- Airborne pollution is deleterious for the cardiovascular system
- Airborne pollution is present both in- and outdoors
- Airborne pollution triggers and empowers deleterious cardiometabolic risk factors
- Exercise should be discouraged in strongly polluted conditions
Fine particulate matter (PM)(≤2.5 μm in diameter [PM2.5]) is likely the uttermost environmental threat to health ]. PM2.5 plays a role in a large variety of noncommunicable diseases. However more than 50% of the deaths related to such diseases are cardiovascular . Taken together, outdoor and indoor air pollution threaten health to a larger extent than soil contamination, water pollution, and occupational pollution .
The most defenceless air pollution victims reside in middle- and low-income countries. Fossil fuel combustion, industrial power generation and manufacturing are the main sources of PM2.5 . More recently, climate changes have further exposed rural areas and their inhabitants to the smoke of extensive and long-lasting wildfires, often spanning more than several hundred kilometres. These new threats exert cardiovascular effects that are PM2.5-alike . As such, the risk of ischaemic heart disease has increased fivefold with coal combustion-derived PM2.5 than with the total PM2.5 . These observations, among many others, underscore the urgent need to diminish fossil fuel combustion, especially coal burning.
Indoor air is often problematic as well. Almost two-thirds of airborne PM are inhaled while people are indoors [1,4]. Seasonal wood burning, whether for heating or recreational purposes, induces intense PM exposure worldwide. In middle- and low-income countries, cooking with biomass fuel is a significant source of intoxication . Whereas in high-income countries, burning candles and incense, aerosol sprays and various vapours from cleaning products together with emissions from gas stoves release PM [1,4]. Compared with clean energy, solid fuels increase cardiovascular mortality by one-third and all-cause mortality by more than one-tenth .
Cardiovascular effects of PM
The cardiovascular effects of PM2.5 inhalation are mediated by multiple processes. Pollution-mediated oxidative stress and inflammation are initiated in the lungs [6,7]. These, in turn, induce endothelial dysfunction, vascular inflammation, coagulation and thrombosis, plaque instability, cardiac arrhythmia and epigenomic changes [1,8]. Repeated exposure to PM2.5 can trigger, empower and exacerbate the deleterious effects of well-known cardiometabolic risk factors (such as hypertension, dyslipidaemia, diabetes, etc.) and thereby accelerate the progression of atherosclerosis and end-organ damage .
PM pollution and the exercising patient
From a cardiologist’s perspective, one could wonder if inhalation of large amounts of PM2.5 negates the favourable effects of physical exercise on cardiovascular health. Evidence of deleterious consequences of exercise on pulmonary function and inflammation, blood pressure and vascular function suggests that exercise should be discouraged in strongly polluted conditions [10,11,12].
The future might become greyer…
An additional important matter of concern is that fossil fuel combustion, greenhouse gas emissions and climate change are mutually reinforcing (Figure 1). Rising temperatures and extreme weather conditions elicit sharp increases in environmental pollution by means of wildfires, floodings and hurricanes, which, in turn, increase PM levels, carbon monoxide and ground-level ozone gas [13,14,15].
Fine PM is a ubiquitous, silent and growing worldwide threat to cardiovascular health. Airborne pollution induces endothelial dysfunction, vascular inflammation, coagulation and thrombosis, plaque instability. It triggers, empowers and exacerbates the deleterious effects of well-known cardiometabolic risk factors (such as hypertension, dyslipidaemia, diabetes, etc.), and thereby accelerates the progression of atherosclerosis and end-organ damage. Until further data are available, exercise should be discouraged in strongly polluted conditions.
Figure 1. Trends in atmospheric carbon dioxide.
The graph below shows monthly mean CO2 measured at Mauna Loa Observatory, Hawaii. CO2 continued to rise during the world-wide COVID-19 pandemic shut-down (growth rate in ppm/year: 2018: 2.85; 2019: 2.49; 2020: 2.31; 2021: 2.38) .
- Landrigan PJ, Fuller R, Acosta NJR, Adeyi O, Arnold R, Basu NN, Baldé AB, Bertollini R, Bose-O'Reilly S, Boufford JI, Breysse PN, Chiles T, Mahidol C, Coll-Seck AM, Cropper ML, Fobil J, Fuster V, Greenstone M, Haines A, Hanrahan D, Hunter D, Khare M, Krupnick A, Lanphear B, Lohani B, Martin K, Mathiasen KV, McTeer MA, Murray CJL, Ndahimananjara JD, Perera F, Potočnik J, Preker AS, Ramesh J, Rockström J, Salinas C, Samson LD, Sandilya K, Sly PD, Smith KR, Steiner A, Stewart RB, Suk WA, van Schayck OCP, Yadama GN, Yumkella K, Zhong M. The Lancet Commission on pollution and health. Lancet. 2018:3;391:462-512.
