The Truth of Air Pollution. Does Woodsmoke Induce Cardiac Hypertrophy?
Authors: Raghad Al-Dulaymi, Prof. Andrew Trafford, Dr. Katharine Dibb, Dr. Aristeidis Voliotis, Prof. Gordon Mcfiggans
Background:
Air pollution from indoor and outdoor sources is a global health problem and is predicted to cause millions of deaths annually. Previous studies demonstrated that short- and long-term exposure to woodsmoke emissions was associated with an increased risk of respiratory diseases. However, the evidence on the association between air pollution from woodsmoke and cardiovascular diseases is not conclusive. Cardiac hypertrophy has been recognised as an independent risk factor for adverse cardiovascular outcomes such as heart failure and sudden cardiac death. Previous evidence suggested the role of tadalafil, a phosphodiesterase 5 (PDE5) inhibitor, in protecting against cardiac hypertrophy in various animal studies.
Objectives:
For this stage of the project, our objective was to measure the effect of woodsmoke particles on the surface area of neonatal rat ventricular myocytes (NRVM) cells to detect any signs of hypertrophy.
Methods:
All experiments and procedures were conducted in accordance with the University of Manchester guidelines for animal care under the Animal (Scientific Procedures) Act 1986 (ASPA). Ethical approval for the work was obtained from the University of Manchester Animal Welfare and Ethical Review Board. Samples of woodsmoke were collected from a modern 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 (Charles River). The effect of pollutants on the cell surface area (hypertrophy) was measured using fluorescent microscopic techniques and software analysis.
Results
Our results showed an increase in cell surface area in response to increasing pollutant concentrations. Incubation of cells with pollutants (from either the flaming or smouldering phases) and a cardioprotective agent (tadalafil 50nM) was associated with a significantly smaller surface area compared to incubation with pollutants alone (P<0.0001). 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.
Conclusions:
Our data showed that woodsmoke-derived pollutants induced cardiac hypertrophy in NRVM in a dose-dependent manner. The cardiac hypertrophy could be prevented and reversed by an antihypertrophic agent ‘tadalafil’. The next phase of the project will be dedicated to exploring the mechanism by which woodsmoke pollutants induce cardiac hypertrophy.