Smoking infection aetiology bronchial mucous gland hypertrophy · MOHAMMED H. EISSA, SAFEIA Z....

T7horax (1967), 22, 271.

Smoking versus infection as the aetiology of bronchialmucous gland hypertrophy in chronic bronchitis

GAMAL E. MEGAHED, GAMAL A. SENNA,MOHAMMED H. EISSA, SAFEIA Z. SALEH, AND

HOUDA A. EISSA

From the Medical, Thoracic Surgery, Pathology, and Bacteriology Departments, Faculty of Medicine,Cairo University, U.A.R.

The smoking habits of 50 proved cases of chronic bronchitis were studied. Bronchoscopy was

done and a bronchial biopsy was taken for histological examination. Bronchial lavage was

obtained under sterile conditions for bacteriological studies. The degree of bronchial mucous

gland hypertrophy was determined, and the presence or absence of infection, as shown by thepresence of potential pathogens in the bronchial lavage, was noted. We think that tobaccosmoking and its resulting irritation to the bronchi is the most important underlying cause ofbronchial mucous gland hypertrophy because there is: (1) a significantly higher incidence ofmucous gland hypertrophy in smokers than in non-smokers among the 50 chronic bronchiticsstudied; (2) a significantly higher accumulated lifetime tobacco consumption in patientsexhibiting mucous gland hypertrophy than in those without hypertrophy of the bronchial mucousglands; (3) a significant association and correlation between the degree of mucous glandhypertrophy and the intensity of smoking; and (4) no difference in the comparative frequencyof occurrence of bronchial mucous gland hypertrophy in subjects with and without demonstrableinfection, as shown by the presence of potential pathogens in the bronchial lavage. We couldnot deny that infection might be having an initiating or potentiating effect.

The characteristic feature of chronic bronchitis isan excessive secretion of mucus, which provokescough and expectoration. This mucus secretion ismainly a function of the bronchial mucous glands.Glynn and Michaels (1960), Reid (1960), andRestrepo and Heard (1963a, b) demonstratedenlargement of the mucous glands in chronicbronchitis. Glynn and Michaels (1960) showedthat the pathological features consisted of anincrease both in the number of mucous relative toserous glands and in the size of the mucous acinidue to swelling of their component cells and theirlumina. They suggested that this mucous changeis probably the result of transformation of serousinto mucous acini, followed by an increase in sizeof the latter. They considered that this mucouschange of the deep glands is the most importantpathological feature of chronic bronchitis. Reid(1960) found that the amount of sputumproduced by the chronic bronchitic was wellcorrelated with the degree of mucous gland hyper-trophy. To investigate the role of smoking ininducing this mucous gland hypertrophy, Thurl-beck, Angus, and Pare (1963) examined bronchifrom necropsies and grouped cases according to

smoking habits. They found that the Reidgland: wall ratio was significantly higher in heavysmokers than in non-smokers.The aim of the present work was to study the

correlation between the degree of hypertrophy ofthe bronchial mucous glands, as shown bybronchial biopsies obtained from chronic bron-chitics, and the smoking habits of these patientsor the presence of infecting pathogens in thebronchial tree, in an attempt to evaluate the rolesof tobacco irritation and infection in the produc-tion of this mucous change in the bronchialglands.

METHODS AND MATERIALS

Fifty men with chronic bronchitis admitted to theMedical Department, Cairo University Hospitals,constitute the subject of the present study. Thisconfinement to the male sex was not due to selectionon our part, for in the period from October 1962 toMay 1964, during which these cases were studied, nota single female chronic bronchitic presented to us.The ages of the patients ranged from 25 to 70 years,with an average of 47-2 years. The diagnosis ofchronic bronchitis was based on the Ciba Guest

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272 Gamal E. Megahed, Gamal A. Senna, Mohammed H. Eissa, Safeia Z. Saleh, and Houda A. Eissa

