TABLE 7. - Means of the numerical values given lung sections at autopsy
    of male former cigarette smokers, standardized for age

  Formerly Smoked


Number of Subjects
Emphysema
Fibrosis
Thickening or arterioles
Thickening of arteries

stopped 2 10 yr.        stopped < 10 yr.


<l Pk.         Pk.      <I Pk.        Pk.


35          66        51          131
0.24         0.70       1.08         1.69
1.14         1.74      2.44        3.30
0.57         0.93       1.25         1.59
0.04        0.16      0.36        0.61

NOTE. - Numerical values for each finding were determined by rating each lung section on
    scales of O-4 for emphysema and thickening of the arterioles, O-7 for fibrosis,
     and O-3 for thickening of the arteries.
Source: Auerbach, O., et al. (2).

bronchiolitis associated with clusters of pigmented alveolar macro-
phages in the lungs of smokers. They found these changes only rarely
in the lungs of nonsmokers (Fig. 1). The smokers were young
(average age 25.7 years), were a heavy smoking population (average
20.1 pack years), but did not differ significantly from the non-
smokers in age, social class, or pollution exposure. However, 12 of
the 19 smokers had had productive cough or frequent cold compared
to only 3 of the 20 nonsmokers. These authors postulated that
bronchiolitis may be responsible for the abnormalities in the tests of
small airway function of smokers.

Pathophysiologic Studies in Humans

  Yeager, et al. (48) showed decreased pinocytosis in human
alveolar macrophages obtained from asymptomatic cigarette smoking
volunteers when compared to those obtained from nonsmoking
controls.

  Warr and Martin (46) studied alveolar macrophages lavaged
from four healthy smokers and four healthy nonsmokers. Only two
members of each group were reactive to delayed hypersensitivity skin
tests for Candida albicans. Macrophages from nonsmokers responded
to Migration Inhibitory Factor (MIF) by a depression in migration of
at least 30 percent, whereas macrophages from smokers did not
respond to MIF. The cells from smokers were noted to migrate three
times faster than those from nonsmokers. When Candida antigen was
added to the medium, cells from the nonreactive subjects (both

76


FIGURE l.-Respiratory bronchiolitis in smokers and control group

c               1
5-         . .    I  . . . . . . . .
                 . . . . . . . .
      t


4,         .    I    . .

                I
       I
3-         .  ? o
       ?

2,      t
             I
      I

l-         o  ?
             ?
       ?

         ? ? ? ? ? ? ?  ?
        ? ? ? ? ? ? ? ?  ?
                ?

NONSMOKERS     SMOKERS

NOTE.-The position of each symbol represents the number of sections
per case in which bronchiolitis was identified.
Source: Niewoehner. D.E., et al. (24).

smokers and nonsmokers) were not inhibited, the cells from the
reactive nonsmokers were inhibited, but the cells from reactive
smokers were not inhibited. Thus, macrophages from smokers did
not respond normally to either MIF or antigenic challenge.

Pathophysiologic Studies in Animals

  Roszman and Rogers (27) noted that either the nicotine or the
water soluble fraction of whole cigarettes smoked suppressed the
immunoglobulin response of lymphoid cell cultures. When concentra-
tions of over 200 micrograms per milliliter of nicotine of the water
soluble fraction were added, they were able to completely suppress
the immunoglobulin response and to observe this suppression even in
cells exposed for 2 hours prior to the antigenic challenge.

  Guinea pigs (29) exposed to the smoke of five cigarettes and
then lavaged 2 hours later had fewer pulmonary macrophages and
leukocytes in the lavage fluid than did controls not exposed to
smoke. The decrease in the number of macrophages was highly
correlated with acetaldehyde, tar, nicotine, hydrogen cyanide, and

77


acrolein concentrations in the cigarette smoke. The decrease in the
number of leukocytes was more closely correlated with pH of the
particulate phase and concentrations of acetaldehyde and tar.

