Assessment of Passive Smoking in Children With Asthma Using Urinary Cotinine Levels and Its Association With Asthma...

Introduction Passive smoking can exacerbate asthma symptoms in children. Although cotinine levels offer an accurate measure of passive smoking, their use in clinical, forensic, and medicolegal documentation remains limited. This study aimed to evaluate passive smoking in children with asthma by measuring urinary cotinine levels and to explore the forensic and medicolegal implications of documenting such exposure. The association of cotinine levels with asthma severity was examined alongside environmental and host-related factors. Cotinine levels were also correlated with demographic characteristics and parental smoking status. Methods Children newly diagnosed with asthma were enrolled in the study and underwent thorough clinical evaluation. To minimize confounding, children with recent respiratory infections, known environmental allergen exposure, or other chronic respiratory conditions were excluded. Parental smoking was assessed through a structured questionnaire. Urinary cotinine levels were measured using the high-performance liquid chromatography method to assess passive smoking. Host factors (age, sex, family history, and associated allergies) and environmental triggers (passive smoking, cold air, dust, seasonal variation, and residential setting) were also evaluated in relation to asthma severity. Results Among 92 children with asthma, 32 (34.8%) had cotinine levels within the passive smoking range. Children aged ≥6 years and those with a family history of asthma showed a significant association with asthma severity (p = 0.001 and p = 0.032, respectively). Cotinine levels within the passive smoking range were significantly correlated with disease severity (p = 0.043). Parental reporting identified only 30.3% of children exposed to passive smoking. In contrast, cotinine biomarker analysis provided objective evidence of environmental tobacco smoke exposure, underscoring the medicolegal importance of such documentation in clinical practice. Conclusions A considerable proportion of children with asthma demonstrated cotinine levels indicative of passive smoking. Passive smoking was significantly associated with increased asthma severity. Compared to parental reporting, urinary cotinine levels offer a more accurate assessment of passive smoke exposure. As a reliable biomarker, urinary cotinine links clinical findings with forensic documentation, reinforcing its role in medicolegal reporting. Integrating cotinine testing into clinical practice may support preventive strategies and strengthen legal advocacy for at-risk pediatric populations.