Symposium (1959) definition--'the production ofphlegm on at least four days a week for three monthsof a year for at least three years'. Plain radiographyof the chest and bronchography was done in eachcase. Cardiac patients presenting with chronic cough,patients with bronchiectasis, genuine asthmatics, andpatients in whom investigations disclosed a specificcause for the chronic cough were excluded. A care-ful history of the smoking habits was obtained by twoof us to cross-check the data. Patients were askedwhether they smoked. Smokers were asked about theduration of their smoking habit and the type ofsmoking practised. Some smoked cigarettes, others'gouza', a peculiar smoking habit prevalent amongour patients, and a third group smoked both cigarettesand gouza. None smoked pipes or cigars. Each timea patient smoked gouza this was considered to beequivalent to the smoking of two cigarettes. Anyerror produced by such an assumption would notaffect the results materially. Patients whose answerswere variable were not included in this study. Theaccumulated lifetime tobacco consumption was cal-culated for each patient by multiplying his average

daily consumption of cigarettes, or cigarette equiva-lent of 'gouza', or both, by the duration of the periodhe smoked. Patients were graded according to theintensity of their smoking habit -as follows:

DAILY TOBACCO CONSUMPTON

Grade Cigarettes/ day0 Non-smokers1 1-2 10-3 30-4 50+

ACCUMULATED LIFETIME TOBACCO CONSUMPTION

Grade0

1234

Cigarettes (thousands)Non-smokers

1-200-400-600+

BRONCHOSCOPIC TECHNIQUE All instruments used inbronchoscopy were sterilized by autoclaving beforeuse. Patients were seen in the morning after a 12hours' fast. They were given a premedication of intra-muscular phenobarbitone and atropine sulphate one

hour before the procedure. The bronchoscope was

introduced under tetracaine hydrochloride surfaceanaesthesia. After general visual endoscopy, bronchiallavage with sterile saline, using a sterile syringe andinjecting it through the bronchoscopic aspirating tubein the main bronchi, was performed. A few seconds

later aspiration was done after asking the patient tocough, and the lavage was collected in a Luken'sspecimen collector, which was then sent to the bacteri-ologist. This laborious aseptic sterile technique wasadopted and bronchial lavage preferred for bacterio-logical studies in our patients, since we were awarethat bacteriological examination of the sputum orthroat swab is misleading due to contamination bypotential pathogens of the nasopharynx, which mayoccur in patients with no bronchial infection, and thusbe a source of error as demonstrated by Masters,Brumfitt, Mendez, and Likar (1958) and Laurenzi,Potter, and Kass (1961). Brumfitt, Willoughby, andBromley (1957) had found that normal bronchiswabbed directly through a bronchoscope weresterile, whereas Haemophilus influenzae was isolatedfrom 18 of 19 chronic bronchitics.A loopful of the bronchial lavage obtained was

inoculated on to duplicate plates of blood agar, oneof which was inoculated aerobically and the otheranaerobically at 370 C. After 24 hours' incubationplates were examined for growth. All organisms wereidentified by visual examination and smear. Staphylo-cocci were tested for ability to produce coagulaseby the tube method using rabbit antiserum. Allcoagulase-positive strains were recognized by theproduction of haemolysin on blood agar plates.Pneumococci were injected into mice and the post-mortem picture was studied. Strains of H. influenzaewere identified by their morphology and indole pro-duction. Gram-negative rods were identified by sub-culture on differential media and biochemicalreaction.H. influenzae, Staphylococcus aureus, and pneumo-

cocci were considered to be the most importantpotential pathogenic organisms for the bronchi, asreported by Dowling, Mellody, Lepper, and Jackson(1960) and Cherniack, Vosti, Dowling, Lepper, andJackson (1959). Neisseria catarrhalis, diphtheroids,and streptococci of the viridans and indifferentvarieties were ignored. Streptococci of the Pl-haemo-lytic variety and Klebsiella pneumoniae, althoughof lesser importance and occurring less frequently,were also considered as potential pathogens. Our 50chronic bronchitics were then classified into twogroups:Group A This group comprised 28 patients. Any

one or more of the potentially pathogenic organismswas isolated from the bronchial lavage.Group B This group consisted of 22 patients.

Infection of the bronchial tree could be excludedbecause none of these pathogens was present in thebronchial lavage.

