A Thai urinary-metabolomics study compared active e-cigarette users, people exposed to secondhand aerosol, and unexposed controls. Direct use was associated with amino-acid, mitochondrial-energy, and glutathione pathways, while secondhand exposure was linked mainly to alanine-aspartate-glutamate metabolism. These are biological-response associations, not proof that exposure caused disease.
Key findings
- Direct use was associated with amino-acid, energy, and redox pathways; glutathione metabolism was prominent and oxidised glutathione was a candidate biomarker. Secondhand exposure was associated with alanine, aspartate, and glutamate metabolism, with L-glutamic acid showing discriminatory potential. Propylene glycol, glycerol, cotinine N-oxide, and nicotine-related metabolites were candidate exposure markers.
Why this matters globally
Systemic evidence on secondhand e-cigarette aerosol remains limited. Metabolomics may distinguish exposure markers from biological-effect markers, informing surveillance and clean-air policy, but it is not ready for individual diagnosis.
Thai researcher contribution
Chiang Mai University, Chulalongkorn University, Payap University, and Chao Phraya Abhaibhubejhr Hospital generated Thai population evidence. Publisher metadata corrects a secondary-database mismatch involving the hospital name.
Limitations to consider
The abstract does not report sample size, age, device type, dose, cotinine levels, or control for diet, medicines, combustible smoke, and comorbidity. A comparative design cannot establish temporality, and multivariate metabolomics is vulnerable to overfitting and multiple testing.