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ronchitis; y a er S. Mitchell, MD, Thomas'N:t:Yincen,i . Of 150 patients with chronic bronchitis and/or diffuse obstructive pulmonary em- ~physema, 143 were cigarette smokers, most of them heavy smokers from an early age. Of the 60 who stopped smoking, 44 noted complete or almost complete relief from coughing. These 44 evidenced a lower mor- tality rate during the 20 years after the onset of their dyspnea than did the 84 who continued to smoke. The lungs of 125 persons who died after age 40 were graded for chronic bronchitis and the quantity of emphysema and black pigmentation. Em- physema and pigment were usually found in close proximity to each other. These three factors correlated well with each other and also with the cigarette smoking histories. The nature of the black pigment is unknown. absolute certainty: by microscopic examination', lung tissue." r ~~'. , ; eviilence. ' In this paper, we will review the °ing smoking and • chronic bronchitis' and ' assemb, our data relating smoking to-::emph}xsema;dia nosed at autopsy. ° A CCUMULATING EVIDENCE indicates that [i cigarette smoking is one of the major causes of chronic bronchitis, outweighing in importance the effects of community air pollution. The ques- tion whether smoking causes emphysema is com- plicated by difficulties of definition and by lack of reliable information on patients studied during life i and post mortem. The bulk of epidemiologic data on smoking and chronic bronchitis comes from Great Britain where "emphysema" almost always has been considered to be a complication of chronic bronchitis. In the US, "emphysema" generally has been the label given to disabling, chronic, obstructive bronchopulmonary disease, and much less attention has been given to • the bronchitis often present or at least antecedent to the disability. Recently workers in both countries have con- curred in the following opinions: (1) chronic bron- chitis may occur without emphysema and vice versa, though the two diseases very commonly coexist; (2) both diseases are associated with ab- normalities in the flow of gas and in the removal of secretions; and (3) emphysema is a morphologic entity characterized by disappearance of alveolar' nary diffusing capacity determined,by'`the'ibrea walls and -the diagnosis can only be made with ;.-holding technique is ;significantly."lower an'sinok -. 17,. „' than in nonsmol{ers. From the Webb-Waring Institute for Medical Research, the Colorado Human 7ung.:and bronchial tissues'obtamed fron0~ sp1 ' tration Hospitel, and the De- ,: r y. ~~~~ . . pa~ent of Medicin® Umversity of Colorado School of Medicine ,t {ha•bit11a1FClgarette +smokers shoW .COnslderRbly' 3nor£? . .,... ,. .. _ . ,. .w~ i. :.cl. Review of the Literature Almost without exception, available!literature suggests association of cigarette . smoking wi chronic broncbitis." Some mention is; also made~; of an increased incidence of respiratory' illnesses in smokers ° The association of smoking with "etpphp- sema" or` breathlessness without' cough has !"beenu stressed much : less . frequently.°.° In ? fa,cb,'r', some; doubt about such an association has been expressed Some mention has also been made of the Very: quent and striking improvement in couglung'noti after smoking has been stopped.l° As in the case of lung cancer, both the;frequenc3~ and severity of chronic bronchitis appear to be~ related to the amount smoked.2'g Also like ;lung cancer, the association is predominantly with ciga= rette and not with cigar or pipe smoking.2•g; incidence of chronic bronchitis is appreciably" less in women than in men, presumably because of con-; siderable difference in their past smoking habits.l'"" Emphysematous subjects are especially Vulner- able to bronchial irritants; smoking tends to aggra vate their airway resistance.12''g. The additive or; synergistic effects of community air pollution'and cigarette smoking have also been stressed `'14 Habitual cigarette smokers have a lower means, ventilatory performance by various methods o# measurement (forced expiratory volume in one.seal ond, maximum midexpiratory flow rate,' and maxi mum breathing capacity) than do nonsmokers .~". In addition, the residual volume, but not total."lurig~ -••capacity, in smokers was moderately elevated'above=; the predicted normal and above that observed in' nonsmokers.'e Inhaling of cigarette smoke causes, an; -acute transient increase in both airway resistance,', -and residual volume 1e;' these observations. ,ha,ye, been made especially in persons mith"ehronic t -structive bronchopulmonary disease:i2 The"pulmq-;r e