Bronchoscopic biopsy was taken with a Brock'sbiopsy forceps under vision from the main carina.The specimens obtained were fixed in 10% formalinsolution, embedded in paraffin, and cut at 5 IAintervals.A record of the main histological features in each

case was made without knowledge of the clinicalhistory or smoking habit of the patient. Broncho-



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Aetiology of bronchial mucous gland hypertrophy in chronic bronchitis

scopic biopsies were also taken in the same way fromfive normal adult males, and were stained and usedas controls in assessing variations seen in the biopsymaterials. The ages of these control subjects were 30,39, 47, 54, and 60 years respectively.The 50 cases studied were graded according to the

state of the bronchial mucous glands as follows:Grade 0 No mucous glands or only a small number

of normal mucous glands were seen in the sectionsexamined. This group comprised 15 patients. In twoof these, serous glands predominated, with a smallnumber of normal mucous glands. In three patientsa small number of serous glands only were seen in thesections. In the remaining 10 patients no serous ormucous glands were present in the sections exam-ined.Grade I Only a slight increase in the number of

mucous glands was seen. This group comprised fourpatients.Grade 2 An increase in the number of mucous

glands was obvious, with numerous serous acini anddemilunes. This group comprised nine patients.Grade 3 The mucous glands were found to be

hypertrophied and of greater diameter than normal.

The cells of the acini were taller and wider and theircytoplasm less basophilic. The cells were also over-distended with mucus rather than showing an exces-sive discharge into the lumen, but occasionally amucous discharge in the lumen was present and thegland therefore appeared as small flat cells enclosinga lumen filled with mucus. In addition, a few serousacini and demilunes were found. This group com-prised 15 patients.Grade 4 Hypertrophied mucous glands, as de-

scribed in grade 3, were seen, but with completereplacement of the normally predominant serousglands, so that there were no serous glands ordemilunes as in grade 3. This group comprised sevenpatients (Figs 1 and 2).

It is worth noting that the five normal controlsubjects showed no evidence of developing eitherhypertrophy or atrophy of the bronchial mucousglands with age.

RESULTS

Statistical comparison of the relative frequency ofoccurrence of mucous gland hypertrophy among

FIG. 1. All deep glands are hypertrophied mucous glands FIG. 2. High-power view of Fig. 1 to show the hyper-with no serous glands or demilunes, i.e., there is an increase trophied mucous glands. The mucous glands are greaterin the number and size of the mucous acini and a dis- in diameter than normal. The cells are taller and widerappearance of serous cells. than normal and are overdistended with mucus.

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TABLE IMUCOUS GLAND HYPERTROPHY IN SMOKERS AND

NON-SMOKERS AMONG CHRONIC BRONCHITICS

Mucous No MucousGland Gland

Hypertrophy HypertrophyTotal p

No. Per No. Percent. cent.

Smokers 33 77 10 23 43 0-02Non-smokers .. 2 29 5 71 7

smokers (43) and non-smokers (7) in the 50 casesof chronic bronchitis studied, using Fisher's exacttest for 2 x 2 tables, has shown a significantlyhigher incidence of mucous gland hypertrophy insmokers (77 %) than in non-smokers (29 %),P= 0-02, as shown in Table I. In fact out of the 35cases showing mucous gland change, only twopatients were non-smokers, and it is of interest tonote that both were workers in dusty occupations,the first an agricultural labourer and the seconda labourer on unpaved dusty high roads in thecountryside.To study the relation between the degree of

mucous change of the bronchial glands and thedegree of intensity of the smoking habit, wecompared statistically the average accumulatedlifetime tobacco consumption of patients showingmucous gland hypertrophy with that of patientsin whom no change was detected in the bronchialglands, using Student's 't' test. It was found thatthe average accumulated lifetime tobacco con-sumption among patients with mucous glandhypertrophy (33 cases)-275,000 cigarettes, S.D.194,000-was significantly higher than among

patients in whom no such hypertrophy wasobserved (10 cases)-133,000 cigarettes, S.D.106,000-P<0-05.As a further study of the association between

the degree of mucous change of the bronchialglands and the degree of intensity of the smokinghabit, we used the chi-square test. We comparedthe relative frequency of incidence of markedmucous change in the bronchial glands (grades 3and 4 of our classification) in non- or light smokers(grades 0 and 1 of our classification-those whoseaccumulated lifetime tobacco consumption was

found to be less than 200,000 cigarettes) and inheavier smokers-those who smoked more than200,000 cigarettes (grades 2, 3, and 4 of our classi-fication). It was found that among those whosmoked less than 200,000 cigarettes (29 cases) onlynine (31 %) showed marked mucous change ofthe bronchial glands, whereas of the 21 patientswho smoked more than 200,000 cigarettes, 13

(62 %) showed marked mucous change of thebronchial glands. This difference was found by thechi-square test to be statistically significant(p= 0 03).

