation of lower FEV, with
increasing emphysema score, but not with the Reid index of
bronchitis. Smokers had lower mean FEV, values than nonsmokers
and ex-smokers among miners with simple pneumoconiosis and

306


grade A PMF, but there was no difference in mean FEV, for smokers
and nonsmokers among workers with more advanced PMF. The
authors suggested that the emphysema is a more important determi-
nant of ventilatory impairment than the radiograph and that the
emphysema is due to coal dust in both simple pneumoconiosis and
progressive massive fibrosis. However, they presented no data to
evaluate the possibility that emphysematous change due to cigarette
smoking may have been responsible for the link between emphyse-
ma score and lung function and for the absence of a correlation with
the radiologic changes of pneumoconiosis.

Leigh and colleagues (1983) described the results of 886 post-
mortem examinations of Australian miners, relating years spent
underground at the coal face to bronchial gland wall ratio, the
presence and extent of emphysema in the lungs, radiographic
findings, and cigarette smoking history. Emphysema was related to
years spent underground at the coal face and to radiological evidence
of CWP. Radiological evidence of pneumoconiosis was negatively
associated with smoking. Even more surprisingly, smoking was not
correlated with gland wall ratio or emphysema. This absence of any
relationship between cigarette smoking and emphysema is unique in
the published literature and suggests a bias in the selection of
subjects who underwent post-mortem examination or in the manner
in which smoking habits were analyzed.

A relatively recent post-mortem study of coal miners and nonmin-
ers from South Wales compared the prevalence and extent of
emphysema in subjects who had died of ischemic heart disease
(Cockcroft, Berry et al. 1982). A greater percentage of smokers and
ex-smokers had emphysema (17/34) than never smokers (l/5) among
the coal miners, but there were too few cases of emphysema among
the nonminers to compare smokers and nonsmokers. Coal miners
were noted to have more emphysema than nonminers, but the
frequency of emphysema in the control population was very low.
While the degree of emphysema in these subjects was quantitated in
the absence of knowledge of the deceased subject's occupation, the
characteristic features of coal miners' lungs (i.e., the formation of
macules and the presence of pigment and the accompanying focal
emphysema) would invariably indicate the deceased subject's occupa-
tion during life. There was a legal requirement for a post-mortem
examination for coal miners. Whether the pigment present also
highlighted and accentuated the emphysema is unknown.

Ruckley and colleagues (1984) examined the lungs of 460 British
coal miners at post-mortem examination for signs of dust-related
fibrosis and emphysema. Smoking habits had been determined
previously by questionnaire. The prevalence of emphysema was 9
percent in the nonsmoking miners whose lungs showed only
circumscribed dust accumulations of which any solid center was less

307


than 1 mm in size, 33 percent in nonsmoking miners with lungs
showing one or more palpable lesions between 1 and 10 mm in size,
and 75 percent in nonsmokers with PMF. The corresponding
prevalences of emphysema among smokers with similar pathologic
findings were 52.7 percent, 70.3 percent, and 85.3 percent, respec-
tively. Ex-smokers generally had intermediate percentages. The
percentage of the population with any emphysema increased with
the increasing content of dust in the lung, but the percentage of the
population with more than one-third of the lung affected showed no
increase with increasing concentration of dust in the lung. These
data suggest that both smoking and coal dust contribute to emphyse-
ma, but that extensive emphysematous change is more closely
related to extent of cigarette smoking.

Morgan and colleagues (1971) examined lung volumes in coal
miners and showed that both cigarette smoking and increasing
simple CWP grade increased the TLC and RV, and the effects
appeared to be additive. This suggests that simple coal workers'
pneumoconiosis is associated with a slight loss of the elastic recoil.
Such an observation is best explained by the presence of so-called
focal dust emphysema (FDE).

In summary, there is little doubt that simple CWP and dust
exposure may lead to the development of focal dust emphysema. The
type of emphysema seen in coal miners is probably still best referred
to as focal dust emphysema, since there is some evidence that it does
not progress to severe centrilobular emphysema (Ruckley et al. 1984)
in the absence of cigarette smoking. Whether a morbid anatomical
distinction between the two conditions is possible is not certain.

