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. 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 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~ )~~! 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