rriean ~iH~ bf ~iterxak~blood 'was 1 :33 'The "meari ~"f~ i`blid'785. ~?hddd ; .a~oearae 'ioo was.e, stanar;~ev.i tion+of'th& stlifferenee~ between arterial blood p_ i ar ldbe bl.qad~iH~Iw-i-"0 02 pH units: f espiratbry,.aK-;alosis was mduced in six.patients.'° ~' thot~ght tivould be`" the widest possflile~ ~di$erencd ' rei3 is i'plot~df. the: pH values for arter,ial an&" tr ' ,; in the resting patient,'• we then"compard "arteria ar lqlie blood in' these patients. The mean pH of;. ; ' ar~eri4 ~blood,~~~inder`ahese ~eircumstances,`was 7 57 .'. tlxe mean pH of ear lobe"blaod was':7.56., e;pl~ iof :blotid obtained from a puncture of e;unwarmed fuirger was compared with the pH ; bf'~arter;al blood in '19 patients. A plot of the com- arisori is shown in Fig 4. The mean pH of arterial ~ kl~w'`745MHf bld frh fi as.,..ean p oooom tenger as"7~'~45:~ The standard deviation of the difference etweeli•-`arterial blood pH and blood from the, riger was -- 0.03 pH units. 'Figure -5 is a plot of pH of arterial blood against central 'venous blood pH. The mean pH of arterial -blood'was 7.47 and the mean pH of central venous blood was 7.43. Comment 'These experiments show that blood obtained ~;•from the warmed ear lobe accurately reflects ar- ;;terial pH and that the pH of blood obtained from Nof 'arteriale blo de Althoughcthepcorrelatio sh we e made in respiratory acidosis and alkalosis, we be- lieve that the same correlation exists in metabolic : acidosis and alkalosis. Some of the patients re- ported did have metabolic acidosis. We suspected that the warmed ear lobe would accurately reflect arterial pH because the ear lobe is thin, can be easily heated, the ratio of blood ., flow to tissue metabolism is large, and the punc- ture of the ear lobe usually results in a free flow of blood. The disadvantage is that warming is re- quired. We wanted to make the technique of obtaining' blood so simple that any laboratory technician could do it. We thought of drawing blood from the finger employing the same technique that is used in drawing blood for routine blood counts. The pH of blood obtained in this way is compa- 'rable to arterial blood pH. Since blood obtained from'the finger is probably a mixture of capillary ,and venous blood we thought that the pH of mixed MclcAL°D~'E~T ; ` F-'~ P °r P~t .tY-; ,If~ . ; venous4 liland must ' approxe Of~~arteria laad ar' ~ve:~ould bave found;;a lat, dlscrepaincy ~Aen :wetcompared,arterial blood`pH w1th'6e.pH, of:' blood" from ;4he finger To ,c~bsexve~~n?hat ;•blood pH with,'the pH •of blood obtained from the ;' y, ~}' pulmonary, artery or right aiuricle Some difEereince: exists, =but it is small In some patients we had difficulty in "obtainin~ blood from a finger puncture. These wereW patients; in circulatory collapse, patients with very thi avascular skin such as that found in scleroderma and in a few patients there was no evident caus for the failure to obtain an adequate sample. When' this problem arose we used ear lobe blood 7 or arterial blood to measure pH. The clinical significance of these studies is ° to'' demonstrate that a direct rather than an indirect ` measurement of blood pH is important in evaluat- ing patients with a disturbance in acid-base bal- ance. The methods we have described should en- able most hospitals and laboratories to make these measurements routinely. We do not mean to imply that the measurement ?:, of pH is all that is needed in a patient with an acid-base imbalance. The carbon dioxide content ~ of venous blood and the pCO2 (which can b'e cal-„-, r culated from a nomogram if pH and CO2 content '" are known e) are needed as well. Estimated arterial pCO2 is needed to discover if the patient has respi- ratory failure for carbon dioxide elimination. While , in the patient with pure metabolic acidosis (eg; diabetic