E  TABLE 2.-Smoking characteristics of silicaexposed workers

                 Number and type
   Study              of population                   Smoking characteristics (percent)                      Comments

Prow          240 gold miners.
(1970)           South Africa

Brinkman et al.     301 automotive industry
(1972)         workers. aged 40-65

SluisCremer       Men expmed to dust,
(1972)          Carletonville. South Africa

Theriault et al.
(3 papers)
(1974)

792 granite workers. Vermont

  Armstrong et al.     Coal and gold miners,
   (1979)           Australia
.

Born et al.
(1963)

Trona miners. Wyoming

Light (I-200)'
Moderate (2Olm)
Heavy (>6CO)

Exposed workers
Nonexpcmed workers

SM
65.8
11
22.3
32.5

70
60.7

SM
60.4

SM           EX'           NS        `Not smoked in
57           30            12         last 6 months

Gold miners

SM
66.3

42.6

NS/EX
34.2

' Numerical rating
of cigs/day x years
smoked

30
39.3

EX           NS
25.6           13.9

NSIEX
33.7

33.6           23.6

NOTJZ.: S.M=Smoker; EX=Ehsmoker; NS=Nonsmoker.


Epidemiological Findings

Early observers of occupational diseases, including Ramazzini in
1713 (1964), wrote about the respiratory problems of miners and
stone cutters, and recognized silicosis among miners, stone cutters or
hewers, and potters. Silicosis, and its previously described associated
health effects, have been given a variety of names that reflect the
several faces of silica exposur&ust consumption, ganister disease,
grinders' asthma, grinders' consumption, grinders' rot, grit consump-
tion, masons' disease, miners' asthma, miners' phthisis, potters' rot,
rock tuberculosis, stonehewers' phthisis, and stonemasons' disease
(Hunter 1955). Greenhow (18781, in his treatise on bronchitis,
recognized that "irritants which act immediately upon the bronchial
membrane may produce inflammation by means of either mechani-
cal or chemical irritation. Fine coal and metal dust, stone and
porcelain grit, and even the flue of cotton wool . inhaled into the
lungs during various industrial processes are all of them mechanical
irritants which become fruitful causes of bronchitis in certain classes
of operatives" (p. 30).

Mortality studies of silica-exposed cohorts have consistently shown
increased mortality rates for tuberculosis and nonmalignant respira-
tory disease, largely accounted for by silicosis (Guralnick 1962;
Registrar General 1958, 1978; Davis et al. 1983; Armstrong et al.
1979; McDonald et al. 1978; Fox et al. 1981). Although none of these
studies accounted for the effects of smoking, the consistency and
magnitude of the increased rates suggest a causal relationship
between silica exposure and these cause-specific mortality rates.
Davis and colleagues (1983) demonstrated dose-response relation-
ships between exposure category, tuberculosis, and silicosis, but
found no excess mortality from bronchitis and pneumonia. Finkel-
stein and colleagues (1982) investigated mortality among 1,190
Ontario miners receiving compensation awards for silicosis and
found nonmalignant respiratory disease (excluding tuberculosis) to
be the most frequent cause of death (standard mortality rate, 765).

NIOSH recently assessed causes of disability among employees of
the mining industry, based on the Social Security Disability Benefit
Awards and Allowances to Workers for 1969-1973 and 1975-1976
(Osborne and Fischbach 1985). The observed proportional morbidity
rate (PMR) for pneumoconiosis from silica and silicates (they were
not distinguished) was found to be somewhat higher (4,894) than for
other mining occupations. Workers employed in boring, drilling, and
cutting jobs appeared to experience increased disability from respira-
tory diseases, specifically pneumoconiosis including silicosis. These
findings, based on somewhat more recent exposures than the
previously cited mortality studies, confirm the major mortality
findings, but suffer from the same methodological problems. Again,
smoking data were not available or analyzed, and it is recognized

327


that those disabled in the mid-1970s very likely were exposed to
silica three or four decades previously; therefore, their disabilities
reflected previous dust exposures.

Early morbidity studies of workers exposed to silica dust focused
on rates of sickness, respiratory symptoms, and physical findings,
supplemented in the 1920s with chest radiography. The U.S. Public
Health Service (US PHS) conducted the first major U.S. silicosis
study of the hard-rock mining industry in 1913-1915 (Higgins et al.
1917; Lanza and Higgins 1915). Their studies reported that 60.4
percent of the 720 miners examined suffered from pulmonary
diseases attributable to mine rock-dust exposure. Dust samples
collected with a Draeger liter bag-granulated sugar filter apparatus
were reported to average from 30 to 50 mg/m3 (Higgins et al. 1917).
Although these concentrations would appear to be quite high, they
are difficult to interpret according to modern-day respirable dust
sampling and analysis (x-ray diffraction for free silica content).

Subsequent US PHS silica studies included Harrington and
Lanza's (1921) 1916-1919 study of copper miners in Butte, Montana,
in which 42.4 percent were judged to have some dust-induced lung
injury and 25.5 percent to have advanced disease. Dreessen and
colleagues (1942) studied 727 metal miners in 1939, and Flinn and
colleagues (1963) studied 67 underground mines employing 20,500
miners from 1958 to 1961, but found varying silicosis prevalence
from mine to mine and widely divergent exposures to free silica. The
silicosis prevalences of 9.1 percent and 3.4 percent, respectively,
were found to be associated with longer duration of exposure and
especially with face work exposures (Dreessen et al. 1942; Flinn et al.
1963). Earlier, Flinn and colleagues (1939) had reported an impor-
tant study (19361937) of West Virginia potteries that included 2,516
workers with an overall silicosis prevalence of 7.8 percent. Free silica
content ranged from 1 to 39 percent, dust concentrations varied from
3 to 440 million particles per cubic foot (mppcfl, and mean particle
diameters were judged to be 1.2 pm (but without data on the
concentration of respirable dust). A strong dose-response relation-
ship between dust concentration, duration of pottery exposure, and
silicosis prevalence was documented. It was suggested that no new
cases of silicosis would occur if dust concentrations in this industry
were brought below 4 mppcf. Renes and colleagues (1950) studied 18
ferrous foundries in 1948-1949, and found 9.2 percent of 1,937
foundrymen to have pulmonary fibrosis. Free silica content averaged
30 percent, with a mean particle size of 3 pm, and 82 percent of the
samples had levels below 6.9 mppcf. Mechanical shakeout operations
were found to have the highest dust concentrations (10 to 75 mppcfl,
and silicosis was noted to be more prevalent among foundrymen with
20 or more years of exposure. It was suggested that conditions had
improved in foundries and that most of the pulmonary fibrosis was

328


due to previous exposures. Early studies of the refractory (silica)
brick industry documented high percentages of free silica, often in
the form of cristobalite and tridymite from burned bricks. Keatinge
and Potter (1949) and Fulton and colleagues (1941) studied 1,035
exposed workers in this industry, finding 52 percent to have some
stage of silicosis. A relationship with dust concentration and
duration of exposure was again documented, as was an apparent
increased risk among men exposed to burned brick dust (Keatinge
and Potter 1949; Fulton et al. 1941).