- DeFlorio-Barker S, Crooks J, Reyes J, Rappold AG. Cardiopulmonary Effects of Fine Particulate Matter Exposure among Older Adults, during Wildfire and Non-Wildfire Periods, in the United States 2008-2010. Environ Health Perspect. 2019;127:37006.
- Thurston GD, Burnett RT, Turner MC, Shi Y, Krewski D, Lall R, Ito K, Jerrett M, Gapstur SM, Diver WR, Pope CA. Ischemic Heart Disease Mortality and Long-Term Exposure to Source-Related Components of U.S. Fine Particle Air Pollution. Environ Health Perspect. 2016;124:785-94.
- Fisk WJ, Chan WR. Effectiveness and cost of reducing particle-related mortality with particle filtration. Indoor Air. 2017;27:909-20.
- Yu K, Qiu G, Chan KH, Lam KH, Kurmi OP, Bennett DA, Yu C, Pan A, Lv J, Guo Y, Bian Z, Yang L, Chen Y, Hu FB, Chen Z, Li L, Wu T. Association of Solid Fuel Use With Risk of Cardiovascular and All-Cause Mortality in Rural China. JAMA. 2018;319:1351-61.
- Araujo JA, Nel AE. Particulate matter and atherosclerosis: role of particle size, composition and oxidative stress. Part Fibre Toxicol. 2009;6:24.
- Rao X, Zhong J, Brook RD, Rajagopalan S. Effect of Particulate Matter Air Pollution on Cardiovascular Oxidative Stress Pathways. Antioxid Redox Signal. 2018;28:797-818.
- Rückerl R, Ibald-Mulli A, Koenig W, Schneider A, Woelke G, Cyrys J, Heinrich J, Marder V, Frampton M, Wichmann HE, Peters A. Air pollution and markers of inflammation and coagulation in patients with coronary heart disease. Am J Respir Crit Care Med. 2006;173:432-41.
- Eze IC, Hemkens LG, Bucher HC, Hoffmann B, Schindler C, Künzli N, Schikowski T, Probst-Hensch NM. Association between ambient air pollution and diabetes mellitus in Europe and North America: systematic review and meta-analysis. Environ Health Perspect . 2015;123:381-9.
- Sinharay R, Gong J, Barratt B, Ohman-Strickland P, Ernst S, Kelly FJ, Zhang JJ, Collins P, Cullinan P, Chung KF. Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study. Lancet. 2018;391:339-49.
- Wauters A, Dreyfuss C, Pochet S, Hendrick P, Berkenboom G, van de Borne P, Argacha JF. Acute exposure to diesel exhaust impairs nitric oxide-mediated endothelial vasomotor function by increasing endothelial oxidative stress. Hypertension. 2013;62:352-8.
- Qin F, Yang Y, Wang ST, Dong YN, Xu MX, Wang ZW, Zhao JX. Exercise and air pollutants exposure: A systematic review and meta-analysis. Life Sci. 2019;218:153-64.
- Sicard P, Paoletti E, Agathokleous E, Araminienė V, Proietti C, Coulibaly F, De Marco A. Ozone weekend effect in cities: Deep insights for urban air pollution control. Environ Res. 2020;191:110193.
- Liu X, Guo H, Zeng L, Lyu X, Wang Y, Zeren Y, Yang J, Zhang L, Zhao S, Li J, Zhang G. Photochemical ozone pollution in five Chinese megacities in summer 2018. Sci Total Environ. 2021;801:149603.
- Rice MB, Thurston GD, Balmes JR, Pinkerton KE. Climate change. A global threat to cardiopulmonary health. Am J Respir Crit Care Med. 2014;189:512-9.
- Global Monitoring Laboratory. Trends in Atmospheric Carbon Dioxide. Full Record (accessed 02/07/2022)
Notes to editor
Philippe van de Borne, MD, PhD, FESC
Faculté de Médecine Campus Erasme, Brussels, Belgium
Address for correspondence:
Professor Philippe van de Borne, Faculté de Médecine Campus Erasme - CP 535, Route de Lennik, 808, 1070 Anderlecht, Belgium
The author has no conflicts of interest to declare regarding this article.
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.