  Tracheal mucous velocity has been shown to be decreased in
purebred beagle dogs (45) exposed to 100 cigarettes per week for
13.5 months. In donkeys (I) low level exposure to whole cigarette
smoke accelerated tracheobronchial clearance, whereas at inter-
mediate and high levels of exposure, clearance was decreased. At high
exposure levels whole cigarette smoke had twice the effect of filtered
smoke in decreasing clearance.

SUMMARY OF RECENT BRONCHOPULMONARY FINDINGS

  1. Cigarette smokers with mild viral respiratory illnesses have
been shown to develop abnormal but reversible changes in certain
pulmonary function tests while nonsmokers show no changes in
these tests. Cigarette smokers have also been shown to have a
significantly longer duration of respiratory symptoms following mild
viral illness than nonsmokers.

  2. Cigarette smoking is more closely related to COPD than is air
pollution under the conditions of air pollution encountered by the
average person. The possibility remains that the two kinds of
exposure may interact to increase the total effect beyond that
contributed by each exposure.

  3. Cigarette smokers without respiratory symptoms have evi-
dence of small airway dysfunction (elevated closing volumes) more
frequently than do nonsmokers without respiratory symptoms.

  4. Autopsy studies have shown a dose-response relationship
between cigarette smoking and the microscopic changes of COPD.
Data from one study indicate that bronchiolitis may be a far more
common finding in cigarette smokers than in nonsmokers.

  5. Pulmonary macrophages from cigarette smokers' lungs have
a decreased ability to respond to in vitro antigenic stimuli as
compared to macrophages from smokers.

78


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81


42 U.S.

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82


CHAPTER 4.
Involuntary Smoking


CHAPTER 4
Involuntary Smoking

Contents

Page

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87

Constituents of Tobacco Smoke  .............................  88
   Carbon Monoxide ...................................  90
   Nicotine  .........................................  97
   Other Substances  ...................................  98

Effects of Exposure to Cigarette Smoke  ........................  98
  Cardiovascular Effects of Involuntary Smoking  ...............  98
  Effects of Carbon Monoxide on Psychomotor Tests  ............  99
  Pathologic Effects of Exposure to Cigarette Smoke .............  99

Summary of Involuntary Smoking Findings .....................  108

Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  109


List of Tables

Table I .-Comparison of mainstream and sidestream            Page
  cigarette smoke . . . _ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89

Table 2.-Measurements of constituents released by
  the combustion of tobacco products in various
  situations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91-94

Table 3.-Median percent carboxyhemoglobin (COHb)
  saturation and 90 percent range for nonsmoker
  by location _ . . _ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96

Table 4.-Effects of carbon monoxide on psychomotor
  functions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  100-101

Table 5.-Admission rates (per 100 infants) by
  diagnosis, birth weight, and maternal
  smoking . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ...104

Table 6.-Pneumonia and bronchitis in the first
  5 years of life by parents' smoking habit
  and morning phlegm . . . . . . . . . . . . . . . . . . . . . . . . . _ . . . . 106


INTRODUCTION

  The effects of smoking on the smoker have been extensively
studied, but the effects of tobacco smoke on nonsmokers have
received much less attention. The 1972 Health Consequences of
Smoking (49) reviewed the effects of public exposure to the air
pollution resulting from tobacco smoke. This exposure has been
called "passive smoking" by many authors, but will be referred to in
this report as "Involuntary Smoking." The term involuntary smoking
will be used to mean the inhalation of tobacco combustion products
from smoke-filled atmospheres by the nonsmoker. This type of
exposure is, in a sense, "smoking" because it provides exposure to
many of the same constituents of tobacco smoke that voluntary
smokers experience. It is also "involuntary" because the exposure
occurs as an unavoidable consequence of breathing in a smoke-filled
environment.

