by a direct effect on pancreatic secretory mechanisms. ;wting a~ a com-
petitive inhibitor of secretin, and by a secondary edect on the duodenal
mucosa, depressing the endo-mnous release of secretin by acid.

Robert (~2) studied the potentiation of active duodenal ulcers by
nicotine administration in the rat. Subcutqneous infusion of pentagas-
trin nnd carbachol resulted in the dose-dependent formation of duo-
denal ulcers within 24 hours. Sicotine alone produced no ulcers
Increasing doses of subcutaneously infused nicotine, in combination
with the other t\vo agents, resulted in a steadily increasing dose-related
incidence and severity of the duodenal ulcers. Robert noted that
Konturek, et al. (9) found that nicotine inhibited pancreatic and
biliary bicarbonate secretian in dogs, and that Thompson, et al. (26)
found that acute dose-s of nicotine in rats eit.her depressed or did not
alter gastric secretion. He concluded that the most. probilble mechsnism
by which nicotine potentiated acute duodenal ulcer formation in the
rat was via a suppression of pancreatic secretion.

Robert, et al. (13) further tested this hypothesis b\- infusing acid
via the esophagus of rats in doses found to cause duodenal ulcers in
one-third of the experimental animals. One group of rats also received
a subcutaneous infusion of nicotine. Another received nicotine, but
only water was infused via the esophagus; 31 percent of the animals
receiving acid but no nicotine had duodenal ulcers; 93 percent of the
nicotine-acid group had duodenal ulcers, while none of the nicotine-
water group had ulcers. The ulcers in the nicotine-ncid group rere
more numerous, extensive, and deeper than those in the animals which
received acid alone.

Summary of Recent Peptic Ulcer Disease Findings

In addition to the findings relating cigarette smoking to peptic ulcer
disease, summarized in previous reports on the health consequences of
smoking (27, 18) and cited in the introduction to this chapter, recent
studies have c0nt.ribute.d further to our understanding of the
association:

1. The finding of a significant dose-related excess mortality from
gastric ulcers among both mnle and female Japan- cigarette
smokers, in a large prospective study, and in the context of the
genetic and cultural differences between the Japanese and pre-
viously investigated IVestern populations, confirms and edends
the association between cigarette smoking and gastric ulcer
mortahty.

476


2. Data from experiments in several different animal species sug-
gest that nicotine potentiates acute duodenal ulcer formation by
mans of inhibition of pancreatic bicarbonate output.
3. Cigarette smoking has been demonstrated to inhibit pancreatic
bicarbonate secretion in healthy young men and women.

Peptic Ulcer Disease References

(1) ALP, X. H, HIS~OP, I. G., GH~NT. A. K Gastric nicer In South Anstralla,
   1954-4X L Epldemlologlcal factors, MedIcal Jonrnal of Australia 2(24) :
   lX%1132, Dee l2,1970.

(0) ALP, M. H., HISLOP, I. G., GBANT, & K. Gastric ulcer ln South AnstralIa.
   BXX-~~. 2. Symptomatology and response to treatment. MedIcal Journal
   of Austrrdh 1 (i) : 372-374, Feb. 13,197L
(9) Brrrola, T. E, SOLOMON, T. E., Jomvson, L. R, ~AcOS8ON, E. D. InhIbition
   of pancreatic secretlon in man by cigarette smoking. Gut 13(5) : 361-385,
   ?dny 19i2.

(4) Cco~4 P., TCLINB. S. II. Relatlonshlp between smoking history and complt-
   cations lmmedlately following surgery for duodenal ulcer. Xount Stnal
   Journal of JledIcine 39(3) : 267-292, MayJune 1072.
(5) FLXG~XD. A., HU~AE, T.. BENLIMVA, J. Contribution to the investigation
   of the effect of cignrette smoking. Sbornlk Vedeckych Pracl Lekarske
   Faknlty Karlovy University v Hradcl Krluove 14(a) : 221-234, 1071.
(6) HIRAYAXA, T. Smoking in relation to the death rates of 265,118 men and
   women in Japan. A report of 5 years of followup. Presented at the Amer-
   lcan Cancer Society's 14th Science Writers' Seminar, Clear-water Beach,
   FlE. Alar- 27.1972.15 pp.