Epidemiological studies of workers in the Vermont granite indus-
try have provided an important and interesting chronology of data
on the natural history of silica-associated respiratory diseases. Early
US PHS studies of this industry (Russell et al. 1929) documented
high dust concentrations (37 to 59 mppcf) and a very high prevalence
of silicosis. On the basis of dust with a free silica content of 35
percent, a presumptive "safe limit" of dustiness was suggested to lie
between 9 and 20 mppcf. A subsequent US PHS study (Russell 1941)
essentially confirmed the findings of the original study, noted an
increased progression of silicosis among the highly exposed cutters,
and concluded that a limit below 10 mppcf for this industry would be
desirable. Subsequent followup studies in 1955 by the US PHS and
the Vermont State Board of Health (Hosey et al. 1957) found that the
prevalence of silicosis had decreased from 45 percent in 1937-1938 to
15 percent in 1956, that the silica content of the dust averaged a
somewhat lower 22 to 25 percent free silica, and that nearly all
workers with silicosis had been exposed prior to implementation of
dust controls in 1937. This report was consistent with an earlier
report by Ashe (19551, and was subsequently supported by a further
followup study by Ashe and Bergstrom (19651, which reported no
cases of silicosis among 1,478 granite workers employed after 1937,
and a study by Davis and colleagues (1983) that reported only one
case in the same population.

All of these early studies of silica exposure concentrated on
radiographic evidence of silicosis and tuberculosis and the associa-
tion with silica content and concentration. These studies formed the
basis for environmental control of silica exposures, demonstrated the
effectiveness of dust control, and provided a widely held impression
that silica exposures, and hence disease arising from silica expo-
sures, were well controlled.

Beginning in the 195Os, British epidemiologists introduced stand-
ardized respiratory questionnaires, field spirometry, and sound
epidemiological methodology to the study of bronchitis and chronic
obstructive lung disease, and were the first to use these methods to
assess respiratory effects among industrial workers. This allowed
assessment of other risk factors, including cigarette smokmg, and
quantitation of major risk factors compared with appropriate

                                             329
157-5L.4 3 - 66 - 1,'


reference populations. At the same time, on the basis of clinical case
series, it was becoming clear that bronchitis and nonspecific airways
obstruction were more common than pneumoconiosis among work-
ers exposed to coal mine dust and silica dust. The significance of
these health effects was not clear. Modern epidemiological studies
began with the Higgins and colleagues (1959) investigation of
Stavely, an English industrial town of 18,000 and home to a
significant number of coal miners and foundry workers. This study
and other cross-sectional studies of silica exposure that have assessed
standardized respiratory symptoms, lung function, smoking, and
occupation (only those with non-coal-mining silica exposures) are
summarized in Table 3.

Review of these studies has found them to be heterogeneous in
regard to workforce composition, free silica content and dust
concentration (if reported), and other associated occupational expo-
sures that may contribute to respiratory symptoms and declines in
lung function. In some instances associated occupational exposures
other than silica dust appear to be as important or more important
than silica dust (Higgins et al. 1959; Gamble et al. 1979; Manfreda et
al. 1982; Graham et al. 1984). Two of these studies found lung
function to be somewhat better among exposed workers than among
reference subjects (Clark et al. 1980; Graham et al. 1984). However,
in both of these studies, one of potash miners and one of taconite
miners, it is very likely that the free silica exposure, although not
documented, was low. One study of fluorspar miners (Parsons et al.
1964) and one of copper miners (Federspiel et al. 1980) suggest a
significant dust effect on bronchitis prevalence and a somewhat
lower lung function among exposed miners. Specific environmental
data on free silica content or dust concentration were not provided in
either study, although most likely some of the dust exposure in these
mines was silica.

Four of the studies reviewed in Table 3 have documented
significant exposures to free silica with the relative absence of other
exposures: the Welsh slate workers study (Glover et al. 19801, the
Vermont granite workers study (Theriault, Burgess et al. 1974;
Theriault, Peters, Fine 1974; Theriault, Peters, Johnson 1974) and
two studies of South African gold miners (Sluis-Cremer et al. 1967;
Wiles and Faure 1977). Silicosis was reported in all four study
populations, ranging from 5 to 33 percent. Sluis-Cremer and
colleagues (1967) surveyed the prevalence of chronic bronchitis in a
mixed mining and nonmining population in Carletonville on the
Witwatersrand, South Africa. Chronic bronchitis was more common
among miners who smoked than among nonminers who smoked, but
there were no significant differences in prevalence of bronchitis
between miners and nonminers who did not smoke. The prevalence
of bronchitis was substantially higher among smokers than among

330


Study,
country

Number and     Age
type of     (mean or
population     range)

Bronchitis (ratio)

S/NS   Exp/Not

       Lung function              P"eum*
                               conic&
S    NS     A     EXP    Not A    (percent)         Comment

Higgine et
al. (1959),
United
Kingdom

Current and ex-   55 to
foundry workera; 64
105 exposed, 81
nondusty
occupations

Not
available
for
foundry
workera
alone

1.2

Not available for foundry   82.1 90    -7.9      14.0   Foundry workera both "pure"
workers alone                          with free silica exposure and
               (Indirect MBC based on          "mixed" with chemical fumes
               FEVd                (HCI. H,SQ, caustic soda,
                                 and benzol) and other dusts;
                               increased respiratory
                               symptoms and decreased lung
                                function mainly in "mixed"
                               foundry workers suggests
                                other dusts and fumes likely
                                more important than "pure"
                                foundry work

Parsons et
al. (1964),
Canada

Fluorspar
mining; 301
ev-4 5%
co"trola

,383
(20 to
70)

Not
available

5.5

Generally higher for nonminers; decreased lung
function in chronic bronchitic me" appeara more
important than dust eategory @a.& on indlrect
MBC, MMF, PFR)

