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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 28  |  Issue : 1  |  Page : 14-17

Detection of early small airway obstruction in male adult smokers of an ethnic community in north east India


Department of Physiology, Regional Institute of Medical Sciences, Imphal, Manipur, India

Date of Web Publication24-Jun-2014

Correspondence Address:
Dr. Govindaraj Yengkhom Singh
Department of Physiology, Regional Institute of Medical Sciences, Imphal - 795 004, Manipur
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-4958.135218

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  Abstract 

Background: Cigarette smoking causes small airway obstruction (SAO) and is the harbinger of developing chronic obstructive pulmonary disease (COPD). However, the prevalence of SAO is reported to vary in different ethnic population and with amount of smoking. Respiratory symptoms are reported to be not reliable for determining early airway obstruction Objective: To find out the relationship of respiratory symptoms and amount of smoking with SAO detected by using spirometer among the smokers of an ethnic community. Materials and Methods: In all, 100 male adult current smokers of the Meitei community of Manipur in north east India performed the spirometry test. Results of forced expiratory flow rate at 25-75% (FEF 25-75%) , forced expiratory volume in 1st second (FEV 1 ) and percentage ratio of FEV 1 to forced vital capacity (FVC), i.e., (FEV 1 /FVC)% were used for determining SAO. A modified validated questionnaire was used for labeling respiratory symptoms of obstructive nature. Statistical analysis was done to test independence of symptom with SAO and also of amount of smoking (in pack year) with presence of SAO. Result: In all, 37% of the total study group (n = 100) were detected as having SAO and 49% of the total as having one or more respiratory symptoms. In all, 29.2% of the smokers who smoked less than 3 pack years (n = 65) were detected having SAO, whereas 51.4 % were observed among those smoking more than 10 pack years (n = 35). SAO varies directly with pack year significantly (P < 0.05). Association of respiratory symptoms with SAO was not significant (P > 0.05). Conclusion: The findings of this study revealed that SAO is common among smokers of the Meitei community. It also supports others' studies, done obviously in different ethnic community, in which development of SAO directly varies with amount of tobacco smoking. Respiratory symptoms would not be reliable in the detection of SAO in this ethnic group also.

Keywords: Ethnicity, Small airway obstruction, Smoker, Spirometry


How to cite this article:
Singh GY, Singh NL, Banik U, Devi GK. Detection of early small airway obstruction in male adult smokers of an ethnic community in north east India. J Med Soc 2014;28:14-7

How to cite this URL:
Singh GY, Singh NL, Banik U, Devi GK. Detection of early small airway obstruction in male adult smokers of an ethnic community in north east India. J Med Soc [serial online] 2014 [cited 2020 Oct 20];28:14-7. Available from: https://www.jmedsoc.org/text.asp?2014/28/1/14/135218


  Introduction Top


Cigarette smoking has been claimed to be the most important risk factor for chronic obstructive pulmonary disease (COPD), which is the second leading cause of death (among male smokers in developing countries) after cardiovascular diseases when estimation of distribution of mortality due to smoking by cause was done. [1] Small airway obstruction (SAO) is strongly related with COPD. [2] A simple yet diagnostic evidence of early stage of COPD is detection of SAO from the spirometry values of forced expiratory volume in first second (FEV1) and the percentage of ratio of FEV1 to forced vital capacity (FVC), i.e. (FEV 1 /FVC%), which are taken as the 'gold standard test' along with certain respiratory symptoms. However, sub clinical SAO had been detected in mild and even moderate COPD without any respiratory symptoms. [3] Prevalence of early SAO was also observed quite variably among smokers due to the variability in bronchial hyper responsiveness (BHR) and mild subclinical inflammatory reaction among different ethnic individuals of different genetic makeup. [4] SAO could also be influenced by the amount of smoking due to the difference in BHR susceptibility to tobacco smoke. [5] It is claimed that if SAO is detected early in diseases like COPD, cessation of smoking would delay its progression in susceptible group, lengthen survival and quality of life, or even reverse the natural course of the disease. [6] This implies the importance of preclinical detection of SAO by office spirometry.

Hence, in this present study, we attempted to detect SAO among the male adult smokers of an ethnic community, the Meiteis, a mongoloid race in north east India with an objective to find out the relationship of respiratory symptoms and amount of smoking with the SAO.


  Materials and Methods Top


The present study was a cross-sectional study of the results of spirometry test performed by 100 male smokers at the Human Research Room of Physiology Department, Regional Institute of Medical Sciences, Imphal, during the period from June 2008 to July 2010. The subjects were between the ages of 18-70 years and had volunteered following recruitment drive by 'verbal information for research participation to any willing smoker coming across' by the members of the research group.

