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PLOS One logoLink to PLOS One
. 2020 Sep 23;15(9):e0239602. doi: 10.1371/journal.pone.0239602

Association between chronic obstructive pulmonary disease (COPD) and occupational exposures: A hospital based quantitative cross-sectional study among the Bangladeshi population

Ahmed Faisal Sumit 1,*,#, Anindya Das 1,#, Ishtiaq Hossain Miraj 2, Debasish Bhowmick 3
Editor: Christophe Leroyer4
PMCID: PMC7510960  PMID: 32966342

Abstract

The association between chronic obstructive pulmonary disease (COPD) and occupational exposures are less studied in Bangladeshi context, despite the fact that occupational exposures are serious public health concerns in Bangladesh. Therefore, this study aimed to evaluate this association considering demographic, health and smoking characteristics of Bangladeshi population. This was a hospital-based quantitative study including 373 participants who were assessed for COPD through spirometry testing. Assessment of occupational exposures was based on both self-reporting by respondents and ALOHA based job exposure matrix (JEM). Here, among the self-reported exposed group (n = 189), 104 participants (55%) were found with COPD compared to 23 participants (12.5%) in unexposed group (n = 184) that differed significantly (p = 0.00). Similarly, among the JEM measured low (n = 103) and high exposed group (n = 236), 23.3% and 41.5% of the participants were found with COPD respectively; compared to unexposed group (14.7%; n = 34), that differed significantly also (p = 0.00). Likewise, participants with longer self-reported occupational exposures (>8 years) showed significantly (p = 0.00) higher proportions of COPD (79.5%) compared to 40.4% in shorter exposure group (1–8 years). Similarly, significant (p = 0.00) higher cases of COPD were observed among the longer cumulative exposure years (>9 years) group than the shorter cumulative exposure years (1–9 years) group in JEM. While combining smoking and occupational exposure, the chance of developing COPD among the current, former and non-smokers of exposed group were 7.4, 7.2 and 12.7 times higher respectively than unexposed group. Furthermore, logistic analysis revealed that after adjustments for confounding risk factors, the chance of developing COPD among the self-reported exposure group was 6.3 times higher (ORs: 6.3, p = 0.00) than unexposed group; and JEM exposure group has odds of 2.8 and 1.1 respectively (p<0.05) for high and low exposures. Further studies are needed to reinforce this association between COPD and occupational exposure in Bangladesh.

Introduction

COPD, a progressive lung disease characterized by airflow limitation, is largely preventable and treatable [1]. According to World Health Organization (WHO), the global prevalence of COPD in 2016 was 251 million, and around 5% of all global deaths in 2015 were attributable to COPD [2]. In South-East Asia, the COPD prevalence varied substantially ranging from 6.5% to 17.9% [3] with 8.6% in China [4] and 9% in India [5]. In Bangladesh, the prevalence of COPD was estimated around 12.5% according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria [6]. Outdoor air pollutions, smoking habit, indoor air pollutions from biomass fuel burning are some of the known factors that contribute to the high prevalence of COPD in Bangladesh [3, 6].

Occupational exposure is considered to be one of the major risk factors of COPD [7, 8]. According to American Thoracic Society (ATS), around 14% of CODP cases were attributable to occupational exposures [9]. In Bangladesh, the prevalence of COPD due to occupational exposures is unknown, although occupational exposure is a serious public health concern here [10]. According to earlier report, an average of 8 million workers from all sectors suffered from workplace hazards whereas occupational exposure is identified as one of the main causes [10]. Several occupational exposures in Bangladesh had been identified, like uncontrolled pesticides exposures in farm [11], hazardous chemical exposures in tanners [12], cotton dust exposures in garments [10], biomass fuel and fumes exposures among the domestic workers [13] etc. The most alarming concern is the lack of awareness among workers, putting them into serious health threats [14].

Although, wealth of evidences had supported the association between COPD and occupational exposures worldwide [7, 8], such study has not yet been established to that extent in Bangladesh. Only COPD status has been observed among the transport workers of Dhaka city [15], and rural women who were exposed to indoor biomass fuel [16, 17]. This study, for the first time so far, attempted to determine the association between COPD and occupational exposures among the Bangladeshi population to a large extent. Here, we aimed to define occupational exposures on the basis of both self-reporting by respondents and job exposure matrix (JEM), and observe its association with COPD. We also investigated the combined effects of occupational exposures and smoking habit on COPD. Furthermore, logistic regression analysis was performed to ascertain whether these associations were influenced by other confounding factors.

Materials and methods

Study participants

This quantitative cross-sectional study, conducted between August, 2019 to February, 2020, included participants who were being followed-up with various respiratory symptoms in the Department of Respiratory Medicine, Dhaka Medical College Hospital, Dhaka, Bangladesh and were assessed for COPD through spirometry testing according to GOLD criteria [18]. We got 373 participants altogether based on their availability and written consent to participate. We interviewed them with the help of a physician from the department of respiratory medicine by using a structured close-ended questionnaire. The questionnaire included participants’ demographic information, occupational details like types of jobs, duration of work, history of occupational exposures etc., smoking status and respiratory symptoms. The participants’ weight and height were measured at the time of data collection and then BMI was calculated accordingly. The study was approved by the Ethical Review Committee of the Faculty of Biological Sciences, University of Dhaka (Ref. no. 89/Biol.Scs.).

Spirometry testing and COPD definition

All participants underwent spirometry test with rolling seal spirometers (Sensormedics 2200, USA). COPD cases and severity were defined according to the earlier study [18]. Shortly, the participants were diagnosed with COPD when the ratio of forced expiratory volume (FEV1) to forced vital capacity (FVC) had been found less than 70% (0.70) at post-bronchodilator spirometry. Post-bronchodilator spirometry was performed 10 to 15 minutes after nebulization with short-acting bronchodilator (5 mg salbutamol). The percent predicted values were estimated based on the US National Health and Nutrition Examination Survey (NHANES) III reference equation with Asian Population corrections [19]. Severity of COPD were defined as stage I (FEV1/FVC<0.70 and FEV1≥80% predicted); stage II (FEV1/FVC<0.70 and 50%≤FEV1<80% predicted); stage III (FEV1/FVC<0.70 and 30%≤FEV1<50% predicted) and stage IV (FEV1/FVC<0.70 and FEV1<30% predicted) [3].