1.93

No specific SiO, expasurea or
dust measurements available;
exposure determined from job
category and tenure

    Sluis     Cold mining;     35 and     1.8      1.22                 Not studied                 5    Free silica content range 5&
    Cremer et   582 expceed, 285   older                                               70%, but generally low dust
   al. (19871,   community                                                       levels; smoking somewhat
    South      controls                                                           more common among miners;
    Africa                                                                 significant increase in chronic
                                                                      bronchitis prevalence among
                                                                      smoking and ex-smoking but
                                                                      not nonsmoking miners
                                                                      suggests possible interaction
                                                                      between smoking and
E                                                                   "underground aerial
w                                                                           pollution"


TABLE 3.-Continued

          Number and    Age     Bronchiti 3 (ratio)              Lung function              Pneume
Study,       type or     (mean or ---                                            coniosie
country      population     range)    SINS   l&p/Not     S    NS     h     EXP    Not h    (percent)         Comment

Higgins et   60 foundry      25 to    Not      Not     Not reported separately     3.49    3.55   -.c6     23.1    No environmental
al. w66),   workers, 100     34     reported   reported   for foundrymen                         measurements, but typical
United     "nondusty"                                                       SiO, foundry exposures; 9-
Kingdom    workers                                                       year followup mortality
                                                                higher among foundry
       43 foundry      55 to                                     2.27    2.36   -39          workers than others,
       workers, 52      64'                                              appreciably higher among
      "nondusty"                                         (FEV7S%)             foundry workers with silicwis
        workers

Theriault   792 granite        44    Not      Not        4.2    4.1    + IO     4.2    4.1   +.10     31    Single "A" radiograph reader;
L al. (3     workers           =pod   repoti                                   dow+response relationship
PapeM                                  (FVC)                             between FVC and granite
(1974).      189 marble        41                                             duet and quartz dust; 2 mL
United     workers                                                       FVClduetyear decline, 9 mL
States                                                              F'VC/smoking-year decline

Wilea and   2,209 gold       4.5ta      2.3      5.3      2.53    3.77    -1.24    3.60    3.64   -.24     6.7    7@-250 particles/cm' dust
Fare      miners with      54
(1977).                                                              counts; 75% free BO,;
       2 10 years'                  (low duet       (MMEF)            flow duet           significant dust
South      service                                                      YS.             exposure/chronic bronchitis
Africa             highYsbust                    high dust           doee-reeponee relationship in
                            C&gOries)                    C&gOrieS)           all smoking categories; much
                                                                stronger smoking effect on
                                                                lung function, but no dase-
                                                       response &lationehip


TABLE 3.-Continued

         Number and     Age     Bronchitis (ratio)             Lung function              Pneume
Study,       type of     (mean or                                               -   conk&
country      population     range)     SINS   Exp/Not     S     NS    A     EXP    Not A    (percent)         Comment

Gamble et    121 talc miners     39.7      3.5      1.2      3.74    4.13    -.39     3.66    3.64   -.14     2.2    2040 w/m' free silica; 0.2%
al. (1979),                                                             talc,   2.96 mg/m' respirable dust;
United     1,077 potash       39.2                     (FEV,)                          .I07   anthophyllite, tremolite, and
States      miners                                                    potash   crysotile asbestos fibers found;
       (reference group)                                                 17/24 jobs ;,2f/cc; decrea..
                                                                lung function and pleural
                                                                thickening significantly
                                                                           aesaciated

Clark et     240 iron ore       49.3    None       1.0     c478.5    61.4    -2.9    861.4   80.0   t1.4     c2    Taconite has iron. quartz.
al. (198X,   miners. 220            among                                            and numerous silicates, esp.
United     yE2X-S              nonsmoking           mv,/Fvc)                        grunerite-cummingtonite; 25-
States     underground            miner8                                          40% total dust quartz;
                      repxted                                       significant smoking effect, no
       86 not exposed     50.1                                                dust effect on lung function
-
Federspiel    133 surface      Not       98.4   None       GM.5 92.5    -7.0    492.5   98.0   -5.5    Not     No dust level or SiO,% data;
et al.      workers       given           among                               reported   no SO, miner exposure. little
(196OJ                          nonsmoking    FEV,)                            or no surface worker SO,
United     112 copper                    nonminers                                  exposure; mining and
States      miners                                                       smoking additive effect on
                                                                bronchitis; signiticantly
                                                                   reduced nonsmoking miner
                                                                   FEV, and FVC and smoking
                                                                           miner FVC


i%   TABLE 3.-Continued

6

             Number and    Age     Bronchitis (ratio)             Lung function              Pneumw
   Study,       type of     (mean or                                                conioaia
    country      population    range)     SINS   Exp/Not     S    NS A     Exp Not A   (percent)         Comment

Glover et
al. (19801,
United
Kingdom

725 slate
workers

530 nonexposed

1.8      4.4

3.06 3.23

mv,1

-.17

3.23

3.53

-30

33

13-325 reepirable quartz in
reapirable dust; no smoking
category/radiographic opacity
association; no dust
concentrations available, but
thought "high"; respiratory
symptoms dependent on
pneumonconiceie category per
multiple regression, except
nonsmokers with previous TB
(in 4&50% of slate workew
age >w

Manfreda
et al.
(1982).
Canada

241 hardrock     25to      9.0      9.5      23     7    +16    0     7     -7      <l   Zinc, copper, nickel mining
miners         54                                             study; 69% silica in dust,
                       (Prevalence of FEY, abnormalities baaed on 95th          20-25% >TLV; some
382 nonexposed                 percentile of nonsmoking general population)           underground worker (95) NO,
men (community                                              exposure, some smelter
sample)                                                     worker (107) SO, exposure
                                                         (10% >TLV); low sulfm?
                                                           worker (39) duet exposure;
                                                    nonsmoking miner bronchitis
                                                    significantly increased;
                                                    significantly reduced lung
                                                           function in smelter workers,
                                                      not miners; probable selection
                                                        processes noted

NOTE: Bronchitin rat& and lung function comparisons are of nonexpwed smokers 6) and nonsmokers (NS) to 888e88 smoking effect and of nonamokiing exposed workers (Exp) and nonexpoeed
worken, (Not) to BBBBBB exposure effezt. Combined smoking and exposure et&& are not shown, but are add- under omxnent.


