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Philip Morris

Biomedical Abstracts

Date: 1980 (est.)
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77'-u1223 Herson. J.: Simpson: C.: Kennedy, j.: K&poor, S. A Theoretical Aporoach to the Evaluation of the Corta.Lizv Effects of a""Lov. Tar" C:zirette. Journal of Claronic Diseases z94112' : 7v7-75a1, Deceaber 1976. Wuolish. Recer,t smof:ina and healza controversv hss centered around the likely the sale of effacts on human aoytslitY' of a federal UL.~i'cq sanetioniaq only low-tar cigarettes. At mresent, verv lit"a data atm available.to documenz the tiortalitv effects of vrolonqed smoi.iny of civarettas at various tar levals. cfiureovmr, ethical and Qracticmlity considiarations preclude the aossibilitv of a controlled clinical tria.L beirna verflormed' to estimate theseefrects. The obtectives or this vap".r are thus to davelov various matzc=aticaL mo&eis to: l1J Estimatc tnm variatiou in various measures of mo`r~3litv by daily saokine f'rzcuencY and civarette tar conzent. (2) Discuss ioplicdtions of the mortality results in taz=s of' public health volicv that Yoinld enicouiraQi3 the US'2 of Zoii!-L9L ciziaL.3Tt2s a;3'.3,/or eZco'uraQe smoiCers' to lo.:r daily sc,ot:ina Erevuency. The tYU ndA.aaeter Govrortz hazard function is aho:jn to fi•.. t1d©moaai"s 1ylo0 American C:oucc~r Socicty life• tables rhich demict survivorstrio of men aceci 25!-1'OG yaars for f ive lovels of smokinq frezuaacv. UsiaJ data on tar, levels oz cic,arettes on the market durinq the period' 13o0-65, various aodels are prooosad to esti'm3te the covariation, of . 'the .7oimrn-~%rtc vardm_t3rs bv smokina freuurucv and tar content. For each molai, ms tima*_ar3 life expectancv and aciE zgijeclfic death rates arp pr.esentvi" fnc_ various smo.:ina treruaBcy/ta'r croups' autd tha mortality coitseane,nces of al law tar and lou freauencv v!ublic hcalth uolicy are discussed. FlultiFle recression analYS'ss.is nsed to summarize tup mo**alitv findiaas and to croviae a auantitative assess,neut ot tne reiative imoortauce of tar content and srruklnq frzcvmmncy, in deteranini,nc lize exvectancy and death rate. E7ijaace froa the models favors a lov-tar, uoticw over a low fra etrt:emcy mal=cv but coasi&er35le benef'its can be o6;.ained from a combined' volicY. (Auth. A os. M'od'. )
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76-11Id1 Hill, P. Hicotiae: kn Etiological F.actor for Coronary Heart Liszase. pp. 313-319. 19761, In: Rynder', E. L. ; Hoffmann, D. ; Gori, G. 8. (c:iitors) . Modifyinq the Risk for the Smo;eer, Volume 1. Proceedings of the 3rd Horld Conferenca on S'moking and Health, New York, June 2-5, 1'975. Dfi?.;i ' Publication .bo. (NIH) 76-1221, EhNlish. Although the relationship of nicotine to, atherosclerosis is unclear, nicotine may be a major factor in sudden death and be responsib le f or the increase in CE'D in women. Concerning the need' to smoke, the environmental coadiLi,ons~ initiatiaq low or hig,h arousal situations may, control the nicotine intake in smokers and the ease of smoking; vithdlrawal. Thus the physiological andibiochzaical changes on smaking withdraval may qive leads on the nicotine "I'demand"' and its relation to, CHD6 Investiq~ation of the daily, patterns of nicotine intake~ an3'i changes in plasma nicotine, cotinine, catecholamines, cortisol and carboxyhemo4lobin (C©Hb) levels in smokers and ex-smokers, shoJed initia:l rapid increase in serum adrenaline on smoking which is not maintained, iiut a prolonged elevation of' cortisol, which was maintained throughout the day in a heavy smoker. These changes were - depenuent on the content and rate of intake of nicotine. 