  The chemical constituents found in an atmosphere filled with
tobacco smoke are derived from two sources - mainstream and
sidestream smoke. Mainstream smoke emerges from the tobacco
product after being drawn through the tobacco during puffing.
Sidestream smoke rises from the burning cone of tobacco. Main-
stream and sidestream smoke contribute different concentrations of
many substances to the atmosphere for several reasons: Different
amounts of tobacco are consumed in the production of mainstream
and sidestream smoke; the temperature of combustion differs for
tobacco during puffing or while smouldering; and certain substances
are partially absorbed from the mainstream smoke by the smoker.
The amount of a substance absorbed by the smoker depends on the
characteristics of the substance and the depth of inhalation by the
smoker. As discussed in the 1972 Report, when the smoker does not
inhale the smoke into his lungs, the smoke he exhales contains less
than half its original amount of water-soluble volatile compounds,
four-fifths of the original  nonwater-soluble compounds and
particulate matter, and almost all of the carbon monoxide (15).
When the smoker inhales the mainstream smoke, he exhales into the
atmosphere less than one-seventh of the amount of volatile and
particulate substances that were originally present in the smoke and
also reduces the exhaled CO to less than half its original concentra-
tion (16). As a result, different concentrations of substances are
found in exhaled mainstream smoke depending on the tobacco
product, composition of the tobacco, and degree of inhalation by the
smoker.

87


  Several minor symptoms (conjunctival irritation, dry throat,
etc.) are caused by levels of cigarette smoke encountered in everyday
life, and serious allergic-like reactions to cigarette smoke may occur
in some sensitive individuals. A major concern, however, about
atmospheric contamination by cigarette smoke has been due to the
production of significant levels of carbon monoxide. Cigarette
smoking in poorly ventilated enclosed spaces may generate carbon
monoxide levels above the acceptable &hour industrial exposure
limits (50 ppm) - set by the American Conference of Government
Industrial Hygienists (I). Exposure to this level of carbon monoxide
even for short periods of time has been shown to reduce significantly
the exercise tolerance of some persons with symptomatic cardio-
vascular disease. There is also some evidence that prolonged exposure
to this level of carbon monoxide in combination with a high
cholesterol diet can enhance experimental atherosclerosis in animals
(Chapter 1, Cardiovascular Diseases).

  In the present chapter, the effects of cigarette smoke on the
environment and on the nonsmoker in that environment will be
examined by reviewing data on (1) the constituents of cigarette
smoke measured under various conditions, and (2) the physiologic
effects of this "involuntary smoking" on individuals.

CONSTITUENTS OF TOBACCO SMOKE

  In a recent workshop on the effects of environmental tobacco
smoke on the nonsmoker (42), Corn (24) presented a compilation
adapted from Hoegg (32) of some of the substances in mainstream
cigarette smoke and the ratio of sidestream to mainstream levels for
some of these substances (Table 1). The actual numerical value of the
sidestream to mainstream concentration ratio will vary with different
types of tobacco tested, but Table 1 gives values generally consistent
with those found by others (34, 42). Many of these substances
including nicotine and carbon monoxide are found in much higher
concentrations in sidestream smoke than in mainstream smoke,
establishing that the smoke exposure received by both the smoker
and nonsmoker due to breathing in a smoke-filled environment
differs qualitatively as well as quantitatively from the smoke
exposure received by the smoker who inhales through a lighted
cigarette. A more comprehensive recent review of the constituents of
mainstream and sidestream smoke has also been provided by
Schmeltz, et al. (42) and Johnson, et al. (34).

88


Compound

Mainstream     Sidestream
(mslcis)     (mdcip)

Ratio
Side&earn/
Mainstream

Comment

General characteristics
Duration of smoke production
Tobacco burnt
Particulates, no. per cigarette
Particulate phase
2Tar (chloroform extract)

Nicotine

Benzo(a)pyrene
Pyrene
Total phenols
Cadmium

Gases and vapors
Water

Ammonia                  0.16           7.4
Carbon monoxide             31.4           148
Carbon dioxide              63.5           19.5
Oxides of Nitrogen            0.014         0.05 1

