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7. INTERACTION BETWEEN SMOKING
AND OCCUPATIONAL EXPOSURES.

National Institute for Occupational Safety and Health


CONTENTS

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..,. . . . . . . . . . . . . . . . . . . . . . . . 5

Illustrative Examples of Different Modes of Action
Between Smoking and Occupational Exposures ............. 5
Tobacco F'roducts May Serve as Vectors by Becoming
  Contaminated with Toxic Agents Found in the
  Workplace, Thus Facilitating Entry of the Agent by
  Inhalation, Ingestion, and/or Skin Absorption ........ 5
Workplace Chemicals May Be Transformed Into More
   Harmful Agents by Smoking.. ............................. 5
Certain Toxic Agents in Tobacco F'roducts and/or
  Smoke May Also Occur in the Workplace, Thus
  Increasing Exposure to the Agent.. ...................... 7
    Hydrogen Cyanide ......................................... 7
     Carbon Monoxide ........................................... 8
    Methylene Chloride ........................................ 8
     Other Chemical Agents.. ................................. 9
Smoking May Contribute to an Effect Comparable to
  That Which Can Result From Exposure to Toxic
  Agents Found in the Workplace, Thus Causing an
   Additive Biological Effect.. ................................. 9
     Coal Dust.. ................................................... 9
     Cotton Dust.. ................................................ 9
     Beta-Radiation .............................................. 10
     Chlorine.. ................................................... .10
   Exposure Among Fire Fighters.. ..................... 10
Smoking May Act Synergistically with Toxic Agents
  Found in the Workplace to Cause a Much More
  Profound Effect Than That Anticipated Simply
  From the Separate Influences of the Agent and
  Smoking Added Together ................................... 11
     Asbestos ...................................................... 11
    Exposures in the Rubber Industry.. ................ .13
     Radon Daughters ......................................... .14
    Exposure in Gold Mining.. ............................ .15
Smoking May Contribute to Accidents in the
  Workplace ....................................................... 15

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Examples Where Action Between Smoking and
Occupational Exposure Has Been Suggested or Only
Hypothesized . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
  Cadmium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
  Chloromethyl Ether . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
Beta-Naphthylamine and Other Aromatic
   Amines . . ., . . . . . . . . . . . . .._.. . . . . . . , . . . . . . . . . . . . . . . . .,. . . . . . 16

Trends in Smoking Habits and in Morbidity and Mortality
Bates for Various Occupational Groups . . . . . . . . . . . . . . . . . . . . . . 1'7

Summary and Recommendations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18
  Recommendations for Research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19


References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

LIST OF FIGURES

Figure 1. -Respiratory cancer rates among uranium
miners by cigarette usage and radiation exposure
compared with rates among nonminers . . . . . . . . . . . . . . . . . . . . . . 14

7-4


Introduction

Despite increasing recognition that both smoking and occupational
exposures contribute independently to the development of certain
disease states, few investigators have addressed the ways in which
these two factors act together to produce disease. Some of the effects
historically attributed to smoking may actually reflect an interaction
between smoking and occupational exposure. This cannot always be
quantified at the present time, but at least six different ways have
been identified in which smoking may act with physical and chemical
agents found in the workplace. These actions are not mutually
exclusive and several may prevail for any given agent.
Six ways in which smoking may act with physical and chemical
agents to produce or increase adverse health effects are:
1. Tobacco products may serve as vectors by becoming contaminated
with toxic agents found in the workplace, thus facilitating entry of the
agent by inhalation, ingestion, and/or skin absorption.
2. Workplace chemicals may be transformed into more harmful
agents by smoking.
3. Certain toxic agents in tobacco products and/or smoke may also
occur in the workplace, thus increasing exposure to the agent.
4. Smoking may contribute to an effect comparable to that which
can result from exposure to toxic agents found in the workplace, thus
causing an additive biological effect.
5. Smoking may act synergistically with toxic agents found in the
workplace to cause a much more profound effect than that anticipated
simply from the separate influences of the agent and smoking added
together.

