Title: Fine Particulate Exposure and Cardiac Autonomic Effects in Boilermakers
Description: Background: Heart Rate Variability (HRV) as a research outcome has the potential for misclassification due to its inability to account for changes in the heart rate. HRV can be parsed into Acceleration Capacity (AC) and Deceleration Capacity (DC) which address these limitations.

Objectives: To investigate the associations between AC and DC with short-term and long-term metal PM2.5 exposures; and examine if these associations are mediated by inflammation.

Methods: A panel of 45-50 male welders, mean age 39-40 years, had continuous PM2.5 exposure during typical welding work shifts for 4-6 hours repeated 2-5 times over sampling periods in 2010-2012. We also obtained continuous recordings of digital electrocardiograms (ECG) over their work shift using Holter monitors during the same time; and analyzed blood samples before and after each welding shift for potential mediators of inflammation.

In our first analysis, we used linear mixed models to assess the association between hourly PM2.5 exposure and each of simultaneously measured hourly AC and DC, controlling for covariates.

Then, mediation analysis was done using linear mixed models to assess the associations between shift PM2.5 exposure, potential mediator levels, and AC and DC, controlling for relevant covariates in order to deduce the direct and indirect effects (via the mediator) of PM2.5 on AC and DC.

In our final analysis, we used linear regression to assess the association between CEI PM2.5 exposure and each of current AC and DC, controlling for confounders.

Results: Negative exposure-response associations were found for AC and DC with increased PM2.5 both in the short-term and long-term exposure after adjusting for covariates. In our mediation models, the proportion of the total effect of PM2.5 on AC or DC (indirect effect) mediated through IL-6 on AC was at best 4%.

Conclusions: There are sustained acute and chronic effects of metal particulates on AC and DC even after exposure has ceased. These findings suggest that there may be more pathways that sustain response following exposure other than a direct effect of metal particulates on AC and DC. Furthermore, there may be complex mediating pathways involving interleukin 6.