(7) KOST~ZFX, 3. J., DALE, J., J~~~oason, E. D., Joaasoiv. I& R. hIechanlsms of
   nicotlneinduced lnhibltlon of pancreatic secretion of bicarbonate in the
   dog. Gastroenterology 62(3) : 425429, 1972.
(8) Ko~.~uamc, S. J, Raoecxr, T., THOR, P., D~MBIX~EI, A., JACOBSON, El. D.
   Effects of nicotine on gastric secretion and ulcer formation in cnts. Pm
   ceedhg~ of the Society for Experimental Biology and Medtclne 138(2) :
   674-67i. November 1971.

(9) Kox~uarx, 9. J, SOLOMON, T. E, MCCBEIOHT, W. G., JOHNSON, IA R,
    JACXXMN. E. D. Edects of nicotine on gastrointestinal secretions. Gastro
   enterology 60(6) : 1093-1105. June 1971.
(lo) MORALES, &, S~LVA, S., &.CALDE, J., WaJSSELUTH, J., &MOB, J., BEY, I%,
   Sdxz. R. Cigarrillo y sec&on gastrica. I. Analisis de la secrecldn-
   gastrica en pacientes digestlvos fumadores p no fumadores. (Clgarettea
   and gastric secretion. I. Analysis of gastric secretion In smoking and non-
   smoking ulcer patients.) Rerista Aledlca de Chile 90(-l) :271-274, Apxll
    197L

(11) MoaaLEa, b. SILYA, S., OEOBIO. G., ALCAJBI; J, WAIB~~LUTR, J. Clgarrlllo y
   secrrdon gastric% II. Efecto de1 clgarrlllo sobre la secreclbn gAstrIca.
   (Cigarettes and ga6trlc secretion. II. Etfect of clgarettes on gastric sea-e-
   Uon) Rwista lkdica de Chile 99(4) : 275-2i9, April 1971.

477


(12) ROBIN. A. Potentlntlon. by nicotine, of duodenal ulcers in the rat. Pro-
    ceedings of the Society for Experimental Biology and Medicine 139( 1) :
    31CL3?2. Jaouan 1972.

(1.9) ROBERT, .I., STOW& D. F.. SEZASIIS, J. E. Possible relationship hetrreeo
    smoking and peptic ulcer. Xature 233(5?20) : 497-493, Ott 15. 19il.
(1-t) SXAIKH. 31. I.. THOMPSOX. J. H.. ALYRES. D. Acute and chronic effects of
    nicotine on nt gastric secretion. Proceedings of the Kestern I'harma-
   cology Society 13: 178-184. 1970.

(1.5) So~ouoa. T. E.. Jacossorv. E. D. Cigarette smoking and duodenal-ulcer dis-
    ease. Sew England Journal of Medicine 286(2'1) : 1012-1~13. June I, 192.
(IG) TI~OSJPSOS, J. H.. GEOEOE, R.. Axarr~o, &I. Some effects of nicotine on gastric
    secretion in rats. Proceedings of the Western Pharmacology Society
   14 : 1X-177. 1971.

(17) U.S. PIXLIC HEALTIX Searxcz. The Health Consequences of Smoking. A Re-
   port of tbe Surgeon Genernl : 1971. U.S. Depnrtmeot of Henltb, Education.
    and Welfare. Washington. DHEW Publication No. (HSN) 71Li513.
   1971, 455 pp.

(18) U.S. PIXILIC HWLTII SEWICE. The Health Consequences of Smoking. A
    Report of the Surgeon General : 1972. U.S. Department of Health, Educa-
   tion, and Welfare. Washington. DHEW Publication No. (HSM) 72-6516,
   1972. 158 pp.

478


Chapter 7
      Involuntary Smoking

Source: 1975 Report. Chapter 4. pages 83 - 112.