20 set
341
1.05 x 10'2

20.8          44.1             2.1
10.2          34.5             3.4
0.92          1.69            1.8
0.46          1.21            2.8
3.5 x 10-s    13.5 x 10-s        3.1
13 x 10-s     39 x lo-5          3.0
0.228         0.603            2.6
12.5 x 10-s    45 x 10-s         3.6

1.5          298

550 set
411
3.5 x lo'*

21
1.2
3.3

Filter cigarette


Filter cigarette

39.7







46
4.7
1.3
3.6

3.5 mg of Mainstream
and 5.5 mg of
Sidestream in
particulate phase,
rest in vapor phase

' Adapted from Hoegg, U.R. (31, 32).
*For 35 ml puff volume, 2 set puff duration, one puff per minute and 23 or 30 mm butt length and 10 percent tobacco moisture.
Source: Corn, M. (14).


  A number of other researchers have attempted to measure the
levels of some of the substances in cigarette smoke encountered in
everyday situations (Table 2). They have also tried to determine the
factors controlling the atmospheric concentrations of these
substances as well as the amount absorbed by nonsmokers under
these conditions. Carbon monoxide, nicotine, benzo(a)pyrene,
acrolein, and acetaldehyde have been of particular concern.

Carbon Monoxide

  Levels of carbon monoxide (CO), a major product of tobacco
combustion, have been studied in a variety of situations, and
concentrations ranging from 2 to 110 ppm have been measured
(Table 2). The major determinants of the CO levels in these
situations are size of the space in which the smoking occurs (dilution
of CO), the number and type of tobacco products smoked (CO
production), and the amount and effectiveness of ventilation (CO
removal).

  The type of tobacco product smoked is important as a
determinant of CO exposure because it has been found that
mainstream smoke from regular and small cigars contains more CO
pre puff and per gram of tobacco burned than filtered or unfiltered
cigarettes (8). This greater production of CO by cigars was confirmed
by Harke (23). He measured the CO produced by 42 cigarettes, 9
cigars, and 9 pipefuls of tobacco, each product evaluated separately
but under the same room conditions. The cigars produced the highest
CO level (60 ppm).

  In addition to the effect of type of tobacco product on CO
levels, data on the effects of room size, amount of tobacco burned,
and ventilation are included in Table 2. Only under conditions of
unusually heavy smoking and poor ventilation did CO levels exceed
the maximum permissible, 8-hour industrial exposure limit of 50
ppm CO (I); however, even in cases where the ventilation was
adequate, the measured CO levels did exceed the maximum
acceptable ambient level of 9 ppm (18).

  Harke (27) also showed that in small enclosed ventilated spaces
(an automobile) the CO level is determined more by the number of
cigarettes being smoked at one given time than by the cumulative
number of cigarettes that have been smoked; also the CO level
decreases rapidly once the smoking stops.

90


`IABLE 2. - Measurements of `consfifuents released by the combustion of tobacco producrs in various situations
          [ Cig = cigarettes; - = unknown; TPM = total particulate matter]

Reference, Location, and
Dimensions If Known

Ventilation

Amount of
Tobacco Burned

Constituents

Harke, H.-P., et al. (27)
Mid-size European car,
engine off, in wind
tunnel at 50 km/hr
wind speed

None

Air jets open &
blower off

9 cig                  30 ppm CO

6 cig                  20 ppm CO

Air jets open &
blower on

6 cig

10ppmCO

Mid-size European car,
engine off, in wind
tunnel at zero km/hr
wind speed

None


None

Air jets open &
blower on

9 cig

6 cig

6 tie.

llOppmC0

80 ppm CO

S-10 ppm CO

Harke, H.-P., Peters, H. (28)
Car in traffic

None

4 cig

21.4 ppm CO

Srch, M. (45)
Car. en `ne off-
   !?
  2.09 m

None

lOcigin hr

90 ppm CO, Smokers  10% COHb
       Nonsmokers 5% COHb

Seiff, H.E. (44)
lntercity buses

15 air changes per hr

23 cig
(burning continuously)

33 ppm CO (at driver's seat)

3 cig
(burning continuously)

18 ppm CO (at driver's seat)


