Dataset Information

Co-exposure to urban particulate matter and aircraft noise adversely impacts the cerebro-pulmonary-cardiovascular axis in mice.

ABSTRACT: Worldwide, up to 8.8 million excess deaths/year have been attributed to air pollution, mainly due to the exposure to fine particulate matter (PM). Traffic-related noise is an additional contributor to global mortality and morbidity. Both health risk factors substantially contribute to cardiovascular, metabolic and neuropsychiatric sequelae. Studies on the combined exposure are rare and urgently needed because of frequent co-occurrence of both risk factors in urban and industrial settings. To study the synergistic effects of PM and noise, we used an exposure system equipped with aerosol generator and loud-speakers, where C57BL/6 mice were acutely exposed for 3d to either ambient PM (NIST particles) and/or noise (aircraft landing and take-off events). The combination of both stressors caused endothelial dysfunction, increased blood pressure, oxidative stress and inflammation. An additive impairment of endothelial function was observed in isolated aortic rings and even more pronounced in cerebral and retinal arterioles. The increase in oxidative stress and inflammation markers together with RNA sequencing data indicate that noise particularly affects the brain and PM the lungs. The combination of both stressors has additive adverse effects on the cardiovascular system that are based on PM-induced systemic inflammation and noise-triggered stress hormone signaling. We demonstrate an additive upregulation of ACE-2 in the lung, suggesting that there may be an increased vulnerability to COVID-19 infection. The data warrant further mechanistic studies to characterize the propagation of primary target tissue damage (lung, brain) to remote organs such as aorta and heart by combined noise and PM exposure.

SUBMITTER: Kuntic M

PROVIDER: S-EPMC9804249 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature

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Co-exposure to urban particulate matter and aircraft noise adversely impacts the cerebro-pulmonary-cardiovascular axis in mice.

Kuntic Marin M Kuntic Ivana I Krishnankutty Roopesh R Gericke Adrian A Oelze Matthias M Junglas Tristan T Bayo Jimenez Maria Teresa MT Stamm Paul P Nandudu Margaret M Hahad Omar O Keppeler Karin K Daub Steffen S Vujacic-Mirski Ksenija K Rajlic Sanela S Strohm Lea L Ubbens Henning H Tang Qi Q Jiang Subao S Ruan Yue Y Macleod Kenneth G KG Steven Sebastian S Berkemeier Thomas T Pöschl Ulrich U Lelieveld Jos J Kleinert Hartmut H von Kriegsheim Alex A Daiber Andreas A Münzel Thomas T

Redox biology 20221218

Worldwide, up to 8.8 million excess deaths/year have been attributed to air pollution, mainly due to the exposure to fine particulate matter (PM). Traffic-related noise is an additional contributor to global mortality and morbidity. Both health risk factors substantially contribute to cardiovascular, metabolic and neuropsychiatric sequelae. Studies on the combined exposure are rare and urgently needed because of frequent co-occurrence of both risk factors in urban and industrial settings. To stu ...[more]

PMID: 36566737

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Project description:BackgroundCycling and other forms of active transportation provide health benefits via increased physical activity. However, direct evidence of the extent to which these benefits may be offset by exposure and intake of traffic-related air pollution is limited. The purpose of this study is to measure changes in endothelial function, measures of oxidative stress and inflammation, and lung function in healthy participants before and after cycling along a high- and low- traffic route.MethodsParticipants (n = 38) bicycled for 1 h along a Downtown and a Residential designated bicycle route in a randomized crossover trial. Heart rate, power output, particulate matter air pollution (PM10, PM2.5, and PM1) and particle number concentration (PNC) were measured. Lung function, endothelial function (reactive hyperemia index, RHI), C-reactive protein, interleukin-6, and 8-hydroxy-2'-deoxyguanosine were assessed within one hour pre- and post-trial.ResultsGeometric mean PNC exposures and intakes were higher along the Downtown (exposure = 16,226 particles/cm3; intake = 4.54 × 1010 particles) compared to the Residential route (exposure = 9367 particles/cm3; intake = 3.13 × 1010 particles). RHI decreased following cycling along the Downtown route and increased on the Residential route; in mixed linear regression models, the (post-pre) change in RHI was 21% lower following cycling on the Downtown versus the Residential route (-0.43, 95% CI: -0.79, -0.079) but RHI decreases were not associated with measured exposure or intake of air pollutants. The differences in RHI by route were larger amongst females and older participants. No consistent associations were observed for any of the other outcome measures.ConclusionsAlthough PNC exposures and intakes were higher along the Downtown route, the lack of association between air pollutant exposure or intake with RHI and other measures suggests other exposures related to cycling on the Downtown route may have been influential in the observed differences between routes in RHI.Trial registrationClinicalTrials.gov, NCT01708356 . Registered 16 October 2012.