Control participants were defined with not having COPD according to GOLD criteria (FEV1/FVC>0.70 and FEV1≥80% predicted at post-bronchodilator spirometry) other than self-reported respiratory symptoms. All control participants had been examined by registered physician and undergone both pre- and post-bronchodilator spirometry procedures. However, potential controls were excluded if they had been diagnosed with asthma, chronic bronchitis, and/or emphysema by registered physician during the time of study or possessing past history of these diseases. Furthermore, control participants with previous history of COPD or taking medications including inhalers that may affect COPD were excluded from the study. However, participants with restrictive lung disease (FEV1/FVC>0.70, and FVC<80% predicted) according to spirometry defined GOLD criteria were included in this study [20, 21].

Evaluation of bronchodilator response

A positive bronchodilator response was evaluated based on an increase of absolute value of FEV1% ≥12% and ≥200 ml after using short-acting bronchodilator according to ATS and ERS guideline [22]. FEV1% reversibility was calculated based on the following formula: (post FEV1-Pre FEV1/ Pre FEV1) X 100 [23].

Assessment of occupational exposure through various means

Self-reported occupational exposures were evaluated based on earlier study [24], where we asked the participants if they were exposed to vapours, gas, dust, fume, smokes, etc. in their workplace. If their self-reported responses were ‘no’, participants were considered as unexposed group. However, in case of positive response, participants further work details including types and duration of exposures were noted. Participants longest job status to whom they claimed exposures were considered only. The reported occupations were then coded according to the International Standard Classification of Occupations (ISCO-88) four-digit classification system [25].

Occupational exposures were also assessed using a JEM. Here, ALOHA JEM for COPD, previously used by several studies to define occupational exposures [2628], were also established for our study. ALOHA-JEM classified all occupations, to which participants were exposed (2, 1, or 0 for ‘high risk’, ‘low risk’ or ‘no’ exposures, respectively), according to ISCO-88 job codes for biological and mineral dusts, gases, and fumes etc. Participants’ years of exposures and category of exposures were then calculated for each job and was multiplied by that score to get cumulative exposures.

Calculation of sample size

Sample size was calculated using this formula: n = z2p (1-p)/d2. Considering prevalence of COPD in Bangladesh (p) = 13.5% = 0.135 according to a previous study [3], z = 1.96, margin of error (d) = 4% = 0.04; sample size (n) became 280. However, considering a large public hospital and various socio-economic classes of patients, we added 20% non-response; the sample size then rose up to 336. Then to cover the holistic dimension of our study area, we took altogether 373 samples.

Statistical analysis

Statistical analysis was performed using SPSS program version 24 software (SPSS Inc., Chicago, USA). Univariate analysis was shown in percentage and numbers. Bivariate comparisons were done using t-test and Pearson's χ2 (chi-square) test for continuous and categorical variables respectively. The level of significance was set at p < 0.05. Binary logistic regression analysis was also performed to determine the adjusted associations between occupational exposures and COPD. Population Attributable Risk (%) or PAR % was determined based on the formula given by previous study [26] to find out the percentage of COPD cases attributable to occupational exposure. The calculation of PAR% was based on the following formula: PAR% = [(AdOR-1)/AdOR] X Pc; where AdOR = Adjusted ORs and Pc = Proportion of COPD cases exposed. The adjusted ORs were obtained from the logistic regression analysis model.

Results

Demographic and health characteristics of the study participants

Table 1” depicts the demographic and health characteristics of the participants. Among the total 373 participants, 127 COPD cases (57.5% GOLD stage I and 42.2% GOLD stage II and II+) and 246 control cases (66% of total) were confirmed. The majority of the participants were aged > 60 years (52% in COPD vs 49.2% in control), male (75.6% in COPD vs 68.3% in control) and in normal BMI (70.1% in COPD vs 67.1% in control). Family history of COPD cases were found among 20.5% of COPD and 24% of control participants. Most of the participants were currently employed (70.9% in COPD vs 76.4% in control). Regarding smoking status, majority of the COPD participants were found smokers (66.9% in COPD vs 39% in control), followed by former smokers (17.3% in COPD vs 17.9% in control) and non-smokers (15.7% in COPD vs 43.1% in control). Furthermore, self-reported dyspnoea, chronic cough, morning phlegm, wheezing, and allergic rhinitis were reported by 76%, 80%, 53%, 57% and 33% of COPD participants respectively, and 60%, 49%, 44%, 47%, and 63% of control participants respectively. No significant differences (p > 0.05) were observed between COPD and control group regarding the participants age, gender, BMI, self-reported morning phlegm and wheezing, and self-reported family history of COPD. However, participants smoking status and self-reported dyspnoea, allergic rhinitis, and chronic cough were significantly differed (p<0.05) between the two groups. Besides, restrictive lung diseases had been found among 6.9% (17) of control participants (“Table 1”).

Table 1. Demographic and health characteristics of the participants.

GOLD Criteria
Variables CODP (n = 127) Control (n = 246) P value
Age £
40–49 years (n = 72) 19 (15%) 53 (21.5%)
50–59 years (n = 114) 42 (33%) 72 (29.3%) 0.30
>60 years (n = 187) 66 (52%) 121 (49.2%)
Gender
Male (n = 264) 96 (75.6%) 168 (68.3%) 0.08
Female (n = 109) 31 (24.4%) 78 (31.7%)
BMI $
Underweight (n = 88) 31 (24.4%) 57 (23.2%)
Normal weight (n = 254) 89 (70.1%) 165 (67.1%) 0.37
Overweight (n = 31) 07 (5.5%) 24 (9.8%)
Self-reported Family history of CODP
No (n = 288) 101 (79.5%) 187 (76%) 0.26
Yes (n = 85) 26 (20.5%) 59 (24%)
Employment status
Currently Employed (n = 278) 90 (70.9%) 188 (76.4%) 0.37
Currently unemployed (n = 56) 22 (17.3%) 34 (13.8%)
Retired (n = 39) 15 (11.8%) 24 (9.8%)
Smoking status
Current Smoker (n = 181) 85 (66.9%) 96 (39%)
Former Smoker (n = 66) 22 (17.3%) 44 (17.9%) 0.00
Non-smoker (n = 126) 20 (15.7%) 106 (43.1%)
Self-reported Symptoms
Dyspnoea 96 (76%) 148 (60%) 0.04
Chronic Cough 101 (80%) 121 (49%) 0.001
Morning Phlegm 67 (53%) 108 (44%) 0.20
Wheezing 72 (57%) 116 (47%) 0.32
Allergic rhinitis 42 (33%) 156 (63%) 0.001
Presence of restrictive disease
Yes 17 (6.9%)
No 229 (93.1%)
COPD stages (GOLD Criteria)
Stage I 73 (57.5%)
Stage II and II+ 54 (42.5%)

$ BMI was categorized into underweight (BMI <18.5), normal weight (18.5–25) and overweight (>25) according to WHO classification [29].

