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. < Stnoking, carbon monoxide and arterial disease i'l 1 ; C'E''R /k .t Jiscascs, lun,g, cigarettes may ,1_s frotn the plain to :otiit. yields. During 390 to 1'9'l0i(TODD, 1972): eftar.ged greatly,, but romen (TOtDta„ 1!97Z).. 160 years but has in- oth men, and women tiglyr CO yield than h t~_.,ypotihesis that :d be attributable !T,**+ART I IE,\RT ~ DCSEASE~ '.~ :ktir Wbmcn. '~~ + JYMA,, O i.kn,.~e . confidence 0 nitc '; limits :2T 0 f43 13 -21 .-22 R 0 r16 . S 1-35 ±12 9. ~, -lxS, - 7 2 -4t - 5 2 .t' 53 _ 5 t"-: f1e,;xtrar uatll 1967. and es.d fro;n Czce: (personal I Rlew•'Aav„ ?art T, Tablts present, no comparable data on CHD. While it is necessary to be cautious in interpretiing secular changes in national mortality figures, the dissociation in death rates from lunm cancer and C:3D among, men over, the la5t 15 ' years is striking. There are no prospective d'ata published to indicate that either change in;death rate is due to'the change from plain cigarettes to filter-tipped, but retrospective data from WYNDEtt et al: (1970) suggest that the risk of developing lung cancer among smokers of filter-tipped cigarettes (for at least 110 years) was about 40% , less than among smokers of plain cigarettes. There are, at DISC'UTSSIOhI (i) On'smoking tables and'CO In February 1973 the Department of Health published Smoking Tables showiing the amount of tar and nicotine produced by' different brands of eigarettes. The reason for publishing this information was to encourage smokers to avoid brar.ds with high tar or nicotine and to change from plain to filter-tipped cigarettes. There, was some presumption of benefit implied in the recommendations, particularly regarding nicotine, for which the evidencaoftoucitywasmuch, less'seeurz than it wass for tar. However, since the tar and nicotine yields of cigarettes tend to vary in, parallel this was'not of great 'significance. Little was known of the effect of changing to low tar andi low' nicotine cigarettes on the absorption of other constituents of tobacco smoke,, such as CO. More recently it has been' suggested' that CO should also appear in the smoking tables (RvssFla, et al., 1'973) on the grounds that the circumstantial evidence incrimi- nating CO was sufficient to encourage the seleetion of brands witlt low CO yiclkLss. However, since, with the exception of cigarettes with ventilated 6llters, there is a negative correlation between the tar andi CO yields of cigarettes, tables listing both sets of figures wouldi be confusing. btoreover, some brands that produce less CO than average are inhaled' more deeply (WALD and Snlrrtt{ 1973). It would, taerefore, seem unwise to publish, of6cial tables of the CO yields of cigarettes until the implica- tions of smoking "low CO" cigarettes~ are understood and it is certain that other toxic constituents will not be absorbed in greater quantities as a result. (ii) On cigarette modiftcation The possibility that the change from plain to filter-tipped cigarettes may account, at least in part, for the rise in national CHD mortality empha:sises' an important problemi arising from the use of filters or tite use of tobacco substitutes. The reduction of one harmful constituent of tobacco'smoke, such as tar, may' result in tlie mcrease of another,,such as CO„and the net egect on rnorbidity and mortality may be just as serious: This problem, may unfortunately not be completely soluble and wiili rc:nain a source of concern to those engaged in the deve[oprvent and testing of safer forms of smoking. (iii) On CO and arteriai cliscaae For many years nicotine has been thought to be involved in the association between smoking and cardiovascular disease. More recently, data have become awailablt; on CO, and while nicotine cannot be regarded as altogether harmdess. 1005052918 .-.,.. ~..,._..~..,_,...~~ ~ ~.._..,......_.......,, •_._.... ' ~ Y. ~ .. .. .

