Smoking remains one of the most important modifiable risk factors affecting respiratory health worldwide. Chronic inhalation of tobacco smoke has long been associated with structural and functional changes in the airways that may culminate in obstructive lung disease. Indeed, longitudinal evidence shows that smokers incur a faster decline in forced expiratory volume in one second (FEV₁) compared with never‑smokers; in one classic 10‑year cohort, current smokers had the greatest annual FEV₁ decrement, particularly those consuming high‑tar cigarettes [1].

However, not all smokers develop clinically overt disease, and differences in smoking intensity, duration, cessation status, and even genetic susceptibility may modulate risk. A recent large pooled‑cohort analysis revealed that even low-intensity smoking or a history of former smoking was associated with accelerated FEV₁ decline compared with never‑smokers [2]. Moreover, a study of young asymptomatic smokers demonstrated that structural lung abnormalities detectable on computed tomography (CT) — even with normal spirometry — were linked to subsequent FEV₁ loss, suggesting that functional decline may lag behind anatomical changes [3].

Conversely, smoking cessation appears to attenuate or partially reverse the accelerated lung-function decline. A recent meta-analysis of cessation interventions among individuals with chronic respiratory conditions reported modest improvements in FEV₁ following smoking cessation, although results were heterogeneous across studies [4]. Similarly, population‑based longitudinal data indicate that the rate of lung-function deterioration in ex-smokers is reduced compared with continuing smokers, even if some residual damage persists [5]. This underscores the clinical importance of early cessation and sustained abstinence.

Given this background — variation in smoking exposure, evolving lung injury even in “healthy” smokers, and partial reversibility with cessation — a systematic synthesis of current epidemiologic evidence is needed to clarify the magnitude, dose‑response, and reversibility of smoking-related lung-function impairment across populations. The present review aims to fill this gap by collating and critically appraising published studies that quantify the effect of smoking on spirometric lung-function parameters.

Study Design and Reporting Framework: This systematic review was conducted in accordance with the core principles of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines []. The methodology was planned prospectively to ensure transparency in study identification, selection, and synthesis.

Eligibility Criteria: Studies were considered eligible if they:

• Included adults or adolescents exposed to active cigarette smoking.
• Reported at least one quantitative lung function parameter (e.g., FEV₁, FVC, FEV₁/FVC ratio, PEFR, or DLCO).
• Used observational (cross-sectional, case–control, cohort) or interventional designs.
• Provided sufficient statistical data for extraction (mean values, effect estimates, or group comparisons).
• Were published in English.

Exclusion criteria comprised:

• Studies exclusively assessing passive smoking or e-cigarette exposure.
• Animal or in vitro studies.
• Review articles, editorials, conference abstracts, and theses.
• Studies lacking extractable numerical lung function data.

Information Sources and Search Strategy: A comprehensive literature search was performed across PubMed, Scopus, Web of Science, and the Cochrane Library. Searches covered all records. A combination of controlled vocabulary terms and keywords was used. A representative PubMed search string included: “smoking” OR “cigarette exposure” AND “lung function” OR “spirometry” OR “pulmonary function tests” AND “FEV1” OR “FVC”. Reference lists of included articles and relevant reviews were also screened manually to identify any additional eligible studies.

Study Selection: All retrieved citations were exported into a reference management software, and duplicates were removed manually and electronically. Two reviewers independently screened titles and abstracts for potential relevance. Full-text review was performed for articles meeting preliminary eligibility criteria. Disagreements were resolved through consensus. Ultimately, 16 studies were selected for inclusion.

Study Selection: A total of 1,462 records were retrieved through database searches, and an additional 18 articles were identified through manual screening of reference lists and related sources. After removing duplicates, 1,109 unique records remained for screening. Titles and abstracts of these 1,109 records were reviewed, following which 74 articles were shortlisted for full-text evaluation. Of these, 47 studies were excluded due to insufficient extractable data, absence of a relevant smoker–nonsmoker comparison, or study designs that did not meet predefined inclusion criteria. Ultimately, 16 studies fulfilled all eligibility requirements and were included in the final qualitative synthesis of this systematic review.

Data Extraction: A structured data extraction form was developed to ensure uniform and systematic retrieval of information from each eligible study. The extracted variables included the first author’s name, year of publication, and country of origin; the study design and characteristics of the sample population; the operational definition of smoking exposure; and the specific lung function parameters assessed. Additionally, summary statistics and effect estimates reported in each study were recorded, along with details regarding any adjustment for potential confounders. To minimize errors and enhance reliability, data extraction was performed independently by two reviewers.

Quality Assessment: Methodological quality and risk of bias were evaluated using the Newcastle–Ottawa Scale (NOS) [7] for observational studies. Each study was scored across selection, comparability, and outcome domains. Studies with scores ≥7 were categorized as high quality.

Data Synthesis: Due to variability in study designs, smoking exposure definitions, and spirometric outcomes, a descriptive synthesis approach was applied. Quantitative pooling was not performed because of substantial methodological heterogeneity. Findings are presented narratively, focusing on consistent trends in lung function impairment associated with smoking.

The included studies were categorized based on study design and focus to facilitate structured synthesis. Table 1 presents nine cross-sectional studies evaluating lung function in smokers versus non-smokers, which consistently demonstrated reductions in spirometric indices (FEV₁, FVC, FEV₁/FVC) among smokers, with additional observations of reduced bronchodilator response in asthmatic smokers and diminished chest expansion and respiratory muscle strength in younger populations.