TABLE 2. - Measurements of constituents released by the combustion of tobacco products in various situations - Continued
           [Cig = cigarettes; - = unknown; TPM = total particulate matter]

Reference, Location, and
Dimensions If Known

Ventilation

Amount of
Tobacco Burned

Constituents

U.S. Dept. Transportation,
et al. (48)
Airplane flights:
   Overseas- 100% filled
   Domestic-66% filled

15-20 air changes per hr       -

do.                   -

2-5 ppm CO, <.120 mg/m3 TPM
<2 ppm CO, <. 120 mg/m3 TPM

Cano, J.P., et al. (I I)
Submarines-66 m3

Yes

157 cig per day
94-103 cig per day

<40 ppm CO, 32 pug/m3 Nicotine
<40 ppm CO, 15-35 ng/m3 Nicotine

Godin, G., et al. (21)

Ferry boat compartments:
Smoking
Nonsmoking

-
-

-
-

18.4 HI.7 ppm CO
3.0~2.4 ppm CO

Theater:
Foyer
Auditorium

-
-

-
-

3.4*0.8 ppm CO
1.4+0.8 ppm CO

Bridge, D.P., Corn, M. (7)
Party rooms:
  145 m3
  101 m3

7 air changes per hr
10.6 air changes per hr

50 cig & 17 cigars in 1.5 hr
63 cig & 10 cigars in 1.5 hr

7 ppm CO
9 ppm CO


TABLE 2. -- Measurements of constituents released by the combustion of tobacco products in various situations - Continued
            [Cig = cigarettes; - = unknown; TPM = total particulate matter1

Reference, Location, and
Dimensions If Known

Ventilation

Amount of
Tobacco Burned

Constituents

Harke, H.-P., et al. (25)
Room-38.2 m3

None              30 cig per 13 min (by machine)

64 ppm CO, 5 10 wg/m3 Nicotine
.46 mg/m3 Acrolein
6.5 mg/m3 Acetaldehyde

5 cig per 13 min (by machine)

11.5 ppm CO, 60 &m3 Nicotine,
.07 m&!/m3 Acrolein,

1.3 mg/m3 Acetaldehyde

Harke, H.-P. (24)
Office Bldg
Office Bldg
Room -78.3 m3

Air conditioned
Not air conditioned
-

-


3 smokers

<5 ppm CO
<5 ppm CO
15.6 ppm CO

Harke. H.-P.. (23:
Room -. 57 m

None
7.2 air changes per hr
8.4 air changes per hr


None
7.2 air changes per hr


None
7.2 air changes per hr

42 cig (by machine)
42 cig     do.
42 cig     do.

9 cigars do.
9 cigars    do.

9 pipes do.
9 pipes    do.

SO ppm CO 530 fig/m3 Nicotine
IO ppm CO' 120 pg/m3 Nicotine
<IO ppm CO: <IO0 fig/m3 Nicotine
60 ppm CO I040 crg/m3 Nicotine
20 ppm CO: 420 pg/m3 Nicotine
10 ppm CO 520 pg/m3 Nicotine
< 10 ppm CO: < 100 fig/m3 Nicotine


a    TABLE 2. - Measurements of constituents released by the combustion of tobacco products in various situartions - Continued
P                [ Cig = cigarettes; - = unknown; TPM = total particulate matter]

Reference, Location, and
Dimensions If Known


Harke, H.-P. (23)
Room-170 m3

Ventilation


None

1.2 air changes per hr

2.3 air changes per hr

Amount of
Tobacco Burned

105 cig

107 cig

101 cig

Constituents

30 ppm CO, Smokers 7.5% COHb
       Nonsmokers 2.1% COHb
5 m-m CO,  Smokers 5.8% COHb
       Nonsmokers 1.3% COHb
75 ppm CO, Smokers 5.0% COHb
       Nonsmokers 1.6% COHb