6. Smoking may contribute to accidents in the workplace.
Exposure to multiple physical and chemical agents in the workplace
can compound these various types of actions.

illustrative Examples of Different Modes of Action Between
gmoklng and Occupational Exposures
Tobacco products may serve as vectors by becoming contaminated
with toxic agents found in the workplace, thus facilitating entry
of the agent by inhalation, ingestion, and/or skin absorption.
Workplace chemicals may be transformed into more harmful
agents by smoking.
Investigations of outbreaks of polymer fume fever provide clear
illustrations of both of these modes of action. Polymer fume fever is a
disease with influenza-like symptoms caused by inhalation of fumes
from heated polytetrafluoroethylene, e.g., Teflon@ (59). Typical
symptoms include chest discomfort, fever, leukocytosis, headache,
chills, muscular aches, and weakness. Since the symptoms are SO
similar to influenza, polymer fume fever may be difficult to diagnose.

7-5


Workers who continue to smoke may experience continuing reexposure
and recurrent symptoms. Although complete recovery has been
reported to occur usually within 12 to 48 hours after exposure is
terminated, an autopsy report has attributed permanent lung damage
to repeated episodes of polymer fume fever (89). Pulmonary edema
following exposure to heated polytetrafluoroethylene has also been
reported (26, 73). Polymer fume fever was first recorded in 1951(38) as
a result of two workers being exposed to the fluorocarbon polymer,
polytetrafluoroethylene, heated to 450-500" C. The particular decompo-
sition product(s) responsible for polymer fume fever have not yet been
identified, but temperatures in excess of 315" C have been sufficient to
cause symptoms. The temperature of the combustion zone of cigarettes
is approximately 875" C (82).

Numerous outbreaks of polymer fume fever among smokers have
been attributed to the decomposition of workplace polytetrafluoroe-
thylene by lit cigarettes and inhalation of the harmful decomposition
products with cigarette smoke. One report (18) describes aviation
employees whose work involved contact with door seals that had been
sprayed with an unspecified fluorocarbon polymer. In one case, a
worker smoking during a break realized by the taste of his cigarette
that it had become contaminated. Although the worker extinguished'
the cigarette, he experienced shivering and chills, which lasted
approximately 6 hours, beginning l/2 hour after this incident. Another
illustrative report (12) describes outbreaks of polymer fume fever
among workers who smoked when their hands were contaminated with
polytetrafluoroethylene used as a mold release agent. There was no
recurrence of symptoms after smoking at the plant was prohibited. An
outbreak of polymer fume fever among workers using liquid fluorocar-
bon polymer in the production of imitation crushed velvet was likewise
attributed to decomposition of fluorocarbon polymer by lit cigarettes
(85). Processing temperatures at this plant were too low to pyrolyze the
polymer. The seven affected workers were all cigarette smokers,
whereas most of the workers without symptoms were nonsmokers.
After work practices were changed to prohibit smoking in the work
area and to require hand washing before smoking, no further
symptoms at this facility were reported. Other outbreaks of polymer
fume fever attributed to cigarette smoking have also been reported (I,
11, 44, 76 90).

The effects of smoking cigarettes contaminated with known
amounts of tetrafluoroethylene polymer have been studied with the
assistance of human volunteers (22). Nine out of ten subjects were
reported to exhibit typical polymer fume fever symptoms after each
had smoked just one cigarette contaminated with 0.46 mg tetrafluoro-
ethylene polymer. Onset of symptoms ranged from 1 to 3.5 hours after
smoking; recovery time averaged 9 hours.

7-6


With respect, to tobacco products serving as vectors, the National
Institute for Occupational Safety and Health (NIOSH) has thus far
identified the following agents as potential occupational contaminants
of tobacco and tobacco products:

Agent
Formaldehyde (61)
Boron Trifluoride (57)

Organotin (66)
Methyl Parathion (65)

Dinitro-otiho-Creosol (60)

Carbaryl (58)
Inorganic Fluorides (63)
Inorganic Mercury (64)

Lead (81, 94)

&fajor Health &jFfecf.s
Respiratory irritant, dermatitis
Respiratory irritant, joint dis-
&iSC?
Respiratory irritant
Reduced erythrocyte cholinester-
ase activity
Kidney damage, peripheral neu-
ritis, CNS disturbances.
Inhibition of acetylcholinesterase
Fluoride osteosclerosis
CNS disturbances, kidney dam-
age, peripheral neuritis
Servous system toxin, renal
toxin, changes in hematopoiet-
ic system

Additional research is clearly warranted to identify other workplace
chemicals which are transformed into more toxic agents by tobacco
smoking.