£ Age was categorized based on earlier study that determined COPD prevalence in Bangladesh [3].

Occupational types and status among the participants

Table 2” shows the frequency of different types of occupations reported by the participants. According to ISCO-88 four digits code, total 13 different job types were reported by the COPD and control participants. Majority of the participants of the COPD group reported their occupations as one of the following: motor vehicle mechanics (65.6%), cleaners (58.8%) and motor driver (57.6%). On the other hand, a large percentage of control reported their occupation as one of the following: manager (92%), clerk (90%), house-keeper (90%), administrative job (85.7%), accountant (83.3%), builder (75%), farmer (68.1%), and salesperson (65.5%).

Table 2. Types of jobs reported by the participants.

Type of Jobs GOLD Criteria
COPD (n = 127) Control (n = 246) P value
Motor vehicle Mechanic (n = 32) 21 (65.6%) 11 (34.4%) 0.00
Tannery Worker (n = 5) 02 (40%) 03 (60%)
Cleaner (n = 51) 30 (58.8%) 21 (41.2%)
Motor driver (n = 33) 19 (57.6%) 14 (42.4%)
Manager (n = 25) 02 (08%) 23 (92%)
Clerk (n = 20) 02 (10%) 18 (90%)
Garment worker (n = 20) 06 (30%) 14 (70%)
Housekeepers and related worker (n = 40) 04 (10%) 36 (90%)
Farmer (n = 47) 15 (31.9%) 32 (68.1%)
Salesperson (n = 58) 19 (32.7%) 39 (67.3%)
Administrative Professional (n = 28) 04 (14.3%) 24 (85.7%)
Accountant (n = 06) 01 (16.7%) 05 (83.3%)
Builder (n = 08) 02 (25%) 06 (75%)

Occupational exposure significantly affected COPD

We found that COPD cases were observed among 55% of self-reported exposed and 12.5% of self-reported unexposed participants (“Table 3”). On the other hand, control cases were found among 45% of self-reported exposed and 87.5% of unexposed participants. While, according to JEM exposure measurement, only 14.7% of the participants with unexposed category developed COPD, whereas the proportion increased to 23.3% and 41.5% for low and high-risk job categories respectively. All these values in COPD differed significantly (p = 0.00) than control group (“Table 3”).

Table 3. Occupational exposures among the COPD and control group.

GOLD criteria
Exposure measurement COPD (n = 127) Control (n = 246) P value
Self-reported exposure measurement 0.00
Unexposed (n = 184) 23 (12.5%) 161 (87.5%)
Exposed (n = 189) 104 (55%) 85 (45%)
^Self-reported exposure-years (Mean ± SD) 11.10 ± 5.52 5.19 ± 3.58 0.00
JEM exposure Measurement 0.00
Unexposed (n = 34) 05 (14.7%) 29 (85.3%)
Low risk (n = 103) 24 (23.3%) 79 (76.7%)
High risk (n = 236) 98 (41.5%) 138 (58.5%)
^JEM Cumulative exposures-years (Mean ± SD) 19.69 ± 11.86 6.94 ± 5.92 0.00

^ Self-reported exposure years and JEM cumulative exposure years (Unit, years) were restricted to exposed participants only.

The duration of exposure (years) among the self-reported exposure group differed significantly as well between the two groups. The mean value of the exposure years for COPD group were 11.10 ± 5.52 years, whereas that for the control group were 5.19 ± 3.58 years. On the other hand, the mean value of JEM cumulative exposure years was around 3 times higher for the COPD group (19.69 ± 11.86 years) compared to the control group (6.94 ± 5.92 years), and that differed significantly (p = 0.00) as well (“Table 3”).

Longer duration of occupational exposure significantly related to COPD

The median value of the exposure years was used as a cut-off point to divide the duration of exposure years into two sub-groups: shorter exposure and longer exposure years. In case of self-reported exposure years, the median value of the exposure years among the 189 self-reported exposure participants was found 8. On the other hand, the median value for the weighted cumulative exposure years (according to JEM exposure probability) among the 339 participants was found 9.

Here, in case of JEM cumulative exposure years, we found that 20.6% of participants with shorter duration (1–9 years) developed COPD compared to 51.5% participants with longer duration (>9 years) (ORs: 4.09, p = 0.00) (“Table 4”). While, in case of self-reported exposure years, 79.5% of participants with longer duration (>8 years) developed COPD compared to 40.4% of participants with shorter duration (1–8 years) (ORs: 12.44, p = 0.00) (“Table 4”).

Table 4. Influence of longer and shorter occupational exposure years (both cumulative and self-reported) on COPD.

GOLD criteria
COPD Control P value ORs
Cumalative Exposure Years*
Shorter Exposure Years (n = 170) (1–9 years) 35 (20.6%) 135 (79.4%) 0.00 4.09
Longer Exposure Years (n = 169) (>9 years) 87 (51.5%) 82 (48.5%)
Self-reported expousre years
Shorter Exposure Years (n = 111) (1–8 years) 42 (40.4%) 69 (59.6%) 0.00 12.44
Longer Exposure Years (n = 78) (>8 years) 62 (79.5%) 16 (20.5%)

* Cumulative exposure year was the multiplicative product of years of exposures and category of exposures (2, 1, or 0 for ‘high risk’, ‘low risk’ or ‘no’ exposures, respectively) defined by ALOHA JEM.

Occupationally exposed COPD participants didn’t show any significance in positive bronchodilator response compared to the unexposed group

Since this study excluded control participants with positive bronchodilator response due to the suspect of asthma, the comparisons were performed among the occupationally exposed and unexposed COPD participants only (“Table 5”). Here, we found that among the self-reported unexposed group, the percentage of participants with positive bronchodilator response were slightly higher (17.4%) than that of the self-reported exposed group (15.4%), but not significantly differed (p = 0.51). Similarly, according to JEM exposure measurement, no significant differences (p = 0.86) were observed among the unexposed, low-risk and high-risk exposed COPD participants in terms of positive bronchodilator response.