3:apid clearance of plasma nicotine occurres, but a, hiq,h plasma cotinine content was maintained from day to, day. Similarly, smokers maintained an elevated~ COHb throughout the day; a, level independent of' the nicotine content of the cigarettes smoked. One week after stopping smokinq, these biochemi:cal parameters are similar to those in nonsmokers. Since smoking withdrawal decreases the risk of CHU1, the effects ot nicotine and C'Ofib, vnich are indeflendent risk factors, appear to be reversible. Although less harmful cigarettes can be develooed only smoking VithdraVal will remove the hazard. (Auth. Abs, ) -79'-o5E@ Hoim-burger, F.; Gori, G. E.; Lynch, C, J. Socially Tolerable Ciq,arette Stoke? (Dettezs) . Jourr.al of the Aaerican nedical Association. ~~2v 1(Zm) : Z'142-21u3, "aY 1s, 1979. Frglish. 100'S052$17' ~This'letter eodments on a study by Gio H. Gori reported in the Wall Street. Journal Xovember 1, 1578,, p. 18' which Lef t the public with the i,pression that some cigarettes are relativelJ safe to! sLcke~ in limited quantity. Results of that study were based on, tar and nicotine values extrapoLa:ted II'rom pre-1960 cigarette smoke. This extrapolation would be justified' only if tfie eompcsiticn of the diliuted smoke remained basically the saae.. The complex naniFulaitioas necessary to obtain lower yields of the six substances studied bi Cori ar,d coworkers aay change the biologic activity of smoke or new sm~oke coc?.onents maY be introduced by addition of flavorings or adaitives not reculated in the United States. Only a, valid lf' c'scrisinate betv h d fl i ee n azar ous saoke. A bioassay of smoke ca previously Fubl'ishedi assay for seasuring the cancer causing potency of various cigarettes is advocated, In his reply, G', 8, Gori.emphasizes that todaY's cigarette pr'eceszina reduces known toxic constituents quantitatively. There is no evidence that the red'uction, of' these constituents is accompanied by an incre3se' in other suspected toxic constituents, Fu'rthezmiore, there is evi3'ence that toda7•s cigarettes produce less tumorigenic tars than Fre-19160 cigarettes, There is no evidence that present flavor addi'itives increase the toxicity of cigarette smoke. Gradual reduction in exFesure to tcxic coastituents remains the reasonable approach until. bi'oassar dat3, are availabl'e fro., onqoiaq buman studies.
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76-1250 Kannel, i. B. ; Castelli, W. P. Siqniiicance of Nicotine, Carbon Monoxine and otaer Smoxe Comiponents in the Development of Cardiovascular Disease. pp. 369-381. 1976, Ia; iyndar, B. L.;, Eioifmaan, D.; Gori, G. g., - (zditors) . nodifying the Bisk for the Smoker, qolume 1. . Proceedings of' the 3rd .orld Conference on Saoking and Bealth, New York', 3.une 2-5, 1975. . D(iE'W Publication do. (.VId) 76-1221, Eaqlish. , There is now, ample evidence to show, that nicotine absorbed from inhaled tobacco has acure, transient effects on the circulation which could explain many of tne observed epidemioloqic faaturzs of tae relation of' cigarette. smokiagi to the d'evelopment of cardiovascular disease. Its actions are comparable with a transient, noncumulative and! reversible triqqerinq effect operative in persons with an already compromised coronary circulation. The hiyh carbioxyh,emoqlobin values qen3rated by cigarette- smokers. also fits this pat:.oa1enetic! conceptualization by causinq further impairment of oxyqen utilization; by isctanic tissues supplied' by critically narrowed' vessels and' catechol stimulated by nicotine. In addition, etfects of nicotine on, -piatelet adhesiveness and other clottinq factors could impair flow in the microvasculature or proaote thrombosis in, near occluded arteries. Evidence which incriminates ciqarettes in the process of atherogenesis is less substantial- and does not explain as well the epidemiological relatioashipss of the cigarette habit to the~occurrencz of cardiovascular disease., altaoulqh, it is quite likelq that severe exposure to carbon, monoxide _pzouotzs ath_rosclerosis in the heavy smoker, it is more. likely that the acute precipitatinq effects of' nicotine an& carbon monoxide are~ responsible for the excess risk in the cardiovascular disease-prome smoker. Giving up smoicinq has been shown to red'uce risk by about half so there is muchl to be qained by abolishinq the use of ciqalrettes or, in reducing their nicotine ana car5on, monozide content. (Auth. Abs.) ~.