nonsmokers in both the dust-exposed and the nonexposed popula-
tions. Evaluation of Vermont granite shed workers (Theriault,
Burgess et al. 1974; Theriault, Peters, Fine 1974; Theriault, Peters,
Johnson 1974) revealed that both smoking and cumulative dust
exposure contributed to the differences in FVC and FEV, among
these workers, but the effect of smoking was larger than the effect of
dust exposure, using a multiple regression technique. A dose-re-
sponse relationship between silica dust exposure and decreased lung
function was demonstrated in both the Vermont granite shed
workers and the South African gold miners (Wiles and Faure 1977).
Glover and colleagues (1980) examined 725 workers and former
workers from the slate mines and quarries of North Wales and 530
men from the same area who had never been exposed. The
prevalence of chronic cough ranged from 5.2 percent in the nonsmok-
ers not exposed to dust to 19.4 percent in the nonsmokers with dust
exposure. Smokers with no exposure to dust had a prevalence of
cough of 27.5 percent; the prevalence was 38.9 percent among the
smokers with dust exposure. FEV, (standardized to a fixed height)
was lower in the smokers than in the nonsmokers. The dust-exposed
nonsmoking workers had a lower mean FEV,, but the values for the
dust-exposed and the nonexposed smokers were similar. The regres-
sion coefficients for FEV, with age were 20 mL per year in the
nonexposed nonsmokers and 38 mL per year in the dust-exposed
nonsmokers, but the coefficients for smokers were similar between
the dust-exposed (40 ml/year) and nonexposed (46 ml/year) men.
The absence of an effect of dust exposure among the smokers in some
of these studies may be the result of the cessation of smoking by
those workers with declining lung function, as suggested by the
observation that the mean FEV, and regression coefficient for
decline in FEV, with age among slate workers was worse in ex-
smokers than in either current smokers or nonsmokers. In contrast,
the values for ex-smokers in the general population were between
those for smokers and those for nonsmokers.

Only a few prospective studies of silica-exposed workers have been
reported in the literature. Four of these studies are summarized in
Table 4 (Higgins et al. 1968; Pham et al. 1979; Kauffmann et al. 1982;
Manfreda et al. 1984). Two other prospective studies of silicaexposed
workers are not included in this table because of methodological
questions. Brinkman and colleagues (1972) followed a group of
foundry workers with silica exposure and with silicosis over an ll-
year period. Only a third of the men known not to have died in that
interval were restudied, however, raising questions about the
validity of the finding of no apparent difference between the silica-
exposed workers and the unexposed workers in decline in lung
function over time. The original cross-sectional study found poorer
lung function among silica-exposed workers and silicotics. Musk and

335


colleagues (1977) conducted a 4-year followup study of Vermont
granite workers and reported a substantially higher annual loss in
lung function than predicted from previous cross-sectional studies of
this population. However, reassessment of some of these data has
raised questions about the adequacy of the pulmonary function
testing (Graham et al. 1981). Reana!ysis of the population revealed
that Vermont granite workers had an annual decline in FEV, of 44
mL per year and those who had left the industry had a decline of 72
mL per year (Eisen et al. 1983). The smoking habits of those who
continued working (20 pack-years) and those who had left the
industry (27 pack-years) were similar. There was no statistically
significant relationship between lifetime dust exposure and decline
in FEV, for either the workers who were still working or those who
had left the industry.

One of the four studies reviewed in Table 4 found no increased
decline in lung function over time among silica-exposed workers
(Higgins et al. 1968). On followup, however, the mortality rate
among the foundrymen in the original study (Table 3) was appreci-
ably higher, particularly among those with silicosis and among older
workers. Smoking habits were recorded in this study, and the
foundry workers who smoked had lower mean FEV, values than the
nonsmoking foundry workers in both the 25 to 34 and the 55 to 64
age groups. Pham and colleagues (1979) found consistently increased
declines with age in all measures of lung function studied (FEV,,
FVC/FEV,, RV/TLC, and fractional uptake of CO) among silica-
exposed steel workers compared with unexposed workers. Results for
smoking and nonsmoking workers were not reported separately.
Lung function of the exposed men in the original survey was
somewhat higher than in the unexposed workers (although they had
much more bronchitis), suggesting that selection processes (healthy
worker effect) occurred in this study. Kauffmann and colleagues
(1979, 1982) also found increased declines in smoking-adjusted lung
function over time among workers exposed to mineral dust (especial-
ly silica), and argued that the mineral dust and silica exposures were
most likely to be causal. Their findings are consistent with this
conclusion, but exposures were assessed by type of job, and informa-
tion on silica dose or interval progression over the 12 years of study
is lacking. Manfreda and colleagues (1984), in a 5-year followup
study of hard-rock miners and smelter workers, reported significant
declines in FEV,/FVC for both smoking and mining industry
exposure. These effects were quantitatively similar, but may reflect
more of a smelter effect than a mining (silica dust) effect, as that was
the finding on their original cross-sectional study. The prospective
study abstract does not address this question.

336


TABLE 4.-Prospective studies of workers occupationally exposed to silica

Study,
country

Number and       Age
type of        (mean or
population        range)

    Annual decline in lung function

s    NS     A     EXP   Not     A                  Comments

Higgins et
al. (19661.
United
Kingdom

60 foundry workers,
100 "nondusty"
workers

43 foundry workers,
100 "nondusty"
workers

25-34

5574

(Ages in
1957)

36' 21    -17       29   30 -1      Somewhat higher increased annual lung function
                          decline in older men, not strongly associated with
                          occupation, but strongly influenced by smoking

32' 54    -22      37 34 +3      ' Heavy smokers only

   (FEV 76)

Pham et
al. 119791,
France

196 steel (foundry
and roll sheet)
workers

166 unexposed
workers

49.5

49.6

(Ages at
first
exam)

7.4% 0.6%   -6.6%    At baseline, bronchitis prevalence significantly
               higher in steel vs. unexposed workers (37.8 vs.
               17.51, lung function somewhat higher in steel
              workers; over Byear followup. somewhat more
  (%FEV          increased steel worker bronchitis prevalence
predicted)         (45.3121.9); more steelworker than unexposed
               worker all-parameter lung function consistent
Matched for age,         decline; no silica content or dust concentration
height, smoking          environmental data
   status


TABLE 4.-Continued

            Number and       Age          Annual decline in lung function
Study,         type of        (mean or
country        population       range)       S    NS     A     Exp   Not     A                  Comments