Table 5. Bronchodilator response among the COPD participants.

Exposure measurement FEV1 Reversibility among the COPD participants P value
(≥ 12% and ≥ 200 ml) <12% and <200ml
Self-reported
Unexposed (n = 23) 04 (17.4%) 19 (82.6%) 0.51
Exposed (n = 104) 16 (15.4%) 88 (84.6%)
JEM exposure measurement
Unexposed (n = 05) 01 (20%) 04 (80%) 0.86
Low risk (n = 24) 03 (12.5%) 21 (87.5%)
High risk (n = 98) 16 (16.3%) 82 (83.7%)

Smoking habit significantly increased the rate of COPD among the occupationally exposed group

The combined influence of smoking habit and self-reported occupational exposures on COPD were shown in “Table 6”. Here, 65.1% COPD cases were observed among the participants with self-reported occupational exposures and current smoking habit, followed by the former smokers (54.8% COPD cases) and non-smokers (34.6% COPD cases). While, 20.3% COPD cases were observed among the self-reported unexposed participants with current smoking habit, whereas that value for the former smokers and non-smokers were 14.3% and 4% respectively. The chance of developing COPD among the current, former and non-smokers of occupationally exposed group were 7.4, 7.2 and 12.7 times higher respectively than those smoking categories of unexposed group. All the differences were significant as well (p<0.05) (“Table 6”).

Table 6. Combined influence of smoking habit and self-reported occupational exposures on COPD.

Exposure and smoking status GOLD criteria
COPD (n = 127) Control (n = 246) P value ORs
Current smoker and Exposed group (n = 106) 69 (65.1%) 37 (34.9%) 0.000 7.4
Current smoker and Unexposed group (n = 74) 15 (20.3%) 59 (79.7%)
Former smoker and Exposed group (n = 31) 17 (54.8%) 14 (45.2%) 0.001 7.2
Former smoker and Unexposed group (n = 35) 05 (14.3) % 30 (85.7%)
Non-smoker and Exposed group (n = 52) 18 (34.6%) 34 (51.5%) 0.000 12.7
Non-smoker and Unexposed group (n = 75) 03 (4%) 72 (96%)

Binary logistic regression analysis

Binary logistic regression analysis was performed considering the presence or absence of COPD as a dependent variable. We found that after adjustments with age, gender, BMI, smoking habit, family history of COPD and cumulative exposure years, the risk of COPD among self-reported exposure group was 6.3 times higher than unexposed group (p = 0.00) (“Table 7”). After considering JEM defined cumulative exposure years, the odds of having COPD among the high and low- exposure years group were 2.8 and 1.1 respectively (p<0.05), compared to unexposed group while adjusting other variables (p<0.05).

Table 7. Binary logistic regression analysis to associate COPD with other independent variables and PAR%.

Variables Category of Characteristics Adjusted ORs (95% CI) P-value PAR%
Age 40–49 years (Reference) 1
50–59 years 1.4 (0.58–2.9) 0.51 9.4
>60 years 1.6 (0.71–3.23) 0.28 19.5
Gender Male (Reference) 1
Female 1.6 (0.82–4.18) 0.13 28.3
BMI Normal (Reference) 1
Underweight 1.6 (0.39–1.46) 0.10 9.15
Overweight 0.6 (0.22–1.85) 0.41 3.7
Smoking habit Never (Reference) 1
Current 5.0 (2.2–12.1) 0.00 53.5
Former 2.8 (1.1–7.4) 0.02 11.1
Family history of COPD Yes (Reference) 1
No 1.0 (0.51–1.96) 0.99 1.8
Self-reported exposure Unexposed (Reference) 1
Exposed 6.3 (2.8–9.2) 0.00 46.2
Exposure Duration (Cumulative years) Unexposed (Reference) 1
Shorter exposure years 1.1 (1.0–12.08) 0.7 2.1
Longer exposure years 2.8 (1.2–13.09) 0.05 26.7

Abbreviation: CI: Confidence Interval, ORs: Odds ratio.

Smoking habit also showed positive significant association (Adjusted ORs = 5.0 and 2.8, p<0.05 for current and former smokers respectively) with COPD when compared to non-smokers. Similarly, gender (female; ORs = 1.6), BMI (underweight; ORs = 1.6), and age (50–59 years; ORs = 1.4 and >60 years; ORs = 1.6) showed positive associations with COPD, but these associations were not found significant (p>0.05) (“Table 7”).

We further calculated PAR% to assess the proportion of the incidence of COPD in Bangladeshi population due to occupational exposure. Here, PAR% for COPD was found 46.2 for self-reported exposure group and 2.1 and 26.7 for JEM defined low and high-exposure years group respectively. For current and former smokers, PAR% for COPD were found 53.5 and 11.1 respectively.

Discussion

This is the first kind of hospital-based quantitative cross-sectional study that determined the association between COPD and occupational exposures among the Bangladeshi population. Here, it is observed that among the total 373 participants, 127 participants (34% of total) were found suffering from spirometry defined COPD. Depending on the assessment measures, COPD cases had been observed among 55%, 41.5% and 23.3% participants with self-reported occupational exposures, JEM exposure defined high and low risk occupation categories respectively. The presence of COPD- occupational exposure relationship was further confirmed after adjusting with cofounding risk factors.

Our results supported other literatures regarding the significant association between COPD and occupational exposures [7, 8]. We got almost 6-folds increased adjusted ORs for self-reported occupational exposures compared to unexposed group. These findings were in accord with previous studies that reported adjusted ORs ranging from 1.3 to 5.9 for COPD due to occupational exposures [9, 26]. Furthermore, the PAR% for COPD among the self-reported, low and high-cumulative exposure years group were found 46.2%, 26.7% and 2.1%, respectively. However, these were slightly higher compared to previous study [26] that reported PAR% for COPD ranging from 25% to 2.3% for self-reported and JEM measured exposures to variable gases, chemicals and dusts.