479


Con tents

Introduction . _ _ . _ _ _ _ _ . _ _ _ _ . _ _ _ _ . _ . _ _ _ _ _ . _ . _ . . _ . . .   483

Constituents of Tobacco Smoke . . _ . . . . . _ _ _ _ _ _ _ . . . _ _ _ . . _ _ _ _   484
   Carbon hlonoxide . _ _ _ _ _ . . . . _ . _ . . . _ _ _ . . . _ _ _ . . . . _ _   486
   Nicotine . _ . . _ _ _ _ _ . _ . _ _ . . _ . . _ _ _ . . . _ _ _ . . , . _   493
   Other Substances . . _ _ _ _ . . _ _ _ _ . _ . . . _ . _ _ . . _ _ . _ _ _ _ . .   494

Effects of Exposure to Cigarette Smoke _ . . . . . . . _ _ . . . _ _ . . . . . .  494
  Cardiovascular Effects of Involuntary Smoking _ _ . . _ _ . _ . _ _  494
  Effects of Carbon Monoxide on Psychomotor Tests _ . . . . _ _ _  495
  Pathologic Effects of Exposure to Cigarette Smoke _ . _ . _ . . _  495

Summary of Involuntary Smoking Findings . . . . . _ . . _ _ . _ _ _ . . _ _ _ _  504

Bibliography _ . . . _ _ . . _ _ _ _ _ . _ _ _ . . . _ _ _ _ _ _ _ _ _ _ . . . _ . _ . _  505

481


List of Tables

Table I.-Comparison of mainstream and sidestream             Pqe
   cigarette smoke . . . . _ . L . _ . _ . . . . . _ _ . . . _ _ _ . . . _ _ _ . . _   485

Table 2.-Measurements of constituents released by
  the combustion of tobacco products in various
   situations _ _ _ _ _ . _ . _ . _ . _ . _ . . . _ _ _ . . _ _ _ . . . . _ . .  4 87-490

Table 3.-Median percent carboxyhemogiobin (COHb)
  saturation and 90 percent range for nonsmoker
  by location . . . _ . _ _ _ . _ . . . _ . . . . _ _ _ . . _ . . . _ _ . . . _ _ _ .    492

Table 4.-Effects of carbon monoxide on psychomotor
   functions . . . . . . . . _ . . . . . . . . . . . . _ . . . . . . . . , . . . . 496-497

Table S.-Admission rates (per 100 infants) by
  diagnosis, birth weight, and maternal
  smoking _ ._. _ ____. _..____ _ _.._ .._.__...........   500

Table 6.-Pneumonia and bronchitis in the first
  5 years of life by parents' smoking habit
  and morning phlegm . _ _ . . _ _ _ . _ . . . . . . . . . . . . . . . .   502

482


INTRODUCIION

    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 (4Y) 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. hlainstream 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 conce'ntra-
tion (16). As a result, different concentrations of substances are
found ih exhaled mainstream smoke depending on the tobacco
product, composition of the tobacco, and degree of inhalation by the
smoker.

483


  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 ihe
production of significant levels of carbon monoxide. Cigarette
smoking in poorly ventilated enclosed spaces may generate carbon
monoxide !eveIs above the acceptable g-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 I, 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 (I) the constituents of cigarette
smoke measured under various conditions, and (2) the physiologic
effects of this "involuntary smoking" on individuals.

CONSTITUENTS OF TOBACCO SXlOKE

  In a recent workshop on the effects of environmental tobacco
smoke on the nonsmoker (41), Corn (14) 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).

484


TABLE 1. - Camparisorr of ntaitrstreuttt atrtl sidesrrearrt cigarerte smoke ' l2

Compound

hfainstream
big/c@

Sidestream
(mg/ck)

Ratio
Sidesbeam/
hfainslrcam

Commcnf

A    Gcncrul charuclcrr~tic\
   Dur.llion of smoke production     20 set         550 KC          27
    1 ooJccu burnt              337          411            1.2
   P,irticulote>, no. cigarette
              per           1.05 x IO"     3.5 x 1o'2         3.3

B   Particulate phase
  2Tar (chloroform extract)        20.8
                          10.2

44.1             2.L
34,s             3.4
I .6Y            1.8
I.27            2.8
13.5 x 10        3.7
39 x 1o-s         3.0
0.603            2.6
4s x 1o-5         3.6

Nrcotine

Benzo(a)pyrene
Pyrene
Total phenols
Cadmium

0.92
0.46
3.5 x 10-s
13 x 1cs
0.228
12.5 x 1cs

Filter cigarette

C   Cases and vapors
    Water                    1.5          295            39.7

Ammonia                 0.16          1.4            46
Carbon mon+ide            31.4          148             4.7
Carbon dioxide              63.5          79.5             1.3
Oxides of Nitrogen           0.014         0 OS1           3.6


  A number of other researchers have sttcmpted to measure the
Ir-:els of some of the substances in ci$!iJKtk 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.