Studies of right ventricular function in coal miners and ex-miners
both during life and at post-mortem examination (Morgan and
Seaton 1984) have shown that car pulmonale or right ventricular
hypertrophy do not occur except in cigarette smokers or in miners
who have PMF (Fernie et al. 1983).

Dust Exposure, Cigarette Smoking, and Ventilatory
Function

In a long-term prospective study of 3,581 miners who worked at
the coal face, Rogan and colleagues (1973) showed that dust exposure
was inversely related to ventilatory capacity. Lifetime cumulative
exposures to coal dust were available. The researchers were able to
demonstrate a progressive reduction in ventilatory capacity with
increasing exposure to dust. The presence of pneumoconiosis was not
associated with an additional decrement of ventilatory capacity
beyond that due to cumulative dust exposure, smoking habits, and
stature. Smokers showed a more rapid decline in FEV, than
nonsmokers, but an effect of cumulative dust exposure was apparent
in both smoking and nonsmoking miners. Among the nonsmokers,

308


FEV, was generally lower in the most dust-exposed group than in
the low exposure group, but the rate of decline per year remained
the same from age 30 to age 60 in both exposure groups. The age-
related regression coefficients were the same in the heavily and
lightly dust-exposed nonsmokers. Subjects with PMF were excluded
from the analysis. Among smokers, the rate of decline in FEV, with
age was greater than for the nonsmokers in each exposure category,
but the absolute FEV, in smokers at a given age was uniformly
lower for the group with high dust exposure than the group with low
dust exposure.

Kibelstis and colleagues (1973) were also able to demonstrate a
slight effect of dust exposure on the ventilatory capacity of their
nonsmoking miners. These investigators divided their population
according to whether the men had worked at the face, in transporta-
tion, in miscellaneous other jobs, or on the surface. Dust measure-
ments performed for these various jobs and work places had shown a
gradient, with the greatest exposure at the coal face and least on the
surface (Doyle 1970). Nevertheless, individual cumulative dust
exposure measurements were not available for the subjects. When
the nonsmoking coal face workers were compared with the non-
smoking surface workers, there was a slight but significant differ-
ence in FEV,. Thus, the coal face workers had an FEV, of 98 percent
of the predicted value; that of the surface workers was 102.4 percent.
The difference in FEV, for the smoking and the nonsmoking coal
face workers was 6 percent; the difference between the smoking
surface workers and the nonsmoking surface workers was 10.5
percent. The effects of cigarette smoking were therefore substantial-
ly larger than those of dust exposure. Among the ex-smokers and
nonsmokers, there was a significant difference in function between
coal face workers and transportation workers and their counterparts
who worked on the surface. Among the smokers, no such difference
was present, with smoking apparently overwhelming the effects of
dust. Airways obstruction was three times more common in the
smokers than in the nonsmokers.

An extensive West German study of 6,700 workers employed in
coal mines, steel works, cement works, asbestos factories, and other
heavy industry related dust exposure to smoking habits and other
factors (Deutsche Forschungsgemeinschaft 1978). Each subject un-
derwent a clinical examination, chest radiograph, and spirometry
along with measurements of airways resistance and arterial blood
gas analyses. The study showed that the most important factors
related to the prevalence of bronchitis and airways obstruction were
age and smoking habits. Among younger workers, there seemed to be
an additive effect of smoking, age, and dust, with the combined effect
of all three equaling the sum of their separate effects. Among older

309


workers, smoking appeared to play a relatively greater role in the
production of airways obstruction.

Hankinson and colleagues (1977) characterized the physiological
impairments that are associated with the inhalation of coal dust and
cigarette smoke. This study relied on flow volume curves as a method
of assessing ventilatory capacity, but in addition to the standard
spirometric measurements, lung volumes were calculated by a
radiological method using posteroanterior and lateral chest films.
Since TLC could be calculated, it was possible to express the flow
rates, not only as a percentage of vital capacity (VC) but also at
absolute lung volumes. Four age- and height-matched groups were
selected on the basis of their smoking history and on the presence of
bronchitis, that is, cough and sputum. Thus the four groups consisted
of smokers with bronchitis, smokers without bronchitis, nonsmokers
with bronchitis, and nonsmokers without bronchitis. Flow-volume
curves of the four groups are shown in Figures 1 and 2. The
differences between the four groups reveal that cigarette smoking
effects the flows at all lung volumes. In contrast, nonsmoking
bronchitics for the most part showed decreased flows at high lung
volumes, although there was some mean reduction in flows at lower
lung volumes, indicating that the small airways were not entirely
spared. When the flows were expressed at absolute lung volumes, it
became evident that smokers had an increased RV and an increased
TLC. In contrast, the nonsmoking subjects with and without
bronchitis had a normal TLC and RV. The increased TLC suggests a
loss of retractive forces in the lung and the presence of subclinical
emphysema. Bronchitis in nonsmoking subjects was not associated
with an increase in TLC.