Kauffmann     178 mineral dust         41      No smokingspecific lung      52 42    -10     la-year followup study of 11 factories, including
et al.       expmd workers (55            function decline given                  several mineral dust exposures, of which only
ww,      expoeed to silica)       (41) o                       (57)   (42)   C-15)    silica is separable; no silica monitoring data;
France                                                 significant FEV, annual adjusted declines in
        177 unexpceed          41                       CFEV,)         mineral dust exposed workers (esp. silica exposed)
          workers                                           interpreted a~ work related and consistent with
                                                   Annual declines       silicaexposed worker original crw-aectional
                                          adjusted for         decreased lung function assessment
                                          smoking statue
                                                    and amount        `Numbers in parentheses, of 55 silica-expceed
                                                       workers only

Manfreda      179 hard rock         2544       3.4% 2.0%  -1.4%     3.1%    1.6%   -1.5%    (See Table 2 for crowsectional results)
et al.       miners, 254                                         Cough and phlegm prevalence greater among
(19&o.      unexpcwd                 (Percentage decrease in   (Percentage decrease in    miners at baseline, no change over time; adjusted
Canada      (community sample)           FJW,/FVC, over 5 years,   FEV,/FVC, over 5 years,   FEV, and FJW,/FVC declines significant for
                           adjusted for age and    adjusted for age, height,    smoking and FEV,/FVC decline significant for
                                  height)          and smoking)      mining expoeure; data suggest FEV,/FVC more
                                                       sensitive indicator; data con.&.ent with mining
                                                     and smelter exposure and smoking additive effect

NCFlW S=Smoker; NS=Nonemoker; Exp=Expaeed; Not=Not exposed.


Pathogenesis of Silica-Related Health Effects

The characteristic pathology of the various forms of silicosis are
well described in recent texts dealing with occupational respiratory
diseases (Parkes 1982; Kleinerman and Merchant 1983). The mature
lesion of silicosis is the hyalinized nodule that is spherical and
typically varies in size from 3 to 12 mm. The nodules are more
commonly found in upper lobes, but are found throughout the lung
and are frequently subpleural. Microscopically, the nodules have a
whorled appearance composed of lamina of acellular hyalin. The
borders of the lesions are typically serpiginous and are composed of
pigment (especially if associated with a coal exposure), chronic
inflammatory cells (mainly lymphocytes and plasmacytes), and
connective tissue extending into the surrounding lung parenchyma.
With phase microscopy, doubly refractile silica particles 1 to 5 urn in
size may be observed within the lesions and within macrophages in
the surrounding infiltrate.

Acute silicosis, or acute silicoproteinosis, differs from classical
nodular silicosis in that the principal finding is alveolar proteinosis
associated with a diffuse interstitial reaction. Scanning electron
microscopy and x-ray microanalysis have demonstrated small bire-
fringent silica and silicate particles (less than 1 urn in diameter) in
these processes (Abraham 1978,1984).

Progressive massive fibrosis may develop on a background of
silicosis through the enlargement and sometimes the coalescence of
the nodular lesions of silicosis into conglomerate silicosis. These
lesions form most commonly in the apical or middle portion of the
upper lobes and are frequently complicated by tuberculosis. Cavita-
tion of these lesions may occur with or without tuberculous infection
(Kleinerman and Merchant 1983).

The mechanisms that produce silicosis, and particularly conglom-
erate silicosis, are still not fully understood. The cellular events
leading to lung injury appear to arise from the cytotoxicity of the
respirable silica particle for a principal lung defender, the alveolar
macrophage. Upon phagocytosis of the silica particle, cell death is
caused by the release of proteolytic and hydrolytic enzymes into
macrophage cytoplasm. The release of these cytoplasmic constitu-
ents, including the still biologically active silica particle and
fibroblast stimulating factor, may then lead to fibrosis (Allison et al.
1966,1977).
As has been noted with other types of pneumoconiosis, silicosis
(and particularly conglomerate silicosis) is associated with a high
prevalence of circulating autoantibodies (ANA and RF) (Jones et al.
1976; Turner-Warwick et al. 1977). Although silica exposure and
particularly silicosis may be associated with rheumatoid arthritis
and several other collagen-vascular diseases, the role of these
antibodies in the etiology, onset, and progression of silicosis is not

339


clear (Parkes 1982). Angiotensin,-converting enzyme (ACE) elevation
has also been reported among silicotics (Gronhagen-Riska 1979;
Nordman et al. 1984). Nordman and colleagues (1984), in a case-
reference study of the Finnish Occupational Diseases Register from
1965 to 1977, reported an association between ACE activity and
progression of silicosis. Smoking, age, and bronchitis .were not
related to ACE activity, which was thought to reflect accumulation
and increased degradation of macrophages. Histocompatibility anti-
gens (HLA) have also been studied as possible genetic risk factors for
silicosis, but with variable results. Koskinen and colleagues (1983)
found that the prevalence of HLA-Awl9 was higher in their Finnish
silicosis patients than in the silica-exposed referent population and
that the highest risk of developing advanced silicosis was associated
with the phenotypic combination Awl9 and B18. However, Sluis-
Cremer and Maier (1984) reported only a decrease in HLA-B40
among 45 South African gold miners. These variable associations are
statistically weak and may be related to the number of statistical
tests performed on the multiple HLA antigens.

The pathogenesis of airways obstruction in silica-exposed workers
is less well understood. Although increased rates of bronchitis and
decreased lung function have been observed in epidemiological
studies comparing silica-exposed and unexposed workers, it appears
that these findings are largely separate from the clinical and
epidemiological picture of silicosis. In the largest and best controlled
study of a reasonably pure silica-exposed sample of 1,973 white gold
miners (Irwig and Rocks 1978), chronic bronchitis was found to be
equally common among those with radiographic evidence of silicosis
and those without. The smoking habits of miners with radiographic
silicosis and of those without silicosis were not significantly different
statistically. Silicotics reported only more days away from work, a
finding the authors suggested may have been as related to their
compensation status as to their disease. Comparison of lung function
between silicotics and their silica-exposed referants revealed equiva-
lent FVC, FEV,, and FEFz~:~~ among silicotics.