Certain toxic agents in tobacco products and/or smoke may also
occur in the workplace, thus increasing exposure to the agent.
Hydrogen Cyanide

Hydrogen cyanide has been found in cigarette smoke at concentrations
as high as 1,600 ppm (83). In 1973 Pettigrew and Fell (69) found the
plasma thiocyanate (a metabolite of cyanide) levels of smokers
significantly elevated as compared to those in nonsmokers. In 1973
Radojicic (71) reported a study of 43 workers in the electroplating
division of an electronics firm in Nes, Yugoslavia. He found that the
majority of workers exposed to cyanide complained of fatigue,
headache, asthenia, tremors of the hands and feet, and pain and
nausea. The urinary thiocyanate concentrations of the exposed group
of workers were higher at the end of the work shift than before
exposure at work. Urinary thiocyanate concentrations were signifi-
cantly higher among exposed smokers than unexposed smoking
controls, significantly higher among exposed nonsmokers than unex-
posed nonsmokers, and significantly higher among exposed smokers
than among exposed nonsmokers. These findings demonstrate that
smoking and occupational exposure can each contribute to a worker's
total exposure to and intake of cyanide.

7-7


Adverse effects from cyanide may occur from sublethal doses.
Hydrogen cyanide and cyanide salts inhibit cytochrome oxidase.
Cyanide can form complexes with heavy metal ions. Formations of
these complexes in the body can rapidly cause disturbances in enzyme
systems in which heavy metals act as co-factors either alone or as part
of organic molecules (2, 15, 27). Thiocyanate itself has toxic effects,
especially inhibition of uptake of inorganic iodide into the thyroid
gland for incorporation into thyroxin (91). The National Institute for
Occupational Safety and Health has estimated that over 20,000
workers in 75 different occupational groups have potential occupation-
al exposure to cyanide (62).

Cigarette smoking causes increased exposure to carbon monoxide (CO).
A CO concentration of 4 percent (40,000 ppm) in cigarette smoke leads
to an alveolar CO concentration of 0.04 to 0.05 percent (400 to 500
ppm), which produces a carboxyhemoglobin (COHb) concentration of 3
to 10 percent (21, 40, 68). Goldsmith, et al. (29) estimated that the
cigarette smoker is exposed to 475 ppm CO for approximately 6
minutes per cigarette.

In a study of COHb levels in British steelworkers, Jones and Walters
(39) found a 4.9 percent end of shift COHb saturation in nonsmoking
blast furnace workers compared to 1.5 percent saturation in non-
smoking unexposed controls. For heavy cigarette smokers, the levels
were 7.4 percent for blast furnace workers and 4.0 percent for smoking
unexposed controls. The COHb levels of blast furnace workers who
smoked were in a critical range. Studies by Aronow (5-g), Anderson (3),
and Horvat (36) and their associates have shown that levels of COHb in
excess of 5 percent can cause cardiovascular alterations which are
dangerous for persons with cardiovascular disease.

Potential occupational exposure to CO is common (37). Since a
significant number of workers have coronary heart disease and many
smoke, additional occupational exposure to CO may increase eardiovas-
cular morbidity and mortality.

Methylene Chloride

Methylene chloride is metabolized to CO in the body (28). COHb levels
in blood increase with increasing environmental concentrations of
methylene chloride as well as with increasing physical activity at the
time of exposure (10, 80). Maximum COHb levels occur 3 to 4 hours
after exposure is discontinued.

Mean methylene chloride concentrations of 778 ppm over a 3-hour
exposure period produced a maximum COHb level of 9.1 percent 4
hours after exposure was discontinued. Twenty hours after this

7-8


exposure the COHb level remained elevated (4.4 percent versus 0.8
percent prior to exposure) (80).

Baaed on this time lag, prohibiting a worker exposed to methylene
chloride from smoking on the job would not be sufficient to protect the
worker who smokes after he leaves work from the additive burdens of
CO from methylene chloride and tobacco smoke.

Other Chemical Agents

Other chemical agents found in tobacco, or in the combustion of
tobacco products, and also.potentially found in the workplace include:
acetone, acrolein, aldehydes, arsenic, cadmium, formaldehyde, hydro-
gen sulfide, ketones, lead, methyl nitrite, nicotine, nitrogen dioxide,
phenol, and polycyclic compounds (83).

