Cigarette smoking remains a global public health concern, contributing to oxidative stress, chronic inflammation, & respiratory dysfunction. Reactive oxygen species (ROS) generated from tobacco smoke overwhelm the body’s natural antioxidant defenses, resulting in lipid peroxidation, DNA damage, & accelerated aging of lung tissue[1].

Antioxidants that neutralize ROS & shield cellular components from oxidative damage include beta-carotene, vitamin C, vitamin E, & selenium. Nevertheless, there is little & frequently contradictory clinical data about their effects on current smokers [2]. The current study was carried out to assess the pulmonary outcomes, biochemical effects (alterations in oxidative stress indicators), & public awareness regarding antioxidant supplements among smokers.

In 2019, smoking accounted for 64.2% of all lung cancer (LC)-related deaths worldwide, making it the leading cause of cancer mortality. Current smoking & LC risk are clearly linked, according to case-control and/or longitudinal studies [3]. Potential risk factors for the development of LC in nonsmokers include secondhand smoke (SHS), other environmental variables, & genetic factors [4-5]. SHS exposure is responsible for about 6% of non-smoker deaths worldwide from LC in 2019.

Cigarette smoking is a major health issue & is the most preventable cause of death in the world. It has been estimated that more than 1.5 billion people smoke cigarettes worldwide [1]. Surveys revealed that there are more than 120 million smokers in India, with five million deaths annually [6]. Various studies have revealed that smoking is responsible for a broad spectrum of dreadful diseases, such as chronic obstructive pulmonary disease, cancer, coronary heart diseases (CHD), & metabolic & neurodegenerative diseases[7].

Study Design & Participants:

A randomized, double-blind, placebo-controlled study was conducted at Deben Mahata Government Medical College & Hospital, Purulia for 01 Year. A total of 100 active smokers (≥10 cigarettes/day for ≥5 years) aged 25–60 years were enrolled.

Inclusion criteria:

• Current smokers without major chronic disease.
• Normal liver & kidney function tests.

Exclusion criteria:

• Alcohol dependence or recent antioxidant use.
• Chronic systemic illness or corticosteroid therapy.

Participants provided written informed consent.

Participants were randomly assigned to two groups (n=50 each):

• Group A (Intervention): Vitamin C 500 mg/day, Vitamin E 200 IU/day, Selenium 100 µg/day, & Beta-carotene 15 mg/day for 12 weeks.
• Group B (Placebo): Identical placebo capsules for 12 weeks.

Both groups received identical dietary advice but no smoking cessation counseling during the study period.

Biochemical Evaluation

Fasting venous blood was collected at baseline & after 12 weeks to determine:

• MDA (µmol/L): via thiobarbituric acid reactive substances (TBARS) assay.
• SOD (U/mL): via spectrophotometric assay.
• TAC (mmol/L): via ferric reducing ability of plasma (FRAP) method.

Respiratory Assessment

Spirometry was conducted using a calibrated digital spirometer, measuring Forced Expiratory Volume in 1 second (FEV₁) & Forced Vital Capacity (FVC) following ATS/ERS guidelines.

Awareness Assessment

A structured, pre-validated questionnaire assessed participants’ knowledge about oxidative stress, dietary antioxidants, & supplementation before & after intervention.

Statistical Analysis

Data were analyzed using SPSS v26.0. Continuous variables were expressed as mean ± SD. Paired & unpaired t-tests compared within- & between-group differences. A p-value <0.05 was considered significant

Table 1: Baseline Characteristics of Participants (n=100)

All participants completed the study. Baseline demographics were comparable between groups.

No significant differences at baseline.

Table 2: Changes in Oxidative Stress Markers After 12 Weeks

After 12 weeks, the intervention group exhibited a significant decline in MDA & increases in SOD & TAC levels.

Table 3: Changes in Pulmonary Function Tests

Spirometric parameters improved in the antioxidant group, while minimal change occurred in the placebo group.

Awareness & Perception

Table 4: Awareness & Perception of Antioxidants among Participants

Baseline awareness of antioxidants was low (39%) but improved significantly after 12 weeks of education & supplementation.

In comparison to a placebo, this study showed that smokers who took antioxidant supplements for 12 weeks experienced a considerable improvement in oxidative stress indicators & a minor improvement in lung function. SOD & TAC rose, indicating enhanced systemic antioxidant defense, but MDA, a measure of lipid peroxidation, significantly decreased [8].

The modest but noteworthy increases in FEV₁ & FVC imply that antioxidant supplements could mitigate the lung deterioration brought on by smoking. Moreover, heightened consciousness underscores the significance of educational initiatives in encouraging healthy lifestyle choices [9].