Since we classified our patients according to thestate of the bronchial mucous glands into fivegrades, 0, 1, 2, 3, and 4, and similarly classifiedthem according to their daily and accumulatedlifetime tobacco consumption, as previously men-tioned, we tried to find out if there was a signi-ficant correlation. In other words, we wanted tosee if the state of the bronchial mucous glandscould be correlated with the intensity of thesmoking habit as measured by the degree of dailyor accumulated lifetime tobacco consumption.This was done by calculating the correlation co-efficient, r, assuming that all readings fall at thecentre of the groups. To make sure that theobtained measure of agreement could not arise bychance, we tested the significance of the obtainedcorrelation coefficient by using Student's 't' test.The t was computed by the formula:

r 2Student's t=

with n-2 degrees of freedom, and thus the level ofsignificance (p) of the correlation coefficient com-puted could be ascertained.The result has shown a significant, moderate

positive correlation coefficient (r+0 335 andP<0-02) between the degree of change of thebronchial glands as detected in the biopsy speci-mens and the degree of intensity of the smokinghabit as measured by the accumulated lifetimetobacco consumption. A similar, significant,moderate positive correlation coefficient (r+0 325and P<0 02) was found between the degree ofmucous change of the bronchial glands and thedegree of intensity of the smoking habit asmeasured by the daily tobacco consumption. Thisfurther clarified the role of smoking in producinghypertrophy of the mucous glands in chronicbronchitis.

In order to test the role of infection as anaetiological factor in bronchial mucous glandhypertrophy, we statistically compared thefrequency of occurrence of mucous gland hyper-trophy in our chronic bronchitic patients with andwithout demonstrable infection, as evidenced bythe isolation of pathogens on culture of bronchiallavage, using a contingency chi-square test, asshown in Table II. It was found that the incidenceof mucous gland hypertrophy in the 28 patientswith demonstrable infection (71-5%) was similar



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TABLE II TABLE IVMUCOUS GLAND HYPERTROPHY IN CHRONIC MUCOUS GLAND HYPERTROPHY IN THOSEWHO SMOKED

BRONCHITICS WITH AND WITHOUT DEMONSTRABLE MORE AND LESS THAN 40,000 CIGARETTES, WHETHERINFECTION BRONCHIAL INFECTION WAS OR WAS NOT FOUND

Mucoua MucousGland- GlandX2trophy Hyper- Total X p

trophy

No.1 No.| %

With demonstrable in-fection .. 20 71-5 8 28-5 28

0005 095With no demonstrable

infection .. 15 68-5 7 31-5 22

to its incidence (68 5 %) in the 22 patients with nopathogens cultured from the bronchial lavage.This difference in incidence is insignificant, andthe two groups are almost identical.To study the role of infection further, and

whether it potentiates the effect of smoking,Table III was constructed. We compared the inci-dence of bronchial mucous gland hypertrophy inpatients who smoked more and less than 40,000cigarettes, among patients in whom infection ofthe bronchial tree was or was not found. Thelevel of significance of the comparative frequencyof incidence of bronchial mucous gland hyper-trophy in the compared groups was calculatedusing Fisher's exact test for 2 x 2 tables. This pairof tables shows that whether infection was or wasnot found, the incidence of mucous gland hyper-trophy was significantly higher in those whosmoked more than 40,000 cigarettes than in thosewho smoked less than this amount.