-.=7'9-1v13 K'och, A.; Roffmann, K',,; Siteck, W,; Horsch, A.; Hengen, 11,,; nberl, H', Einffluss von 2igarettenrauchinhalationi aluf Kreislauf- und' :-,S'toffrechselgrossen. [ Ef'fect of' Cigacette Saoke Inhalation on Circulatio,-, -,and netalbolism, ] Yerhandl'uagen, der Deutschen Gesellschaf t fur Innere redizia 84; 1397-1I400, 1976, G'erman. 10il 52 5 0 ~918. Biochemical and b1!ood circulation parameters were eas.uredl in. a g,roup of six healthy men, 20 to 30 years old before and after they smoked' txo 6.5 ca. lona cigarettes, each in 12 iin, Nicotine content of one saoked cigarette was either 1, 54 (hig,h-nicotine) or 0!.08 mg (""nicotine-f ree "') . A .""shamsmoking'" test was also d!one. The aeasuresents were made 1!, 10, 20, 45, and 120 aia after smoking. Pulse rate was directly proportional to thie nicotine variations in plasma after smoking either two high-nicotine or two "'"nicotine-free''' cigarettes, The spstolic Fressure increased considerably with the high-nicotine cigarettes and to a smaller extent with "'"nicotine- free" cigarette.s, The pulse wave velocity decreased significantl7, with high-nicoltine cigarettes. The blood flow through the calf increased slightly for a short time with hish-nicotinle cigarettes but retained unchanged with "'"nicotine-f'ree''' eigar'ettes, The acral flow decreased ;ignificantly with high-nicotine cigarettes and less so with: ""nicotine- '' ; f t Th 2' i ' ` ~ ree acta e c giarettes. e to ppruvaite ratio and blood sugar Iievel increased significantly and continuously with high-nicotine cigarettes, but onlr slightly with ""nicotine-free" c'igarettes.
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7'6-1 2'66I M'aaaing, P. A. ; Feyerabend, C'. Cigarette Smoking and F'etal : 3reathinq !lovements, Obstetzical and Gynecoloqiical Survey 3'1 j10) : 7'1I6-71d', October' 1976. Enqlish. The present study investigated the factor in cigarette smok;e responsible for tae depression of fetal breathing. Ultrasound recordings were mad'e of' ' the fetal chest wall movement. Fetal breathing movements were measured before and after smoking two consecutive cigarettes in 19 vomen Vith normal pregnancies, 10 rrith Preeclampsia, 12 with diabetic pregnancies, and 6 vcmen who ultimately delivered small-ior-date babies. In the normal preqnancy group fetal brea.thing movements were present for 69.7 percent of the time before smoking. There was a significant reduction in the. proportion of time d:urinQ which fetal breathing movements were present within 5 minutes after the start of smoking. The reduction was progressive rea :hinq a nadir of 5!0 percent at 3'0 minutes. Plasma nicotine level rose from an initial value of .6' nq/ml to 15'.1' nq,/nl after, the second' ciqarette. There was a siqniticant correlation between the rise of pLasma nicotine 'i-i after simoking and the fall in the amount of fetal breathinq,. This correlation was also evident in, the diabetics and small-for-date preqinain:.ies.. T'hie preeclamptics showed no reductionl in fetal breathing moveaents. Correlations between fetal breatainq movements and' chalnqes in blood sugar or carbozyhemoqlobin levels were not observed. Hence, nicotine appeared to be the ractoz in cigarette smoke responsible tor the reduction, in the incidence of fetal breathing movements. 