Similar biochemical advantages of antioxidants in lowering oxidative damage have been demonstrated in earlier research; however, the clinical impact is still negligible in the absence of concurrent smoking cessation.

The comparatively brief length, the absence of long-term follow-up, & the lack of dietary intake monitoring are among the limitations. In spite of this, the study suggests that antioxidants may have an additional function in smokers [10].

The existence of varied cigarette consumption patterns in India presents serious difficulties [11]. Concerns are raised by the higher rates of cigarette exposure among men, those with less education, & those in lower socioeconomic groups, particularly considering their limited ability to address the health consequences of this habit. A significant portion of everyday users smoke more than 10 cigarettes a day [12].

Most commonly, MDA is used as a biomarker to measure oxidative stress in a variety of health threats, from mental health disorders & cancer to chronic obstructive pulmonary disease, asthma, & cardiovascular diseases [13]. Reactive species such nitrogen alkoxyl & peroxyl radicals, as well as elements like ROS, are important components of cigarette smoke [14]. Their presence in the smoke triggers additional issues by generating other substances, such free radicals, which are naturally inclined to start processes like lipid peroxidation, which ultimately leads to endothelial cell dysfunction. There are numerous research that support the finding that free radicals harm chronic smokers & secondhand smokers by increasing oxidative stress..

Antioxidant supplementation significantly improves oxidative balance & respiratory function in smokers while enhancing awareness about oxidative stress. Public health strategies combining antioxidant education with smoking cessation could be more effective in reducing smoking-induced oxidative damage.

1. Rahman I, MacNee W. Oxidative stress & regulation of glutathione in lung inflammation. Eur Respir J. 2000;16(3):534–554.
2. Lykkesfeldt J, et al. Smoking & antioxidants: impact on oxidative stress & inflammation. Curr Drug Targets. 2007;8(7):545–553.
3. Devaraj S, Jialal I. Antioxidants & smoking-induced oxidative stress. Clin Chem Lab Med. 2005;43(11):1203–1208.
4. Halliwell B, Gutteridge JMC. Free radicals in biology & medicine. 5th ed. Oxford University Press; 2015.
5. Marklund S, Marklund G: Involvement of the superoxide anion radical in the autoxidation of pyrogallol & a convenient assay for superoxide dismutase. Eur J Biochem. 1974, 47:469-74. 10.1111/j.1432-1033.1974.tb03714.x
6. Sinha AK: Colorimetric assay of catalase. Anal Biochem. 1972, 47:389-94. 10.1016/0003-2697(72)90132-7
7. Rotruck JT, Pope AL, Ganther HE, Swanson AB, Hafeman DG, Hoekstra WG: Selenium: biochemical role as a component of glutathione peroxidase. Science. 1973, 179:588-90. 10.1126/science.179.4073.588
8. Singh A, Arora M, Bentley R, Spittal MJ, Do LG, Grills N, English DR: Geographic variation in tobacco use in India: a population-based multilevel cross-sectional study. BMJ Open. 2020, 10:e033178. 10.1136/bmjopen-2019-033178
9. Shaikh R, Janssen F, Vogt T: The progression of the tobacco epidemic in India on the national & regional level, 1998-2016. BMC Public Health. 2022, 22:317. 10.1186/s12889-021-12261-y
10. Yang DQ, Zuo QN, Wang T, et al.: Mitochondrial-targeting antioxidant SS-31 suppresses airway inflammation & oxidative stress induced by cigarette smoke. Oxid Med Cell Longev. 2021, 2021:6644238. 10.1155/2021/6644238
11. Goel R, Bitzer ZT, Reilly SM, Foulds J, Muscat J, Elias RJ, Richie JP Jr: Influence of smoking puff parameters & tobacco varieties on free radicals yields in cigarette mainstream smoke. Chem Res Toxicol. 2018, 31:325-31. 10.1021/acs.chemrestox.8b00011
12. Frijhoff J, Winyard PG, Zarkovic N, et al.: Clinical relevance of biomarkers of oxidative stress. Antioxid Redox Signal. 2015, 23:1144-70. 10.1089/ars.2015.6317
13. Anand A, Gupta PK, Prabhakar S, Sharma S, Thakur K: Analysis of smoking & LPO in ALS. Neurochem Int. 2014, 71:47-55. 10.1016/j.neuint.2014.04.004
14. Rai RR, Phadke MS: Plasma oxidant-antioxidant status in different respiratory disorders. Indian J Clin Biochem. 2006, 21:161-4. 10.1007/BF02912934.