Subjects having known cardiovascular diseases, COPD, lung cancer, bronchial asthma, ex-smokers, and other recent or current respiratory tract infections were excluded from the study. Informed consents were taken from all the subjects and approval of the Institutional Ethics Committee taken.

A modified European Community Respiratory Health Study (ECRHS) questionnaire used by the Differential Diagnosis Between Asthma and COPD (DIDASCO) study was followed for recording symptoms suggestive of obstructive lung disease. [3] We added two extra questions, one for sputum production and the other for smoker's cough with hawking.

Flow volume detection by pneumotach sensor (MEDSPIROR, Model RMS Pvt Ltd, Chandigarh) was used for recording the spirometry values. The test performances were done following the norms laid down by ATS/ERS Task Force. [7] The parameters used for diagnosis of SAO were the FEV 1 , FVC, FEF 25-75% (forced expiratory flow rate at 25-75%) and (FEV 1 /FVC) %. The reference values for diagnosis were followed from the computer-generated predicted values in percentage, which was drawn from data taken from Indian subjects and considered valid for the study. [8] Abnormal low value of FEF 25-75% were determined when it was <70% of predicted value or/and the FEV 1 was <80% predicted value and (FEV 1 /FVC) % was <70% of predicted value as in GOLD (Global Initiative for Obstructive Lung Disease) classification. [9]

For statistical studies of airflow function in relation to amount of smoking, the subjects were divided into the following two groups.

Group A1: Smoking five cigarettes or less per day.
Group A2: Smoking more than five cigarettes per day.

Student's t-test was applied to test for significance in the difference of means of the various parametric values in each of the above two groups.

For studying the relationship of SAO with respiratory symptoms, all the smokers were again grouped into

Group S1: Those symptomatic, i.e. symptoms being suggestive of respiratory disease.
Group S2: Those asymptomatic, i.e. without symptoms that may suggest respiratory diseases.

The development of SAO was then analyzed for its association with respiratory symptoms and also with amount of smoking by applying Pearson's chi-square test.

All values were expressed in mean ± standard deviation (SD) and the level of significance was drawn at P < 0.05.


  Results Top


All the smokers performed the test successfully without any unwanted event, and the best result from three performances of each subject was chosen for data entry. Sixty-five smokers of the study group gave a history of regular smoking for a mean 10.55 ± 7.26 years at the rate of mean 4.3 ± 0.76 cigarettes per day and were included in the group A1 with the amount of cigarette consumption of mean 2.3 ± 1.71 pack year. The remaining 35 smokers classified as group A2 were smoking at the rate of mean 14.57 ± 3.76 cigarettes per day for a period of mean 15.68 ± 7.27 years and were calculated as consuming mean 11.9 ± 6.43 pack year. When the differences of means in the various recorded spirometry values between the two groups were tested by applying Student's t-test, we found significantly low values in all the spirometry parameters of Group A2 smokers when compared with their counterparts of Group A1 [Table 1].
Table 1: Comparison of values of different spirometry parameters that determine small airway obstruction between the smokers of groups A1 and A2

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Interpretation of the recorded data of spirometry test revealed 37% of the total study groups were having SAO [Table 2]. A break up of the 37 smokers with SAO detected by different spirometry parameters are also shown according to the parameters used.
Table 2: Detection of SAO diagnosed by the results of different spirometry parameters of the smokers

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SAO was detected in 19 smokers among the 65 smokers of the A1 group (i.e. 29.2%) and in 18 of 35 smokers (51.4%) of the A2 group.

A chi-square test applied in a test of independence between the number of smokers with SAO among the two groups A1 and A2 revealed detection of SAO among the group A2 being significantly (P < 0.05) higher than those in group A1 [Table 3].
Table 3: Distribution of smokers with SAO and without SAO in relation to their pack years consumption of cigarettes and their association tested (P < 0.05)

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Of the total 100 smokers, 49 gave presenting history of one or more respiratory symptoms, the rest were asymptomatic. A total of 18 smokers were detected having developed SAO among this symptomatic group (S1). Almost a similar number of smokers (19 smokers) were found with SAO among the asymptomatic group (S2). Chi-square test was applied to test the relationship between the respiratory symptoms association with SAO status and observed that association of SAO with presence of symptoms was insignificant (P > 0.05) [Table 4].
Table 4: The symptom status among the smokers in relation to the SAO detection tested for independence (P > 0.05)

