Abstract
BackgroundTo 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 (PM2.5) and in exposure-related decreases in heart rate variability (HRV). We examined the association between daytime exposure to the metal content of PM2.5 and night HRV in a panel study of boilermaker construction workers exposed to metal-rich welding fumes.MethodsTwenty-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 PM2.5 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 PM2.5 metal exposures both with and without adjustment for total PM2.5. 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 PM2.5 and metal content, we used a two-step approach that treated the residuals from linear regression models of each metal on PM2.5 as surrogates for the differential effects of metal exposures in models for night rMSSD.ResultsThe median PM2.5 exposure was 650 μg/m3; median metal exposures for iron, manganese, aluminum, copper, zinc, chromium, lead, and nickel ranged from 226 μg/m3 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/m3 increase in manganese. However, even after adjusting for individual metals, increases in total PM2.5 exposures were associated with declines in night rMSSD.ConclusionThese results support the cardiotoxicity of PM2.5 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.
Highlights
To better understand the mechanism(s) of particulate matter (PM) associated cardiovascular effects, research priorities include identifying the responsible PM characteristics
We examined the association between workday heart rate variability (HRV), a measure of cardiovascular autonomic control, and workday PM2.5 metal exposures and found statistically significant increases in the 5-min SDNN, averaged over the 8–10 hour workday with personal lead and vanadium exposures [9]
Regression models included a continuous covariate for non-work, night rMSSD to control for participant specific risk factors for HRV such as age and health status that don't vary over the time frame of interest
Summary
To better understand the mechanism(s) of particulate matter (PM) associated cardiovascular effects, research priorities include identifying the responsible PM characteristics. As we seek to better understand the mechanisms, research priorities include identifying the PM characteristic(s) responsible for the observed cardiovascular health effects [1,4,5]. Evidence from epidemiological and toxicological studies suggest that composition may play a role in particle-associated cardiovascular responses [4,5]. Some studies have focused on identifying air pollution sources responsible for the observed health effects, and there is growing evidence linking traffic-related particle exposures to cardiovascular responses [6]. Through source-related studies and toxicological evidence, particulate matter components including soluble organic compounds and metals, transition metals, have been linked to cardiovascular outcomes [4]. The role of metals is further implicated by a study of air pollution exposures among older men finding that metal processing genes modified cardiovascular autonomic responses to PM2.5[8]
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.