Our study also investigated combined influence of occupational exposures and smoking on COPD. Our unadjusted data showed that joint effect of occupational exposure and current smoking habit was associated with nearly 7-folds increase in case of developing COPD, similar to previous study that showed nearly 5-folds increase in the risk of developing COPD [30], but slightly lower than another study that showed nearly 14-folds of increase [9]. However, for adjusted data, it was observed that current and former smoking habit were associated with 5.0 and 2.8-times higher risks of developing COPD respectively than non-smokers, which was almost consistent with previous study [31] that showed 4.40-times of higher risks. The PAR% for COPD due to current smoking habit was found 53.5%, which supported previous data that showed 56% for combined current and past smoking habit [32].

The duration of occupational exposures required to develop COPD is still in ambiguity. According to earlier report, minimum 15 years of exposures were required to develop COPD [33], whereas another study showed 6–10 years of exposures [27]. Here, we defined low and high exposure years based on the previous study where median value of the cumulative exposure years was used as cut off point to categorize exposure duration [28]. Here, our adjusted data revealed that longer and shorter duration of cumulative exposure years increased the risk of COPD by 2.9 and 1.2-folds respectively compared to unexposed group which was also correlated with pervious study that showed 1.3 to 2.2-folds increase of COPD due to low and high cumulative exposure years respectively [26].

The association between occupational exposure and bronchodilator response among the COPD participants were also assessed in our study. Here, similar to earlier study [34], our study showed that 12–20% of COPD participants exhibited positive bronchodilator response, although the association was not significant when compared to occupational exposure. Our finding was in contrast with previous study showing the significant association between %FEV1 reversibility with occupational exposure among the COPD participants [23]. However, such assessment in the previous study [23] was performed only based on the increase of average %FEV1 predicted values among the exposed group rather than on positive bronchodilator response.

We, similar to other studies [3, 35, 36], found correlations between COPD and low BMI (Adjusted ORs: 1.6); and between COPD and age (Adjusted ORs: 1.6 for age>60 years and1.4 for age 50–59 years), although those were not significant. Furthermore, similar to previous study [28], we also found positive association between COPD and gender (female). However, unlike other studies [37, 38], we did not find positive association between COPD and family history of COPD. This might happen because we noted self-reported response without checking authenticity, and most of our participants were not educated enough.

Our study had few limitations. This was hospital-based study that might not represent the global scenario of Bangladesh. Many of the variables including smoking habit, age and family history of COPD were self-reported without testing their authenticity. We could not verify occupational exposures reported by the participants. However, this limitation was addressed by checking participants job identity card and moreover by conducting JEM exposure measures. Besides, exposure assessment from longer job durations in our study helped to ensure that occupational exposure led to the development of COPD. Another limitation of our study was to define COPD according to GOLD criteria only which was reported previously to overestimate COPD cases [3]. This was also reflected in our study as well since both prevalence and ORs of developing COPD for most variables were found higher from the similar studies [9, 26].

Our study guided us to conclude that occupational exposures in the workplace was significantly associated with COPD among Bangladeshi population. Additional factors including smoking habit, age, BMI and gender should also be kept in mind as those became important risk factors of COPD too. Further research is needed to look over this association into more detail to mitigate COPD cases among Bangladeshi people.

Supporting information

S1 Table. Spirometry values of control participants according to self-reported occupational exposure.

(PDF)

S2 Table. Spirometry values of COPD participants according to self-reported occupational exposure.

(PDF)

Acknowledgments

We are thankful for the support and help from the staff and attendants of the Dhaka Medical College Hospital, Dhaka, Bangladesh. Furthermore, we are grateful to the participants and their family who have agreed either to participate or give consent in the study.

Data Availability

All relevant data are within the manuscript and its Supporting Information files.

Funding Statement

The author(s) received no specific funding for this work.