Anderson, G., Dalhamn, T. (3)
Room-80 m3

6.4 air changes per hr      46 cig & 3 pipefuls

4.5 ppm CO, 377 pg/m3 Nicotine,
3.0 mg/m3 TPM

Russell, M.A.H., et al. (40)
Room-43 m3

None

80 cig & 2 cigars per hr

38 ppm CO, Smokers 9.6% COHb
       Nonsmokers 2.6% COHb

Harmsen, H., Effenberger, E.
(30)
Room-93 m3

None

62 cig in 2 hrs

80 ppm CO, 5200 rg/m3 Nicotine

Hoegg, U.R. (31, 32)
Sealed test chamber-25 m3

None

4 cig
8 cig
16 cig
24 cig

12.2 ppm CO, 2.28 mg/m3 TPM
25.6 ppm CO, 5.39 mg/m3 TPM
47.0 ppm CO, 11.41 mg/m3 TPM
69.8 ppm CO, 16.65 mg/m3 TPM


  One must be careful when using the levels recorded in Table 2
as measures of individual exposure because the CO levels were
usually measured at points several feet from the nearest smoker and
probably would have been higher if measured at points correspond-
ing to the position of a person sitting next to someone actively
smoking (17, 3.5). In addition, it is the CO absorbed by the body
that causes the harmful effects and not that which is measured in the
atmosphere. This absorption can vary from individual to individual,
depending on factors such as duration of exposure, volume of air
breathed per minute, and cardio-respiratory function.

  Several investigators have tried to determine the amount of
carbon monoxide absorbed in involuntary smoking situations by
measuring changes in carboxyhemoglobin levels in nonsmokers
exposed to cigarette smoke-tilled environments. Anderson and
Dalhamn (3) were unable to find any change in the COHb levels of
nonsmokers in a well ventilated room where the CO level was 4.5
ppm. When Harke (2.3) studied nonsmokers under similar conditions
(good ventilation and less than 5 ppm CO), he was able to show an
increase in COHb level from 1.1 to 1.6 percent; without ventilation
the CO levels rose to 30 ppm and the COHb level increased from .9
to 2.1 percent in 2 hours. Russell, et al. (40) also found that COHb
levels increased from 1.6 to 2.6 percent in nonsmokers exposed to a
smoke-filled room where the CO level was measured at 38 ppm;
however, he cautioned that nearly all persons in the room felt that
the conditions were worse than those experienced in most social
situations.

  Stewart, et al. (46) measured COHb levels in a group of
nonsmoking blood donors from several cities and found that 45
percent exceeded the Clean Air Act's Quality Standard of 1.5
percent with the 90 percent range as high as 3.7 percent for
individual cities (Table 3). These levels represent the total CO
exposure from all sources, involuntary smoking, and other sources of
pollution as well as establishing the levels which would be added to
any new involuntary smoking exposure.

  Increases in the COHb levels of this magnitude are probably
functionally insignificant in the healthy adult, but in persons
with angina pectoris, any reduction of oxygen-carrying capacity is of
great importance. In this disease, the volume of blood able to be
pumped through the diseased coronary artery is already unable to
meet the demands of the heart muscle under exercise stress. Aronow,
et al. (4) examined the effect of exposure to carbon monoxide on
persons with angina pectoris. They exercised persons with angina

95


W
m

TABLE 3. - Median percent carboxyhemoglobin (COHb) saturation and 90 percent
          range for nonsmokers by location

Location

Anchorage
Chicago
Denver
Detroit
Honolulu
Houston
Los Angeles
Miami
Milwaukee
New Orleans
New York
Phoenix
St. Louis
Salt Lake City
San Francisco
Seattle
Vermont,
New Hampshire
Washington, D.C.