Project description:BackgroundPrevious observational studies have shown that the prevalence of cardiovascular diseases (CVDs) is related to particulate matter (PM). However, given the methodological limitations of conventional observational research, it is difficult to identify causality conclusively. To explore the causality of PM on CVDs and cardiovascular biomarkers, we conducted a Mendelian randomization (MR) analysis.MethodIn this study, we obtained summary-level data for CVDs and cardiovascular biomarkers including atrial fibrillation (AF), heart failure (HF), myocardial infarction (MI), ischemic stroke (IS), stroke subtypes, body mass index (BMI), lipid traits, fasting glucose, fasting insulin, and blood pressure from several large genome-wide association studies (GWASs). Then we used two-sample MR to assess the causality of PM on CVDs and cardiovascular biomarkers, 16 single nucleotide polymorphisms (SNPs) for PM2.5 and 6 SNPs for PM10 were obtained from UK Biobank participants. Inverse variance weighting (IVW) analyses under the fixed effects model were used as the main analytical method to calculate MR Estimates, followed by multiple sensitivity analyses to confirm the robustness of the results.ResultsOur study revealed increases in PM2.5 concentration were significantly related to a higher risk of MI (odds ratio (OR), 2.578; 95% confidence interval (CI), 1.611-4.127; p = 7.920 × 10-5). Suggestive evidence was found between PM10 concentration and HF (OR, 2.015; 95% CI, 1.082-3.753; p = 0.027) and IS (OR, 2.279; 95% CI,1.099-4.723; p = 0.027). There was no evidence for an effect of PM concentration on other CVDs. Furthermore, PM2.5 concentration increases were significantly associated with increases in triglyceride (TG) (OR, 1.426; 95% CI, 1.133-1.795; p = 2.469 × 10-3) and decreases in high-density lipoprotein cholesterol (HDL-C) (OR, 0.779; 95% CI, 0.615-0.986; p = 0.038). The PM10 concentration increases were also closely related to the decreases in HDL-C (OR, 0.563; 95% CI, 0.366-0.865; p = 8.756 × 10-3). We observed no causal effect of PM on other cardiovascular biomarkers.ConclusionAt the genetic level, our study suggested the causality of PM2.5 on MI, TG, as well HDL-C, and revealed the causality of PM10 on HF, IS, and HDL-C. Our findings indicated the need for continued improvements in air pollution abatement for CVDs prevention.

Project description:Exposures to ambient particulate matter (PM) are associated with increased morbidity and mortality. PM2.5 (<2.5 μm) and ozone exposures have been shown to associate with carotid intima media thickness in humans. Animal studies support a causal relationship between air pollution and atherosclerosis and identified adverse PM effects on HDL functionality. We aimed to determine whether brief exposures to PM2.5 and/or ozone could induce effects on HDL anti-oxidant and anti-inflammatory capacity in humans.Subjects were exposed to fine concentrated ambient fine particles (CAP) with PM2.5 targeted at 150 μg/m(3), ozone targeted at 240 μg/m(3) (120 ppb), PM2.5 plus ozone targeted at similar concentrations, and filtered air (FA) for 2 h, on 4 different occasions, at least two weeks apart, in a randomized, crossover study. Blood was obtained before exposures (baseline), 1 h after and 20 h after exposures. Plasma HDL anti-oxidant/anti-inflammatory capacity and paraoxonase activity were determined. HDL anti-oxidant/anti-inflammatory capacity was assessed by a cell-free fluorescent assay and expressed in units of a HDL oxidant index (HOI). Changes in HOI (ΔHOI) were calculated as the difference in HOI from baseline to 1 h after or 20 h after exposures.There was a trend towards bigger ΔHOI between PM2.5 and FA 1 h after exposures (p = 0.18) but not 20 h after. This trend became significant (p <0.05) when baseline HOI was lower (<1.5 or <2.0), indicating decreased HDL anti-oxidant/anti-inflammatory capacity shortly after the exposures. There were no significant effects of ozone alone or in combination with PM2.5 on the change in HOI at both time points. The change in HOI due to PM2.5 showed a positive trend with particle mass concentration (p = 0.078) and significantly associated with the slope of systolic blood pressure during exposures (p = 0.005).Brief exposures to concentrated PM2.5 elicited swift effects on HDL anti-oxidant/anti-inflammatory functionality, which could indicate a potential mechanism for how particulate air pollution induces harmful cardiovascular effects.

Dataset Information

Co-exposure to urban particulate matter and aircraft noise adversely impacts the cerebro-pulmonary-cardiovascular axis in mice.

Publications

Co-exposure to urban particulate matter and aircraft noise adversely impacts the cerebro-pulmonary-cardiovascular axis in mice.

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