References

  • 1.López-Campos JL, Soler-Cataluña JJ, Miravitlles M. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease 2019 Report: Future Challenges. Arch Bronconeumol. 2020; 56(2):65–7. 10.1016/j.arbres.2019.06.001 [DOI] [PubMed] [Google Scholar]
  • 2.World Health Organization. Chronic obstructive pulmonary disease (COPD) fact sheet 2017. Last updated: December 1 2017. Available from: https://www.who.int/news-room/fact-sheets/detail/chronic-obstructive-pulmonary-disease-(copd).
  • 3.Alam DS, Chowdhury MA, Siddiquee AT, Ahmed S, Clemens JD. Prevalence and determinants of chronic obstructive pulmonary disease (COPD) in Bangladesh. COPD. 2015;12(6):658–67. 10.3109/15412555.2015.1041101 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Wang C, Xu J, Yang L, Xu Y, Zhang X, Bai C, et al. Prevalence and risk factors of chronic obstructive pulmonary disease in China (the China Pulmonary Health [CPH] study): a national cross-sectional study. Lancet. 2018; 391(10131):1706–17. 10.1016/S0140-6736(18)30841-9 [DOI] [PubMed] [Google Scholar]
  • 5.Shanmugananth E, Singh S, Ahlawat R, Nambi G, Sperjan G, Abraham M, et al. Prevalence of Chronic Obstructive Pulmonary Disease (COPD) among Indian Population. RJPT. 2019;12(11):5285–9. [Google Scholar]
  • 6.Sutradhar I, Gupta RD, Hasan M, Wazib A, Sarker M. Prevalence and Risk Factors of Chronic Obstructive Pulmonary Disease in Bangladesh: A Systematic Review. Cureus. 2019; 11(1): e3970 10.7759/cureus.3970 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Doney B, Kurth L, Halldin C, Hale J, Frenk SM. Occupational exposure and airflow obstruction and self-reported COPD among ever-employed US adults using a COPD-job exposure matrix. Am J Ind Med. 2019;62(5):393–403. 10.1002/ajim.22958 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Kurth L, Doney B, Weinmann S. Occupational exposures and chronic obstructive pulmonary disease (COPD): comparison of a COPD-specific job exposure matrix and expert-evaluated occupational exposures. Occup Environ Med. 2017;74(4):290–3. 10.1136/oemed-2016-103753 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Blanc PD, Annesi-Maesano I, Balmes JR, Cummings KJ, Fishwick D, Miedinger D, et al. The Occupational Burden of Nonmalignant Respiratory Diseases. An Official American Thoracic Society and European Respiratory Society Statement. Am J Respir Crit Care Med. 2019;199(11):1312–34. 10.1164/rccm.201904-0717ST [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Tasnim F, Rahman I, Rahman M, Islam R. A review on occupational health safety in Bangladesh with respect to Asian Continent. Int J Pub health safe. 2016; 1:102. [Google Scholar]
  • 11.Miah SJ, Hoque A, Paul A, Rahman A. Unsafe use of pesticide and its impact on health of farmers: a case study in Burichong Upazila, Bangladesh. IOSR-JESTFT. 2014; 8(1): 57–67. [Google Scholar]
  • 12.Hossain MA, Islam LN. Effect of occupational exposure on allergic diseases and relationship with serum IgE levels in the tannery workers in Bangladesh. BRC. 2016;2(1):158–63. [Google Scholar]
  • 13.Alim MA, Sarker MA, Selim S, Karim MR, Yoshida Y, Hamajima N. Respiratory involvements among women exposed to the smoke of traditional biomass fuel and gas fuel in a district of Bangladesh. Environ Health Prev Med. 2014;19(2):126–34. 10.1007/s12199-013-0364-4 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Islam MS, Razwanul I, Mahmud MT. Safety Practices and Causes of Fatality in Building Construction Projects: A Case Study for Bangladesh. JJCE. 2017;11(2):267–78. [Google Scholar]
  • 15.Mahfuz M, Ahmed T, Ahmad SA, Khan MH. Altered Pulmonary Function among the Transport Workers in Dhaka city. Health. 2014; 6(16):2144–53. [Google Scholar]
  • 16.Biswas RS, Paul S, Rahaman MR, Sayeed MA, Hoque MG, Hossain MA, et al. Indoor biomass fuel smoke exposure as a risk factor for chronic obstructive pulmonary disease (COPD) for women of rural Bangladesh. Chattagram Maa-O-Shishu Hosp Med College. J 2016;15(1):8–11. [Google Scholar]
  • 17.Siddharthan T, Grigsby MR, Goodman D, Chowdhury M, Rubinstein A, Irazola V, et al. Association between household air pollution exposure and chronic obstructive pulmonary disease outcomes in 13 low-and middle-income country settings. Am J Respir Crit Care Med. 2018;197(5):611–20. 10.1164/rccm.201709-1861OC [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18.Pauwels RA, Buist AS, Calverley PM, Jenkins CR, Hurd SS. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary. Am J Respir Crit Care Med. 2001;163(5):1256–76. 10.1164/ajrccm.163.5.2101039 [DOI] [PubMed] [Google Scholar]
  • 19.Miller A. Lung function testing: selection of reference values and interpretative strategies. Am Rev Respir Dis. 1992; 146:1368–9. [DOI] [PubMed] [Google Scholar]
  • 20.Eriksson B, Lindberg A, Müllerova H, Rönmark E, Lundbäck B. Association of heart diseases with COPD and restrictive lung function–results from a population survey. Respir Med. 2013;107(1):98–106. 10.1016/j.rmed.2012.09.011 [DOI] [PubMed] [Google Scholar]
  • 21.Vandevoorde J, Verbanck S, Schuermans D, Kartounian J, Vincken W. Obstructive and restrictive spirometric patterns: fixed cut-offs for FEV1/FEV6 and FEV6. Eur Respir J. 2006; 27(2):378–83. 10.1183/09031936.06.00036005 [DOI] [PubMed] [Google Scholar]
  • 22.Sim YS, Lee JH, Lee WY, Suh DI, Oh YM, Yoon JS, et al. Spirometry and bronchodilator test. Tuberc Respir Dis. 2017;80(2):105–12. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 23.Minov J, Karadzinska-Bislimovska J, Vasilevska K, Risteska-Kuc S, Stoleski S, Mijakoski D. Chronic Obstructive Pulmonary Disease in Never-Smoking Bricklayers. Maced J Med Sci. 2013;6(4):397–403. [Google Scholar]
  • 24.Caillaud D, Lemoigne F, Carré P, Escamilla R, Chanez P, Burgel PR, et al. Association between occupational exposure and the clinical characteristics of COPD. BMC Public Health. 2012;12(1):302. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 25.International Labour Office. International Standard Classification of Occupations: ISCO-88. Geneva: International Labour Organization, 1990. [Google Scholar]
  • 26.Govender N, Lalloo UG, Naidoo RN. Occupational exposures and chronic obstructive pulmonary disease: a hospital based case–control study. Thorax. 2011;66(7):597–601. 10.1136/thx.2010.149468 [DOI] [PubMed] [Google Scholar]
  • 27.Mehta AJ, Miedinger D, Keidel D, Bettschart R, Bircher A, Bridevaux PO, et al. Occupational exposure to dusts, gases, and fumes and incidence of chronic obstructive pulmonary disease in the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults. Am J Respir Crit Care Med. 2012;185(12):1292–300. 10.1164/rccm.201110-1917OC [DOI] [PubMed] [Google Scholar]
  • 28.Matheson MC, Benke G, Raven J, Sim MR, Kromhout H, Vermeulen R, et al. Biological dust exposure in the workplace is a risk factor for chronic obstructive pulmonary disease. Thorax. 2005;60(8):645–51. 10.1136/thx.2004.035170 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29.World Health Organization. Physical status: the use and interpretation of anthropometry. Report of a WHO Expert Committee. World Health Organ Tech Rep Ser. 1995; 854:1–452. [PubMed] [Google Scholar]
  • 30.de Meer G, Kerkhof M, Kromhout H, Schouten JP, Heederik D. Interaction of atopy and smoking on respiratory effects of occupational dust exposure: a general population-based study. Environ Health. 2004;3(1):6 10.1186/1476-069X-3-6 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 31.Pallasaho P, Kainu A, Sovijärvi A, Lindqvist A, Piirilä PL. Combined effect of smoking and occupational exposure to dusts, gases or fumes on the incidence of COPD. COPD. 2014;11(1):88–95. 10.3109/15412555.2013.830095 [DOI] [PubMed] [Google Scholar]
  • 32.Trupin L, Earnest G, San Pedro M, Balmes JR, Eisner MD, Yelin E, et al. The occupational burden of chronic obstructive pulmonary disease. Eur Res J. 2003;22(3):462–9. [DOI] [PubMed] [Google Scholar]
  • 33.Jaén Á, Zock JP, Kogevinas M, Ferrer A, Marín A. Occupation, smoking, and chronic obstructive respiratory disorders: a cross sectional study in an industrial area of Catalonia, Spain. Environ Health. 2006;5(1):2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34.Janson C, Malinovschi A, Amaral AF, Accordini S, Bousquet J, Buist, AS, et al. Bronchodilator reversibility in asthma and COPD: findings from three large population studies. Eur Respir J. 2019;54(3):1900561 10.1183/13993003.00561-2019 [DOI] [PubMed] [Google Scholar]
  • 35.Zhou Y, Wang D, Liu S, Lu J, Zheng J, Zhong N, et al. The association between BMI and COPD: the results of two population-based studies in Guangzhou, China. COPD. 2013;10(5):567–72. 10.3109/15412555.2013.781579 [DOI] [PubMed] [Google Scholar]
  • 36.Schirnhofer L, Lamprecht B, Vollmer WM, Allison MJ, Studnicka M, Jensen RL, et al. COPD prevalence in Salzburg, Austria: results from the Burden of Obstructive Lung Disease (BOLD) study. Chest. 2007;131(1):29–36. 10.1378/chest.06-0365 [DOI] [PubMed] [Google Scholar]
  • 37.Perret J, Matheson M, Johns D, Lowe A, Lodge C, Burgess J, et al. The interaction between family history of COPD, personal smoking and post-bronchodilator airflow obstruction: A cohort study. Eur Res J. 2015; 46(59): PA1111. [Google Scholar]
  • 38.De Marco R, Accordini S, Marcon A, Cerveri I, Antó JM, Gislason T, et al. Risk factors for chronic obstructive pulmonary disease in a European cohort of young adults. Am J Respir Crit Care Med. 2011;183(7):891–7. 10.1164/rccm.201007-1125OC [DOI] [PubMed] [Google Scholar]