A number of longitudinal studies have been carried out with
groups of coal miners. Love and Miller (1982) followed 1,677 men
from five British collieries for 11 years. Loss of FEV, was found to
increase with cumulative dust exposure, after allowing for age,
smoking, and colliery effect. The investigators classified smoking
according to the smoking status that was recorded in all three
surveys, that is, as nonsmokers, ex-smokers, or current smokers.
Miners who were recorded as smokers at the first survey and as ex-
smokers at the second and third surveys were designated as
intermittent smokers. According to Love and Miller (1982), the
average decrement in FEV, from the effects of dust was about one-
third of that due to smoking. They further stated that if men left the
industry because of ill health and respiratory impairment, the
average loss of FEV, would have been underestimated. This could
apply to men who retired from the workforce because of the effects of
dust, cigarette smoking, or both in combination.

There are several problems with this study. First, only 1,677
subjects were studied, 29 percent of the population of 6,191 in the

310


(n)= 428

d
G

30    40    50    60    70

Volume, percent forced wtal capacity

FIGURE l.-Mean flow volume curves expressed as
       percentage of forced vital capacity
SOYRCE Hankmson et al lYT:i

first survey. No data were provided to establish that the 1,677
survivors had similar characteristics to the original 6,191 subjects. It
is essential to know that the ventilatory capacities, age, height, and
smoking habits of the survivors did not differ from those of the
original cohort. Second, no quantification of smoking was available.
FEV, was regressed against age, regular smoking habit, and dust.
Unfortunately, smoking was treated as an unchanging variable such
as height, although Fletcher and colleagues (1976) had shown that
the effects of cigarette smoking increase with pack-years. Similarly,
Kibelstis and colleagues (1973) showed that while cough and sputum
relate well to current smoking habits, pack-years are a better
predictor of the prevalence of airways obstruction.

Attfield (1985) examined changes in ventilatory function among
smoking and nonsmoking miners in the United States. They
recorded the decline in FEV, over an ll-year period in a group of
1,072 U.S. miners. Over that time the loss in FEV, was 0.1 L more in

311


(n)=426

7 -

6t

P
8   5-
P
2
1
=   4
4
Il.

  3
2 ;
1 i

  " I

/
6       7       6       5       4       3       2       1

                 Absolute lung volume. lhS

FIGURE 2.-Mean flow volume curves expressed as
       absolute lung volumes
SOCRCE Hankrnson et al 119771.

the smoking miners than in the nonsmoking miners, in a multiple
regression model. The effect of coal dust exposure over the 11-year
period ranged from 0.036 to 0.084 L, depending on the regression
model used for the coal dust exposure.

The relative importance of cigarette smoking versus dust and
other factors in occupational lung disease has been reviewed by
Elmes (1981). He concluded that while control of occupational
exposure to coal dust remains critical, substantial future improve-
ment in respiratory health can be achieved by reducing the
prevalence of smoking among miners.

Summary and Conclusions

1. Coal dust exposure is clearly the major etiologic factor in the
production of the radiologic changes of coal workers' pneumo-
coniosis (CWP). Cigarette smoking probably increases the
prevalence of irregular opacities on the chest roentgenograms

312


of smoking coal miners, but appears to have little effect on the
prevalence of small rounded opacities or complicated CWP.
2. Increasing category of simple radiologic CWP is not associated
with increasing airflow obstruction, but increasing coal dust
exposure is associated with increasing airflow obstruction in
both smokers and nonsmokers.

3. Since the introduction of more effective controls to reduce the
levels of coal dust exposure at the worksite, cigarette smoking
has become the more significant contributor to reported cases
of disabling airflow obstruction among coal miners.
4. Cigarette smoking and coal dust exposure appear to have an
independent and additive effect on the prevalence of chronic
cough and phlegm.