Smoking may contribute to an effect comparable to that which
can result from exposure to toxic agents found in the workplace,
thus causing an additive biological effect.
Coal Dust

Coal dust and cigarette smoking appear to act in an additive fashion to
produce obstructive airway disease. Although dust exposure alone
plays a significant role in the development of this disease, there is a
significantly higher prevalence of obstructive airway disease in
smoking miners than in nonsmoking miners with the same dust
exposure (41). Flow volume curve data suggest that nonsmoking
miners with dust-induced chronic obstructive airway disease have
decreased flow rates primarily at higher lung volumes, whereas
smoking miners have decreased flow rates at all lung volumes (32).

cotton Dust

Many investigators have noted that among cotton workers, cigarette
smokers show increased prevalence of byssinosis when compared to
nonsmoking cotton workers (13, 53, 54, 55). Cotton dust inhalation
produces an acute clinical syndrome consisting of chest tightness,
cough, and shortness of breath in cotton workers (34). This was
formerly known as "Monday morning fever" since symptoms develop
on the first day of work after an absence. The clinical syndrome may
be accompanied by significant reduction in pulmonary function (52).
The acute clinical and functional abnormalities produced by cotton
dust gradually become more frequent as the disease progresses,
eventually resulting in chronic obstructive airways disease (34).

In the acute phase of the illness there is a significantly greater
diminution in pulmonary function in smokers than in nonsmokers (55),
and the relationship of cotton dust and smoking to pulmonary
dysfunction appears to be additive.

7-9


In the more severe phave of chronic obstructive airway disease, the
relationship between smoking and cotton dust exposure appears to be
synergistic (5.5).

Beta-Radiatim

In studies in mice when both beta-radiation and cigarette tar were
applied to produce carcinomas in the skin, cancers appeared 6 to 7
months earlier than when radiation was administered alone. The
shortened latent period gave an illusion of synergism which was
reported in a preliminary analysis based on tumor yield at 18 months.
However, at the conclusion of the experiment, the authors felt there
was actually nothing more than an additive biological effect of
cigarette tar and beta-radiation (23).

Chlorine

Exposure to chlorine and cigarette smoke may cause an additive
biological effect. Chester, et al. (20) examined 139 men in a plant
producing chlorine and sodium hydroxide by electrolysis of brine. Of
the 139 workers, 55 had been accidentally exposed one or more times to
chlorine at high concentrations and had required oxygen therapy at
least once during their employment. The maximal mid-expiratory flow
(MMF) values of workers with accidental chlorine exposure was
compared with those of nonexposed workers for smokers and
nonsmokers. A significant difference in MMF was seen when chlorine
and smoking were considered as additive@xic agents. MMF values
decrease in the sequence from unexposed nonsmokers (4.36) to
unexposed smokers (4.13) to exposed nonsmokers (4.10) and to exposed
smokers (3.57).

Capodaglio, et al. (19) studied the diffusing capacity of the lung in
workers employed in a plant for electrolytic production of chlorine and
soda. He compared 52 exposed workers to 2'7 unexposed workers. The
diffusing capacity of the lung was significantly lower in exposed
smokers than in nonexposed smokers (P<O.OZ), lower in exposed
smokers than in exposed nonsmokers, and lower in exposed smokers
than in unesposed nonsmokers (P <ON.

These studies show the additive effects of cigarette smoking and
chlorine exposure.

Exposwe d trwng Fire Fighters
A study of the prevalence rates of chronic nonspecific respiratory
disease among 2.000 Boston fire fighters showed a contribution from
both occupation and smoking (77). Rates of chronic nonspecific
respiratory disease in young fire fighters increased with amount
smoked: however, new fire fighters had lower rates for all smoking
categories than experienced fire fighters. The experienced fire fighter

7-10


who was a light or nonsmoker had more than a threefold higher rate of
chronic nonspecific respiratory disease than the new fire fighter in the
same smoking category.

Smoking may act synergestically with toxic agents found in the
workplace to cause a much more profound effect than that
anticipated simply from the separate influences of the agent and
smoking added together.
Asbestos

Asbestos provides one of the most dramatic examples of adverse health
effects resulting from interaction between the smoking of tobacco
products and an agent used in the workplace. Asbestos, the generic
term used to describe chain-silicates, was first used in Finland to
strengthen clay pottery about 2500 B.C. (79). Modern industrial use of
asbestos is relatively more recent, dating from 1880 when it was used
to make heat- and acid-resistant fabrics (35, 72). From that beginning
its usefulness has grown immensely, output having increased over one
thousandfold in the past 69 years (79).
With increasing industrial importance has come an increasing
awareness of the adverse health consequences incurred by working
with asbestos. Asbestosis was first reported early in the twentieth
century, and subsequent individual observations and epidemiological
studies have well defined the association of this nonmalignant
respiratory disease with asbestos exposure.`In 1935 Lynch and Smith
reported a suspected association between asbestosis and lung cancer
(49). Succeeding epidemiological studies have given significant support
to these early reports.
In 1968 a prospective study of insulation workers by Selikoff, et al.