acidosis) the pH is acid, and the pCO2 and CO2 content are low, and in the patient with pure respiratory acidosis (eg, pulmonary emphysema with lung failure) the pH is acid and the pCO2 • and CO2 content are high, it is possible to have confusing combination of acidosis and alkalosis. In the patient with an acid-base imbalance it is neces- sary to have measurements of both blood pH and serum CO2 content. University Hospitals, Iowa City, Iowa 52241 (Dr. Bedell ). This investigation was supported by research grant H-7104 from the National Heart Institute of the US Public Health . Service and in part by Public Health Service Research Career Program award HE-K3-4007 from the National Heart '~ Institute, and was aided by grants from the Iowa Tuber-'` eulosis and Health Association and Iowa Heart Association. References -1. Brooks, D., and Wynn, ' V.: Use of Venous Blood for 4. Gambino, S.R.: Collection of Capillary Blood for .. H and Carbon-Dioxide Studies, Lancet 1:227-330 (Jan 31) Simultaneous' CO$ ' '' 4959. Determinations of Arterial pH,Content, w p :; Pco$ and Oxygen Saturation, Amer J Clin Path 35:175,183 2 Gambino S R.: Comparisons of pH in Human Arterial, ( Feb ) 1961. :, 9M '!Venous,6d Capillary Blood, Amer J Clin Path 32:298-300 5. Cooper, E.A., and Smith, H.: Indirect Estimation `of'': " ( Sept )"1959. Arterial Peo4, Anaesthesia 16:445-460 ( Oct ).1961. ' 3 Maas, A .H.J., iieijst, A.N.P.van: Comparison of. ; 6: Singer, R. B., and Hastings, A.B.: `Improved Clinical" '± pH of Artenal BIood Frem Ear Lobe With Astro's Micxo 11+Iethodfor Estimationof Disturbances "of Acid-Base BaT ` , r p Glass Electr(yde,yClin`Chirri~Aeta 63133;=19'61 ance;of Human Wood, Medxcine (Ba1t)a27 ,- ir

, GAR~~TE { u eY `a ' + tholo c chan es , uamous~meta lasi gtg >g sq p ~lo f cilia,, fibr`osis, at postmorte~n ea~aminatiob than o'thos'e from°nonsmokers or'ex-smokers.1g App'lica~ on of cigarette "sinoke condensate to the broncl~ial~~'!~,, ~" :: ~`. ~; rt, nc osa of laboiatory dogs caused similar pathologic ssive 3s ~~oysprle,c ' C11an~eS. Asthmatid'~ fthlilll fro thy~ e cilia o epiea cesme respirator, ~ Etraets of man and various animals in tissue cultune ~~ a he one noncigarette smoker ~s, a{reEufar p~re srni show complete temporary inhibition after exposur ~~. . ~ i. r~ . f . . At M o c3garette smoke or to cigarette smoke cond,en- ~~.but 22 of the 1~ smokers frirthrs'pati~n~~p ~sate. Habitual smokers and persons recently ca~-~ ~~ ulation 'averaged at"least:`2U cigaret#es' a~'day, tnaui 'itdithi h filih d ,' ce w pneumonaaveewer ca tano, .; t~oked 40 and even GO cigarettes `a'clay ~ or . : others21 Smokers over 40 had shorter cilia thari; ` '~' ~° ~eage at which they started to smoke variei . ronsmakers of the same age.22 The self-cleansing ~ 4 to"50 with a,anean of 1$ The'ntimberaof -,,.: ~ trnechanism of the human tracheobronchial tree is ~ years" (20 cigarettes a day forone year as;;lalaelldT - ~ a'!impaired in persons with chronic obstructive bron''k)kdy - one pac up to th anset of Ad year smoee,s chopulmonary disease as compared to normal per- varied from 10 to 77 with a mean of 31 . '9 sons. Humans with chronic bronchitis almost The expected frequency of smoking in this popu- always show extensive loss of their cilia-bearing lation composed predominantly of~ males : ' aged "5, bronchial epithelium18 Healing of ciliated respira- t 75 (' 48)d' .omean 'years at onset'accoin!td^' ,,rg~ tory epithelium in dogs was delayed by exposure to 1958 US Pbli Hlh Suodt uceatervice 25 srvey; wu2 cigarett24 e smoke condensate. have been approximately 75o to 80%; the obv Recently application of cigarette smoke to lung f h ,requency of 95% therefore was appreciabli yg extracts which were considered to represent the In addition these smokers were very much' more normal alveolar lining caused a decrease in surface apt to be heavy smokers than an average US popu-~ i tension; in addition lung extracts from rats exposed lti Thkfidh ~ ,aon.e nonsmoers were conne anast- clusively to those with an early history of broncliial~ asthma. All patients were admonished to stop s,tna Numerous techniques were utilized, always''incT ing a frank statement that smoking was unques= tionably harmful. Success in stopping smoking'i~t this patient population is shown in Table 2 ~i'vvoyia . Frequency of SmokingBetween July 1956 and observations recorded in Table 2 are emphasized,:~ .