Smoking primes the metabolomic response in trauma

Area of Science:

• Biochemistry
• Trauma Medicine
• Metabolomics

Background:

• Smoking is a significant public health issue linked to oxidative stress and related diseases.
• Tobacco use increases the risk of trauma morbidity, including acute respiratory distress syndrome.
• The specific impact of smoking on metabolic heterogeneity in trauma remains under-examined.

Purpose of the Study:

• To investigate the mechanistic effect of smoking on metabolic heterogeneity in injured patients.
• To analyze metabolic differences in trauma patients stratified by smoking status (nonsmoker, passive smoker, active smoker).
• To compare metabolic profiles of high injury/high shock patients with healthy controls.

Main Methods:

• Plasma samples from injured patients at a Level 1 trauma center were analyzed using mass spectrometry-based metabolomics.
• Patients were stratified by cotinine intensity into nonsmoker, passive smoker, and active smoker groups.
• Substratification by Injury Severity Score (≥15) and base excess (<-6) identified high injury/high shock patients.

Main Results:

• Elevated metabolites in active smokers (controls) indicated chronic inflammation and oxidative processes.
• Active smokers with high injury/high shock showed enrichment in malate-aspartate shuttle, tyrosine metabolism, carnitine synthesis, and very long-chain fatty acid oxidation.
• Forty-eight high injury/high shock patients and 95 healthy controls were included in the analysis.

Conclusions:

• Smoking amplifies oxidative stress and mitochondrial dysfunction, exacerbating the inflammatory response in trauma.
• Smoking is associated with impaired utilization of long-chain fatty acids, aspartate, and tyrosine, increasing oxidative stress post-injury.
• Altered metabolic profiles in smokers offer potential therapeutic targets for reducing oxidative damage in trauma patients.