4 The truth of air pollution. Does woodsmoke induce cardiac hypertrophy?

<h3>Background</h3> Air pollution is a global health problem and is predicted to cause millions of deaths annually.<sup>1</sup> Previous studies demonstrated that exposure to woodsmoke emissions was associated with an increased risk of respiratory diseases.<sup>2</sup> However, the evidence on the association between air pollution from woodsmoke and cardiovascular diseases is not conclusive. Previous evidence suggested the role of tadalafil, a phosphodiesterase 5 (PDE5) inhibitor, in protecting against cardiac hypertrophy in various animal studies.<sup>3</sup> <h3>Objectives</h3> Our objective was to measure the effect of woodsmoke particles on the surface area of neonatal rat ventricular myocytes (NRVM) to detect any signs of hypertrophy. <h3>Methods</h3> Samples were collected from a wood-burner based at the University of Manchester. Woodsmoke was collected from 2 phases of combustion: flaming and smouldering. Emission particles were immersed in cell maintenance media before cell exposure. NRVM were harvested from 1-2 days old Wister rats. The effect of pollutants on the cell surface area was measured using fluorescent microscopic techniques and software analysis. <h3>Results</h3> Our results showed an increase in cell surface area in response to increasing pollutant concentrations. Incubation of cells with pollutants and a cardioprotective agent (tadalafil 50nM) was associated with a significantly smaller surface area compared to incubation with pollutants alone. Moreover, incubation of the cells with pollutants first then with a combination of pollutants and PDE5 inhibitor reversed the hypertrophy for both the flaming and smouldering phase groups. <h3>Conclusions</h3> Our data showed that woodsmoke-derived pollutants induced cardiac hypertrophy in NRVM. The cardiac hypertrophy could be prevented and reversed by a PDEF5 inhibitor. The next phase will be dedicated to exploring the mechanism by which woodsmoke pollutants induce cardiac hypertrophy. <h3>References</h3> Landrigan PJ, Fuller R, Acosta NJR, Adeyi O, Arnold R, Basu N (Nil), <i>et al</i>. The lancet commission on pollution and health. <i>Lancet</i> 2018;<b>391</b>(10119):462–512. Hutchings DC, Anderson SG, Caldwell JL, Trafford AW. Phosphodiesterase-5 inhibitors and the heart: compound cardioprotection? <i>Heart</i> 2018.

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Published
2024-12-01
DOI
https://doi.org/10.1136/heartjnl-2024-bscr.9
Primary Topic
Air Quality and Health Impacts
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article
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article

4 The truth of air pollution. Does woodsmoke induce cardiac hypertrophy?

Aristeidis Voliotis, Andrew W. Trafford, Gordon B. McFiggans, Katharine M. Dibb et al.
Air Quality and Health Impacts
article

4 The truth of air pollution. Does woodsmoke induce cardiac hypertrophy?

Aristeidis Voliotis, Andrew W. Trafford, Gordon B. McFiggans, Katharine M. Dibb, Raghad Al-Dulaymi
article en

Abstract

<h3>Background</h3> Air pollution is a global health problem and is predicted to cause millions of deaths annually.<sup>1</sup> Previous studies demonstrated that exposure to woodsmoke emissions was associated with an increased risk of respiratory diseases.<sup>2</sup> However, the evidence on the association between air pollution from woodsmoke and cardiovascular diseases is not conclusive. Previous evidence suggested the role of tadalafil, a phosphodiesterase 5 (PDE5) inhibitor, in protecting against cardiac hypertrophy in various animal studies.<sup>3</sup> <h3>Objectives</h3> Our objective was to measure the effect of woodsmoke particles on the surface area of neonatal rat ventricular myocytes (NRVM) to detect any signs of hypertrophy. <h3>Methods</h3> Samples were collected from a wood-burner based at the University of Manchester. Woodsmoke was collected from 2 phases of combustion: flaming and smouldering. Emission particles were immersed in cell maintenance media before cell exposure. NRVM were harvested from 1-2 days old Wister rats. The effect of pollutants on the cell surface area was measured using fluorescent microscopic techniques and software analysis. <h3>Results</h3> Our results showed an increase in cell surface area in response to increasing pollutant concentrations. Incubation of cells with pollutants and a cardioprotective agent (tadalafil 50nM) was associated with a significantly smaller surface area compared to incubation with pollutants alone. Moreover, incubation of the cells with pollutants first then with a combination of pollutants and PDE5 inhibitor reversed the hypertrophy for both the flaming and smouldering phase groups. <h3>Conclusions</h3> Our data showed that woodsmoke-derived pollutants induced cardiac hypertrophy in NRVM. The cardiac hypertrophy could be prevented and reversed by a PDEF5 inhibitor. The next phase will be dedicated to exploring the mechanism by which woodsmoke pollutants induce cardiac hypertrophy. <h3>References</h3> Landrigan PJ, Fuller R, Acosta NJR, Adeyi O, Arnold R, Basu N (Nil), <i>et al</i>. The lancet commission on pollution and health. <i>Lancet</i> 2018;<b>391</b>(10119):462–512. Hutchings DC, Anderson SG, Caldwell JL, Trafford AW. Phosphodiesterase-5 inhibitors and the heart: compound cardioprotection? <i>Heart</i> 2018.

University of Manchester (GB)
Openalex Percentile: Top 67%
Air Quality and Health Impacts
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