-,, (1) overall success in stopping smoking was iovi~, July, 1961, 150 patients with well documented ie, 42% in this group of patients; and (2) three~ chronic obstructive bronchopulmonary disease were fourths (77%) of those who stopped did so, befoi;e~~ studied clinically and physiologically with great being exposed to the efforts of the authors . The authors arrived at the impression =fihat a' considerable portion of these smokers were' truly addicted to cigarettes. With almost no exceptions;; those who continued to smoke admitted that smok- ing was probably harmful to them. In ',support".o this opinion broadly held by these patients, '44'"v'o the 60 (66M) who succeeded in stopping 'smok'; also experienced striking relief from coughing.l^In; fact, most of these 44 patients repeatedly sta;t , that they stopped coughing altogether. M. `I' We were unable to identify any particular to cigarette smoke during life have been found to have lower than normal surface tension.14 Some observers have found areas of emphysema in close proximity to deposits of "soot," although the exact nature of this "soot" is unknown. il ~p133 Moderately Severe and Severe Chronic Obstructive Bronchopulmonary Disease care. Each patient had a maximum breathing ca- pacity of less than 50% of predicted normal. All were followed for the ensuing two to six years. Smoking histories were obtained by personal in- terviews conducted by one of the authors at the original examination for this study. Each patient was asked the age at which he started to smoke, whether he smoked cigarettes, pipe, or cigars, whether he inhaled, his maximum and average daily consumption, and when (if at all) he perma- nently stopped smoking. These questions were asked again at each subsequent visiti ' of individual who was either successful,orurts'nc Frequency of smoking among these 150 patients ;. T~ is shown in Table 1, subdivided by our clinical Table 2.-Success in Stopping`Smoking classification of them. Those who coughed for from "2 to 41 (mean 21) years before onset of dyspnea on '~exertion are labelled "tussive"; those who denied cough prior to onset of their dyspnea on exertion were labelled "dyspneic"; and those who gave a history of episodic wheezing dyspnea almost always starting in childhood and prior to onset of persis- tent dyspnea on exertion were labelled "asthmatic." ~Stopped- before onset of dyspnea ....,.:..1i..:.;.v Stopped* before initial study examination Stopped' after initial study examination Smoking continued to present ........ .:...:. ~~ '83 Pipe smoker ~;. . ................................... Nonsmokers ................................... 'b, •W}thoutA resumptiori,,to, date. ys, `-a;. . . .....•~, .,. , ~~

A0...j15, 20 5 10 15 20 YfARS AFTER ONSET OF DYSPNEA / Fiq 1. Inffuenceof stopping smoking and coughing on ex- !"tss '20.year mortality and loss of exercise tolerance as sxhibited in 128 patients suffering from chronic obstructive ~b,ronchopulmonary d'isease. • u.,.. . 5 10 15 20 AFTER ONSET OF DYSPNEA Fig 2.-Improvement in excess mortality from stopping smoking and coughing is indicated by shaded area. 125: '59 14 12 AitExTE-SIVIO t'u!~ 8A CQN'T 13 Fig 3.-Cornlation of morphologic evidence of pigment deposition, chronic bronchitis, and emphysema an 125 per- sons more than 40 years of age who died of various causes. For definitions of quantity of emphysema, chronic bronchitis, and smoking history, see text. I 11 16 ° MITC1' HEI,L~a,~~ 8,19 q N~ -cessful in.sto-pping s~ok'ing~ Women"vvexe get~er,ally 0, more successful in sta~ping" than men, ;Pgtiextts~~_ . a.a. . k ~ ere ' already tatally disabled appeazetl more A1 ~ :_~:to stop than individuals wwith .Iess,`disali~t~; ' in 'better socioeconomic positions and ~'~those ". i y; greater intelligence appeared more able,°to stop.:,.;{+4 Effect -of Stopping Smoking on Mortadity.:Ihe' ;.prognosis for these 150 .patients was measured• by ¢; both mortality and loss of eiercise 'tolerance, ,1,ov i f an observation period of from two to six years,; date of onset of persistent dyspnea ( consciousness of respiratory discomfort) on exertion was based„ upon the patient's subjective statement and ante- dated the authors' original examination by, fr,om;' s• 1 to 38 years. Exercise tolerance of each patient was estimated from symptoms and work capacity and, after ac- cession to the study, from the objective pulmonaiy ., function tests. Exercise tolerance was categorized `.