7'9-1v78 Rabinovitz, B'. ID.; T'horpi, 1t.: Huber, G„ L.; Abelnann, W, H. Acute i ".:-Sixteen healthy, sub jects, ages 18-351 rears,' were studied in the supine. .: HemocTnamic Eff''ects of Cigarette Simok,ing in Can Assessed by Systolic Time , Intervals and EchocardiograFhi. Circulaition 60 ('u) : 75Z-76'0, October 19719. ~--k':'aad after smoking a hi'gih-nicotine cigarette (2.5 mg nicotine) and a lov- :'f+?9''posi'tion by means of systolic time intervals and echocardiography before ;•~ nicotine cigarette (<0.02 mg nicotine) to assess and comFare the immediate effects upon left ventricular function. Smokers (a-12) and nonseckess (n=4) behaived alike. Righ- and low-nicotine cigarettes both caused significant i'ncreases in heart rate, systolic and diastolic blood pressure and the triple product (systolic blood pressure x left ventricular ejection, (LVET) x heart rate) , prolonged LY'ET, and decreased the pre-eji,ection period ('PE'P). and FE'P/LV'E:. In add'ition, smoking a aicotine reference cig,arette increased the eehoeardiographicallr-derived' LV enid-diastolic volume by 7.5 percent and augmented ejection fraction by u percent, while significantly enhancing meaa normalized circumferential fiber shortening by 12.5' percent and mean . normalized posterior wall relocity by 91 percent. Smoking a tobacco - cigarette of ultra-Zow nicotine content resulted in comparable inczeases in ejection fraction and mean circumferential fiber shortening, albieit on the basis o-f a significant decrease in end-systolic volume without alteration in end-diastolic volume. These data suggest that s3oking, a high-nicotine cigarette Mhile in the supinie position acutely increases venous return and augments the principal determinants of myocardial oxygeni consumption. (i.e.,, heart rate, contractility, preload and afterload) and that cigarette smoke ma7 contain inotropic and chronotropic substances other than nicotine. (Auth. Abs.) 1005052819
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6-068'.4 &awbone, 3. G. . Closing Volume. The Effects~ of' Acute Exaosure to Tobacco and Tobacco~ Substitute dixtures. (Su©olement y5) - 9'1-916, 1976. In: l Closiaa YoLume. Phvsiolomy, tilethodolovy, c,pideaiolo4v and Clinical Invastiaacioas. An International Svmposium fdeLd' in: od'ense October 20-21, 1975. Scandinavian Journal of' Respiratory Diseases Eaglishi. Tae ef'fects of tobacco cigarette smokina on oulmonary function vere. comioared to the eftects of ciaa~rettes containinq tobacco-substitute material. Twenty-nine male snbiects were aivided into 4 studv crouvs: nonsmokers, normal ciuarette smokers, (whose averaae consumption was greater than 20 middle tar cicarettes containing 17-22 mq tar, per day), substituta simo7cers A and substitute smokers B. Twenty-four hours before , Jarette smokers did exist.,y . attending the laboratory s!ubj~ects (,who~ were smokers) were given a supply of unmarked cigarettes to sAoke for the intervening neriod. Otaon arrival all subiects were aiven a pulmonary function test. The~ test groups ta11 sumiects except nonsmokers) were then asked to t''chain-smoute" five cigarettes followinc which the pul- monarv function test was reajainistered'. All cic:arettes were filter tipped and idl ntical in apoaaranca. Control cigarettes contained'1010 percent flue-cured tobacco while the test cigarettes contained one ot two substitute materials in a mixture of 4 0~ percent sub•szitute to 60 percent control tobacco. Both nitroQen and araon closing volumes were measured to indicate pulmonarY funntioa. The subiect coefficient of' vari3tion •ras nreat: u~c to 3© percent in zonsmakers~ and up to 50 Percent in smo,cers. For the nitroQen closing volume no sicnificant_ d.ifference existed between the 4 groups; hovever, for 'i3 arvon•test a sianificant difference between nonsmokers and the control 7,3-095'9. Russell, xilson, C'. , Cole, P. V., idle, !i. , Feyerabend', r Comparison of Increases in Calrboxy'hiaemoglobia After' Smoking "Extra.