S3118 Secondhand Smoke: A Silent Culprit Behind Peptic Ulcer Disease

Introduction: Peptic ulcer disease (PUD) is a prevalent gastrointestinal disorder with multifactorial etiologies. While direct smoking is a known risk factor, the impact of secondhand smoke (SHS) is understudied. Our retrospective case-control study investigates the association between SHS exposure and PUD. Methods: We conducted a retrospective case-control study at a tertiary care center (January 2022-October 2024) including 524 PUD cases (diagnosed via endoscopy/imaging) and 524 age- and sex-matched controls without GI complaints. Data on SHS exposure were collected via structured interviews, categorizing duration as <5, 5-10, and >10 hours per week. Additional variables (H. pylori, nonsteroidal anti-inflammatory drug use, alcohol, comorbidities) were extracted from records. Conditional logistic regression was used to calculate adjusted odds ratios (ORs) and 95% confidence intervals (Cis) for the association between SHS exposure and PUD. Subgroup analyses examined SHS duration and PUD risk, while Chi-square tests assessed links between SHS and PUD complications like bleeding ulcers. Results: SHS exposure was significantly more prevalent in cases (68.5%) compared to controls (43.1%; χ² = 94.63; P < 0.001). Adjusted logistic regression revealed SHS exposure as an independent risk factor for PUD (OR 1.48; 95% C 1.19-1.76; P < 0.001). Subgroup analysis showed a dose-response relationship. Individuals exposed to >10 hours per week of SHS had an OR of 1.41 (95% CI 1.05-1.77), while those exposed 5-10 hours per week had an OR of 1.50 (95% CI 0.91-2.10). Exposure <5 hours per week showed an OR of 1.37 (95% CI 0.68-2.06). Although not statistically significant, exposure durations <10 hours per week showed a consistent trend toward increased risk. SHS exposure was not significantly associated with severe PUD complications, such as bleeding ulcers (χ2 = 0.59; P = 0.44). Conclusion: SHS constitutes an independent risk factor for PUD, with evidence indicating a dose-response relationship. Our findings emphasize the necessity for focused public health interventions aimed at decreasing SHS exposure and its effects on gastrointestinal health. Subsequent investigations have to examine the biological mechanisms that underpin this association.