~ into one of four different degrees for each patient for each year after the onset of dyspnea. Group 1 included patients able to walk indefi-;~ nitely at a regular pace on level ground, and able''" to climb more than one ordinary flight of stairs ',';::; without stopping, but in the patient's opinion, be- coming shorter of breath on exertion than expected A for average individuals of the same age, weight, 4=;: and sex. Group 2 was composed of patients able to walk no more than approximately one block ;i -- ( approx 500 feet ) on level ground and/or able to f-' climb one flight of stairs slowly without stopping. : Patients in group 3 were able to walk no more than 50 feet on level ground without stopping and a~^ ' were unable to climb one flight of stairs without.. stopping. Those in group 4 experienced dyspnea °.' at rest. 'nr One of these categories was applied to each pa- ' tient for each calendar year after the onset of dyspnea. This categorization was intended to char- acterize one entire year and was necessarily some- what arbitrary, especially for those years before the patients were seen by the authors. However, different observers have had little or no difficulty in agreeing on the categorization of cases after accession to the study. Furthermore, improvement in exercise tolerance sufficient to justify a lower numerical classification has not been observed in this group of patients after accession to the study. Reports from hospital records and other physicians and the observed status when first examined all aided materially in determining the categories as- signed before observation. The 150 patients were divided into three groups: (1) 44 whose coughs disappeared or were ' pressively improved after stopping smoking, . (2) 84 who continued to smoke, and (3) 6 who were nonsmokers plus 16 whose coughs did not disappear or improve greatly after cessation of . smoking. The severity of disease as measured by objective ' pulmonary function tests was ,approgi-ve

w'. ~niately' the ;'same m`;~he' first two' , gro.ups uwhic' were 'oompared: The cumulative' expected morEali for a standarc1=17S: population,.of the same ;age,an ex! distribu.tion was determined.' This, was sub,, cfied-iIrom;Ahe cumulative observed mortality., cumulati ve , excess' mortality and loss of exer ~ ' ek tolerance',over;the two- to six-year perio~p~ „ ' e first two ;'of these three' groups is 'shown, 7n'~ g: 1. The improvement in mortality in those who"'F ;'stopped smoking and coughing is illustratei3, izi °'2. #~Emphysema and Black Pigment in Lungs We made a postmortem study of one lung from 125 persons dying with and without clinical evi- idence of chronic obstructive bronchopulmonary disease; these included 18 , of the above patients whom we studied very carefully during life. The group does not include any persons under 40 at death and excludes five coal miners, three of whose lungs were markedly "anthracotic." Most of the patients in this study had been lifelong or longtime Tesidents of Colorado, many coming from rural areas. A few had emigrated to Colorado from east- ernm cities for their health. Historical information was obtained from hospital charts and from replies to letters sent to nearest of kin and to referring physicians. A few patients available for these spe- cial studies on whom reliable smoking histories were not available were excluded. The amount of black pigment deposited through- out the lung on gross and microscopic inspection was quantitated on the following scale: 0, +, ++, +++; it tended to be located in areas of lung departitioning or damage, along the pleurae and surrounding blood vessels, bronchi and bronchioles. All lungs in this study were found to contain pig- ment. We have never seen a lung from a person older than 13 years of age that did not contain at least small amounts of black