As urbanization accelerates, indoor air quality has emerged as a critical determinant of population health. To systematically evaluate the relationship between indoor air quality (IAQ) and human physiological responses, we conducted a comprehensive review of 63 experimental studies retrieved from three major databases (ScienceDirect, Google Scholar, Web of Science) spanning the years 2000–2023. This systematic review synthesizes evidence from experimental studies examining the physiological impacts of indoor air contaminants, including gaseous pollutants, particulate matter (PM), and volatile organic compounds (VOCs). Through an analysis of cardiovascular biomarkers (heart rate variability, blood pressure), respiratory parameters, and neurological indicators (electroencephalogram patterns), we identify the mechanisms linking air quality degradation to impaired physiological functioning. Our findings demonstrate that optimized ventilation systems and high-efficiency particulate filtration can mitigate exposure risks, potentially enhancing cardiovascular efficiency, pulmonary capacity, and cognitive performance. The evidence further suggests that sustained improvements for indoor environments may decrease incidence rates of respiratory pathologies and neurological disorders.

Elevated indoor carbon dioxide (CO₂) concentrations are increasingly recognized as a critical determinant of occupant health and cognitive performance; however, the neurophysiological mechanisms linking CO₂ exposure to daytime sleepiness remain a subject of debate. This study investigated the effects of dynamically rising CO₂ concentrations on subjective sleepiness and neural oscillation patterns in a controlled environment. A within-subject repeated-measures experiment was conducted with 18 healthy university students exposed to CO₂ levels gradually increasing from a baseline of ~800 ppm to ~2000 ppm over a 40-min period. Subjective sleepiness was assessed using the Karolinska Sleepiness Scale (KSS), while electroencephalogram (EEG), heart rate (HR), and heart rate variability (HRV) were monitored continuously. Results indicate a significant increase in subjective sleepiness scores concurrent with rising CO₂ levels (p < 0.001). Power spectral density (PSD) analysis revealed that elevated CO₂ exposure significantly enhanced power in low-frequency EEG bands (δ, θ, and α), indicative of a transition from alertness to drowsiness. Specifically, α-band power peaked between 20 and 30 min (increasing by 0.15 uV² relative to the 0–10 min baseline), while θ and δ bands peaked earlier (10–20 min) and sustained elevated levels through 30 min. Topographic mapping identified the central, parietal, and occipital regions as the primary loci of this low-frequency activity. Additionally, HR and HRV measures showed upward trends, suggesting autonomic modulation. It is noted that low-frequency EEG power declined during the final 30–40 min interval, potentially reflecting physiological saturation or acclimatization. These findings provide objective neurophysiological evidence that dynamic CO₂ accumulation accelerates drowsiness onset, underscoring the necessity of optimized ventilation strategies in educational settings. However, these findings should be interpreted with caution due to the small sample size and the absence of a control group with constant CO₂ concentration. Future studies with larger, diverse samples and stable-concentration control groups are recommended to validate these trends.