- Lancet 2(7831) : 687-694, Septem er , arettes ld" Ci - d "H " ' . ai g on an mild ~. ; ~ T~*nk1973',.. English. carbozyhemoglobin (COH'b) after smoJting, "extra-mild'' and "'nonmild" cig'arettes. The mean increase after smokingi a single nonmild cigarette A"c'ross-over, comparison was aade, in 22 smokers, of increases in , yas 1.45 percent for the standard-size brand (ten puffs) and 1.091percent ~' for the small-size brand (seven puffs) . The meanincrease after a, single extra-mild cigarette was 01.64 percent for the: standard and 0.75 percent for the small brand',. The low Co, absorption from the standard-size mild cigarette was less than half the amount absorbed~ from the similar-sized nonmild cigarette. . This low CO brand' also has a. low tar and nicotine yield. CoHb increases after smoking were g,reatere in tae women than in the men, and there was an inverse! relation betYeen C'D8b increase and hemoglobin level.. The health implications of variations in CO yield of cigarettes are probablp as iaportant as those of' differences in tar and nicotine yield; the C0lyield'f of cigarettes should thus be pubsished! together with tar and! nicotine yield. See Abstract 73-G9©7. ,(Auth. Abs.) 1-110050'52820
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75-0788. Eussall, lY.b.H.;' ~ilson, C.;' Patel, U'. R.; Fryerabi:r.d, C.;~ Cole, P. v. Plasma Niicotina Levals After SmcJcizg Cigarettes Uith Hiyh, and Low Nicotine TiElds. British Cedieal .Icurnal 2(5'y168): 414-416, Cay 24, 1975, English. which have been saoked over the preceding few hours. (,Ault:h. Abs.) v_y the cigarette is smoked than on its r.icotine yield' or the number showed mark_d individual variation. The findings suggest that the Flasm3 nicotine level occurring j',usit after cigarette snoking depends more on the morning and afternocn while smoking usual or high-nicotine cigarettes 3ropped to an average of 52.4 nnol/i (8.5 ng;/'ml) . The changes between . respectively) were not siguificantly, hhigher than the morning levels, but after switching to lov-nicotine cigarettes~ (0.14 mg) the plasZa nicotine with their carboxyhemoglohin levels. After ccntinutng~ to saoke their usual brandi or switching to a high-nicotine b_and (3.2' m3 ) avbrage afternoon levels of 185.6 and 180.0' nimol/1 (30.1 and 2'9.2 ng,/m1, Plasma nicotine occurring three minutes after smoking a cigarette was measured in ten sedentary workers in sid-morniiig and five hours latzt on four typical workir.g days. The averagie mid-tcorning level after they had baen smoking, their usual cigarettes (dean nico ina yield 1.34' mg) was 150.4 nmol/1 (;24.4 ng/dl) (range 95.6-236.7 nmol/1 ('15.5-38.u ng,/ml))- t Diespite great variation betwczn smokers the ctid-morni'nig levels of each ' smoker were fairly consistent over the four mornings and cozrelatcd 0.62 72-0575. Sclunahl, D. Review of Current Research in Gerntany on Less Harmful Ways of Smoking. Journal' of the National Cancer Uutitute 48(6):1'77S-ITl7, June 1972. Research et7brts of the German cigarette rttanufacturers'to reduce the tar and nicotine levels in cigarettes are briefly reviewed. Fractions from cinrette smoke condensates are being tested on mouse skin to define and eliminate those fiacriona in which tumor initiators are eonr~entrated. Smoke condensates frorn ci¢arettes modified by various procedures ~j to reduce or eliminate their turnorigenicirty are being tested' on mouse skin and in the subcutaneous tissue of rats. To titnd ~' °' out whether tumori8enicity could also be reduced in the total smoke, a new expertmentall technique has been develboe,l' by which the total smoke of cigarettes is inhaled by hamsters. A:s a resuat of pressure on the German tobacco industry too reduce the yield of total eondensate and nicotine per cigarette, the condensate pe cigarette was 36 percent less and'the' nicotine 31 percencless in 1970 compared with those in 1961. '79-1ta23 Spohr, 0,; Hofraainn, K.; S'teck, Harenberg, J.; walter, E.; 'Athier'osclerosis 33 (3)' : 2'71-28'3, July 1979, English, Evaluation of' Smoking-Induced Eff'ects on Sympathetic, H'erod'ynacic and H'etabolic Variables with, Respect to Plasma Nicotine and COHb Levels, He'ngen', X'.,; llugust'in, J'.,; lSoerT, H.; 1CocA, A.,; F:OrSCls, A.; xeber, E. per cigarette and of shiam-saoking was studied in six healthy habituall smokers,. Levels of •carboxThemog7obin (CO'Hb) and plasma nicotine were measured sicultaneously• vith heoodynamic variables, such as heart rate and blood