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  Discussion Top


This study was taken up with three simple and a more generalized approach to detection of tobacco smoking-related SAO, which obviously would include the early potential stage of COPD. First, in this study, because FEF 25-75% alone had been projected as a good tool for determining early SAO, [10],[11] we included it along with the other standard spirometric parameters to increase the sensitivity of diagnosis of SAO that might associate with any obstructive respiratory disease including COPD. FEF 25-75% alone independently detected 16% of the smokers as having SAO in our study, whereas in a similar study in a different ethnical community, Joseph et al.,(1991) found a much higher percentage of the total smokers having SAO. [11] Another 9% of the total smokers evident of mixed pattern in this study could be because of other interstitial pathology induced by cigarette smoke, like the genetically related idiopathic pulmonary fibrosis. [12] Second, the analysis of SAO among the smokers of this ethnic community was also tailored to their presenting symptoms, as the sputum production and smokers' cough was frequent among smokers. Though variably experienced, they are often presented as an annoyance relevant to their respiratory problem. We considered the addition of these symptoms would increase the sensitivity of the questionnaire and would not affect its validity as the study did not confine only to COPD. Third and finally, the study gave importance to the psychology on smoking that prevails among the smokers in relation to the amount consumed. In the interaction while taking history, we found majority of the smokers answered that they believed smoking a few cigarettes, i.e. two or three cigarettes per day will not harm them much. We fixed the number of cigarettes smoked at five per day as the watershed for the two groups to be analyzed on the basis that many of those who stated smoking few admitted of consuming sometimes one or two more cigarettes than their usual amount per day. Hence, in this study we considered it pertinent to analyze the development of SAO between those smoking five or fewer cigarettes per day and those smoking more than five per day.

The 12% obstructive pattern (COPD suggestive) and 9% mixed pattern detected by using FEV1 and FVC % parameters, and the 16% early SAO detected by low FEF 25-75% , were clubbed together as smokers with SAO (altogether totaling 37%), as features of small airways obstruction were a common denominator and because of a common etiologic agent, i.e. tobacco smoking. Joshi had highlighted that the prevalence of smoking-related obstructive small airway could be somewhere between 15 to 45%. [13] Our detection of 12% of the smokers having spirometric evidence of mild COPD was lesser than that of Lundbback et al., [14] but was slightly higher than the finding by Dosman et al., who used a multiple number of diagnostic criteria. [15] Further, this 12% of our study was similar with those of Tattersall et al., [16] in percentage prevalence, though the authors conducted the tests in population obviously of different races using different diagnostic parameters. Though studies by using spirometric parameters and other methods that are time consuming and useful for academic purpose only could be found abundantly, research in relation to a simple yet potentially useful method for screening SAO by using a combination of the spirometric parameters as in the present studies are few.

In this study, the detection of a high proportion of smokers with SAO (18 of 35) among those consuming higher amount of cigarette at mean 11.9 pack years implies that this ethnic population share similar characteristics with the findings of Movahed and Milne. [17] Encompassing the age influence and by using the FEV1 and FVC parameters only, Jan and Michael reported airway obstruction in 30.6% among those who smoke more than 10 pack years and aged 40 years or more but significantly less in those younger smokers with lesser pack years. [18] In our study, 29.2 % of the smokers who smoked less than three pack years were detected having SAO, whereas it was 51.4 % among those smoking more than 10 pack years. The higher percentage detection could be either because of ethnicity factor or because of using one more sensitive parameter or both.

The DIDASCO study had concluded respiratory symptoms are not reliable as an indicator of mild COPD. [3] In our study also, association of respiratory symptoms with detection of SAO among the smokers were insignificant. This disagree with Movahed and Milne who had the opinion that pulmonary symptoms increase in frequency once 10 pack years history is reached. [17] A weak point of the study in relation to the symptom study was the encompassing of any respiratory discomfort or production of phlegm considered as related with smoking, which is difficult to validate as cause related as some may be subjective and psychological.


  Conclusion Top


Development of early SAO is common among the smokers of Meitei community of Manipur. SAO develops more commonly in smokers with large amount of cigarette consumption and affecting as high as 51% smokers at 10 pack years or more. Respiratory symptoms would not be a reliable determinant of early detection of SAO as observed in other ethnic communities. The study brings out the necessity for screening of smokers by spirometry to detect development of SAO, especially for smokers consuming more than 10 pack years. The findings and awareness would help discourage smoking and help the health care givers in planning strategies for prevention of respiratory diseases like COPD and other obstructive diseases.