  Levels of carbon monoxide (CO), a major product of tobacco
combustion, have been studind in a variety of situations, and
concentrations ranging from 2 to 1 10 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 (S). Tllis 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 haximum permissible, &hour industrial exposure limit of--f0
ppm CO (I); however, even in cases where the ventilation was
adequate,  the measured CO levels did exceed the maximum
acceptable ambient level of9 ppm (18).

  Harke (-37) 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 cumula\ive
number of cigarettes that have been smoked; also the CO level
decreases rapidly once the smoking stops.

486


Rcfcrcncc, Location, and
Dlmenslons If Known

VcnlilJtion

Conslilllcnls

Ilarkc, IL-P., Cl 31. (7)
hlid-size European cur,
cng~ne off, in wind
tunnel at so km/h1
wind speed

Nvne

Air jets open Sr
blower off

9 c,g

6 cig

30 ppm CO

20 ppm CO

Air jets open &
blou'er on

6 cig

10ppmCO

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

None

NOW

Air jets open &
blower on

9 cig

6 cig

6 cit.

llOppmC0

80 ppm CO

8-10 ppm CO

Ilarke, H.-P., Peters, H. (28)
Car in trafl'tc

Srch. hf. (a)
Car, en Tine off-
   $
2.09 n,

NOllC              4 cig

None              10 cig in I hr

21.4 ppm CO

90 ppm CO, Smokers  I O'I (`Ollh
       ?ionvnokcrr 5'): UIllb

Scilf, I1.E. (~4)
   Intcrcity busts

23 cig
(burning conlinuou\ly)


fs
0)   TABLE 2. - Measuremenrs of constiruenfs released by rhe combustion of tobacco products in various sirlrarions - COnrilrfled
02                 [ Cig = cigare t (es; - = unknown; TPhl = 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% filed
   Domestic-66% filled

15-20 air changes per hr
do.

2-S ppm CO < 120 mg/m3 TPM
<2 ppm CO: <:I20 mg/m3 TPhf

Cano, J.P., et al. (I 1)
Submarines-66 m3

Godin, G, et al. (21)
Ferry boat compartments:
   Smoking
   Nonsmoking

Yes

157 cig per day
94-103 cig per day

<40 ppm CO, 32 up/m3 Nicotine
<40 ppm CO, 15-35 pg/rn3 Nicotine

18.4 i8.7 ppm CO
3.Oi2.4 ppm CO

`Iheater:
Foyer
Auditorium

3.4tO.8 ppm CO
1.4iO.8 ppm CO

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

7 air changes per hr
1) 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 = tot31'pa~ticthte matter]

Rcfcrence, Location, and
Dimensions If Known

Ventilation

Amount of
Tobacco Burned

ConstiWents

llarke, H.-P., et al. $ 25)
  Room-38.2 m              None             30 cig per 13 min (by machine)    64 ppm CO, 510 ug/m3 Nicotine
                                   .46 mg/m3 Acrolein
                                       6.5 mg/m3 Acctaldehydc

5 cig per 13 min (by machine)

Il.5 ppm CO, 60 rg/m3 Nicotine,
..07 mg/m3 Acrolcin,

1.3 mn/m3 Acctaldchydc

Harkc. H.-P. (24)
Office Bldg
ofrlcc Illdg
Roum-78.3 m3

Air conditioned
Not air conditioned

3 smokers

<5 ppm CO
<5 ppm co
! 5.6 ppm CO

   Harkc, IL-P., (23,
    Room-57 m3              None              42 cig (by machine)
                      7.2 air changes per hr       42 cig     do.      50 ppm CO, 530 pg/rn: Niculinc
                     8.4 air charlgcs per hr       42 cig     do.     < ;; ;;; ;;I :-:",;y;,,3";;.;;::;lc

                          None              9 cigars do.         60 ppm CO, 1040 tig/rn3 Nlcorinc
                     7.2 air changes per hr      9 cigxr do.         20 ppm CO, 420 pg/rn' NILU~IIIE

                           None              9 pipes do.         10 ppm CO, S20 pg/m3 Nicolinc
E                      7.2 air changes per hr      9 pipes    do.        <lO ppm CO, <IO0 lip/m3 Nicollne
Q