, l2 N. WALD and S. Howiutm (particularly in patients with heart disease),,, the evidence implicating CO would, now seem to be stronger. CO exposure from tobacco smoking can exacerbate angina pectoris and intermittent claudication, which affect about 15: _C9 i; of men aged 55-60 years. Whether CO1 exerts this acute effect on coronary or peripheral arteries directly, by for example inhibiting cytpchrome P-350 (CooPElt et ol:, 1970); or indirectly through hypoxia is not:of great practical importance. It would be of interest however, to repeat the studies by ANDERSON et al. (1'973) and ARoNow and ISBELL (1973);,but exposing patients with CHD to air containing oxygen at a reduced partiai pressure instead'of exposing them to CO. The level of'liypoitia that would'correspond' to a given COHb level could be determined empirically by rneasuring the shift in the oxygen dissociation curve. CO may be a cause of'human atherosclerosis, although before this conclusion is accepted more data are needed from experiments on primates exposed' to lower levels of'CO'than have usually been administered hiilierto, and with both continuous and intermittent exposure, as is typical of the human situation. Atherosclerosis iss also related to many factors such a$ diet, family history, hypertension, and physical activity„ and assessing the role of another factor such as CO is dill'iculit. Prospective studies in which COHb levels are measured and the brands of cigarettes used, are recorded may help provide an answer. From such studies it wi1U be possible to see whether CHD is more closely associated with the nicotine yields of the bratids. of' cigarettes smoked, or with the CO yields. Even then the matter would still, not' be settled because the CO and! nicotine yields as measured by the smoking machine would not reflect any systematic differences in the way different brands of cigarettes are smoked. If it became practical to measure blood nicotine levels accurately and at the right time in relation to smoking, many of the difficulties -would' be solved. For the present, however, it is necessary to reserve jjud;Qment on whether CO is a cause of arterial disease, while at the same time suspecting that it may be the principal agent in tobacco smoke. drkotowfedqetrtent--We thank MrJohn Evans of the National Coal Board, Edinburgh, for deter- mining the CiJ yields of the cigarettes. We also thank Profts:sorSir Richard Doll, Professor Vlartin Vessey and ,4tr Peter Smith for tlieir 'hcipful' advice, and Cathy Harwood for her assistance in the preparation of the manuscript and 6gur+es. REFERENCES t#rmetesonr„ E. W., ArtnEt.+wnt; R. J., Srtwttcx, J. lvi., FoRnttrt, N. J. and Kr>a,sotv, J: H. (1!973) Ann. iatern. Med. 79, 46. Axortow, W. S: and Isnu.L, MLW.,(1973) Antt.,intern. Aled:79, 392. Aaotrow, W. S. and'Rbt:Aw,,S. N. (19711) Circulation 44, 78Z tAROavow, W. S.,,STL%istEte, E. A. and I3BELL, M. W. (i1974) Circulation 49, 415. A1TeutP, P. (1973) Circulation 48. 11,67: Asrntur, P:, K.Et.asrrt; K. andi WAmrRUP; J. ('1967) !. .ltluroscfer. {tes. 7, 343. r,YxFS. S. M., GtrwELU, S. Jr., and MUrLLeR„ H. (1970) ,(vue. ,V: Y. Aond. Sci. 174, 263. BrJT, E. W. R. ('t96i6) A Canadian St:rd,v of Srnnking anrl'ldealth. Deparrtmenrof Nutional licalth and Welfare, OttaM1Sa. &x)r¢isr, W. Ni., BsuKSOV, J. and Dtr:v„ H. L. (1936) .dm. J: P1tysiof: 11'S, 463. IIUCHAVALtt, Ei. (1963)riPn. hd.bfy'r'.J: 29~,57U~. Burrm, J., Dnsirs, G: M.. Jor*ES. J. G. and StNcLatx; A. (19'r4),Ann. occup. Fl)•s. 17.57. Cnszietae*+, C. M : and CpLS. P. V. (1973) Lancer2, 21. Conutatr„ R. F. (Editor) (1970) Biological effects of carbon monoxide. Auut. 11.Y. Acad. Sci: 1174, 1-430. 1005,105.2919 ...^...__.,...__