(75) defined cigarette smoking as an additional hazard to the health of
workers exposed to asbestos. In a study of 370 asbestos insulation
workers, 1963-196'7, Selikoff found that of 87 men with no his&y of
cigarette smoking, none died of bronchogenic carcinoma, while 24 of
283 cigarette smokers did die of that disease. This study suggested that
@btoS workers who smoke have 8 times the lung cancer risk of all
other smokers and 92 times the risk of nonsmokers not esposed to

ahe&os. This same group of insulation workers was restudied 5 years
later (92). At that time 41 of the 283 smokers had died of bronchogenic
caner. In a larger prospective study involving 11,656 insulation
workers in the United States and Canada, 134 deaths due to lung
*Lncer were found among 9,591 men with a history of regular cigarette
smoking (31). Of the 2,066 noncigarette smokers followed over the
same &year period, only two deaths were due to lung cancer.

Over a lo-year period, Berry, et al. (14) studied 1,300 male and 480
female asbestos factory workers in whom a smoking history was
known. The male and female groups were then evaluated on whether
they had low to moderate or high asbestos exposure. Thp rc+lJnrchers


found no significant excess deaths from lung cancer in either smoking
or nonsmoking groups at low to moderate exposures. However, a
highly significant increase in lung cancer deaths was seen in the
severely exposed who also smoked.

The above mentioned studies and other similar studies have shown
that cigarette smoking and asbestos exposure together are associated
with extremely high rates of lung cancer. But what role does each play
in this process? Two general hypotheses have been proposed to answer
this question (14). The additive hypothesis suggests that asbestos
exposure and cigarette smoking act independently to produce lung
cancer and that the excess risk seen when both are experienced
together is due to the sum of their risks. The multiplicative
(synergistic) hypothesis contends that each of the involved risk factors
has a certain value for its risk and that the product of these two risks
(asbestos exposure x cigarette smoking) describes how they work
together to bring about a certain result (lung cancer). Selikoff's data
suggest a synergistic effect. However, in the study by Berry, et al. (I,$),
the male data do not fit either hypothesis while the female data easily
support the multiplicative hypothesis. A more recent study by
Martischnig, et al. (50) of 201 men with confirmed bronchial carcinoma
was much less consistent with the multiplicative hypothesis and
pointed more closely to the additive hypothesis. However, the smoking
histories were obtained retrospectively, smoking-specific estimates
were not available, and the data are difficult to interpret. Regardless
of whether the action is additive or synergistic, a substantial risk faces
smokers who are exposed to asbestos. The extraordinary increase in
lung cancer resulting from the interaction of cigarette smoking and
asbestos exposure has led the Johns-Manville Corporation to ban
smoking in its asbestos plants (38).

Other neoplasms have been associated with exposure to asbestos but
appear to be independent of smoking habits. Eighty-five to ninety
percent of mesothelioma has been attributed to exposure to asbestos
(84). The relationship of pleural and peritoneal mesothelioma to
smoking and asbestos exposure was investigated by Hammond and
Selikoff (91). Calculations from their studies reveal 0.38 deaths from
pleural mesothelioma per 1,000 man years of observation among
asbestos-exposed cigarette smokers and 0.39 for exposed nonsmokers.
Rates for peritoneal mesothelioma were 0.73 for smokers and 0.33 for
nonsmokers (74). On the other hand, esophageal cancer rates were
significantly increased, but only among smokers. Rates for stomach
and colon cancer showed no such restriction (31, 75).