5. Increasing coal dust exposure is associated with a form of
emphysema known as focal dust emphysema, but there is no
definite evidence that extensive centrilobular emphysema
occurs in the absence of cigarette smoking.

6. The majority of studies have shown that coal dust exposure is
not associated with an increased risk for lung cancer.

7. Reduction in the levels of coal dust exposure is the only method
available to reduce the prevalence of simple or complicated
CWP. However, the prevalence of ventilatory disabilities in
coal miners could be substantially reduced by reducing the
prevalence of cigarette smoking, and efforts aimed at reducing
ventilatory disability should include efforts to enhance success-
ful smoking cessation.

313


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reference to lung cancer. British Journal of Industrial Medicine 36t3):199-205,
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ASHFORD, J.R., MORGAN, D.C., RAE, S., SOWDEN, R.R. Respiratory symptoms in
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CHAPTER 8

SILICA-EXPOSED WORKERS


CONTENTS

Silica Exposure

Population at Risk

Smoking Behavior of Silica-Exposed Workers

Definitions of Health Effects

Epidemiological Findings

Pathogenesis of Silica-Related Health Effects

Silica Exposure and Cancer
Epidemiologic Studies of Smoking, Silica Exposure,
   Silicosis, and Cancer
    Silica-Exposed Cohort Studies
     Metal Ore Mining
      Steel Industry
     Workplaces With Exposure to Silica Only
    Followup of Silicotics

Research Recommendations

Summary and Conclusions


References

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Silica Exposure

The oxides of silicon (SiO,) are found in a number of polymorphic
structures consisting of three-dimensional networks of silica tetrahe-
dra (Zoltai and Stout 1984). When SiO, is bound with cations, it is
considered to be "combined" silica. When not combined, it exists in
its "free" forms-polymorphic crystalline, cryptocrystalline (minute
crystals), and amorphous (noncrystalline) (Parkes 1982). Whether
SiO, is in a free form is important from the standpoint of
occupational toxicity. The crystalline phases of SiOz, including
quartz, tridymite, and cristobalite, are recognized as causative
agents in silicosis. Diatomite tends to form amorphous silica, and
crystalline lenses are found in diatomaceous earth deposits. Diatom-
ite is converted to the biologically active cristobalite with calcining
at temperatures from 1000" C to 1723" C (Parkes 1982).

Occupational exposures to free silica are diverse. Major industries
with recognized significant silica exposures include metal mining,
coal mining, and nonmetallic mineral extraction, stone, clay, and
glass processing, iron and steel foundries, and nonferrous foundries.
A more complete listing of occupations with potential exposure to
silica is found in Table 1. Some of these exposures, including silica
flour production and use, sandblasting and certain mining, quarry-
ing and tunneling operations, result in exposure predominantly to
silica. However, many silica exposures, including most mining
operations and foundry exposures, are mixed-dust exposures, which
has implications for the type and extent of biological response seen
among exposed workers.

A general pattern of noncompliance with the current permissible
exposure limit (PEL) for free silica has been documented in recent
papers appearing in the American medical literature. These reports
have included the Occupational Safety and Health Administration
(OSHA) compliance data for 205 foundries in which 40.6 percent of
samples exceeded the PEL (Oudiz et al. 1983); OSHA data showing a
53 percent rate of noncompliance with the silica PEL in 27 silica
flour mills (Banks, Morring, Boehlecke 1981; Banks, Morring,
Boehlecke et al. 1981); and gross excesses (greater than hundredfold)
of the silica standard in sandblasting operations, which remain a
poorly regulated industrial process in the United States but are
banned in several other developed countries (Samimi et al. 1974).

