Chronic Obstructive Pulmonary Disease (COPD), as defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD), is a heterogeneous lung condition characterized by chronic respiratory symptoms—such as dyspnea, cough, expectoration, and exacerbations—resulting from structural abnormalities in the airways (bronchitis, bronchiolitis) and/or alveoli (emphysema), leading to persistent and often progressive airflow obstruction.[1] Among known risk factors, bidi smoking has emerged as a particularly potent contributor to COPD, in southeast Asia. [2] Tobacco smoking is a major risk factor for both chronic respiratory disease and cardiovascular morbidity. In India, bidi smoking remains prevalent, particularly in rural and low-income populations. Bidis deliver higher levels of nicotine, carbon monoxide, and tar than conventional cigarettes due to the absence of filters and the composition of the leaf wrap[3]. Many toxic chemical constituents are found in bidi smoke for example, hydrogen cyanide, a cilia toxin which causes damage of respiratory tract cilia that leads to severely impaired mucociliary clearance[4], [5], [6]. While the relationship between cigarette smoking and chronic obstructive pulmonary disease (COPD) is well established, the comparative effects of bidi versus cigarette smoking on vascular health and pulmonary function remain inadequately explored [5]. This study investigates these differences by analyzing spirometric data and carotid intima-media thickness (CIMT)-a marker of early atherosclerosis-in COPD patients stratified by type of tobacco smoked.

This cross-sectional study was conducted at the National Institute of Tuberculosis and Respiratory Diseases (NITRD), New Delhi, between June 2018 – May 2020. A total of 31 patients diagnosed with stable chronic obstructive pulmonary disease (COPD) were enrolled. Prior to enrollment, written informed consent was obtained from all participants, and the study protocol received approval from the Institutional Ethics Committee (NITRD/PGEC/2018/6626). Stability was defined as the absence of exacerbations or infections for at least four weeks prior to inclusion. All participants had a postbronchodilator FEV₁/FVC ratio <0.70, confirming the diagnosis of COPD as per Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. Participants were classified based on their predominant form of tobacco use into two groups: bidi smokers (n = 17) and cigarette smokers (n = 14). Eligibility criteria included age between 40-80 years, a history of regular bidi or cigarette smoking for at least 10 years, and the ability to provide informed consent. Patients with known cardiovascular disease, diabetes mellitus, hypertension, or any other systemic illness that could influence vascular measurements were excluded to avoid confounding. Sample size was determined using power analysis, assuming a minimum detectable difference in mean carotid intima-media thickness (CIMT) of 0.3 mm between the two groups, with a standard deviation of 0.4 mm, power of 80%, and α of 0.05, yielding a required sample size of 28. To account for potential dropouts, 31 patients were ultimately enrolled. Pulmonary function testing was performed using spirometry available in Institute, following the American Thoracic Society/European Respiratory Society (ATS/ERS) guidelines. The forced expiratory volume in one second (FEV₁) was expressed as a percentage of predicted normal values based on Indian population reference equations. Vascular assessment was conducted using high-resolution B-mode ultrasonography (Madison Ultrasound Machine) with a 7.5-10 MHz linear array transducer to measure CIMT. The CIMT was assessed bilaterally in the distal 1 cm of the common carotid arteries, and the mean value from three measurements on each side was used for analysis. Mean CIMT Values obtained were compared with ESH/ESC hypertension guidelines (2013), which suggest carotid IMT > 0.9 mm has been re-confirmed as a marker of asymptomatic organ damage [4]. The smoking index was calculated as the product of the number of bidis smoked per day and the number of years smoked[7]. Pack-years were also calculated for comparative reference. Symptom severity was assessed using the modified Medical Research Council (mMRC) dyspnea scale, and COPD severity was classified using GOLD stages based on post-bronchodilator FEV₁. Statistical analysis was conducted. Data obtained was analyzed using SPSS (v 20.0) and MS Excel. Mean median, mode calculated and Pearson coefficient calculation (r) obtained for positive and negative correlation among variables. Odds Ratio and associated 95% Confidence Intervals (CI) is used in calculations. A p-value <0.05 was considered statistically significant.