Decision Letter 0

Christophe Leroyer

16 Jul 2020

PONE-D-20-16525

Association between chronic obstructive pulmonary disease (COPD) and occupational exposures: A hospital based quantitative cross-sectional study among the Bangladeshi population.

PLOS ONE

Dear Dr. Sumit,

Thank you for submitting your manuscript to PLOS ONE. After careful consideration, we feel that it has merit but does not fully meet PLOS ONE’s publication criteria as it currently stands. Therefore, we invite you to submit a revised version of the manuscript that addresses the points raised during the review process.

==============================

ACADEMIC EDITOR: Please insert comments here and delete this placeholder text when finished. Be sure to:

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==============================

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Christophe Leroyer

Academic Editor

PLOS ONE

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Reviewer #2: Yes

**********

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Reviewer #1: The authors examine the relation between occupational exposures and COPD in a respiratory clinic based population in Bangladesh. They find a higher rate of COPD in Occupationally exposed population.

Major comments:

As all of the patients were being evaluated for respiratory problems, the authors need to be very cautious in how these results are presented and interpreted. For example- what diagnoses did the patients in the control group actually have?

Also- the authors should present the proportion of patients with restriction ( normal ratio and low FEV1)- As I suspect there would be a high proportion of patients with this abnormality.

Was pre bronchodilator lung function assessed? This might be important and including an assessment of bronchodilator responsiveness would be helpful.

Reviewer #2: The authors present original results concerning the share of professional origin in the etiology of COPD in Bangladesh. The text is well written apart from 2 minimal mistakes. The document is understandable and meets the criteria of a good scientific article. The publication is original and will allow to deepen later among the trades found, the pathogens at the origin of these respiratory diseases.

**********

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Reviewer #1: Yes: David Mannino

Reviewer #2: Yes: DEWITTE, J.D.

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PLoS One. 2020 Sep 23;15(9):e0239602. doi: 10.1371/journal.pone.0239602.r002

Author response to Decision Letter 0


22 Aug 2020

Dear Respected Reviewers,

Many thanks for reviewing our paper. We really appreciate that you gave us response in such a short time. We have edited the manuscript according to your suggestions. We are grateful enough to receive the inputs you both have given for our manuscript. We strongly believe that your inputs will help us improving the quality of our manuscript substantially.

Please find the responses here:

Response to Reviewers' Comments

Reviewer 1 comment:

1. As all of the patients were being evaluated for respiratory problems, the authors need to be very cautious in how these results are presented and interpreted. For example- what diagnoses did the patients in the control group actually have?

Response: Initially, all the control participants were examined by registered physician after complaining about respiratory problems. They all were confirmly diagnosed without COPD based on the spirometry results that was FEV1/FVC>0.70, and FEV1% ≥ 80 predicted.

Based on the suggestions by registered physician, some of the control participants were also undergoing other tests like chest x-ray, serum IgE test, blood eosinophil count, etc, to confirm the diagnosis of asthma, bronchitis, emphysema, restrictive problems and/or other respiratory diseases. We have excluded those control participants who had been diagnosed with asthma, chronic bronchitis, and/or emphysema by registered physician during the time of study or if they had past history of these diseases. This information has been added in the manuscript now.

We have not excluded control participants if they had been diagnosed with restrictive problems. Besides, control participants with doctor diagnosed allergic rhinitis, wheezing, mild/chronic cough, morning phlegm, dyspnoea were also included in our study. However, majority of the control participants were diagnosed as normal by registered physician.

In our study we have only assessed self-reported respiratory symptoms of the participants (“Table 1”) rather than registered physician diagnosed respiratory diseases since we found majority of the control participants were diagnosed as normal by registered physician.

2. Also- the authors should present the proportion of patients with restriction (normal ratio and low FEV1)- As I suspect there would be a high proportion of patients with this abnormality.

Response: According to your suggestion, we have included the proportion of control participants with restriction (normal ratio, but FVC<80% predicted) according to GOLD criteria.

3. Was pre bronchodilator lung function assessed? This might be important and including an assessment of bronchodilator responsiveness would be helpful.

Response: According to your suggestion, we have included pre bronchodilator response data in our manuscript.

Since we excluded all control participants who have shown positive bronchodilator response due to the suspect of asthma, bronchodilator response was shown only for the COPD participants.

Reviewer 2 comment:

The text is well written apart from 2 minimal mistakes.

Response: We have addressed short grammatical mistakes and corrected accordingly.

Attachment

Submitted filename: Resonse to Reviewers.docx

Decision Letter 1

Christophe Leroyer

3 Sep 2020

PONE-D-20-16525R1

Association between chronic obstructive pulmonary disease (COPD) and occupational exposures: A hospital based quantitative cross-sectional study among the Bangladeshi population.

