Environment International (Dec 2022)
Short-term PM2.5 exposure and cognitive function: Association and neurophysiological mechanisms
Abstract
Background: Although converging evidence has demonstrated that exposure to fine particulate matter (PM2.5) caused adverse effects on brain structure and cognitive function, the association between the short-term exposure to PM2.5 and cognition dysfunction remained underexplored, especially possible neurophysiological mechanisms. Methods: We conducted a longitudinal observational study with four repeated measurement sessions among 90 young adults from September 2020 to June 2021. During each measurement session, we measured participants’ personal-level air pollution exposure for one week with portable monitors, followed by executive function assessment and electrophysiological signal recording at an assessment center. Standard Stroop color-word test was used accompanied with electroencephalogram (EEG) recording to assess performance on executive function. We used linear mixed-effect model with lagged values of PM2.5 levels to analyze the association between PM2.5 exposure and changes in executive function, and mediation analysis to investigate mediation effect by EEG signal. Results: Adjusted mixed-effect models demonstrated that elevated PM2.5 exposure three days prior to cognitive assessment (lag-3) was associated with (1) declined performance in both congruent and incongruent tasks in Stroop test, (2) reduced lower and upper alpha event-related desynchronization (ERD) during 500–1000 ms after stimuli, both indicating impaired executive control. Lower and upper alpha ERD also mediated observed associations between short-term PM2.5 exposure and executive function. No significant associations were found between short-term PM2.5 exposure or aperiodic exponents in tonic and phasic states, or periodic alpha oscillations in tonic state. Conclusion: Our results provided evidence that short-term PM2.5 exposure was associated with executive dysfunction. Reduced alpha ERD was likely to be the underlying pathway through which PM2.5 induced adverse effects on neuron activities during cognitive tasks.