In 1971 Weiss (87) explored the relationship of asbestosis to cigarette
smoking. He examined 100 asbestos textile workers by chest X-ray and
questionnaire. Pulmonary fibrosis was found in 40 percent of 75
workers who smoked and 24 percent of 25 nonsmokers. Weiss
determined that age, sex, and duration of exposure to asbestos were

T-12


not responsible for the difference noted. Seventy-three of the above
cigarette smokers were then questioned concerning amount and
duration of smoking. The prevalence of fibrosis was 23 percent of 13
workers who smoked less than one pack per day and 43 percent of 60
who smoked one or more packs per day. Of 18 workers who smoked a
pack or more per day for less than 20 years and had less than 20 years
of asbestos exposure, 28 percent had fibrosis. Of 19 workers who
smoked more than 20 years and with more than 20 years of exposure to
asbestos, 74 percent had fibrosis. This study suggested that the
prevalence of pulmonary fibrosis increases with an increasing amount
and duration of cigarette smoking as well as with an increasing
duration of exposure to asbestos. Due to the small size of the observed
group, Weiss was unable to determine whether cigarette smoking and
asbestos exposure were working in an additive or multiplicative
manner. A study recently published by Weiss and Theodos indicates
that type of asbestos as well as smoking habits are factors in the
development of pleuropulmonary disease in asbestos workers (88).

In summary, workers exposed to tobacco smoke and asbestos
experience far greater levels of lung cancer than would be expected
from the contribution of either tobacco smoke or asbestos alone.
However, other adverse health effects of occupational exposure to
asbestos (for example, mesothelioma) appear to be independent of
smoking habits. Thus, smoking varies in its contribution to the
development of different adverse health effects resulting from
occupational exposure to a particular occupational agent.

Exposures in the Rubber Inohstry

In a study of rubber workers, Lednar, et al. (47') reported that smokers
exposed to fumes and dust, particularly talc and carbon black, had a
significantly higher risk of developing a pulmonary disability than did
nonsmokers. The combination of smoking and occupational exposure
significantly elevated the probability of developing an early pulmonary
disability. The authors reported that a rubber worker exposed to dust
and smoking was associated with 10 to 12 times the risk of pulmonary
disability retirement compared to the risk of a nonsmoking, nonoccupa-
tionally-exposed rubber worker. This elevated risk was found where
there were exposures to respirable particulates and/or solvents. This
study suggests that smoking and occupational exposures in the rubber
industry are synergistic since the authors report that a rubber worker
who smoked and was exposed to talc had an excess relative risk of 3.40,
whereas an excess relative risk of 1.77 would be expected if the effects
of smoking and work exposure were additive. The mechanism of this
interaction is not yet understood.

7-13


FIGURE l.-Respiratory cancer rates among uranium miners by
cigarette usage and radiation exposure compared with rates among
nonminers
SOURCE: Archer, Y.E. (4).

Radon Darqhfers

A substantial excess of lung cancer, reduced pulmonary function, and
emphysema has been reported among uranium miners (48). The excess
has been attributed primarily to irradiation of the tracheobronchial
epithelium by al&~ particles emitted during the decay of radon (Rn)
and its daughter products. In a study of uranium miners, Archer, et al.
(4) found that respiratory cancer rates among smoking and non-
smoking uranium miners were six to nine times greater than among
nonminers with similar smoking habits. The lung cancer rate for
nonsmoking uranium miners was 7.1 per 10,000 person years compared
to 1.1 for nonminers who did not smoke. The lung cancer rate for
uranium miners who smoked was 42.2 per 10,000 person years
compared to 4.4 for nonminers who smoked two or more packs of
cigarettes a day (Figure 1). There was also a definite association
between the prevalence of emphysema and the cumulative amount of
cigarettes smoked, as well as with accumulative radiation exposure.

7-14


Smoking may contribute to accidents in the workplace.
In a g-month study of jot) accidents, lb.. ifbLa! ;lcci~i~nt ra!c W:LS more
than twice as high among smokers as atn~ng ncitljrnohers I ~1. Other
authors have suggested Lhar injurie: ;.~~trihttifh. XI smoking were
caused by loss of attention, ~>rectit~~;~)at.i*:~ iti ! he, h:d for smoking,
irritation of the eyes, and cough !/;:i.

Smoking can also contribute to fire ant1 cxlda4ons in occupational
settings where inflamma% and t>sltLisive c&mical ag<!ntd are used. In
many of these areas smoking is pmhibitecl. For esample. smoking is
not permitted in coal mines and miners arc' (X!rs~Jrd\ :`ineti if found in
violation of this provision.