. , . ~ r. now :c: batc aI ,ina '~ ; of rncn' aged ,.r rcril+iteta[ arteries t~ x.•a aL, 1970), or It would be of interest _(, Ax(,Now and IsBELL. •:n at a reduced partial .nat wuuld correspond ,surit' ; the shifc ia the +nr.a.this conclusion is ':cs' cr posed to lower t with lnoth continuous -wtt. eillurosclerosis is :rtensi.)u. and physical -ult. Prospective of`ctelrettes used are rilli bc possible to see ieltis of the brands of tter would still not be', thc sraokin; machine ut brands of cigarettes xvcls a'ccurately and at would be solved. For alyt'r: (.0 is' a cause of ; prinL•ipal agent •S Fd:::huqat. for deter- •d Dol.. frui~:.csor 11,lartin • u*n ccn assistanc-c in she . 3;3'. SCi: t' 1. 263, -j~f K,:io:•taf' Ftcalth and .46S. Llpr,. 17: 57. ,:ar. N: Y. A cad. Scf. 174, . ..~~..~ Smoking, carbon monoxide and arterial disease 13 CottuRNi R'. F.,,FoRStER, R'. E. and KAtvE. P. B. (1965) J: cGn. Invest. •3;4, 1899. Cotll:rt, S. I., DoRtoN, G':, GoLDSAam, J. R. and Pi:mUrr, S. (1971) Archs. envir. fJfdth = 47. CroMMtrrEE ON EfFECTS or ATbtosPHF.Ric CONTAMINACdTS o1c HLliVtAN HEAi.TtE ANID WELFAR.?:(i96g) Egects'of Chronic Exposure to Low Letels of Carbon 14fonoxide on Hummr'Healtly Behaviour, ortd Performance. Nat. Acad. Scii, Nat. Acad. Eng., \Wasiiington, D.C. CooPEx; D. Y., SCHLEYER. H. and RosExrt'1IAL. 0. (1970) Ann. Y. Y. Acad: Sci. 174, 205. Cuwte, J., Stt:LErr, R. W: and BAt.L, K. P. (1973) Lancer 1„1033. DEAnre„M. and PERtuNs, N. (Unpublished) Presented at the 7th Internationat'Scientitic'Yteeting of' the International Epidtmiological Associationi Brighton. August 1974. ' DoLt., R. and~ Htta.:, A. B. (1964) Br. mcd:J: 1, 1399; 1450. Doual:As, C. G., Hitt.DANE„J. S. and HACiDAhE,1. B. S. (19t2)! Physiol. 4•i, 275. DrDYt:E, J. T., DAWBER, T.,R., KANt•rta., W. B., Kr.tclt, S. H. and KAttti, H. A. (1964) 1. Am. med. Ass.190, 886, Got:DS:,urH„J. RL and [1AtvDAw, S. A. (1'968) Science 162, 1'352. GREE3LSPAN, K.,,EDMANDS, 1L. E., KNoEBEL, S. Bl and Ftsarr, C. (1969) Arclts: fttrern. jTlcd. 123, 707. HAMtotvm; E. C.,('1972) Proceedin;s of the Second World Conference on Smokurg ond'ffealth, 1971. (Edited by RzcttARDsort, R. G.) Pitman, London. JntvES, R. D., Coatattxs, B: T. and CF.RN-itc; A. A. (1972) Lmtcet 2,302. KAHN, H: A. ('1966) i.b'atn. Cancer Itet. Monogr. 19, 1.: - K.trrtvF.u., W. B.,,CASaES+u, W. P. and McNAatARA, P. M. (1968) MMain. Cancer litst. Monogr. 28, 9: -KJE1.DsESV, K., AsTRUP, P. and' WA'NsrRUP, J. (1969) J. Arheroscler. Rea. 10, 173. KjEwsetv{ K., AsrstuP„P. and W;..~ts-rRtur„Ji (1972) A'rh'erosclerosis 16, 67. KnzosErq K., THOMSEN, H. K. and A'szxi uP, P. (Il9'74) Circulation Res. 34,339. KIEt.nsEN, K:,,WA,4s'r¢tuP, J: and'As'rttuP, P. (1963) J.Atheroscler. Res: 8, 335. •MoRxts; J: N., CitavE, S. P. W., ADAm, C., StREY, C., EPSOEnc, L. and! SHEEt+tA t. D. J. (1973) Lancer 1,333. MoRRts: J. N!, KAGAN, A., PArrLsoN, D. C., GARDNER, M. J: andi RAFFZ:E, P. A. B. (1966) Latrcet 2, 553. PASSMORE, R. and DtrRNtN,J. V. G. A. (1955) Physiol. Rev:35, 301. RAnysEy, I: h3. (1967) Archsienvir. liLlth 15, 580. RoritwElit:, K. and GRAtvT, C. A. (Editors) (1972) Tobacco Research Council, London. Research Paper IL RoucrtroN„F. J. W. and DARLI;NO,,R. C. (1'944) Arn. J: PbysioL 141, 17. RussEt.t,, M. A. H., Wttson+, C., CoLE, P. V., IDLE, M. and FEYERABEND, C. (1'973) Lcncer'2, 683. SIGGAARD-ANDER:SES'~„J:, BoNDE PEtERSEN, F:, Hnt+sEn+, T. 1. and MEt.tFwaAARtD;,K. (1968) Scand. J. clihn. Lab. Invest. SuppL 103'22, 39. _ SsosrltAt+D, T. (1949) Scand. J: clin. Lab. Invest. 