Recent pathological evidence of a nonfibrous mineral dust small
airway lesion has been provided by Churg and Wright (1983). This
pathological process, which they labeled mineral dust airways
disease (MDAD), is similar to that produced by tobacco smoke. This
pathological process involves primarily respiratory bronchioles, with
a lesser extension into alveolar ducts. This lesion generally involves
more pigmentation and more thickening of the bronchiole walls than
is typically found in cigarette smokers. In a recent study by Churg
and colleagues (1985) of 13 cases of patients with MDAD, 7 had
occupational histories consistent with a primary silica exposure.
Only 1 of 121 cases without a clear history of dust exposure was
found to have MDAD. Those. with MDAD, matched for age and

340


smoking habit with 13 cases without MDAD, were found to have
significantly poorer lung function, including clinically relevant
lower mean levels of FEVI, FEF25-75~1, and FVC and increased
RV/TLC and AN, per liter as percentages of that predicted. It was
also noted that significantly more membranous and respiratory
bronchiole fibrosis occurred among subjects with MDAD. The
similarity in location, morphology, and physiological impairment
between the pathology induced by mineral dust and that observed
with cigarette smoking suggests that the cellular events giving rise
to them may be similar. Although a good deal is known about the
pathogenesis of the process arising from cigarette smoke (US DHHS
1984), systematic experimental studies of mineral dust airways
disease have not been reported.

Silica Exposure and Cancer

Initial concerns about the association between silica exposure and
cancer arose during the 1930s among investigators in England,
Canada, and South Africa. In the early research on this topic, the
focus was on the proportion of lung cancers arising among autopsied
cases of silicosis compared with that among nonsilicotics or members
of the general public. All of the early research (Dible 1934: Anderson
and Dible 1938; Kennaway and Kennaway 1947; Klotz 1939; Irvine
1939) was characterized by the lack of any data on smoking.

Early assessments of the association between silicosis and lung
cancer were summarized by Hueper (1966). More recently, Hepple-
ston (1985) summarized the autopsy findings from South Africa
(Becker and Chatgidakis 1960; Chatgidakis 19631, from Switzerland
(Ruttner and Heer 19691, and from Germany (Otto and Hinuber
19721, but again no smoking data were presented. The reports from
South Africa and Switzerland showed no differences in the ratio of
lung cancers between silicotics and controls. However, Otto and
Hinuber (1972) showed that porcelain workers with silicosis had
more than twice the proportion of lung cancers as the noncases.
Early studies suggested that silicotics have an increased lung cancer
risk (Dible 1934; Klotz 1939; Mittmann 1959) or that silicotics with
respiratory cancer have greater concentrations of silica in lung
tissue (Anderson and Dible 1938). However, data from Bridge (19381,
Heppleston (19851, Hueper (1966), and Irvine (1939) suggested that
lung cancer risk among silicotics is less than or equal to that of men
without silicosis, regardless of their occupation. In reviewing the
evidence, Hueper (1966) observed that the data support the idea that
lung cancer is a coincidental finding among silicotics and that there
is no etiological relationship.

None of these studies addressed the smoking status of the subjects,
a crucial omission in any study of lung cancer. Furthermore, age was

341


not adjusted, nor were there any quantitative estimates of the silica
exposure or assessments of the severity of the silicotic lesions.

Epidemiologic Studies of Smoking, Silica Exposure,
Silicosis, and Cancer
Silica-Exposed Cohort Studies

Occupational silica dust exposure is common in many industries;
therefore this section is organized so that exposure studies in work
settings that are similar can be examined together, i.e., metal ore
mining, the steel industry, and workplaces where exposures are to
silica only.

Metal Ore Mining

McDonald and colleagues (1978) conducted an enlarged followup
study from 1937 to 1973 of the Homestake Veterans Association
cohort that included 1,321 men with at least 21 years of employment
at the mine. Standardized mortality ratios (SMRs) were calculated
using South Dakota mortality rates as opposed to U.S. rates. The
South Dakota lung cancer rates were lower than those for the United
States as a whole. Using dust exposure data from company midget
impinger samples, the authors examined the pneumoconiosis (mostly
silicosis) and cancer risks in five categories of dustiness, collapsing
them when indicated owing to small numbers. The data showed
striking trends for pneumoconiosis and tuberculosis, but no gradi-
ents emerged for respiratory cancer.

Brown and colleagues (1985) also conducted an assessment of the
Homestake gold miners. The cohort included 3,328 white male
miners employed at least 1 year between 1940 and 1965 and followed
until June 1, 1977. The authors calculated SMRs using person-years
and contrasted mine mortality rates with rates for U.S. white men.
An index of dust exposure by job location was assembled for the
purpose of assessing dose-response gradients. The SMR for malig-
nant neoplasms of the trachea, bronchus, and lung was 100, with no
trends in latency or dust exposure by length of employment.

Katsnelson and Mokronosova (1979) examined the mortality at a
U.S.S.R. gold mine and at several brick plants from 1948 to 1974.
Dust concentrations were not specifically stated for workers in the
gold mine, and an approximation of the SMR (which the authors
termed "relative risk") was calculated to compare the cancer risk
among gold miners with the cancer risk of residents of a nearby town
(excluding those who worked with chromate dusts and adding to the
comparison group those who worked less than 3 years in the plants
under study). The authors reported a relative risk (RR) of 7.9
(p < 0.001) for lung cancer among the male underground gold miners;
without the silicotics, the RR was 3.1 (~~0.02). Surface workers had

342


a nonsignificant RR of 1.6. No lung cancer deaths occurred among
women during these years. No smoking data were presented for gold
mine workers, although data presented for workers at a silica
firebrick plant and an aluminosilicate brick plant indicated that two-
thirds to three-fourths of the men smoked, whereas only 0 to 15
percent of the women did. There appeared to be an inverse gradient
of the proportion of lung cancers by stage of silicosis or silicotubercu-
losis (although no standard classification such as that of Internation-
al Labour Office (1980) is given).

Armstrong and colleagues (1979) followed 1,974 Kalgoorlie gold
miners from Western Australia (whose smoking habits were mea-
sured between 1960 and 1962) for silicosis incidence and mortality
through 1975. Expected death rates were obtained from the age-
specific death rates of Western Australia during 1963-1967, 1968-
1972, and 1972-1976. There were significant (p<O.Ol) mortality
excesses for respiratory cancer (SMR 140) and for pneumoconoisis
and silicosis (SMR 640). The authors compared the cancer risk of the
underground miners and the surface miners and also the association
between silicosis, smoking, and lung cancer. They observed a 40
percent excess of lung cancer among underground workers and a 13
percent excess risk of pulmonary cancer among silicotics (both
nonsignificant). In 1961-1962, the Kalgoorlie miners had a greater
prevalence of smoking (66.3 percent) than either the coal miners
(58.7 percent) or the male residents of Busselton, Australia, in 1966
(53.2 percent) and tended to smoke more cigarettes per day. The
authors stated that the lung cancer risk was probably a function of
the heavier cigarette smoking habits of the miners and that there
was little evidence to link experience underground (and thus
exposure to silica) to lung cancer risk.