pressure, and with the metabolic parameters, plasaia dopasine-beta- liydr'oxylase (IDBH) , cortisol, bl!ood glucose, lactate, and free fatty acids. All variables, with the exception of COHb, were dose rellated, to Flasca nicotine levels. Blood pressure, heart rate, and' lactate showed simultaneous peaks together with oaximal nicotine levels, vhi,le DEH and cortisol', blood glucose, and free fatty acids shovedl a del'alyed' reaction compared to nicotine concentrations. No effects of' COHibi, even 'With levels up to 5.6plus or, miaus0,5 peFcent, were observed on the varialbles investigated. Results demonstrate that it is nicotine that induces considerable hemod'ynaeic and metabolic alterations after smoking. (Auth, A' bs.~ the effect of smoking cigarettes containingi 1.5 mg and' 0,08' mg nicotine 1005052821
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7'9-0291 Tachmes, L.; Pernandez, E.J.;* Sackae.r, a. 3. Hemodynamic Effec;s of Smoking Cigarettes of High and Lov N3cotine Content. Chest 7 4(3!) : 243- 24'.6 , Sep tember 1978. Eaglish The heaodynamic effects of smoking cigarettes with high and lcv, contents f of nicot iRe in young smokers free! of corona ry arterial disease were studied'. The sample consiste& of fivemen and, three women, ranging in a~ge from 18 to 30 years, with a smoking history of 2-15, pack-y,ears. The smoking . of', one cigarette with a high content of nicotine produced a pea.k rise in cardiac output of 32 percent above baseline values, and the effect pers_sted f~or1 hour. Smoking, a cigaretteyith~ a low cont~en~tof nicotine,. . produced a peak rise of' 13 percent above ba-seline values, Yith a duration of' 5 minutes. T'he, rise in cardiac output was almost, entirely att_;'butable to: tachycardia,, since stroke volume remained relatively constant. Smoking a cigarette with high nicotine content also caused greater and more sustained elevation in systemic, blood prEssure- than smoking a cigarette with low n,icotine cfontent. After smoking, there were no statistical]:p significant changes in consumption of', orygen, diffusing capacity,, volume of~ blood in pulmonary tissue: plus capillaries, functional residual capacity,, 'or flow of' bloodl in calf. Thus, there vas a responsiveness to the, dose of nicotine in cigarettes smoked bT yomng. smokers~ free•of cprona.r7 a~rterial disease, in heart rate and blood pzessare. (Auth. lbs. Bod. ) 10050528022. - 74-1312. Turner, J.1.2l.; Sillett, 8. W.; Ball, K. P. Some Effects~ of Ch.anging to Lor-Tar and Lo!Y-Eicotine Cigarettes. Lancat 2(7'883) : 737-739,. Saptember 2,8, 1974, English.. . Cigarette consumption and biood carboxyhemoglo.bin. (CpHib), levels were maasured during three consecutive periods of one week in ten volunteers smoking ciga.:ettes of prngressivelY lower tar/nicotine content (from 20 mq tar~/1.5 mq. nicotine to 4 mg tar/O. 14 mg, aicotine) . Cigarette consumptioz inc_eased'significantlp (P < 0.01) d'uringthe lov period and vary low period compared with the medium, period. The mean COt[b levelsfzll from 6.34 percent in the medium period', to 6.25 percent in the low p2riod and to 3.80'percent, in the very 1'ow period (low to very low, P<. 0.01). There was a decrease in butt 1'ength from 8.84m mm in the medium period to 7.20 mm in the low and. 4.54 msin the very lov period' (low to very loY, P < 0.01). , There vas~ a rise in the obsarved!/ezpected filter- nicotine ratio fro.m 0.62 in the medium to 0.7'7' in the low and 1.23 in the vary low period. These~ results suggest a change in: the smoking pattern. The fall in CoHb lev_l's did not correlate with the fall in the expected' carbon monozida (C0) dose as predicted by the smoking machine. When the- Co dose Yas corrected for changes in the smokiag pattern the values obtained: showed a close correlation with COBb levels., It is~ concluded-- that, on, changing to very low tar and very low nicotine cig,arettes, consumption increases, smoking patterns change, but COfHb levels fall. (Auth., Abs.)