1, 201. STAAI`n.ER, J.. BERKSON, D. M., LEvrrnoN, ML J., MotoNt+TEtt, L., EksrEtY, ,Lt. B!. HALt., Y., BuRUCEx, F., SoxucE-Nc; R. and'A.wDELStAN, S: L. (1'968) Ann. N. Y..-1cad. Sci.149; 1022. THOmEat, H. K. (1974).9tJrerosclerosis 20, 233. TODD, G. F. (Editor) (1972) Tobacco Research Council, London. Rcsearch'Paper'I.. U.S. DEPAn1h/ENT OF HEALTIH, EDUCAT1toN AnD WELFARE (IS71'):The I'dCalth CvnSOQaeitces of Sinokvtg, A Report to the Surgron Gcncra:. Table A23, p.1.:0-12°_.' L'SDHEtiY, \ti'ashington, D.C. ULS. DEPARTMENS OF HLALTkt; EDUCATION AND WELFARE (1'972). Occapurionrd Erpos:tra to Carbon Monoxide, USDHEW, Washington, D.C. WALo,,N., HowARD, S.. S.mrx, P. G. and BAILEY; A. (in rress) 77wrax. WwLD, N., HowARDi S., SMtTH. P. G. and KJELDSEN, K. (1973) Br. med: J: 1, 76L l WALD, N. and SnaRtt, P. G. (t973)'Lancer2; 907. WAtasrauP, J., KjEtlDSta;t,,K. and AsTrtuP; P. (1969) Acta path: mkrobiol.,scarrd:75,,353. WEasnER, W. S., Ct.ARxson, T. B. and LOFLAtaD, H. Bl (1968) fxp. 6rmo1: Parhoh 13, 36. WnaDEx, E. L., NLA'eucltr, K: and BEArrIZ:, E.1: (1970) J. Am. med. Ats. 213, 2'221. DISCUSSION Dr P. CoLE (St B'arrholomew's Hpspi tal. London): I do r.ot agrec that it would be unvfise to )nu blish the'CO yields of cigarettes along with the tar and nicoiine yields. P1:blicatien af tar attd' nicotine yieldfr pre-supposes that both these substances are harmful ; in fact, unc evidcnce that nicouine is Darmful is very slim. There is very strong evidence that cribon monoxidt3 is harmful, and I would suggest that publication of'CO tables would therefore lead to /ess public oonfssion as to the real harm from tobacco smoking. Dr WAto: I have already givcn my reasons for disagresiag with Dr Cole. Although, I agree that the evidence that nicotine is harnrtful! is not great, I' do not think that it can be considered harmless. 1005052920 :r.; ,..

A'. 1 ,. 14 N. Wkt.m and S. HowAten Also, I' do not th;nk that the evidence thai the carbon monoxide exposure from tobacco smoke is harmful is as compelling; as Dr Cole believes. Therefore, I think action on this matter should be postponed until, satisfactory information is available. There is a further practical point. At present, cigarettes wibh low CO yiclds have ventilated fiitcrsS which are often, unacceptable to heavy smokers. Promotion of cisarettes with low CO yi-.lds is therefore unlikely to have an appreciable impact on smokers who have the highest risk of diseases associated with smoking. Mr VMDtn (Analysis Automation, Oxford): is tfiere a major difference between the elfects of tar and carbou monoxide, in that thesmoker alone suffers from the effecrof tar, but that others will be affected by the smoker's production of earbon monoxide? Dr Wu:n: It is true that there will be passive smoking by persons in close proximity to a smoker. However, at present the evidence suggests that passive smoking is not of inedical'significance. In one study, the rise in carboxyhaemogiobin among non-smokers in, a smoke-filled room was only equivalent to smoking one cigarette or less. Therefore the difference referred to by Mr Verdln is probably nor great. --~-.~..-..... - .-.~......._ .. .. ,--.--._-._.~.-