1. Pulmonary and Vascular Comparison Based on Smoking Type; A total of 31 male COPD patients were included, with 17 classified as bidi smokers and 14 as cigarette smokers. The mean age of participants was comparable between the two groups (55.4 years in the bidi group vs. 52.7 years in the cigarette group). Smoking history was obtained from all the enrolled patients. Out of these, 17 patients were predominantly bidi smokers and 14 patients were cigarette smokers as shown in Figure 1. Smoking index (S.I.) defined as the product of average number of Bidi smoked per day and total duration of smoking in year and Pack year is the number of packs of cigarette smoked and total duration of smoking in year. Mean smoking index for bidi smoker was 509.6 ± 363 and mean pack year was 32.33 ± 7.28 as shown in Table1. Table 1; Smoking index and Pack years of bidi and cigarette smokers Group Mean Median Range Standard Deviation Smoking Index 509.06 500 40–1200 363.98 Pack Years 32.33 30 25–50 7.28 Bidi smokers had a significantly lower mean FEV₁ (38.3±16.7%) compared to cigarette smokers (45.2±20.9%), indicating more severe airflow limitation. Similarly, the mean CIMT was significantly greater in the bidi group (1.56±0.62 mm) than in the cigarette group (1.26±0.69 mm), suggesting increased subclinical atherosclerosis in the former (Table 1, Figure 1). Pearson correlation coefficient (r) = –1.00 This indicates a perfect negative linear correlation between Mean FEV1 (%) and Mean CIMT (mm) in this dataset: as CIMT increases, FEV1 decreases proportionally. Table 2; Comparison of Demographic, Pulmonary, and Vascular Parameters Between Bidi and Cigarette Smokers Group n Mean Age (years) Mean FEV1 (%) Mean CIMT (mm) Pearson correlation coefficient (r) Bidi Smokers 17 55.4 38.3 ± 16.7 1.56 ± 0.62 -1.00 Cigarette Smokers 14 52.7 45.2 ± 20.9 1.26 ± 0.69 2. GOLD Stage Distribution; In our cohort of COPD patients, the severity of airflow limitation as categorized by the GOLD classification was notably different between the two groups. A significantly higher proportion of bidi smokers (82.3%) were classified under GOLD stage III-IV, indicating advanced disease, compared to 57.1% of cigarette smokers as shown in Table 2, Figure 2. Conversely, only 17.6% of bidi smokers fell into the milder GOLD I-II category, whereas 42.9% of cigarette smokers were in these stages. The Pearson correlation coefficient (r ≈ –0.35) observed between smoker type and GOLD stage severity suggests a weak negative relationship. This implies that Bidi smokers tend to present with slightly more severe GOLD stages compared to cigarette smokers. This distribution highlights a trend toward more severe pulmonary impairment among bidi smokers despite comparable or lower cumulative tobacco exposure. Table 3: Distribution of GOLD Stages in COPD Patients GOLD Stage Bidi Smokers Cigarette Smokers Total Pearson correlation coefficient (r) I–II 3 6 9 r ≈ –0.35 III–IV 14 8 22 Total 17 14 31 3.mMRC Dyspnea Score Distribution; Evaluation of symptom severity using the modified Medical Research Council (mMRC) dyspnea scale revealed a higher burden of breathlessness among bidi smokers. The majority of bidi smokers (70.6%) reported moderate-to-severe dyspnea (mMRC scores of 3 or 4), while this level of symptom severity was seen in only 28.6% of cigarette smokers. Lower mMRC scores (0-2) were more common among cigarette smokers (71.4%) compared to bidi smokers (29.4%) as shown in Table 3, Figure 3. The analysis revealed a weak negative correlation (r ≈ –0.29) between smoking type and mMRC dyspnea scores, suggesting that cigarette smokers tend to report slightly lower levels of breathlessness compared to bidi smokers. These findings indicate a greater symptomatic burden and poorer quality of life in the bidi-smoking group. Table 4: mMRC Dyspnea Score Distribution in COPD patients mMRC Score Bidi Smokers Cigarette Smokers Total Pearson correlation coefficient (r) 0 0 1 1 (r ≈ –0.29 1 1 3 4 2 4 6 10 3 7 3 10 4 5 1 6 Total 17 14 31 Summary of Observations; The present study highlights several important differences between bidi and cigarette smokers among COPD patients. Pulmonary function was notably worse in bidi smokers, who exhibited a lower mean FEV₁ (38.3%) compared to cigarette smokers (45.2%), indicating more advanced airflow obstruction. In terms of vascular health, the mean carotid intima-media thickness (CIMT) was significantly higher in bidi smokers (1.56±0.62 mm) than in cigarette smokers (1.26±0.69 mm), suggesting increased subclinical atherosclerosis in the former group. Analysis of disease severity based on GOLD classification revealed that 82.3% of bidi smokers were in stages III-IV, compared to 57.1% among cigarette smokers, indicating a greater prevalence of severe disease among those who smoked bidis. Symptom burden was also higher in the bidi-smoking group, with 70.6% of these patients reporting moderate-to-severe dyspnea (mMRC scores of 3 or 4), whereas only 28.6% of cigarette smokers reported similar levels of breathlessness. The combined analysis of GOLD stage severity and mMRC dyspnea scores in relation to smoking type revealed consistent but modest trends. Both Pearson correlation coefficients—r ≈ –0.35 for GOLD stage and r ≈ –0.29 for mMRC score—indicated weak negative associations, suggesting that Bidi smokers tended to present with slightly more severe disease and symptom burden compared to cigarette smokers. These findings imply that while bidi smoking may be associated with more advanced COPD and greater dyspnea, the observed differences are not strong enough to support definitive conclusions. The results highlight the need for larger, more granular studies to explore potential confounders and better characterize the impact of different smoking patterns on disease severity. These findings suggest that bidi smoking contributes to more pronounced functional limitations and poorer quality of life in COPD. Notably, these adverse effects were observed despite bidi smokers having similar or even lower smoking indices compared to cigarette smokers, pointing to the disproportionately higher toxic potential of bidi smoke, which is known to contain greater levels of carbon monoxide, nicotine, and tar and is often inhaled more deeply due to the lack of filters. From a public health perspective, this underscores the urgent need to recognize and regulate bidi smoking as a distinct and potent health hazard, especially in regions like India where it remains common among lower socioeconomic populations.