  Several investigators have tried to determine the amount of
carbon monoxide absorbed in involuntary smoking situations by
measuring changes in carbosyhrmozjobin 1-.2vels in nonsmokr:rs
exposed to cigarette smoke-filled environments. Anderson and
Dalharnn (3) were unable to find any change in the COHb levels of
nonsmokers in a well ventilated room where the CO level \vas 4.5
ppm. \Vhen Harke (23) studied nonsmokers under similar condltrons
(good ventilation and less than 5 ppm CO), he w;ts able to show an
increase in COHb level from I, I to I .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 at. (40) also found that COHb
levels increased from 1.6 to 3.6 percent in nonsmokers exposed to a
smoke-filled room where the CO !~rl was measured at 35 ppm:
however, he cautioned that nearly ail pzrsons 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 Ic~els 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 unabk to
meet the demands of the heart nluscle 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

491


TABLE 3. -Median percent carboxyhemoglobh (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.

I /

T

Nonsmokers

hledian      Range

No. of
Nonsmokers

Pcrccnl of
Nonsmokers
With COtlb
> 1.5%

1.5        0.6 - 3.2             152              56
1.7        1.0 - 3.2            401              74
2.0        0.9 - 3,7            144              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.s - 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           53s              55

1.2
1.2

!

0.8 - 2.1            959
0.6 - 2.5            850

18
35

I-

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


pectoris before and after rxposure to carbon monoxide. `TII? sverase
amount of exercise that was able to be performed before a person
developed chest pain was significantly shortened from 226.7 sc~onds
before exposure to 157.6 seconds after CO exposure. This change:
occurred after a Z-hour exposure to SO ppm CO and with an increase
in COFIb level from I .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 prctoris. 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.

h'icotirle

  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 wilt 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 pg/m'; 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, 1 10 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. Cane, ef
at. (II) studied urinary excretion of nicotine by persons on a
submarine. Despite very low levels measured in the air (I 5 to 32
pg/m3), nonsmokers did show a small rise in nicotine excretion;
however, the amount excreted was still less than I 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 I 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.

493


  Acroleill and acetafdcflycl~ fuve also been measurctf in hrnoke-
lill~d rooms (2.5. Table 2) and may contnbute to tl~e eye irritation
commonly experienced in tfirse sitiutlons.

EFFECTS OF EXPOSURE TO CIGARETTE SIIOKE

   Tfle effects of cis;rrct tc` ~1rloki11~ on tflr c;ll-rtio\~~~~~~ltar syhtem of
tile 5moher are well cstablihlicd. fut very littfc is kno\vn about tire
cardiovascril2r response 01` tfle nonsmohcr to ci~;ireffc aruoke. ffarke
and Bl~icllcrt (Z'6) studied IS adults ( I I smokers antI 7 nonsmokers)
in 3 room I70 m3 larzit in which I50 cigarettes \vcrc` smoked or
allowed to bL1r11 in ashtrays for 30 minutes. Tfl<y noted that the
subjects wflo smoked during  tfle experiment fud 3 significant
lowering of skin ternpt:rattlre and a rise in bfoocf pressure. Non-
smokers who were exposed  to the same smoke-contaminated
environment showed no cltarl_ge in ei tlier of tlirse parameters.
Luquetts. et 31. (36;) p2rformd a 5iIIlifar exfwrifllenf witfl 40
cltildren exposed afterfutefy to smote-contalninatctl and clean
stmospfteres. but otflerwise under identical experimtY1 taf conditions.
T11ey found that exposure to tile smoke causecf i~lrrsaes in lleartra te
(5 beats per minute) an11 in systolic (4 mm 11:) 3lld cliahlOlk r> Inn1
HF) hfood pressure. Tfle cfiffer-erlces i11 results betwecrl tf~e\c httldit`s
may be due, in part. to tile ase of IlIe subject5 - i.e.. cfiildrcii may IW
Inore s2nsjtjv2 to tile ~.frcfior~r~cufar effects of il~~0l~rJlt:ll)' SlllOkill~
ill311 3tJults. or tile incrrahe in lIt23rt rutc and I~lOo~f pl-hburc Il1.l) fW
dus to a difference bct\vre~~ cflifdren atlcf aLl~~fr\ ill 111~ )~~!<flL~fO:lC
response to being in 2 ~mo~z-t~ifl4 .ltmO~f~fkhr~~.