Examples where action between smoking and occupetionnl
exposure has been suggested or only hypothesized
Gzd nt'u nt

several studies of the effects of c~cupational exposure 10 ixlmium on
smokers and nonsmokc:1~s cla\-c lcc'ti msluctv~i i&J .:ci. ii;. 51. 70).
Pulmonary function is poorer in smoke* :han in nonsmokers cspo.4
to cadmium, and smokers al.~o had LL hig!lcr incitlencc: ul' i)roteir.uria
than did nonsmokers in a cadmium-espo+cd popiation in a Swedish
battery factory. An additive rather than a poxntiating effect seems
more likely from the limited data.


degree of exposure to chloromethyl ether and an exposure index was
calculated for each man by cumulating the total exposure.

Chronic cough and expectoration showed a dose-response relation-
ship to chemical exposure. Chronic cough was also related to smoking,
but for each smoking category chronic cough was more common for
exposed than for unexposed men.

The l&year incidence of lung cancer was dose-related to chemical
exposure but not to cigarette smoking. All cancers were small cell
carcinomas, occurred in men younger than 55, and had an induction-
latent period of 10 to 24 years. The lo-year mortality rate in this group
of workers was 2.7 times that expected, and lung cancer accounted for
the excess number of deaths.

Bronchogenic carcinomas linked to cigarette smoking are most often
squamous cell in type with long induction-latent periods and, in the
absence of occupational agents, tend to recur after the age of 60. The
cancers which tend to occur in workers exposed to chloromethyl ether
are small cell in type, have short induction-latent periods, and tend to
appear before the age of 55. The absence of a relationship between
cigarette smoking and lung cancer in this study may be due to the
competing effect of chloromethyl ether which results in lung cancer in
exposed workers before the long-term carcinogenic effect of cigarette
smoking could be demonstrated. However, cough related to cigarette
smoking appears earlier in exposed workers, thus demonstrating the
action of cigarette smoking with exposure to chloromethyl ether in the
development of chronic cough symptoms. This case study also points up
the complex issues involved in understanding the actions between
smoking and occupational exposures.

Beta-Naphthylamine and Other Aromatic Amines

Doll, et al. found an excess risk of bladder cancer in a series of studies
(2~~2.9 of men employed in coal gas production in England and Wales.
Most of the gas workers were smokers. Chemical studies showed that
inside the retort houses gas workers inhaled beta-naphthylamine and
other aromatic amines (known bladder carcinogens). Since aromatic
amines are also found in cigarette smoke (83), the gas workers who
smoked received exposure to bladder carcinogens from two sources.
This evidence is difficult to interpret at the present time. There are
reports of associations between cigarette smoking and bladder cancer
(30,92); however, occupational exposures were generally not controlled
in these studies. There is a need to assess further the action between
smoking and exposure to aromatic amines.

7-16


Trends in Smoking Habits and in Morbidity and Mortality Rates
tor Various Occupational Groups

Surveys (56) have shown that male blue-collar workers are much more
likely to smoke cigarettes than white-collar workers. While in 1970
only 3'7 percent of white-collar workers were reported to be current
smokers, 51 percent of those in blue-collar occupations smoked. Also,
more ex-smokers are found among white-collar workers than among
blue-collar workers (35 percent and 23 percent respectively). Smoking
among white-collar workers dropped from 43 to 37 percent between
1966 and 1970; during the same time period smoking among blue-collar
workers dropped from 62 percent to 51 percent.

The pattern among female employees is quite different (56). There
was little difference in smoking rates between white- and blue-collar
female workers, 36 and 33 percent respectively, in 1970. In addition,
the smoking rates for 1966 were the same as those for 1970 in both
groups of female workers. During the period studied, the increased
cessation of smoking among female workers was offset by the
increased initiation of smoking in the same group.