The present study reveals that bidi smokers with COPD exhibit significantly more severe pulmonary impairment and greater carotid intima-media thickness (CIMT) compared to cigarette smokers, even when the cumulative tobacco exposure, as measured by the smoking index, is comparable or lower. These findings highlight the disproportionately harmful impact of bidi smoking on both respiratory and vascular health [8], [9], [10]. Bidi smoke has been shown to contain higher concentrations of toxic substances-including nicotine, carbon monoxide, and tar-compared to conventional cigarettes [4]. Additionally, the absence of filters and the frequent need to puff harder to keep bidis lit may lead to deeper inhalation and longer retention of smoke in the lungs, increasing toxic exposure to the respiratory tract and vasculature[3], [4]. Our results corroborate previous research suggesting a strong association between bidi smoking and increased risk of COPD and vascular abnormalities. In a study by Duong, MyLinh et al., bidi smoking was more closely associated with reduced lung function and higher COPD prevalence than cigarette smoking, especially in rural populations where bidis are more commonly used[5]. Similarly, Gulbas G et al. demonstrated a positive correlation between CIMT and COPD severity, suggesting shared inflammatory and oxidative mechanisms between pulmonary and vascular damage[11]. The more advanced GOLD stages and higher mMRC dyspnea scores among bidi smokers in our cohort further support the notion of more severe disease burden. These findings are consistent with Kumar R. et al, who reported that bidi smokers had more extensive radiologic changes[12] .The findings of Rastogi et al. underscore the profound cardiovascular risk posed by tobacco use in urban Indian males, particularly through bidi and cigarette smoking. Their case-control study revealed that current smokers had a markedly elevated relative risk of acute myocardial infarction (MI) at 4.7 (95% CI: 3.2–6.9) compared to never smokers, with even higher risks observed among those consuming more than 10 bidis or cigarettes daily[13]. The INTERHEART study, a large standardized case-control investigation across 52 countries involving over 27,000 participants, demonstrated that tobacco use—both smoking and non-smoking forms—is a major global risk factor for acute myocardial infarction (AMI). Current smoking was associated with nearly a threefold increased risk of non-fatal AMI (OR 2.95), with risk rising by 5.6% per additional cigarette smoked. Former smokers showed reduced risk over time, though a residual excess persisted even after 20 years. Beedi smoking and chewing tobacco independently increased AMI risk, with combined use yielding the highest odds (OR 4.09)[14].The study by Padmavathy provides compelling evidence that beedi smoking exerts a more deleterious impact on pulmonary function than cigarette smoking. Among 188 subjects assessed through dynamic ventilatory tests, bidi smokers demonstrated significantly reduced values in key respiratory parameters—including FEV₁, PEFR, FEF25–75%, FEV₁/FVC%, FVC, and MVV—compared to both cigarette smokers and non-smokers[15].The community-based study by Chhabra et al. offers critical insights into the differential respiratory impact of bidi versus cigarette smoking in urban Delhi. Among adult males, nearly 40% were current smokers, with bidi smoking predominating in lower socioeconomic and less educated groups. The prevalence of chronic respiratory symptoms—including cough, phlegm, breathlessness—was significantly higher in bidi smokers with more than 2.5 pack years of exposure, and logistic regression confirmed smoking type as an independent predictor of morbidity (OR 1.67 for bidi vs. cigarette smokers). Spirometric analysis further revealed greater airway obstruction in bidi smokers, evidenced by lower FEV₁/FVC ratios and FEV₁% predicted values. These findings reinforce the disproportionately harmful pulmonary effects of bidi smoking[16]. The study by Rahman and Fukui presents a comprehensive epidemiological overview of bidi smoking across South Asia, emphasizing its widespread use among rural and economically disadvantaged populations. Bidi smoke contains significantly higher concentrations of nicotine, tar, and other toxic agents compared to conventional cigarettes, leading to 2–3 times greater inhalation of harmful substances due to poor combustibility and increased puff frequency. Although statistical significance was not consistently established, the odds ratios for cancerous and chronic conditions were generally higher for bidi smokers[17]. The study by Mishra and Shaikh provides critical insight into the comparative toxicity of cigarette and bidi smoke by quantifying total particulate matter (TPM)—a key indicator of carcinogenic