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. 2023 Apr;30(2):665-679.
doi: 10.1007/s12350-022-03003-7. Epub 2022 Aug 1.

The combined effect of air and transportation noise pollution on atherosclerotic inflammation and risk of cardiovascular disease events

Michael T Osborne  1   2 , Shady Abohashem  1   2 , Nicki Naddaf  1 , Taimur Abbasi  1   2 , Hadil Zureigat  1 , Kenechukwu Mezue  1   2 , Ahmed Ghoneem  1 , Tawseef Dar  1   2 , Alexander J Cardeiro  1 , Nehal N Mehta  3 , Sanjay Rajagopalan  4 , Zahi A Fayad  5 , Ahmed Tawakol  6   7
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The combined effect of air and transportation noise pollution on atherosclerotic inflammation and risk of cardiovascular disease events

Michael T Osborne et al. J Nucl Cardiol. 2023 Apr.

Abstract

Background: Air pollution and noise exposures individually associate with major adverse cardiovascular events (MACE) via a mechanism involving arterial inflammation (ArtI); however, their combined impact on ArtI and MACE remains unknown. We tested whether dual (vs. one or neither) exposure associates with greater ArtI and MACE risk and whether MACE risk is mediated via ArtI.

Methods: Individuals (N = 474) without active cancer or known cardiovascular disease with clinical 18F-FDG-PET/CT imaging were followed for 5 years for MACE. ArtI was measured. Average air pollution (particulate matter ≤ 2.5 μm, PM2.5) and transportation noise exposure were determined at individual residences. Higher exposures were defined as noise > 55 dBA (World Health Organization cutoff) and PM2.5 ≥ sample median.

Results: At baseline, 46%, 46%, and 8% were exposed to high levels of neither, one, or both pollutants; 39 experienced MACE over a median 4.1 years. Exposure to an increasing number of pollutants associated with higher ArtI (standardized β [95% CI: .195 [.052, .339], P = .008) and MACE (HR [95% CI]: 2.897 [1.818-4.615], P < .001). In path analysis, ArtI partially mediated the relationship between pollutant exposures and MACE (P < .05).

Conclusion: Air pollution and transportation noise exposures contribute incrementally to ArtI and MACE. The mechanism linking dual exposure to MACE involves ArtI.

Keywords: 18F-FDG-PET/CT; Air pollution; arterial inflammation; transportation noise pollution.

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Figures

Figure 1.
Figure 1.
Study subject selection.
Figure 2.
Figure 2.
Relationship between number of heightened pollutant exposures and arterial inflammation. Error bars represent 95% CI.
Figure 3.
Figure 3.
Relationships between types of heightened pollutant exposures and arterial inflammation. Error bars represent 95% CI, and the unadjusted P-value for the relationship between the number of pollutant exposures and arterial inflammation is shown.
Figure 4.
Figure 4.
(A) Histogram showing the distribution of MACE by number of pollutant exposures. Error bars represent 95% CI, and P-values are unadjusted. (B) Point estimates of hazard ratios are represented by black squares with 95% CI depicted by horizontal lines. * P-values are fully adjusted with backwards selection.
Figure 5.
Figure 5.
Kaplan-Meier MACE-free survival plot by number of pollutant exposures. Log-rank P-values are provided.
Figure 6.
Figure 6.
Single mediator model adjusted for age and sex for the role of increased arterial inflammation in the relationship between the number of pollutant exposures and MACE.
Figure 7.
Figure 7.
The hypothesized biological mechanism linking combined air and transportation noise pollution to major adverse cardiovascular events through heightened atherosclerotic inflammation. Black dotted lines refer to paths highlighted in previous studies, while the solid red line depicts the common path highlighted by the current study’s findings.
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