r

Nonsmokers

r

Median      Range

Percent of
Nonsmokers
Wi$tlCt$Hb
    . 0

1.5        0.6 - 3.2             152               56
1.7        1.0 - 3.2             401               74
2.0        0.9 - 3.7            744               76
1.6        0.7 - 2.7          1,172               42
1.4        0.7 ~~ 2.5            503              39
1.2        0.6 ~ 3.5             240              30
1.8        1.0 - 3.0          2,886               76
1.2        0.4 - 3.0            398               33
1.2        0.5 - 2.5         2,720               26
1.6         1.0 - 3.0             159               59
1.2        0.6 - 2.5          2,291               35
1.2        0.5 ~ 2.5            147               24
1.4        0.9 - 2.1             671               35
1.2        0.6 - 2.5            544               27
1.5        0.8 - 2.7             660               61
1.5        0.8 - 2.7            535               55

1.2        0.8 - 2.1            959               18
1.2        0.6 - 2.5             850               35

No. of
Nonsmokers

Source: Stewart, R.D., et al. (46).


pectoris before and after exposure to carbon monoxide. The average
amount of exercise that was able to be performed before a person
developed chest pain was significantly shortened from 226.7 seconds
before exposure to 187.6 seconds after CO exposure. This change
occurred after a 2-hour exposure to 50 ppm CO and with an increase
in COHb level from 1.03 percent to 2.68 percent; these COHb levels
are within the range produced by involuntary smoking.

  These data indicate that exposure to CO at levels found in some
involuntary smoking situations may well have a significant impact on
the functional capacity of persons with angina pectoris. Carbon
monoxide has also been shown to decrease cardiac contractility in
persons with coronary heart disease at COHb levels similar to those
produced due to involuntary smoking situations (5). It is reasonable
to assume that any significant CO exposure to the diseased heart
reduces its functional reserve.

Nicotine

  Nicotine in the atmosphere differs from CO in that it tends to
settle out of the air with or without ventilation (thereby decreasing
its atmospheric concentration), whereas the CO level will remain
constant until the CO is removed. The concentrations of both
substances are decreased substantially by ventilation. As can be seen
from data in Table 2, under conditions of adequate ventilation
neither exceeds the maximum threshold limit values for industrial
exposure (nicotine, 500 gg/m 3; CO, 50 ppm, I); whereas in
conditions without ventilation, smoking produces very high con-
centrations of both (nicotine, up to 1,040 pg/m3 ; CO, 110 ppm).

  Nicotine in the environment is of concern because nicotine
absorbed by cigarette smokers is felt to be one factor contributing to
the development of atherosclerotic cardiovascular disease. Several
researchers have attempted to measure the amount of nicotine
absorbed by nonsmokers in involuntary smoking situations. Cano, et
al. (II) studied urinary excretion of nicotine by persons on a
submarine. Despite very low levels measured in the air (15 to 32
wg/m3), nonsmokers did show a small rise in nicotine excretion;
however, the amount excreted was still less than 1 percent of the
amount excreted by smokers. Harke (23) measured nicotine and its
metabolite cotinine in the urine of smokers and nonsmokers exposed
to a smoke-filled environment and reported that nonsmokers
excreted less than 1 percent of the amount of nicotine and cotinine
excreted by smokers. He feels that at this low level of absorption
nicotine is unlikely to be a hazard to the nonsmoker.

97


Other Substances

  In two studies environmental levels of the experimental
carcinogen benzo(a)pyrene were measured. Galuskinova (20) found
levels of benzo(a)pyrene from 2.82 to 14.4 mg/m3 in smoky
restaurants, but it is not clear how much of this was due to cooking
and how much was due to smoking. In a study of the concentration
of benzo(a)pyrene in the atmosphere of airplanes (48), only a
fraction of a microgram per cubic meter was detected. The effect of
chronic exposure to very low levels of this carcinogen has not been
established for humans.

  Acrolein and acetaldehyde have also been measured in smoke-
filled rooms (25, Table 2) and may contribute to the eye irritation
commonly experienced in these situations.