Costello (1982) conducted a followup study of 12,258 white "metal
ore" miners who were part of a 1958-1961 U.S. Public Health
Service (US PHS) survey of silicosis and the metal mining industry.
SMRs were calculated using as expected values the 1968 through
1970 white male mortality rates in the 16 States where the mines
were located. The results showed that the cohort as a whole had an
all-causes SMR of 105.9 (p < 0.01); the SMR for cancer of the trachea,
bronchus, and lung was 126.6 (p < O.OOl), and the SMR for pneumoco-
niosis (mostly silicosis) was 343.6 (p<O.OOl). Both digestive tract
cancers and hypertensive heart disease were significantly reduced.
Costello presented several cause-specific and ore-specific SMRs that
were all significant at ~~0.05. Respiratory cancer SMRs were 130.0
among lead zinc miners, 354.6 for mercury miners, and 346.5 for
chromium miners. Highly statistically significant SMRs for pneumo-
coniosis were obtained among copper, lead zinc, molybdenum, and
gold or silver ore miners. In the US PHS 195%1961 survey, 14.5
percent of the metal miners were nonsmokers, 10.9 percent were ex-

343


smokers, 70.5 percent were current smokers, and 37 percent were
pipe and cigar smokers. The smoking status of 0.4 percent was
unknown. Costello argued that on the basis of a relationship between
lung function tests and lung cancer, cigarette smoking was the major
predictor of excess lung cancer in these metal ore miners.

Steel Industry

Gibson and colleagues (1977) conducted a retrospective cohort
study of the Dofasco steel mill workers in Hamilton, Ontario,
Canada, from 1967 to 1976. The authors compared foundry workers
with nonfoundry workers and reported a lung cancer SMR of 250
(p < 0.0005). They used metropolitan Toronto male mortality rates to
calculate expected values. The authors noted that the finishing area
had the highest mean level of total suspended particulates (much of
it silica), respirable particulates, and benzene-soluble fraction of
total suspended particulates. The molding and furnace work areas
had similar industrial hygiene characteristics. No smoking histories
were available for the cohort as a whole. However, 22 of the 24 men
with lung cancers were cigarette smokers. The authors proposed that
smoking and particulate exposure (containing adsorbed organic
material) might be an explanation for the excess lung cancers.

Blot and colleagues (1983) conducted a case-control study of lung
cancer among white men in eastern Pennsylvania to assess the
association with employment in the steel industry. Interviews with
next of kin provided information about residential, occupational, and
smoking histories. The authors demonstrated a smoking-adjusted
odds ratio of 2.2 for usual employment in the steel industry (95
percent confidence interval, 1.5 to 3.3). The odds ratio for lung cancer
was also calculated by smoking category and was significantly
elevated for light smokers and heavy smokers but not for nonsmok-
ers or for moderate smokers.

Workplaces With Exposure to Silica Only

In contrast with workers in the foundry and mining industries,
where silica exposure is most likely to be "contaminated" by
combination with organic foundry fumes or asbestiform materials, or
radon in the case of mining, some workers are exposed to "pure"
silica. These workers are found in several industries, including
ceramics or firebrick manufacture, granite quarrying, or tunnel
digging.

Katsnelson and Mokronosova (1979) examined lung cancer at two
aluminosilicate fireclay plants and at a silica firebrick plant.
Although the firebricks and the fireclay dusts contain high levels of
quartz, no dust samples were collected in the plants. The relative
risk (RR) for lung cancer for the male workers was 4.0 (p < 0.01) and

344


4.5, respectively, at the fireclay plants, and a nonsignificant SMR of
5.1 was reported for the female workers at the first plant. At the
firebrick plants the RR was 2.0 (p < 0.05) for male workers and 0.8 for
the female workers.

Vermont granite workers are exposed to quartz dust with a
concentration of approximately 30 percent free silica. Davis and
colleagues (1983) conducted a proportional morbidity rate (PMR)
study of 969 deceased white granite workers whose x rays were on
file at the Vermont Division of Industrial Hygiene and who had died
between 1952 and 1978. The authors developed a dust exposure
index for the purpose of assessing exposure profiles for their study
subjects. They analyzed the data, excluding tuberculosis and silicosis
after both of these causes of death showed powerful excess disease
risks. Slight excesses for digestive tract, lung, larynx, and prostate
cancers were reported, including a PMR of 1.3 for general respira-
tory cancer (95 percent confidence intervals, 1.0 to 1.6). No apparent
trends emerged relating dust exposure categories with either diges-
tive cancer, respiratory diseases, or lung cancer. Smoking data were
not available for the subjects.

Costello and Graham (19851 conducted a cohort study of 5,414
Vermont granite workers from 1950 to 1982. The authors used the
personnel information on tile in the Occupational Hygiene Division
of the Vermont State Health Department to ascertain date of hire
and date of death. Significant overall excess mortality was observed
for silicosis (SMR 586.6) and tuberculosis (SMR 473.81, but the
excesses were confined to workers hired before 1940. However, no
increased risks were observed for either respiratory system cancer or
lung cancer. The latency time may have been too short to determine
the lung cancer risk among granite workers hired after 1940.
Information was lacking on smoking and dust exposure, and the
Vermont records regarding employees at risk were incomplete.

Selikoff (1978) examined a 932-man cohort of unionized New York
City tunnel workers from 1955 to 1972. These men were exposed to
silicious dusts containing sizable amounts of quartz, schists, and
gneises, but there was little likelihood of exposure to asbestos. There
was an SMR of 495 for pulmonary tuberculosis, an SMR of 160 for
lung cancer, and a gradient in the risk of respiratory cancer
according to the number of years worked. No smoking data were
available, and it is possible that this elevated risk may be a reflection
only of long-term smoking habits and not of silica exposure.