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79'-1i114 Yu2uc, C,; Kuinze, !!'. Aauclagewohnheiten von BSasenkrebs-Patienten• Versuch zur Quantifizierung der Schadstoffexposition. (Smoking Habits of' - Blaid3'er Cancer Patients: Am AttemFt to Quantif'7 Tar Exposition. ], aktue2le ' Orol ogie 10 (3) : 159-16,2, C:aY 197a:, German. There were significantly more cig;3rette smokers among eale bladder cancer patients than in the corresponding population g'ro~up, rhe tar expiosure of' =' _the average smoker in Jlustria has gone down as a result cf the decrease in sales of' nionfiltere3 cigarettes anithe decrease in tar content of cigarettes, Bladder cancer patients di3 not follow this trenid: 96 percent had' coasumeC' cig,arettes Yith high tar contents most of the tive; 52' percent saoked only high tar cigarettes. The iapSeaentation of a maximur limit of tar'content per cigarette would be of aajor iaportance for'the prevention :of,,.tobacco-assoc'iate3'.cancers and other diseases. (Aluith, Abs.,) 75-1252'.*W31d, N.; EHolward, S. ; Smita, P. G. ; Bailey, A. Use of. Carboxyhaemoglobia Levels to~ P.edict the Development of' Diseases Assoc_ated with Cigarptte S,aoking,. Thorax 30: 133-140, 1'97,5', Eng'lish. Carhoxyhecoglobin(CC1ib) levels in tobacco smokers vary thrcughout the day accordinig to the pattern of cigarette consmmFtion and the rate at which CCEb is eliminiatedl. A method is described whereby a single COSibt measuremer.t together with a recent ssoking history may be ased to est:mata the average C0Hb increase produced by each cigarette, the tctal dlaily carbon aoncxide (C'0), uptake from smoking, and the mean COr7b level throughout the day. These three indicas of tobacco! smoke absorFtioa ve.rr estimated in nz'nc healthy cigarette smokers on different days. The indices were reasonably reproducible withia the same person, and the differzmces betwefnl people were statistically sig,nificaat (p < 0.0011).. Thee s timat~esof ineand'aily C0Bb level resultin3~ from sm~ok~ingraniged f~rca; 0.7 to 9.3 percent in smckzrs yho sm~oked 15 to 40 cigarettes per day. These difie_er.ces are suf'ficiently large to distinguish possible differeacros iL the risk of developing' diseases such as iscfiemic heart disease~ which may result fzcm the inhalation andi absorrtion~ of tobacco saoke. ( AutS . Abs. Nod'. ) 100Si052823
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76r011i9. L'a1d, N.; Howard, S. Smoking, Carbon Honoxide and' Arterial @isease. Annals of Occupational Hygiene 1'S (1) : 1~-1u, 1975, English. .. The role of carbon monoxide (CO) as a measure of' tobacco smoke absorption and as a possible cause of arterial disease in man is reviewea. Smoking is thie most important single source of exposure to Co, and, ~' frequently leads to carboxyhemloglobin (CO11b) levels above eight percent. liiost filter-tipped cigarettes produce more CO' than plain cigarettes. The miain factors affecting the uptake and elimination of CO are considered; a single COHb mleasurement combined with a recent smoking and, exercise history can be used to estimate the CO'Eb*derived from each cigarette. In one study in a factory population in Copenhagen, the proportion of' sub jects with coronary heart disease and/or intermittent claudication increased not only with tobacco consumption (11 percent among heavy, smokers and one percent among light smokers) but also with CClilo level (18 percent among heavy smokers with a CoHb level of eight percent or mcte). C0 exposure from smoking has been shosrn to be harmful in persons who already have coronary