EFFECTS OF EXPOSURE TO CIGARETTE SMOKE

Chrdiovascular Effecis of Involtm fary Smoking

  The effects of cigarette smoking on the cardiovascular system of
the smoker are well established, but very little is known about the
cardiovascular response of the nonsmoker to cigarette smoke. Harke
and Bleichert (26) studied 18 adults (1 1 smokers and 7 nonsmokers)
in a room 170 m3 large in which 150 cigarettes were smoked or
allowed to burn in ashtrays for 30 minutes. They noted that the
subjects who smoked during the experiment had a significant
lowering of skin temperature and a rise in blood pressure. Non-
smokers who were exposed to the same smoke-contaminated
environment showed no change in either of these parameters.
Luquette, et al. (36) performed a similar experiment with 40
children exposed alternately to smoke-contaminated and clean
atmospheres, but otherwise under identical experimental conditions.
They found that exposure to the smoke caused increases in heart rate
(5 beats per minute) and in systolic (4 mm Hg) and diastolic (5 mm
Hg) blood pressure. The differences in results between these studies
may be due, in part, to the age of the subjects - i.e., children may be
more sensitive to the cardiovascular effects of involuntary smoking
than adults, or the increase in heart rate and blood pressure may be
due to a difference between children and adults in the psychologic
response to being in a smoke-filled atmosphere.

98


Effects of Carbon Monoxide on Psychomotor Tests

  Carbon monoxide from tobacco smoke, automobile exhaust,
and industrial pollution is an important component of air pollution.
There has been some concern over the effect of relatively low levels
of carbon monoxide on psychomotor functions (the ability to
perceive and react to stimuli), especially those functions related to
driving an automobile (Table 4).

  Carbon monoxide levels occasionally reached in some involun-
tary smoking situations result in measurable cognitive and motor
effects, but these effects generally are measurable only at the
threshold of stimuli perception. One study (Wright, et al., (50))
found that the safe driving habits measured on a driving simulator
did not improve as much with practice in a group exposed to CO as
did the habits of a control group. Another study (37) with a
different experimental design but at the same levels of CO did not
find any effect on complex psychomotor activity such as driving a
car. Thus, the role of CO alone in motor vehicle accidents remains
unclear. The effect on judgement and reactions of CO in combina-
tion with factors such as fatigue and alcohol, conditions known to
influence judgement and reaction time, has not been determined.

Pathologic Effects of Exposure to Cigarette Smoke

  The effect of involuntary smoking on an individual is deter-
mined not only by the qualitative and quantitative aspects of the
smoke-filled environment, but also largely by the characteristics of
the individual. Reactions may vary with age as well as with the
sensitivity of an individual to the components of tobacco smoke. The
severity of possible effects range fiom minor eye and throat
irritations experienced by most people in smoke-filled rooms, to the
angina1 attacks of some persons with cardiovascular disease.

  The minor symptomatic irritation experienced by nonsmokers
in a smoke-filled environment is influenced by the humidity of the
air as well as the concentration of irritating substances found in the
atmosphere. Johansson and Ronge (33) have shown that irritation
due to cigarette smoke is maximal in warm, dry air and decreases
with a small rise in relative llumidity. A change from acceptable to
unpleasant was reported at 4.7 mg/m3 of particulate matter for
nonsmokers and eye irritation was noted at 9 mg/m3 for both
smokers and nonsmokers. The authors concluded that a ventilation
rate of 12 m3/hr/cig was necessary to avoid eye irritation and 50
mj/hr/cig was necessary to avoid unpleasant odors.

99


TABLE 4.- Effects of carbon monoxide on psychomotor functions

co        COHb

Reference

Test or               level
Measurement          (wm)

level
(Percent)

Effect

McFarland, R.A.
(37)



Ray, A.M.,
Rockwell, T.H.
(39)

McFarland R.A.
(38) '

                a
Ability of drivers to stay
between two-lane markers
while being permitted only
brief glimpses of the road

Reaction time to
car taillights


Performance of two tasks at
same time

Dark adaptation and glare
recovery
Peripheral vision at 10'
and 30"
Peripheral vision at 20o
Depth perception
Time perception

700

6       None
11       None
17        None



10      Prolonged




17       None

Stewart, R.D., et al.
(47)

700             17        None



700            17       None



700            17       Decreased

700            17       None

500            20       None