TABLE IIIMUCOUS GLAND HYPERTROPHY IN CHRONIC

BRONCHITIS WITH AND WITHOUT DEMONSTRABLEBRONCHIAL INFECTION, IN THOSE WHO SMOKED MORE

AND LESS THAN 40,000 CIGARETTES

Total Grade of Mucous GlandsCigarette Total p

Consumption 0 1,2,3,4

Infection found>40,000 3 18 (85 7%) 21< 40,000 5 2 (28-5%) 7 0-017

8 20 (71-7%) 28

No infection found>40,000 3 15 (833%) 18<40,000 4 0 (0%/) 4 0-008

7 15 (68 2%), 22

This also shows that those who smoked morethan 40,000 cigarettes had a similar incidence ofhypertrophy of the mucous glands, whetherinfection was or was not present, i.e., theincidence of mucous gland hypertrophy was notaffected by the presence or absence of infection

Cigarette Grade ofMucous GlandsConsumption 0 1, 2, 3,4

> 40,000Infection 3 18 (85-7°/) 21No infection 3 15 (83-3%) 18 0-67

6 33 (846%) 39

< 40,000Infection 5 2 (28 5 %) 7No infection 4 0 (0%) 4 0-76

9 2 (18-1'%) 11

as shown by the next pair of tables (Table IV).Although this table does not show statisticallysignificant evidence that in patients who smokedless than 40,000 cigarettes infection has a poten-tiating effect, yet the apparent effect is potentia-tion. Mucous gland hypertrophy was observed in28-5% of patients (two out of seven) when infec-tion was found. When no infection was found(four patients) no case showed mucous glandhypertrophy. This apparent potentiating effect ofinfection cannot be dismissed simply because thenumber of patients in this group is small.The fact that the effect of infection is non-

significant does not permit infection to be dis-missed, for non-significance does not mean non-existence. In order to dismiss infection as a factorone would need a confidence integral for a para-meter which describes the effect of infection, andwould need to show that only a negligible effect iscompatible with the observations.However, suppose that one writes:

p1=probability that the mucous glands are normalin an infected light or non-smoker

p,=probability that the mucous glands are normalin an uninfected smoker

p3= probability that the mucous glands are normalin an infected smoker

Then consider the evidence for or against thefollowing hypothesis:P3 =PlP2 (i.e., smoking and infection act inde-

pendently)Tables III and IV can be rearranged as a table

of the incidence of normal mucous glands, asfollows:

CIGAREITE CONSUMPTION

<40,000 >40,000Infection 5/7=0-71 3/21=0-14No infection 4/4=l100 3/18=0-17

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The data suggest that hypertrophy is rare whenboth infection and heavy smoking are absent, andthat Pi = 071, P2 0.17. These two values givepip,=0 12, giving an expectation of 2-52 normalcases in the 21 infected heavy smokers accordingto the hypothesis P3=PiP2. The observed numberis three (i.e., 14% against the theoretical 12%),which agrees well with the hypothesis. Thereforeone should not dismiss infection as an associatedaetiological agent.

DISCUSSION

The present study clearly shows that smoking isan important underlying aetiological basis for themucous gland hypertrophy seen in chronicbronchitics as evidenced by:

(1) the significantly higher incidence of mucousgland hypertrophy in smokers than in non-smokers among the 50 chronic bronchiticsstudied. In fact, out of the 35 cases with mucousgland hypertrophy only two, i.e., 5 7%, were non-smokers. These two patients were found to belabourers in dusty occupations, where the irrita-tion of inhaled dust replaced the irritation ofinhaled tobacco smoke in producing mucousgland hypertrophy;

(2) the significantly higher average accumulatedlifetime tobacco consumption in patients withmucous gland hypertrophy than in those withoutsuch a change;

(3) the significant association between thedegree of mucous change of the bronchial glandsand the intensity of the smoking habit as shownby the chi-square test;

(4) the significant correlation between thedegree of mucous gland hypertrophy and thedegree of intensity of the smoking habit, asmeasured by the daily or accumulated lifetimetobacco consumption.