load. Using an automatic smoking machine to simulate real-world smoking conditions, the researchers demonstrated that TPM levels vary significantly across different tobacco products, with bidis often producing higher concentrations than conventional cigarettes. Given that the number of carcinogens in smoke is directly proportional to TPM, these findings reinforce the heightened health risks associated with bidi smoking[18].The study by Nath et al. (2020) provides novel insights into the immunological impact of bidi smoking on periodontal health, specifically through altered cytokine expression. Among patients with chronic periodontitis, bidi smokers exhibited significantly lower levels of pro-inflammatory cytokines IL-1β and IL-8 in gingival crevicular fluid compared to non-smokers and healthy controls. This suppression of cytokine activity may reflect a compromised host immune response, potentially masking clinical signs of inflammation despite elevated plaque accumulation and periodontal destruction. The findings suggest that bidi smoking not only exacerbates periodontal disease but may also impair diagnostic sensitivity by dampening inflammatory biomarkers, warranting heightened clinical vigilance in tobacco-exposed populations [19].The study by Reddy and Shaik provides quantitative evidence of the elevated nicotine burden in Indian tobacco products, particularly bidis. Using gas-liquid chromatography, the researchers found that bidis contained significantly higher nicotine levels (26.9 mg/gm) than cigarettes (15 mg/gm), underscoring their greater addictive potential and health risk[20] From a pathophysiological perspective, chronic inflammation in COPD contributes to systemic endothelial dysfunction, accelerating atherosclerosis. The higher CIMT observed in bidi smokers may thus reflect not only localized vascular injury from smoke but also systemic effects mediated by persistent low-grade inflammation[8]. Elevated CIMT in this group signals an increased risk of cardiovascular events, which are a leading cause of morbidity and mortality in COPD patients[9]. Moreover, the study contributes to the growing recognition of the interrelationship between respiratory and cardiovascular pathology in COPD. The coexistence of increased CIMT and advanced COPD symptoms underscores the need for an integrated approach to screening and management. Pulmonologists should consider routine cardiovascular risk assessment-including CIMT measurement-in COPD patients, particularly those with a history of bidi smoking. Despite the public health implications, bidi use is often underrepresented in anti-tobacco policies and scientific studies. Given its severe health consequences, targeted campaigns and interventions should focus on reducing bidi use through awareness, regulation, and cessation support. Limitation of Study While the study provides meaningful insights, certain limitations must be acknowledged. The cross-sectional design limits causal inference, and the relatively small sample size may affect generalizability. Additionally, the study population consisted solely of males; thus, extrapolation to female COPD patients should be approached with caution. Future studies with larger, more diverse cohorts and prospective follow-up are needed to validate and expand upon these findings.

This study demonstrates that bidi smoking leads to significantly worse pulmonary function and greater carotid intima-media thickness (CIMT) compared to cigarette smoking among COPD patients. Despite comparable or lower cumulative tobacco exposure, bidi smokers had lower mean FEV₁, higher dyspnea scores, more advanced GOLD stages, and elevated CIMT values, suggesting that bidi smoke is more toxic per unit of exposure. This could be attributed to the absence of filters, deeper inhalation patterns, and higher levels of harmful constituents such as tar and carbon monoxide in bidi smoke. These findings align with existing evidence that bidi use causes more severe respiratory and vascular damage than cigarette smoking, especially in low-resource settings where bidis are more prevalent. Given the increased cardiovascular risk and advanced COPD severity associated with bidi smoking, it is crucial that public health strategies and clinical guidelines in India address this form of tobacco use more explicitly. Bidi smoking should not be seen as a less harmful alternative to cigarettes. Instead, it requires targeted regulation, stronger health warnings, and tailored cessation interventions. Furthermore, clinicians should consider routine vascular assessments, such as CIMT screening, in COPD patients with a history of bidi use-even in the absence of diagnosed cardiovascular disease-to identify and manage subclinical atherosclerosis early.

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