Followup of Silicotics

Westerholm (1980) conducted a followup study from 1931 to 1969
of silicotics from the Swedish Pneumoconiosis Register. For those
whose silicosis arose from employment in mining, quarrying, or
tunneling (MQT) and whose silicosis was diagnosed between 1931

345


and 1948, the lung cancer PMR was 590 (p<O.Ol); for MQT workers
whose silicosis was diagnosed between 1949 and 1969, the PMR was
380 (p<O.Ol). The other significant finding was among workers in
the steel and iron industry (SII) whose silicosis occurred between
1949 and 1969; their PMR was 220 (p <0.05). Westerholm and
colleagues (1985) extended the study from 1961 to 1980 to follow up
712 silicosis cases and 810 noncases from the Swedish silica exposure
registry, matched for age, industry, and occupation. For MQT
workers, the SMR was 538 (p< 0.05) and for SII workers, 385
(p< 0.05). Smoking was not adjusted in the first study, and in the
second, it was indirectly accounted for by the selection of controls
from the same cohort as the silicosis cases.

Finkelstein and colleagues (1982) studied 1,190 Ontario, Canada,
silicotic miners diagnosed between 1940 and 1975. The authors
reported an overall SMR of 198 (p < 0.011, with SMRs of 303 (p < 0.011
and 195 (p < 0.05) for silicotics diagnosed between 1940 and 1949 and
between 1950 and 1959, respectively. No smoking data were collect-
ed.

Schuller and Ruttner (1985) examined the mortality from 1960 to
1978 of 2,399 cases of silicosis in Switzerland. To account for the
sequelae of silicosis isuch as tuberculosis and car pulmonale), the
authors calculated age- and period-specific mortality odds ratios
(MOR). The lung cancer MORs by industry were as follows: miners
229 (p < 0.01); stone workers 118 (p < 0.61; foundrymen 327 (p< 0.001);
others plus ceramic workers 237 (p < 0.05); and ceramic workers 205
(p=O.25). The overall MOR for all Swiss silicotics was 223 (p< 0.05).
The authors noted that smoking is a major cofactor because smokers
have more chest symptoms, thus making silicosis more easily
detected, and because a high proportion of workers in silica-exposed
jobs are smokers, ranging from 60 percent to 85 percent. Because of
the lack of significant lung cancer risk among stone workers with
silicosis (having less confounding exposure to polycyclic aromatic
hydrocarbons than workers in foundries), the authors argued against
silica being a carcinogen, but postulated an interaction of occupation
and smoking. The authors cited the need for cohort studies of
workers in these industries with silica exposure, including detailed
smoking information. An additional question is the relation of lung
cancer risk by degree of silicosis.

Neuberger and colleagues (1985) examined the relative risk for
lung cancer among Austrian silicotics from 1955 to 1979. The overall
risk adjusted for age and sex was 1.4 (p< 0.05). The lung cancer
relative risk increased from 1.31 in the 1955 to 1959 period to 1.42 in
the 1975 to 1979 period. No information was provided on smoking, on
industry-specific risks, or on possible silica exposure levels.
Kurppa and colleagues (1985) examined the subsequent mortality
of 961 cases of silicosis diagnosed in Finland between 1935 and 1977.

346


Using the Finnish male population as a comparison group, they
observed 80 lung cancer deaths instead of the age-adjusted expected
number of 25.6, a SMR of 312 (99 percent confidence interval, 230 to
414). The authors also found SMRs of over 700 for pulmonary disease
and tuberculosis. When the lung cancer risk was examined by
industry, the SMR results were as follows: mining 436 (p<O.Ol);
stone industry 271 (p<O.Ol); steel casting 184; iron foundries 225;
and other industries 343 (p<O.Ol). The authors demonstrated that
the SMRs for each industry showed a 40 percent or more risk
increase (despite small numbers) regardless of whether the silicosis
was diagnosed between 1935 and 1959 or between 1960 and 1977.
The authors did not have smoking data.

Zambon and colleagues (1985) examined a cohort of 1,234 silicotics
from the Veneto region of Italy who were diagnosed from 1959 to
1963, and followed them through 1980. Complete occupational and
smoking histories were available. Overall, the cohort had striking
excesses of infectious disease (tuberculosis) and respiratory disease
(silicosis) mortality, with SMRs of 1,960 and 741, respectively. There
was a significant (p<O.O5) lung cancer SMR of 228 and a nonsignifi-
cant SMR of 206 for cancer of the larynx (based on only seven cases).
There was a gradient of lung cancer risk using years since first silica
exposure as a surrogate for dose (risk did not begin to rise until 20
years after the first exposure). The gradient was maintained across
mining and tunneling industries; tunneling and quarrying industries
had significant overall SMRs of 239 and 569, respectively. The
authors reported that only 13.2 percent of the cohort were nonsmok-
ers and only 3 of 49 deaths occurred in this group; thus, they believed
that the excess mortality was very likely due to smoking.

Research Recommendations

1. Further prospective dose-response studies on chronic bronchi-
tis and airways obstruction assessing silica concentration,
smoking, and airway reactivity should be undertaken.
2. Systematic, well-controlled studies of lung tissue from silica-
exposed workers to assess the pathology and associated impair-
ment of small airways disease should be undertaken.
3. Experimental studies of the interaction of cigarette smoke and
silica dust on the pathogenesis of small airways disease should
be undertaken.

4. The potential for silica to act as a carcinogen alone or in
combination with other exposures should be investigated in
carefully controlled studies that include a detailed examina-
tion of the smoking habits of the participants.
5. Priority should be given to compliance with the current silica
permissible exposure limit.

347


6. Systematic surveillance of silica-exposed populations to docu-
ment silica dose and silica-associated health effects should be
extended by government agencies, unions, and industry.

Summary and Conclusions

1. Silicosis, acute silicosis, mixed-dust silicosis, silicotuberculosis,
and diatomaceous earth pneumoconiosis are causally related to
silica exposure as a sole or principal etiological agent.

2. Epidemiological evidence, based on both cross-sectional and
prospective studies, demonstrates that silica dust is associated
with chronic bronchitis and chronic airways obstruction. Silica
dust and smoking are major risk factors and appear to be
additive in producing chronic bronchitis and chronic airways
obstruction. Most studies indicate that the smoking effect is
stronger than the silica dust effect.

3. Pathological studies describe mineral dust airways disease,
which is morphologically similar to the small airways lesions
caused by cigarette smoking.

4. A number of studies have demonstrated an increased risk of
lung cancer in workers exposed to silica, but few of these
studies have adequately controlled for smoking. Therefore,
while the increased standardized mortality ratios for lung
cancer in these populations suggest the need for further
investigation of a potential carcinogenic effect of silica expo-
sure (particularly in a combined exposure with other possible
carcinogens), the evidence does not currently establish whether
silica exposure increases the risk of developing lung cancer in
man.

5. Smoking control efforts should be an important concomitant of
efforts to reduce the burden of silica-related illness in working
populations.

348


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