Summary: | <p>Abstract</p> <p>Background</p> <p>To better understand the mechanism(s) of particulate matter (PM) associated cardiovascular effects, research priorities include identifying the responsible PM characteristics. Evidence suggests that metals play a role in the cardiotoxicity of fine PM (PM<sub>2.5</sub>) and in exposure-related decreases in heart rate variability (HRV). We examined the association between daytime exposure to the metal content of PM<sub>2.5 </sub>and night HRV in a panel study of boilermaker construction workers exposed to metal-rich welding fumes.</p> <p>Methods</p> <p>Twenty-six male workers were monitored by ambulatory electrocardiogram (ECG) on a workday while exposed to welding fume and a non-workday (baseline). From the ECG, rMSSD (square root of the mean squared differences of successive intervals) was summarized over the night (0:00–7:00). Workday, gravimetric PM<sub>2.5 </sub>samples were analyzed by x-ray fluorescence to determine metal content. We used linear mixed effects models to assess the associations between night rMSSD and PM<sub>2.5 </sub>metal exposures both with and without adjustment for total PM<sub>2.5</sub>. Matched ECG measurements from the non-workday were used to control for individual cardiac risk factors and models were also adjusted for smoking status. To address collinearity between PM<sub>2.5 </sub>and metal content, we used a two-step approach that treated the residuals from linear regression models of each metal on PM<sub>2.5 </sub>as surrogates for the differential effects of metal exposures in models for night rMSSD.</p> <p>Results</p> <p>The median PM<sub>2.5 </sub>exposure was 650 μg/m<sup>3</sup>; median metal exposures for iron, manganese, aluminum, copper, zinc, chromium, lead, and nickel ranged from 226 μg/m<sup>3 </sup>to non-detectable. We found inverse linear associations in exposure-response models with increased metal exposures associated with decreased night rMSSD. A statistically significant association for manganese was observed, with a decline of 0.130 msec (95% CI: -0.162, -0.098) in night rMSSD for every 1 μg/m<sup>3 </sup>increase in manganese. However, even after adjusting for individual metals, increases in total PM<sub>2.5 </sub>exposures were associated with declines in night rMSSD.</p> <p>Conclusion</p> <p>These results support the cardiotoxicity of PM<sub>2.5 </sub>metal exposures, specifically manganese. However the metal component alone did not account for the observed declines in night HRV. Therefore, results suggest the importance of other PM elemental components.</p>
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