The Time Course of Changes in Heart Rate Variability Subsequent to Metal-Rich Workday Particulate Exposures

Abstract

ISEE-203 Objective: Although recent research demonstrates associations between particulate exposures and decreased heart rate variability (HRV), the time course of the response following exposures remains unclear. In a cohort of boilermaker welders, occupationally exposed to high levels of metal-rich particulate, we investigated the time course of hourly HRV changes subsequent to workday exposures. Material and Methods: We conducted a repeated measures panel study among 36 men who were monitored by 24-hour ambulatory electrocardiograms (ECG) over both a workday (exposure period) and nonworkday (control period). ECGs were analyzed and the standard deviation of normal-to-normal beats index (SDNNi) was calculated from 5-minute data and summarized over hourly periods up to 17 hours postwork. Matched measurements from nonwork days were used to control for diurnal fluctuations and the associations with workday particulate exposures were assessed using linear regression. Results: Welders were exposed to a mean (SD) workday PM2.5 concentration of 1.14 (0.76) mg/m3. Mean hourly postwork SDNNi was consistently lower than nonwork SDNNi during the same time period. HRV was negatively associated with workday particulate in most of the 17 hours postwork. The hourly associations by time since exposure suggested an early and later phase response, with the largest regression coefficients observed 2 to 3 hours after exposure, [eg, third hour −6.40 (95% CI: −11.69 to −1.12) ms/1 mg/m3], and then 9 to 13 hours [eg, 11th hour −8.31 (95% CI: −17.37 to 0.75) ms/1 mg/m3], after adjusting for baseline HRV over the same time period. Conclusions: Our research supports the cardiotoxicity of occupational particulate exposures. In addition, results suggest a multiphase, cardiovascular autonomic response subsequent to high levels of workday particulates, including an early phase response, 2 to 3 hours postexposure, followed by a stronger late phase response, 9 to 13 hours postexposure. Supported by NIEHS grants ES009860 and ES00002, and NIOSH grant T42 OH008416.