pigment. The amount of departitioning, ie, disappearance of alveolar walls, damage, or emphysema, was also graded. Lungs were fixed in the inflated state by the formalin-fume method of H. Boren or by the Zenker-formol liquid method of R. R. Wright. Lungs were sliced into 1 cm thick slabs. Both sides of all slabs from a lung were examined grossly and with a hand lens and an estimate of the degree of gross departitioning was made. Those with less than 5% of the lung departitioned were graded 0; those with from 5% to 25% involved were graded +; those with from 25% to 66% were graded ++; and those with over 66% departitioned were graded Departitioning was always confirmed by examining selected sections under the stereoscopic microscope. Our change from the formalin-fume, air-drying technique to the liquid Zenker-formol method was made after we discovered that the dried tissues = often made -evaluation of the bronchial mucosa,. l °{9!i~~n ,!~~f j " ~cultt and nnrelrableOura.v,~e~ x pqrtance of~'chronic bronchitis~r ~ ~~cleath=~~; ~ed~o care£~il effor[~ ; "clf" eacli' pariet °s follos:% u ' o:n.':.~ * ' ', chronic ~Tperplas~ic ,En ~ b~n ; . ' present bq. all' standa7rd `` "oritea~a' ~,' as* mucus tglandS and,gOlileti z~l~s, etaplasit~,~ ulcerations and pa~ch~ loss of' ~ated h>Y 'mucoceliular plugs, aud' chronie'~u~flaYnmatory ' ^ changes ° in the' ; subepithehal tissues "S - some of, these abnarmal:~uidings, ; enough to justify a diagnosis ° of; ~etiive' e ; ' bronchitis. a A- no evidence of chronic'xoncluhs A total of 197 lungs';have .. been `studied ;~g but only 125 are included in ': this' ;r,e.'port bec firm conclusions 'regarding the" status of ; the ' chi were not available in the others, mosdy anitial 51. The quantity of smoking was graded,.as none for nonsmokers; "slight" for ''those ' smoking: up' to five cigarettes a day _ and/or a;pipe' „or cigars; "moderate for patients smoking 15 .to 25"cigarette'; ~,. wa day, average~ ab.ou.t. 20; 'arid "heavy..,,~foir` ~os smoking more than 30 cigarettes' a T day, ~ usna 40 or more. Smoking habits appeared, to; be } markably consistent with the exception that of those with chronic obstructive bronchopnlm nary diseases tended to cut down in the last uionths of their lives. We had the impression that,'the, "slight" smokers were not too differerit `from'x" nonsmokers. We felt that the "moderate ;'''.-a ably ." . "heavY" smokers tended to be rou ` " their exposure to cigarette smoke. ;' The correlation of the findings of pigment, chroa~c; bronchitis, and emphysema with the smoking 4 tories is shown in Fig 3. Of 40 patients with .rnore~ than 25% emphysematous lung destruetion, and +++ emphysema ), all except 2 were xe lar "moderate" to "heavy" cigarette smokers. 28 patients with definite diagnoses of chronie.-bron-a, chitis all except one were again regulax' rn erate to heavy cigarette smokers. This one^was! a`~ The non- and sli' pipe and cigar smoker.ght,au~c ;t ,. ,ers tended to have light (-- ) lung pigmentation _, and postmortem examination tended not to 'ea :chronic bronchitis or emphysema. ~Bronchitis; physema, and no obstructive disease , were fduni 'to be distributed at random among moderate-;an ''Ieavy" smokers (Fig 3). ~~: . ... .~ Comment The correlation between the amount of smd and the presence and degree of c1n•onic bronih'itis `and emphysema and of lung'; pigmentation wwhiehti :wwe have demonstrated by no I means° proyes '~t hypothesis that the inhalation of cigarette" smttkeA -is tlie only or even one, of the causes of:enxphys -a` 'disease' clearly described°, in ;the anineteeni ceryy; before""cigarettes~vvexe.' gene~a~availa !!,Y "tiTm

