Analysis of 9,214 U.S. adults from NHANES 2015-2018 reveals current smoking elevates HbA1c levels by 0.067% in non-diabetic individuals, while former smokers show no such elevation. The effect was confirmed using both self-reported smoking status and serum cotinine measurements, with active smoking defined as cotinine levels ≥3.0 ng/mL. This finding illuminates smoking's direct metabolic impact on glucose regulation, even before diabetes develops. The reversible nature of this effect offers encouraging evidence for smoking cessation benefits beyond cardiovascular health. While a 0.067% HbA1c increase may seem modest, it represents meaningful metabolic dysfunction that could accelerate progression toward prediabetes. The mechanism likely involves nicotine's interference with insulin sensitivity and chronic inflammation from tobacco exposure. However, this cross-sectional study cannot establish causation, and the effect size, while statistically significant, remains relatively small. As a preprint awaiting peer review, these results require validation. The research reinforces that smoking cessation delivers immediate metabolic benefits, providing compelling evidence for healthcare providers counseling patients about diabetes prevention strategies.