Effects of exposition to glycol ethers on heart rate recovery, parasympathetic modulation and oxygen diffusion at rest and during exercise

Abstract

Introduction

Daily exposition to ether glycols is common. Caretakers using cleaning products are critically exposed by combining physical activity with exposition to highly concentrated products. Previous animal studies showed hemato-, respiratory and autonomic nervous system toxicity amongst others. Yet, no controlled study explored the combination of an exposition to glycol ethers with physical activity in humans.

Methods

30 young healthy participants were exposed a control condition (ambient air) and to one of three vaporized glycol ethers: propylene glycol n-propyl ether (PGPE, 25 ppm, n = 10) or propylene glycol ethyl ether (PGEE, 35 ppm, n = 10) or propylene glycol monomethyl ether (PGME, 35 ppm, n = 10) in a single-blind cross-over design. They performed an orthostatic test (5-min supine, 5-min standing) and a 6-min steady-state exercise at 1.5 W/kg followed by 10-min recovery in PGPE/PGEE conditions. In addition, an incremental exercise to exhaustion followed in PGME condition. Heart rate variability (HRV) was measured throughout the protocol, Heart rate recovery (HRR) was assessed during the 10-min recovery post steady-state exercise. Root-mean-square of the successive differences (RMSSD), power spectrum of the low- (LF) and high-frequency (HF) bands, tau, amplitude and T30 were computed for HRR. Near Infrared spectroscopy (NIRS) and cardiac output (using thoracic impedance) were measured for PGME exposition. PO₂, PCO₂ and pH were measured regularly via arterialized and venous blood sampling.

Results

Resting values of supine LF (1,180 ± 851 vs. 2,993 ± 2,259 ms²) and standing RMSSD (32 ± 17 vs. 41 ± 17 ms) increased under PGEE. Supine and standing HR decreased under PGPE (65.5 ± 4.8 vs. 61.3 ± 6.9 and 83.8 ± 7.0 vs. 76.1 ± 10.0 bpm) whereas standing RMSSD (26.6 ± 10.0 vs. 37.0 ± 14.9 ms) and LF (825 ± 474 vs. 2,028 ± 1,471 ms²) increased.  Parasympathetic reactivation (e.g., RMSSD, LF and HF) was increased post-exercise under exposition to all three glycol ethers. In addition, amplitude significantly increased when exposed to PGEE. However, unexpectedly, HRR was neither slowed nor speeded. Finally, no differences were observed in any NIRS variables or cardiac output. Accordingly, the modelled muscle oxygen diffusion coefficient was not modified between any solvent conditions. Arterialized blood pH (7.35 ± .06 vs. 7.39 ± .04) and PaCO₂ (34.1 ± 5.0 vs. 35.7 ± 4.3 mmHg) increased whilst PaO₂ (81.8 ± 9.7 vs. 77.9 ± 10.6 mmHg) decreased.

Discussion/Conclusion:

The decrease in supine/standing HR associated with a general increase in HRV during recovery likely indicate an increase in parasympathetic modulation, which is compatible with the sedative effects of glycol ethers previously described in animal models. However, HR recovery was not altered. Despite no change in the O₂ diffusion coefficient, there was an increase in PaCO₂, a decrease in PaO₂ and an increase in blood pH, all indicative of potential impaired blood oxygenation during exercise, to be further investigated. To conclude, exposition to different glycol ethers induced an enhanced parasympathetic activation without any changes in HR recovery or O₂ diffusion.