heart disease or intermittent cLaudication. The evidence that CO is also harmfulin persons without arterial disease is inconclusive, but animal data suggest that this may be the case. Some implications relating to the use of "'smoking tables'" and thE odification of cigarettes are corsidered. (guth. bbis. ltod.) 70-if149: Wynder, E. L„hiabuchi, K., Beattie, E. J. (7r.) The EpidernioloMr of Lung Cancer. Journal of the American. Medical Association 213(13):2221-2228, September 2'8,197CD. A retrospective epid:atiologie investig3tion of 350 lung cancer patients of the Memorial Sloan -Kettering Cancer Center observed between Noszmber 1'966 and August 1969, confirmed the close association between ci;arette smoking and lung eancer,, particularly of the squamous and oat cell types. New trends in this'stntdy show that, there is a decrease in relative risk for those patients developing lung eance'r ten years after they have switched to fi7ter cigarettes, possibly due to the lower "tar" content in fdter cia3rettes smoked by theu patients. The risk also deciunes after complete cessation of smoking snd appears to approach the level!of nonsmokers after 1'3'years of not smoking. It is su,;;ested that further efforts to produce less harmful tobmcco products be continued and' expanded' aPthou,lt no smoking or cessation of smoking is the most effective prevention av,ietsc lung cancer. (Auth. Abs. Mod.) ~_~e,. . . . 72-0578. Wynder, E. L., HotTmann, D. (Editors)' Less Harmful Ways of Smoking, A Workshop of the Second, World Conference on Smoking and Health, London„ September 20-24, 1'97'1. Journal of the Nationai' Cancer Institute 4'S(6):1739-1891, June 1972. This workshop was condttczed' to deI'ine what constitutes a less harmful tobacco product and'less harmful smoking habits and to seelc the cooperation of the scientific community and the tobacco industry toward further progress in this area. The pzpers presented cover international'research in tobacco and health, epidemiolo}cal'znd biochemical'studies on tobacco and liealth,and'model studies in tobacco czrcinogenesis. 72-0579. Wynder, E. L., Hoffirrtartn, D. Less Harmfuli Ways of Smoking. Joutnal' of the National Cancer Instiiute 48(6):1749-1758, Jur3e 11972. This communication sureests introducing ways of smoldngtha!t may be less harmful and that are based on the principle of bringing less smoke in contact with lung tissue which wi.tl result in less absorption of tobacco smoke. The discussion shows that cig3r and pipe smoking is generally amsocinted' with a lower risJc'for smoke-related disease, larD ly becatts', ci:zr and' pipe smokers rarely inhale deeply, and that certain types of cigarettes are less instrumennal' in the induction ot' ;ung cancer than others and' are also likely to offer a Iower risk for' other to'bacco-related diseases. Continuous mt:nitori:.g of human smoking habits is vital to the appropriate evaluation of tobacco products presently avaiInblz as well'as chanc:rt tnd. modified' products that may be offercd in the future. This information sliould provide appropriate guidelines anti incrn- tives for tobacco, industnes and governments interested in producing prmdlucts dtrsigricd to make tobacco smoking as hsmless 3s possible by scrting maximum permissible levels of the diffierent harmful components in the smof::. While in some countrics the tobacco industries are already movin;, in, this direction on their own, appropriate goverttm<tttal, directives to accontplish this end are favored where necessary.

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