Table 2 summarizes four longitudinal and predictive cohort studies, highlighting the long-term impact of smoking on lung function; these studies reported accelerated FEV₁ decline, poorer pulmonary function trajectories in persistent smokers, and predictive associations between early adult lung function and future airflow obstruction.

Table 3 focuses on three studies examining smoking duration, severity, and cessation response. These studies indicate that longer smoking duration correlates with progressive lung function deterioration, while smoking cessation results in measurable improvements in FEV₁, particularly in individuals with lower baseline obstruction and younger age, though smoking continues to impair outcomes in asthma. Collectively, these findings underscore the dose-dependent and potentially reversible effects of smoking on pulmonary function.

Table 1: Cross-Sectional Studies Evaluating Smoking and Lung Function (n = 9)

Table 2: Longitudinal and Predictive Cohort Studies (n = 4)

Table 3: Studies Focused on Smoking Duration, Severity, or Cessation Response (n = 3)

Our systematic review consolidates evidence that cigarette smoking exerts a robust, deleterious effect on lung function across diverse populations and study designs. The cross‑sectional studies underscore the presence of impaired spirometric indices (reduced FEV₁, FVC, FEV₁/FVC) in smokers compared with non‑smokers, even among asymptomatic individuals or younger age groups. The longitudinal and cohort data strengthen this by demonstrating accelerated decline in

FEV₁ over time among smokers, and predict future airflow obstruction. Additionally, studies on smoking duration and cessation suggest that the magnitude of lung-function impairment correlates with cumulative exposure, while quitting smoking can attenuate (though not always fully reverse) decline. These observations align with results from large population-based studies outside of our included dataset.

A major strength of prior large‑scale data lies in the demonstration that even low-intensity or former smokers have significantly faster FEV₁ decline than never‑smokers. In a pooled analysis of several US cohorts, investigators reported mean annual FEV₁ declines of ~31.0 mL/year among never‑smokers versus ~39.9 mL/year among current smokers; importantly, former smokers still exhibited a modest but significant excess decline (~34.97 mL/yr), suggesting persistent vulnerability despite cessation [24]. This supports our review’s observation of residual functional impairment in former smokers; findings suggest that cessation slows—but does not always normalize—decline, especially with long-term or heavy prior smoking exposure.

More recent evidence further indicates that structural lung changes may precede overt spirometric abnormalities. In a cohort of young smokers with normal baseline spirometry, quanti­tative thoracic computed tomography (QCT) revealed early radiological abnormalities (small‑airway disease, vascular remodeling, ground‑glass opacities) that predicted accelerated FEV₁ decline over follow-up [25]. Such findings highlight a window of subclinical lung injury, undetectable via conventional spirometry at initial stages, which could evolve into measurable functional loss over time. This supports the biological plausibility of smoking-induced lung injury even before symptomatic or spirometric disease becomes manifest.

Environmental and host‑related modifiers can further influence smoking‑related lung-function trajectory. For example, exposure to indoor air pollutants (e.g., particulate matter, NO₂) in former smokers has been associated with additional decline in FEV₁, underscoring that cessation alone may not halt deterioration if other exposures remain uncontrolled [26]. Moreover, non‑smoking factors such as body composition — notably reduced muscle‑to‑fat ratio — have also been linked to accelerated decline in lung function and increased risk of airflow obstruction [27]. These observations suggest that lung-function decline is multifactorial, with smoking as a central, but not exclusive, determinant.

The cumulative evidence — including our review — reinforces the critical need for early smoking cessation and prevention efforts, ideally before irreversible structural changes develop. The identification of subclinical radiological changes in smokers with preserved spirometry suggests the utility of advanced imaging (e.g., QCT) and longitudinal monitoring in at-risk populations. Additionally, interventions should consider co‑existing environmental exposures (indoor air pollution) and modifiable host factors (body composition, physical activity) to maximize lung health outcomes. For researchers, future prospective studies with long-term follow-up are needed — integrating spirometry, imaging, and environmental assessments — to delineate trajectories of lung injury and recovery post-cessation.

While our synthesis draws on a broad range of studies, variability in study designs, definitions of smoking exposure (intensity, duration, former vs current), and outcome measures (spirometry parameters, bronchodilator response) limits the ability to perform a quantitative meta-analysis. Further, many included studies lack detailed data on pack‑years, environmental exposures, or comorbid conditions (e.g., obesity, occupational hazards) that might modulate the effect of smoking on lung function.

The evidence from the included studies demonstrates that cigarette smoking has a consistently deleterious effect on lung function, reflected by reductions in FEV₁, FVC, and FEV₁/FVC ratios across diverse populations and age groups. Cross-sectional studies confirm early functional impairment even in adolescents and young adults, while longitudinal analyses reveal accelerated lung-function decline and long-term risk of airflow obstruction in persistent smokers. Importantly, smoking cessation mitigates some of these effects, leading to measurable improvements in pulmonary function, particularly among younger individuals and those with less baseline airway obstruction. The duration and intensity of smoking further exacerbate functional impairment, underscoring a clear dose-response relationship. These findings highlight the critical importance of early prevention, smoking reduction, and cessation interventions to preserve lung health and prevent chronic respiratory morbidity.

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