HPLC Cotinine Analysis to Assess Passive Smoking Exposure in Pediatric Asthma

Researchers at the Dr. Ram Manohar Lohia Institute of Medical Sciences (Lucknow, India) evaluated passive smoking in children with asthma by measuring urinary cotinine levels and to explore the forensic and medicolegal implications of documenting such exposure. These levels were measured using high-performance liquid chromatography (HPLC) to assess passive smoking. A paper based on their work was published in Cureus (1).

Among the most common chronic disease in children, asthma presents with a wide range of respiratory symptoms that vary in severity, with acute exacerbations sometimes being fatal (2,3).

The World Health Organization (WHO) has reported that more than 700 million children worldwide are exposed to passive smoking (2). Children are especially vulnerable to passive smoke’s harmful effects due to their narrower airways, higher respiratory rates, and underdeveloped immune systems (3).

Among the most common chronic disease in children, asthma presents with a wide range of respiratory symptoms that vary in severity, with acute exacerbations sometimes being fatal (2,4). Children with asthma are even more open to its negative impact, as passive smoke exposure is linked to more frequent exacerbations and increased bronchial hyperreactivity (5), as well as possibly contributing to an increase in disease severity (6). The reduction of a child’s exposure to passive smoking has been shown to assist in both the prevention and management of asthma (7).

A metabolite of nicotine, cotinine is widely recognized as the most reliable biomarker for assessing tobacco smoke exposure, preferred over even nicotine due to the alkaloid remaining in the body for a longer period, making it easier to detect (8,9). From a forensic medicine perspective, urinary cotinine levels serve not only as clinical indicators of environmental tobacco smoke (ETS) exposure but also as objective evidence in medicolegal contexts, including custody disputes, child neglect investigations, and public health litigation involving tobacco-related harm. In contexts such as these, quantifiable biomarkers like cotinine offer concrete proof, bridging the gap between clinical assessment and legal accountability (10).

For this study, children newly diagnosed with asthma were enrolled in the study and underwent thorough clinical evaluation. Parental smoking was assessed through a structured questionnaire. Urinary cotinine levels were measured using the HPLC 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. Among the 92 children with asthma accepted into the study, 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. 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 (1).

The results of the study reveal a significantly high proportion of children with asthma who have urinary cotinine levels indicative of passive smoking exposure, which the researchers believe underscore a substantial association between passive smoking and the severity of asthma in children. Among the host factors, older age and a positive family history were significantly linked with more severe forms of the disease. The study also highlights the value of urinary cotinine assessment as a more accurate and objective measure of tobacco smoke exposure compared to parental self-reporting (1).

The researchers acknowledged that their study had some limitations. As they were conducting a pilot study, the sample size was relatively small and calculated based on the known prevalence of asthma. Additionally, the cross-sectional design limited causal inference. Furthermore, recall bias on the part of the parents may have affected the accuracy of their reporting, and the single-center setting may have introduced selection bias. Also, potential confounding factors, such as indoor pollution and ventilation status, were not assessed. Finally, the location where the smoking took place (indoor vs. outdoor environment) was also not specifically defined. However, despite these limitations, in addition to informing effective clinical management, the researchers believe that their findings illustrate the need for further research into the underlying causes of pediatric asthma, and more importantly, should serve as a wake-up call for the healthcare community to strengthen public health initiatives aimed at shielding children from the harmful effects of ETS (1).

References

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