494


  Carbon monos~de from tobclccn <nioke. ~utornollil~ ~sll;~ust.
and industr~nl pollurion is 2n important component 01`air pollution.
There 113s been some concern over the ellct of rcl;lt~v?ly low Icvels
of carbon monoxide on psychomoror functions t tll? aljllit]: to
perceive and ri`3cf to stimuli). especially those functions rzlatzcl to
driving an automobile (Table 4).

  Carbon monoxide levels occasionally reached in some involun-
tary smoking situations result in measurable cosnitii.e and motor
effects, but these effects generally are measurable only at the
threshold of stimuli perception. One study (Wright. t`t al.. (JO))
found that the safe driving habits me3surrd on a tlri\*iil_r simulator
did not improve as much with practice in a group expo5cd to CO 3s
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. Tllus, the role of CO alone in motor vehicle accidents remains
unclear. The effect on judgernent 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.

P~tlrologic Effects of Exposure to Cigarette Smoke

  The effect of involuntary  smokin g on an individual is deter-
mined not only by the qualitative and quantitative aspects of the
smoke-filled environment, but also largely by (lie cl\aracteristics of
the individual. Reactions may vary with age as well as with tile
sensitivity of an individual to the components of tobacco smoke. The
severity of possible effects range from 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 nonsmo_kers
in a smoke-tilled environment is influenced by the humidity of the
air as well as the concentration of irtitating substances found in the
atmosphere. lohansson and Ronge (33) have shown tllat irritation
due to cigarette smoke is maximal in warm, dry air and decreases
with a small rise in relative llumidity. A change frown acceptable to
unpleasant was reported at 4.7 m_E/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 I?_ m'/hr/cig was necessary to avoid eye irritation and 50
m3 /hr/cig was necessary to avoid unpleasant 0Jors.

495


TABLE 4.- Effects of carbon rnorloxide on psychomotor ftlnctions

Reference

Test or
Measurement

co
level
(mm)

COllb
level
(Percent)

Effect

hfcF.uland. R.A.
(3 7)

Abdify of drivers to stay                        6       None
between two-lane markers                       II       N 0 n c
while being permiflcd only                      17       NOilC
brick glimpsx of the ro;ld

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

hlcFarland, R.A
(38)

Reaction time to
car tdllllglll>

IO

Prolonpcd

Pcrformancc of two tasks at        700             17       None

sune time

Dark adaptallon and glare
rrcovery
Peripheral vision at IO0
and 30"

700

700

17       None

17       None

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

Peripheral vision at 20"          700            17       l)L'uc;I\cd

Depth perception             700             17       Nnnc

Time perception              500           20       None


IIcndcr, W., el al.       Tllre>llold for trrnpordl
(6)               ICbolullorl of vi\u.il rllmull

100          7.25        K~iwl


  Tnfo rovernmell t q~~nsor~d ~tt~diz\ II;IL.T ;IIICJII~~C~I to L~t.:~~~~.l~~
tile degree of minor irritation due to ciyJrc'ttc \mokc ~\peri~niz~l I>\
bus and plane passengers. TIw U.S. Ikp~rt~n~~~~r ol Tr.ln\porr;,tlo;l
t-C-!) studied the environment on t\vo venr~l.ttcd IJII~Y -~ 011~` w1t11
simulated unrestricted smokin: and anotiter wit11 ~imul2tzd srnokirlg
limited to the rear 20 pcrccnt of tlls seats. In one bus. l~~litc'il
cigarettes were placed at every otllcr seat (23 c1~3rette5) to simulate ;I
bus filled wit11 smokers. In tlic otller bus. cis.irettcs were placed 0111).
in [lie rear 20 percent of tile bus (five ciprzttcs) to simulate ;I bus
where smoking waslimited to the r&ar 10 percent of the sests. \\`llen
smoking was limited. the CO level at the driver's seat was only IS
pprn (ambient air I3 ppm) compared to l11e level of 33 ppm
(ambient air 7 ppni) nira5ured in the nnrestrictcd sniokin: situation.
Four of tf~e 5i.x Lubjects seated in tile bus reported eye irritation
durln_r tile unrr5tricted smokin: simulation. None of tile six subjects
reported any eye irritation in the restricted sniokin_c situation (not
even tllose se3tetl in the rear 70 percent of the bus).