Population at Risk

Estimates of the population at risk for potential silica exposure are
available from the National Institute for Occupational Safety and
Health (NIOSH) National Occupational Hazard Survey, which was
based on a probability sample of 5,000 industries between 1972 and
1974 (NIOSH 1978). From these survey results, NIOSH estimated


TABLE l.-Occupations with potential exposure to silica

Abrasive blasters
Abrasive makers
Auu, garage workers
Bisque-kiln workers
Brick layers
Buffers
Burhstone workers
Carborundum makers
Casting cleaners (foundry)
Cement makers
Cement mixers
Ceramic workers
Chemical glass makers
Chippers
Coal miners
Construct workers
Cosmetic makers
Cutlery makers
Diatomaceous earth calciners
Electronic equipment makers
Enamellers
Fertilizer makers
Flint workers
Foundry workers
Furnace liners
Fused quartz workers
class makers
Glaze mixers (pottery)
Granite cutters
Granite workers
Grinding wheel makers
Grindstone workers
Hard rock miners
Insecticide makers
Insulators
Jewelers
Jute workers
Kiln liners
Masons
Metal buffers
Metal burnishers
Metal polishers
Miners
Mortar mixers
Mortarmen

Oil purifiers
Oilstone workers
Optical equipment makers
Paint mixers
Polishing soap makers
Porcelain workers
Pottery workers
Pouncers (felt hat)
Pulpstone workers
Quarry workers
Quartz workers
Refractory makers
Road constructors
Rock crushers
Rock cutters
Rock drillers
Rock grinders
Rock screeners
Rubber compound mixers
Sand cutters
Sand pulverizers
Sand blasters
Sandpaper makers
Sandstone grinders
Sawyers
Scouring soap workers
Silica brick workers
Silicon alloy makers
Silver polishers
Slate workers
Smelters
Sodium silicate makers
Spacecraft workers
Stone bedrubbers
Stone cutters
Stone planners
Street sweepers
Subway construction workers
Tile makers
Toothpaste makers
Tube mill liners
Tumbline barrel workers
Tunnel construction workers
Whetstone workers
Wood tiller workers

SOCRCE Aspen Systems 119781

that 3,200,OOO active workers in 238,000 plants were potentially
exposed to silica; however, this estimate was based on workers in an
area where free silica is used, and the number of workers with
clinically significant exposures would be appreciably lower. This
estimate excluded former workers who were retired, working
elsewhere, or disabled and the large industrial sector of agriculture
where some silica dust exposure occurs (Popendorf et al. 1982).

324


Significant physical factors for occupational respiratory disease
risk include the percentage of free silica, the respirable fraction of
the mineral dust (which may have a higher silica content (Ayer et al.
197311, and the concentration of dust (total and respirable) in the
worker's breathing zone. In addition, other workplace contaminants
may combine with silica particles to alter the toxicity of the given
mineral dust exposure. Individual factors such as pulmonary deposi-
tion and clearance, atopic status, genetic constitution, and immune
response may also be important risk factors in silica-related disease;
however, they are sometimes difficult to measure and have been less
well studied. Hence, studies of workers exposed to silica must
provide clear documentation of the exposures in the workplace as
well as documentation of other personal and environmental factors
that may influence biological response.

Smoking Behavior of Silica-Exposed Workers

The smoking behavior of workers in a variety of settings where
silica exposure can occur is detailed in Table 2. These studies in the
United States and abroad indicate that a very large proportion of
people who are exposed to silica are also smokers.

Definitions of Health Effects

Several health effects are associated with occupational exposure to
silica dust. The causal role silica plays in some disease responses,
namely silicosis and silica-induced alveolar lipoproteinosis ("acute
silicosis"), is quite clear and widely accepted. Silica is recognized as
playing an important causal contributing role in a second group of
pulmonary responses-silicotuberculosis, mixed-dust fibrosis (usual-
ly mixed with iron oxides), and the fibrosing alveolitis arising from
exposure to calcined diatomaceous earth (diatomite pneumoconiosis)
(Parkes 1982). Smoking appears to play no significant causal role in
the etiology of the first two categories of silica-induced diseases. In a
third group of health effects, silica dust appears to be a risk factor in
simple chronic bronchitis as characterized by mucus hypersecretion
and in chronic airways obstruction, which is often associated with a
progressive decline in expiratory flow rates and is largely irrevers-
ible. This last group of pulmonary responses is nonspecific, recog-
nized to be multifactorial and causally linked to cigarette smoking. A
causal relationship between silica dust and chronic bronchitis or
chronic airways obstruction is less clear. This issue is of considerable
importance because of the prevalence of chronic bronchitis and
chronic airways obstruction in modern society and the large size of
the population at potential risk of silica exposure.