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. 2024 Oct;132(10):107702.
doi: 10.1289/EHP14806. Epub 2024 Oct 28.

Mechanisms Underlying Acute Cognitive Impairment following Carbon Dioxide Inhalation in a Randomized Crossover Trial

Frederic T Lu  1   2 , Disha Gupta  3   4 , Nancy Fiedler  2   3 , Usha Satish  5 , Kathleen G Black  3 , Alicia Legard  3 , Adriana De Resende  3 , Changjiang Guo  3   4 , Andrew J Gow  3   4 , Howard M Kipen  2   3
Affiliations

Mechanisms Underlying Acute Cognitive Impairment following Carbon Dioxide Inhalation in a Randomized Crossover Trial

Frederic T Lu et al. Environ Health Perspect. 2024 Oct.
No abstract available

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Figures

Figures 1A to 1E are line graphs titled task management, focused activity, information management, crisis responsiveness, and basic strategy, plotting score, ranging from 80 to 160 in increments of 80; 0 to 16 in increments of 2; 0 to 16 in increments of 2; 0 to 14 in increments of 2; and 0 to 30 in increments of 5 (y-axis) across control (600 parts per million) and intervention (2500 parts per million) (x-axis), respectively.
Figure 1.
Changes in cognitive function in 12 healthy individuals in a randomized crossover exposure to 2 h of CO2. Participants underwent a 2-h inhalation session under normal conditions (600 ppm, control) and with a raised level of CO2 (2,500 ppm, experimental). During each exposure, participants engaged with the computer-based SMS program as a measure of cognitive functioning. Each graph represents one performance metric assessed in the SMS, reported as raw scores on a positive linear scale. Each colored line and shape represent an individual participant. The mean and SEM for each measurement are shown as vertical bars next to the individual-level data. Data were analyzed for statistical significance (*, α<0.05; actual p-values are given within each graph) by paired t-test comparing intervention and control by participant. Note: CO2, carbon dioxide; SEM, standard error of the mean; SMS, Strategic Management Simulation.
Figures 2A to 2C are line graphs titled Basal oxygen consumption rate, total stimulated oxygen consumption, and time to peak oxygen consumption, plotting picomole per minute, ranging from 0 to 50 in increments of 10; nanomole, ranging from 0 to 20 in increments of 5; and time (minute), ranging from 0 to 150 in increments of 25 (y-axis) across control (600 parts per million) and intervention (2500 parts per million) (x-axis), respectively.
Figure 2.
Changes in metabolic activity within the PMNs of 12 healthy individuals following a randomized crossover exposure to 2 h of CO2. Participants underwent a 2-h inhalation session under normal conditions (600 ppm, control) and with a raised level of CO2 (2,500 ppm, experimental). Blood samples were taken by venipuncture into EDTA tubes 4 h after exposure ended. Basal OCR was measured for 30 min prior to the addition of PMA. Both the time to peak oxygen consumption and the total oxygen consumed (post PMA) were calculated. Measurements were performed in triplicate. Each colored line and shape represent an individual participant. The mean and SEM for each outcome are shown as vertical bars next to the individual-level data. Data were analyzed for statistical significance (*, α<0.05; actual p-values are given within each graph) by paired t-test comparing intervention and control by participant. Note: CO2, carbon dioxide; EDTA, ethylenediaminetetraacetic acid; OCR, oxygen consumption rate; PMA, phorbol myristate acetate; PMN, polymorphonuclear neutrophil; SEM, standard error of the mean.
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References

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