  Acknowledgement Top


The authors gratefully acknowledge the statistical advice of Mr. P. Jasawanta of 3 Sigma Statistical Consultants, Proactive Academy Building, Kwakeithel Bazar, Imphal, PIN-795 001, Manipur, India.

 
  References Top

1.Majid E, Alan DL. Smoking and oral tobacco use. In: Majid E, Alan DL, Anthony R, Christopher JL, editors. Comparative Quantification of Health Risks - Global and Regional Burden of Disease Attributable to Selected Major Risk Factors. Vol. 1. World Health Organization; 2004. p. 883-957.  Back to cited text no. 1
    
2.McDonough JE, Yuan R, Suzuki M, Seyednejad N, Elliott WM, Sanchez PG, et al. Small-airway obstruction and emphysema in chronic obstructive pulmonary disease. N Eng J Med 2011:365:1567-75.  Back to cited text no. 2
    
3.Buffels J, Degryse J, Heyrman J, Decramer M; DIDASCO Study. Office spirometry significantly improves early detection of COPD in general practice: The DIDASCO Study. Chest 2004;125:1394-9.  Back to cited text no. 3
    
4.He JQ, Connett JE, Anthonisen NR, Paré PD, Sandford AJ. Glutathione S- transferase variants and their interaction with smoking on lung function. Am J Respir Crit Care Med 2004;170:388-94.  Back to cited text no. 4
    
5.Burrows B, Knudson RJ, Cline MG, Lebowitz MD. Quantitative relationships between cigarette smoking and ventilatory functions. Am Rev Respir Dis 1977;115:195-205.  Back to cited text no. 5
    
6.Bohadana A, Nilsson F, Martinet Y. Detecting airflow obstruction in smoking cessation Trials: A rationale for routine spirometry. Chest 2005;128:1252-7.  Back to cited text no. 6
    
7.Miller MR, Hankinson J, Brusasco V, Burgos F, Casaburi R, Coates A, et al.; ATS/ERS Task Force. Standardization of spirometry. Eur Resp J 2005;26:319-38.  Back to cited text no. 7
    
8.Hughes JMB. Presentation of pulmonary function test results to the clinician. In: Hughes JMB, Pride NB, editors. Lung function Tests- Physiological Principles and Clinical application. London: W. B. Saunders. First Publication; 1999. p. 287-95.  Back to cited text no. 8
    
9.Gross NJ. The GOLD standard for chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2001;163:1047-8.  Back to cited text no. 9
    
10.Milanka B, Milanko B, Milanka V. Our experience with the early detection of small respiratory diseases. Bronchpneumologie 1980;30:521-8.  Back to cited text no. 10
    
11.Joseph CM, Sridhar CB, Raphael M. Spirometric indices of early airflow obstruction. J Indian Med Assoc 1991;89:135-7.  Back to cited text no. 11
    
12.Steele MP, Speer MC, Loyd Je, Brown KK, Herron A, Siifer SH, et al. Clinical and pathological features of familial interstitial pneumonia. Am J Respir Crit Care Med 2005;172:1146-52.  Back to cited text no. 12
    
13.Joshi JM. Chronic obstructive pulmonary disease: Knowing what we mean, meaning what we say. Indian J Chest Dis Allied Sci 2008;50:89-95.  Back to cited text no. 13
    
14.Lundbback B, Lindberg A, Lindstorm M, Ronmark E, Jonsson AC, Jonsson E, et al.; Obstructive Lung Disease in Northern Sweden Studies. Not 15 but 50% of smokers develop COPD ? - Report from the obstructive lung disease in Northern Sweden Studies. Respir Med 2003;97:115-22.  Back to cited text no. 14
    
15.Dosman JA, Cotton DJ, Graham BL, Hall DL, Li R, Froh F, et al. Sensitivity and specificity of early diagnostic tests of lung function in smokers. Chest 1981;79:6-11.  Back to cited text no. 15
    
16.Tattersall SF, Benson MK, Hunter D, Mansell A, Pride NB, Fletcher CM. The use of tests of peripheral lung function for predicting future disability from airflow in middle aged smokers. Am Rev Respir Dis 1978;118:1035-50.  Back to cited text no. 16
    
17.Movahed M, Milne N. Association between amount of smoking with chronic cough and sputum production. The Internet Journal of pulmonary Medicine 2006;7, number 1. Available from: www.ispub.com/ostia [Last accessed on 2013 Sept 16].  Back to cited text no. 17
    
18.Jan Z, Michael B and the know the age of your lung study group. Early detection of COPD in a high - risk population using spirometric screening. Chest 2001;119:731-6.  Back to cited text no. 18
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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