Since we obtained histological material fromeach patient on a single occasion only, we cannotstate whether the glandular hypertrophy that westudied is permanent or reversible. If the hyper-trophy is irreversible, it may be argued that therewill tend to be more hypertrophy in persons witha large total of cigarettes smoked, simply becausethis total is also irreversible, that is, hypertrophyand the total smoking will tend to have a positivecorrelation because both tend to be higher inolder than in younger people. To answer thisargument, the average age of smokers withbronchial mucous gland hypertrophy (33 cases)was found to be 49-3 years (S.D. 109), and theaverage age of smokers with no mucous gland

hypertrophy (10 cases) 42-7 years (S.D. 12). Thedifference of 6-6 years between the two means,however, tested by the 't' test proved to be insig-nificant (p 0-1). Similarly, a calculation of 95%confidence limits for the true mean age of bothgroups of smokers with or without bronchialmucous gland hypertrophy was carried out. The95% confidence interval of the true mean age forsmokers with mucous gland hypertrophy wasfound to be from 45-43 years to 53-17 years, andfor smokers with no mucous gland hypertrophyfrom 34-12 to 51-28 years. The difference in truemean ages may be as large as 19 years in onedirection or, alternatively, as much as 5 85 yearsin the opposite direction. The usual theory of con-fidence limits is a little shaky on data such asthese, but the essential point is that although theobserved difference (6-6 years) is not significantone cannot discount the existence of a real differ-ence in the same direction. The question, how-ever, is whether hypertrophy tends to increasewith age so fast that the difference of 6-6 yearscan account for the observed differences in theincidence of bronchial mucous gland hypertrophy.Our five normal control subjects showed no evi-dence of either hypertrophy or atrophy of thebronchial mucous glands developing with age.We similarly compared the incidence of bron-

chial mucous gland hypertrophy, using contin-gency tables based on two dividing lines for theages of the patients, namely, 45 and 55 years, andapplied Fisher's exact test for 2 x 2 tables, to findif there was any significant difference in theincidence of mucous gland hypertrophy above andbelow these dividing lines (Table V). The differ-ences again were found to be not significant.

TABLE VMUCOUS GLAND HYPERTROPHY IN SMOKERS UNDER

OR OVER 45 AND 55 YEARS

Grade ofMucous Glands

Age (yrs) Total P0 1,2,3,4

<45 7 9 1645+ 3 24 27 0-2

10 33 43

< 55 8 22 3055+ 2 11 13 0-51

10 33 43

This lack of correlation between age andmucous gland hypertrophy may be explainedby the variability of age when smoking wasbegun and of the average daily cigaretteconsumption in the different patients. The



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average age at starting to smoke was 22years, but the range extended from 8 years(case 32) to 50 years (case 2). Thus it is clearthat the total cigarette consumption is not acombined index of smoking and age but of thedaily cigarette consumption and the duration ofthe smoking habit. In other words, the correlationbetween smoking and bronchial mucous glandhypertrophy is a true one and is not simply afunction of the age of the patient.

Since some occupations may predispose tochronic irritation of the tracheobronchial tree andmight be the underlying cause of hypertrophy ofthe bronchial mucous glands rather than smoking,we compared the occupations of the patients withand without mucous gland hypertrophy, asshown in Table VI, and no difference wasobserved between the two groups.

TABLE VIOCCUPATION OF CHRONIC BRONCHITIC PATIENTSSTUDIED, WITH AND WITHOUT BRONCHIAL MUCOUS

GLAND HYPERTROPHY

No. with No. withoulOccupation Mucous Gland Mucous Gland

Hypertrophy Hypertrophy

General unskilled 7 3Farmer 6 5

(4 non-smokers)Furnaceman .. 3 2Donkey-car driver .. IPoliceman .CarpenterSalesman 2 lClerk .. .. .. .. - I

(non-smoker)Building labourer 3Shoe-maker 3Door-keeper..2Tailor I.Mattress-maker .. ..Waiter IAgricultural labourer

(non-smoker)Labourer in a brick factory. ILabourer on unpaved high

roads(non-smoker)

Total 35 15

That chronic bronchitis observed during theperiod of this study was confined (without selec-tion on our part) to the male sex is also furtherevidence in favour of the role of smoking. In ourcountry, smoking is very rare in women and isalmost unknown in our hospital class of femalepatients.Our findings are in agreement with the necropsy

study of the bronchi carried out by Thurl-becket al. (1963), who grouped cases according to theirsmoking habits and found that the Reid (1960)gland: wall ratio was significantly higher in heavy

smokers than in non-smokers. Glynn andMichaels (1960) found smoking to be morecommon (7 out of 16) among patients havingmucous gland excess than in those with serousgland excess (2 out of 14). They commented, how-ever, that information about smoking habits intheir patients was incomplete and that it wouldbe unwise to stress the difference between the twogroups. They also could find no relation betweensmoking and the degree of mucous conversion,and suggested that tobacco is not the immediatecause of mucous change of the bronchial glands.