In a study by Boucot, et al. (16), I.21 new lung cancers developed
among 6,136 men aged 45 and older who volunteered to report
semiannually for chest X-ray J and answer questionnaires about
symptoms, smoking habits, and so forth, over a lo-year period
beginning in 1951. The risk of developing lung cancer increased with
increasing age, was higher in nonwhites than in whites, and bore a
dose-response relationship to cigarette smoking. The highest lung
cancer risk was among asbestos workers, 42.9/1000 man-years (crude
rate). The risk was 2.2/1000 man-years (crude rate) for men in
occupational categories not thought to be associated with an increased
risk of lung cancer. When adjusted for age, race, and smoking, these
rates were respectively 23.0/1000 and 1.4/1000 man-years. Occupation-
al categories showing somewhat increased risk were metal workers,
cooks, and automobile drivers. A higher percentage of nonwhites (226
percent) than whites (13.5 percent) worked in occupations thought to
be at increased lung cancer risk. The excess lung cancer rate in
nonwhite males could not be attributed to smoking.
The smoking habits in various occupational groups demonstrate
ample opportunity for interaction between cigarette smoking and
physical and chemical agents in the workplace. In general, those who
have the highest smoking rates also have the highest risk for industrial
exposures. Both the consumption of tobacco products and exposure to
industrial agents increased steadily from 1920 to 1960. This is reflected
in certain mortality trends. For example, the United States age-
adjusted mortality rate from carcinoma of the pancreas has been
reported to have risen from 2.9 to 8.2 per 100,000 population from 1920
to 1965, an increment of 233 percent. The rise was found to be real and
threefold in magnitude when adjustments were made for the aging of

7-17


the population. A literature review on pancreatic'cancer was conducted
by Krain to help identify real causes or associations for pancreatic
cancer. His report indicated th;tL only the data on industrial carcinogen
esposurc and cigarette smoking show both the trend and the statistical
magni tudc of association to consider them as real causes or associations
i $3).

Since 1966 the consumption of tobacco products has decreased in
blue-cohar workers whi!e the number of industrial exposures has
continued to increase (f7, i6j. The increasingly higher rates of lung
cancer in nonwhite males, independent of smoking habits, may reflect
the late entry of nonwhites into industrial settings and the fact that
they hare jobs with higher risk for occupational exposure to toxic
agents.

Summary and Recommendations

Although precise relationships betKeen smoking and occupational
exposures cannot always` be quantified, the necessary data are
beginning to accumulate.

From 1920 to 1966 tobacco consumption increased as did the
introduction into the workplace of chemicals with unstudied biologic
effects.. Workers with the greatest risk of exposure to industrial agents
in many cases had the highest smoking rates. Since 1966 the
consumption of tobacco produc+a has decreased in male blue-collar
workers `while the introduction of new `cheinicals into the workplace
has continued to increase.

At !east six different ways have been illustrated by which smoking
may act with physical and chemical agents in the workplace to produce
or increase adverse health effects. These actions need not be mutually
esclusive, and exposure to multiple physical and chemical agents in the
workplace can compound these various types of actions.

The examples of the interactions between the smoking of tobacco
products and industrial esposures cited in this report indicate that a
curtailment of smoking in certain occupational settings would
contribute to the rculuction of specific disease processes. The National
Institute for Occupational Safety and Health has .therefore recom-
mended in certain circumstances that workers exposed to particular
agents refrain from smoking. However. it is important to note that in
some situations (for csample, radon daughters and chloromethyl ether)
the contribution of occupational esposurcs to adverse health effects,
was greater than the contribution of cigarette smoking. Therefore,`the
curtailment of smoking in the workplace should be accompanied by
simultaneous control of occupational exposures to toxic physical and
chemical agents. Both are needed!

7-18


Recommendations for Research
1. Studies on the health effects of smoking should take occupational
exposures into consideration and \-ice versa. Wheneser possible, studies
should include data on nonsmoking workers as we!1 as unexposed
smoking and nonsmoking controls.
2. The increasing rates of lung cancer in nc)n\t-bite males compared to
white males should be investigated further with reqec: to iiccupation-
al exposures and smoking habits.
3. The change in smoking habits of blue-cctllar workers over the last
decade provides an opportunity to assess more critically the contribu-
tion of smoking versus occlupational ~qmurct to certain di+easse states.
Cohorts should be identified and followed prospectively for this
purpose.
4. Workplace agents which interact with the smoking of tobacco to
produce adverse health effectj should 1~' identified.
5. Investigation of the mechanisms of synergism between smoking
and occupational exposures is needed.
6. The impact of the combination of smoking and workplace
exposures upon reproductive experience merits further study.
`7. The impact of smoking in the workplace upon accidents merits
further study.
8. The lack of information on the effecrof sidestream smoke in the
development of occupational disease in nonsmoking workers merits
attention.
9. The effects of cessation of smoking upon lung cancer risk among
those occupationally exposed to toxic workplace agents requires
investigation.


Interaction Between Smokind and Occupational Exposures:
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