PLOS ONE

Dear Dr. Sumit,

Thank you for submitting your manuscript to PLOS ONE. After careful consideration, we feel that it has merit but does not fully meet PLOS ONE’s publication criteria as it currently stands. Therefore, we invite you to submit a revised version of the manuscript that addresses the points raised during the review process.

==============================

ACADEMIC EDITOR:

My comment refers to the discussion section:

"The association between occupational exposure and bronchodilator response among the COPD

300 participants were also assessed in our study. Here, similar to earlier study [34], our study showed that

301 12-20% of COPD participants exhibited positive bronchodilator response, although the association was

302 not significant when compared to occupational exposure. Our finding was in contrast with previous

303 study showing the significant association between %FEV1 reversibility with occupational exposure

304 among the COPD participants [23]. However, such assessment was performed only based on the

305 increase of average %FEV1 predicted values among the exposed group rather than on positive

306 bronchodilator response."

The last sentence is unclear to me: do you refer to your study or to the previous one ?

many thnaks to elucidate this point

==============================

Please submit your revised manuscript by Oct 18 2020 11:59PM. If you will need more time than this to complete your revisions, please reply to this message or contact the journal office at plosone@plos.org. When you're ready to submit your revision, log on to https://www.editorialmanager.com/pone/ and select the 'Submissions Needing Revision' folder to locate your manuscript file.

Please include the following items when submitting your revised manuscript:

  • A rebuttal letter that responds to each point raised by the academic editor and reviewer(s). You should upload this letter as a separate file labeled 'Response to Reviewers'.

  • A marked-up copy of your manuscript that highlights changes made to the original version. You should upload this as a separate file labeled 'Revised Manuscript with Track Changes'.

  • An unmarked version of your revised paper without tracked changes. You should upload this as a separate file labeled 'Manuscript'.

If you would like to make changes to your financial disclosure, please include your updated statement in your cover letter. Guidelines for resubmitting your figure files are available below the reviewer comments at the end of this letter.

If applicable, we recommend that you deposit your laboratory protocols in protocols.io to enhance the reproducibility of your results. Protocols.io assigns your protocol its own identifier (DOI) so that it can be cited independently in the future. For instructions see: http://journals.plos.org/plosone/s/submission-guidelines#loc-laboratory-protocols

We look forward to receiving your revised manuscript.

Kind regards,

Christophe Leroyer

Academic Editor

PLOS ONE

[Note: HTML markup is below. Please do not edit.]

[NOTE: If reviewer comments were submitted as an attachment file, they will be attached to this email and accessible via the submission site. Please log into your account, locate the manuscript record, and check for the action link "View Attachments". If this link does not appear, there are no attachment files.]

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PLoS One. 2020 Sep 23;15(9):e0239602. doi: 10.1371/journal.pone.0239602.r004

Author response to Decision Letter 1


9 Sep 2020

Reviewer comment:

The association between occupational exposure and bronchodilator response among the COPD participants were also assessed in our study. Here, similar to earlier study [34], our study showed that 12-20% of COPD participants exhibited positive bronchodilator response, although the association was not significant when compared to occupational exposure. Our finding was in contrast with previous study showing the significant association between %FEV1 reversibility with occupational exposure among the COPD participants [23]. However, such assessment was performed only based on the increase of average %FEV1 predicted values among the exposed group rather than on positive bronchodilator response."

The last sentence is unclear to me: do you refer to your study or to the previous one?

Response:

The last sentence refers to previous study and we have added this in our manuscript as follow:

“However, such assessment in the previous study [23] was performed only based on the increase of average %FEV1 predicted values among the exposed group rather than on positive bronchodilator response.”

Attachment

Submitted filename: Resonse to Reviewers.docx

Decision Letter 2

Christophe Leroyer

10 Sep 2020

Association between chronic obstructive pulmonary disease (COPD) and occupational exposures: A hospital based quantitative cross-sectional study among the Bangladeshi population.

PONE-D-20-16525R2

Dear Dr. Sumit,

We’re pleased to inform you that your manuscript has been judged scientifically suitable for publication and will be formally accepted for publication once it meets all outstanding technical requirements.

Within one week, you’ll receive an e-mail detailing the required amendments. When these have been addressed, you’ll receive a formal acceptance letter and your manuscript will be scheduled for publication.

An invoice for payment will follow shortly after the formal acceptance. To ensure an efficient process, please log into Editorial Manager at http://www.editorialmanager.com/pone/, click the 'Update My Information' link at the top of the page, and double check that your user information is up-to-date. If you have any billing related questions, please contact our Author Billing department directly at authorbilling@plos.org.

If your institution or institutions have a press office, please notify them about your upcoming paper to help maximize its impact. If they’ll be preparing press materials, please inform our press team as soon as possible -- no later than 48 hours after receiving the formal acceptance. Your manuscript will remain under strict press embargo until 2 pm Eastern Time on the date of publication. For more information, please contact onepress@plos.org.

Kind regards,

Christophe Leroyer

Academic Editor

PLOS ONE

Acceptance letter

Christophe Leroyer

14 Sep 2020

PONE-D-20-16525R2

Association between chronic obstructive pulmonary disease (COPD) and occupational exposures: A hospital based quantitative cross-sectional study among the Bangladeshi population.

Dear Dr. Sumit:

I'm pleased to inform you that your manuscript has been deemed suitable for publication in PLOS ONE. Congratulations! Your manuscript is now with our production department.

If your institution or institutions have a press office, please let them know about your upcoming paper now to help maximize its impact. If they'll be preparing press materials, please inform our press team within the next 48 hours. Your manuscript will remain under strict press embargo until 2 pm Eastern Time on the date of publication. For more information please contact onepress@plos.org.

If we can help with anything else, please email us at plosone@plos.org.

Thank you for submitting your work to PLOS ONE and supporting open access.

Kind regards,

PLOS ONE Editorial Office Staff

on behalf of

Dr. Christophe Leroyer

Academic Editor

PLOS ONE

Associated Data

    This section collects any data citations, data availability statements, or supplementary materials included in this article.

    Supplementary Materials

    S1 Table. Spirometry values of control participants according to self-reported occupational exposure.

    (PDF)

    S2 Table. Spirometry values of COPD participants according to self-reported occupational exposure.

    (PDF)

    Attachment

    Submitted filename: Resonse to Reviewers.docx

    Attachment

    Submitted filename: Resonse to Reviewers.docx

    Data Availability Statement

    All relevant data are within the manuscript and its Supporting Information files.


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