  Several Federal agencirs (4s) cooperated to survey tile symp-
toms experienced by travelers on botli military and commercial
aircraft. They distributed 3 questionnaire to passengers 011 20
military and S commercial fligltts; 57 percent of the passengers on
tile military fli$if5 and 45 percent of the passcn_cers on the
commercial tli$jth were smokers. The planes were well ventilated
and C-0 levels were always bciow 5 ppm witll low levels of other
pollutants as well. In 5pile 01. tile low level of measurable pollution,
over GO percent ot' tile nonsmoking passengers and IS to 12 percent
of tile smokers reported being annoyed by tile other passengers'
smoking. Seventy-tllree percent of the nonsmoking passengers on the
commercial flights and 67 percent of the nonsmoking passengers on
tlla military tlights sug_rested that some remedial action be taken; 84
percent of tl,ore su~,uestin, 0 remedial action felt that segregatjng the
smokers from nonsmokers would be a satisfactory solution. These
feelings were even more prevalent amon, 0 those nonsmokers who had
a history of respiratory disease.

  Children have been found to have a higher incidence of
respiratory infections than adults and are thou$t to be more
sensitive to tile effects of air pollution due to their greater minute
ventilation per body wei$t than adults. Several researchers have
investigated the effects of parental smokinr on the health of
children. Cameron. ct al. conducted two telephone surveys of Detroit
families to determine tile relationship bet!v<crt cllildren's respiratory
illness arid parental smoking habits. III IIK fir\t \urvc`y (0) 01ey found
a statistically significant rrlation~l~ip lJclwc'~*n 111~* ;\~~-v;r/~`llce Of`

498


  Colley (12) also found 3 relationsllip between parental stnokin:
habits and the prevalence of respiratory il!ness in the chlicircn. iIe
found an even stronger relationship between parental cough and
phlegm production and respiratory  infections in children. tie
postulates this latter relationship to result from the :reatsr infcc-
ti\.lty of these parents due to their cough and plll<:rn production.
Ths relationship between parental cigarette smokin: and respiratory
ir.t`ection in thsir children would then occur because cigarette
smoking caused the parents to cough and produce phlegm and would
not be indicative of a direct effect of cigarette smoke-filled air on the
ClllldI?Il.

  Harlap and Davies (29) studied infant admissions to Hadas~ah
Hospital in West Jerusalem and found a relationship between
admissions for bronchitis and pneumonia in the firs1 !`ear of life and
marernal smoking habits during pregnancy. Data on maternal
smoking habits after the birth of the child were not obtained, but it
can be assumed that most of the mothers who smoked during
preynancy continued to smoke durin g the first year of the infant's
life. 3, relationship between infant admission and maternal smoking
habits was demonstrable only between the sixth and ninth months of
iniant life and was more pronounced during the winter months
(when the effect of cigarette smoke on the indoor environment
would be greatest). Ifothers who smoke during pregnancy are known
to have infants with a lower average birth weight than the infants of
nonsmoking mothers. The relationship between maternal smoking
and their infants' admission to the hospital found in this study was
greater ior low birth weight infants, but was also found for normal
birth \veight infants (Table 5) (3). Harlap -and Davies (139)
demonstrated a dose-response relationship for maternal smoking and
infant admission for bronchitis and pneumonia; however, they also'
found a relationship between maternal smoking and infant admis-
sions for poisoning and injuries. This may indicate a bias in tllr study

499


TABLE 5. - Admission rates (per IO0 infants) by diagnosis, birth weight, and maternal smoking

Diagnosis

<2,999

Birth weight(g)
3,000 - $499

3,500+

   Total
(including unknown)

Bronchitis and
pneumonia

All other

Total

s       NS       s       NS       S       NS           S       NS
(297)    (2,326)    (415)    (4,098)   (264)   (3,195)        (986)    (9,686)

19.2      12.3      9.6      8.2      12.1      9.0          13.1       9.5

22.6      19.9      14.5      14.6      15.2      13.3          16.9      15.5

41.8      32.2      24.1      22.8      27.3      22.3          30.0      24.9

NOTE. - S=Smokers; NS=Nonsmokers.
Source: Harlap, S., Davies, A.M. (29).