Si, data presented in F"ag "~ad~oapg6ar `to Indxcate ? ose ian-qssooiahon -between smoking and em-' ~ema~ as" ~etuv smoku~g `-sand chroruc brqn ; ' ';~tR ~e~qaki~ # ~ I; ry0st~ii8 ~'~~ 4~~") almt~st~l aur~ patients ' lived in lCoiorado; + . ~a ;~~tliough" same ~for ~~only `a , few` years, it does not " m dustrial';air poilution was a major '':;ahat' in 4causef;of 'the pigmi.~nt'we found in their lungs..The black~~pigrr~ent`v~?dhich''is, found in all adult -human ungs;: bas''beeri labelled. anthracosis. However, v1i'ilea~f4:studies of'i'ts nature have been made, ; 4`very little is really known. It could be harmless ~'ca'rbon or soot; the carbon could act as a carrier ~RA f noxious substances such as 03, 502, or NO2; er hand, it could be a tar from petroleum ~,~'aon theoth . ra nd/or , cigarette smoke or some other biologically s:!~active"arid potentially harmful substance. It is very iikely to be a mixture of materials, depending upon "'the individual's past environment. The fact that ,;t is. seen in some areas without associated damage i could mean relatively recent arrival of a noxious substance at that location, or that it is a harmless substance. Its presence in all lungs of persons from 13 years of age on up certainly suggests that sources other than smoking are responsible at least in part. Its absence from some damaged, ie, em- ; v',physematous, areas could mean that damage oc- curs in its absence or that the material had once `been #here; had; caused dama'ge,yand alici~, the -aged, lung and pi.gment had been.X ernoved vza' "'nhati b ' r yzpcs ory ;expectoration.x ' Our'°methods of' assessing the amount n£ ~?gmen in and the"degree of'_departitioning?, of;the,'~un "have been called quantitative even thouugli nnr~ have used only -an "ordinal scale" of ineasurementt `(aris=" ing from the operation of rank-ordering).'`However,;', , it has ' been clearly shown that ordinal as well as 4 interval and ratio scales have their merits. Measure=, ment is never better than the empirical operations by which it is carried out. We have been more concerned with the reproducibility of our empirical"V~~ ~ operations than the numerical methods of express- ing our results. Very little evidence has been accumulated re=,°, garding the importance of inhaling tobacco smoke': ; as an influence on its ability to do harm. The nose is a remarkably effective filter, humidifier, and warmer of the air we breathe. Industrial and com- munity air pollutants are inhaled mostly through the nose; this is not true of tobacco smoke. And not one of our 95% of smokers denied inhaling his smoke. 4200 E 9th Ave, Denver 20 (Dr. Mitchell). This investigation was supported by Public Health Ser- vice Research Grants No. HE-06067-02 and No. A1-04152. References 1. Chronic Bronchitis in Great Britain. National Survey 14. Miller, D., and Bondurant, S.: Effects of Cigarette Carried Out by Respiratory Diseases Study Group of College Smoke on Surface Characteristics of Lung Extracts, Amer of General Practitioners, Brit Med J 2:973-979, 1961. 2. Edwards, F.; McKeown, T.; and Whitfield, A.G.W.: Association Between Smoking and Disease in Men Over Sixty, Lancet 1:196-200, 1959. Rev Resp Dis 85:692-696, 1962. 15. Flick, A.L., and Patou, R.R.: Obstructive Emphy- sema in Cigarette Smokers, Arch Intern Med (Chicago) ' 104:518-526, 1959. 3. Fletcher, C.M.: Chronic Bronchitis: Its Prevalence, Na- 16. Blackburn, H.; Brozek, J.; and Taylor, H.L.: Lung ture and Pathogenesis, Amer Rev Resp Dis 80:483-494, 1959. Volume in Smokers and Non-Smokers, Ann Intern Med 4. Ogilvie, A.G.: Social and Environmental Factors in 51:68-77, 1959. Chronic Bronchitis in Newcastle-Upon-Tyne, Postgrad Med 17. Wilson, R.H., et al: Pulmonary Pathologic Physiology J 36:261-269, 1960. of Persons Who Smoke Cigarettes, New Eng J Med 5. Oswald, N.C., and Medvei, V.C.: Chronic Bronchitis: 262:956-961, 1960. Effect of Cigarette Smoking, Lancet 2:843-844, 1955. 6. Van Proosdy, C.: Smoking: Its Influence on Individual and Its Role in Social Medicine, Houston: Elsevier Press, Inc., 1960. 7. Brinkman, G.L., and Coates, E.O., Jr.: Effect of Bron- chitis, Smoking and Occupation on Ventilation, Amer Rev Resp Dis 87:684-693, 1963. 8. Higgins, I.T.T.: Tobacco Smoking, Respiratory Symp- toms, and Ventilatory, Capacity: Studies in Random Samples of Population, Brit Med J 1:325-329, 1959. 9. Dysinger, P.W., and Lemon, F.R.: Pulmonary Emphy- sema in Non-Smoking Population, Dis Chest 43:17-25, 1963. .. 10. Leese, W.L.B.: Investigation Into Cause of Bron- chitis, Lancet 2:762-765, 1956. 11. Anderson, D.O., and Ferris, B.G., Jr.: Role of Tobacco Smoking in Causation of Chronic Respiratory Disease, New Eng J Med 267:787-794, 1962. 12. Attinger, E.O.; Goldstein, M.M.; and Segal, M.S.: ' 23. 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