Since mucous gland hypertrophy, as suggestedby Glynn and Michaels (1960), is the cardinalpathological feature in chronic bronchitis, thepresent study points to the importance of smok-ing as an aetiological factor in this disease. Thisagrees with the observations of Oswald andMedvei (1955) and Palmer (1954) that bronchitisis more common among smokers than non-smokers.The present study could not show that infection

has a role in the causation of mucous change ofthe bronchial glands in chronic bronchitis. Thismay point to the greater importance of smokingas an aetiological factor in this disease and is inagreement with the views of Greene andBerkowitz (1954), who reported smoking to befour to seven times more common a cause ofchronic bronchitis than all other causes combined.In fact, in a study of the role of smoking inchronic bronchitis in Egyptians, one of us(G. E. M.) found by comparing the smokinghabits of chronic bronchitics and control non-bronchitic subjects that a critical upper limit valueof accumulated lifetime tobacco consumptionequivalent to 300,000 cigarettes existed, abovewhich all smokers were chronic bronchitics. Thisis equivalent to the smoking of two packets ofcigarettes daily for 20 years. Yet one cannot com-pletely rule out the role of infection, which mightbe having an initiating or potentiating effect thatis difficult to ascertain on the basis of the presentdata.

REFERENCESBrumfitt, W., Willoughby, M. L. N., and Bromley, L. L. (1957). An

evaluation of sputum examination in chronic bronchitis. Lancet,2, 1306.

Cherniack, N. S., Vosti, K. L., Dowling, H. F., Lepper, M. H., andJackson, G. G. (1959). Long-term treatment ofbronchiectasis andchronic bronchitis. Arch. intern. Med., 103, 345.

Ciba Guest Symposium (1959). Terminology, definitions, and classi-fication of chronic pulmonary emphysema and related condi-tions. Thorax, 14, 286.

Dowling, H. F., Mellody, Margaret, Lepper, M. H., and Jackson,G. G. (1960). Bacteriologic studies of the sputum in patientswith chronic bronchitis and bronchiectasis. Amer. Rei. resp.Dis., 81', 329.

Glynn, A. A., and Michaels, L. (1960). Bronchial biopsy in chronicbronchitis and asthma. Thorax, 15, 142.

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287 Gamal E. Megahed, Gamal A. Senna, Mohammed H. Eissa, Safeia Z. S&leh, and Houda A. Eissa

Greene, B. A., and Berkowitz, S. (1954). Tobacco bronchitis: ananesthesiologic study. Ann. intern. Med., 40, 729.

Laurenzi, 0. A., Potter, R. T., and Kass, E. H. (1961). Bacteriologicflora of the lower respiratory-tract. -New Engl. J. Med., 265,1273.

Masters, P. L., Brumfitt, W., Mendez, R. L., and Likar, M. (1958).Bacterial flora of the upper respiratory tract in Paddingtonfamilies, 1952-54. Brit. med. J., 1, 1200.

Megahed, Gamal E. (1967). The role of smoking in chronic bronchitisin Egyptians-to be published.

Oswald, N. C., and Medvei, V. C. (1955). Chronic bronchitis, theeffect of cigarette-smoking. Lancet, 2, 843.

Palmer, K. N. V. (1954). The role of smoking in bronchitis. Brit. nmed.J., 1, 1473.

Reid, L. (1960). Measurement of the bronchial mucous gland layer:a diagnostic yardstick in chronic bronchitis. Thorax 15, 132.

Restrepo, G. L., and Heard, B. E. (1963a). Mucous gland enlargementin chronic bronchitis: extent of enlargement in the tracheo-bronchial tree. Ibid., 18, 334.-- (1963b). The size of the bronchial glands in chronic

bronchitis. J. Path. Bact., 85, 305.Thurlbeck, W. M., Angus, G. E., and Pare, J. A. P. (1963). Mucous

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