Written by Joyce Smith, BS. Acute and chronic exposure to iron-rich airborne nanoparticles contribute to mitochondrial dysfunction of heart tissue and the subsequent development of cardiovascular disease that has its origins in early childhood.
Iron is the most abundant metal in the solid (non-volatile) fraction of the ultrafine particles present in urban air pollution. Studies have shown that inhaled or ingested nanoparticles can travel to major organs and damage the cardiovascular system as witnessed by autopsies revealing air pollution nanoparticles in the human brain 1 and heart 2. A current study found that 790,000 people die annually of which 40-80% are attributed to cardiovascular events 3. Another study found that short term PM2.5 exposure raises the risk of acute myocardial infarction up to 5% within a few days of exposure 4. Today, traffic exhaust emissions and iron oxides emissions from the wearing down of vehicle brakes 5 are common contributors to iron-rich air pollution. Currently there is no monitoring and regulating of these ultrafine particles; furthermore, their concentrations do not correlate with PM2.5 measurements, thus regulating PM2.5 does little to reduce nanoparticle concentrations in air pollution 6.
Researchers Barbara Maher from the University of Montana and Lancaster University and Lilian Calderón-Garcidueñas of the Universidad del Valle de Mexico, 7 identified metallic nanoparticles, including iron-rich nanoparticles and other pollution-derived metals such as titanium, in the autopsied hearts of a 3-year-old child killed in a car crash and a 26-year-old adult. For both study subjects there were no potential confounding variables such as obesity, smoking, alcohol or drug use, occupational hazards, and chronic or age-related diseases; however, both lived in metropolitan Mexico City where PM2.5 levels frequently exceed U.S. Environmental Protection Agency (EPA) standards almost 40% of days and World Health Organization (WHO) standards almost 75% of days. Nine subjects, who had previously resided in less populated and polluted locations (Veracruz City, in Veracruz, Mexico), provided the control samples. Through the use of energy-dispersive x-ray analysis and high resolution transmission electron microscopy, the research team found that the heart tissue mitochondria of the two test subjects contained predominantly iron-rich nanoparticles. Theses nanoparticles appeared damaged and had deformed, fragmented or missing inner membranes and altered, and sometimes even ruptured membrane structures. Even in the very young three-year-old Mexican child, increased levels of markers of cardiac oxidative stress were present.
According to Maher and team, the impacts of iron overload in mitochondria have major implications for heart health. The iron-rich nanoparticles have an affinity for ventricular tissue. They attack the mitochondria that drive ATP synthesis, and by modifying cell signaling via Fenton reaction, they facilitate the production of reactive oxygen species (ROS) such as superoxide anions and hydrogen peroxide 8,9. Thus, iron -driven myocardial mitochondrial dysfunction and uncontrolled ROS production may be key players in the initiation and progression of cardiovascular disease 10.
This study adds to the available knowledge concerning the association of air pollution with the development of heart disease. Heart damage can begin in early childhood as evidenced by the inhalation of iron-clad particles and their progressive damage to heart mitochondria and increased oxidative stress in a 3-year-old child. The researchers recommend that since childhood exposure to air pollution is a modifiable risk factor for cardiovascular disease, it is critical that we as individuals, along with our governments, take action on a global scale to reduce PM2.5 and to monitor, regulate and reduce the emissions of these damaging ultrafine iron-rich components of worldwide urban air pollution.
Source: Maher Barbara, A., A. González-Maciel, R. Reynoso-Robles, R. Torres-Jardón, and L. Calderón-Garcidueñas. “Iron-rich air pollution nanoparticles: an unrecognised environmental risk factor for myocardial mitochondrial dysfunction and cardiac oxidative stress.” Environmental Research.
© 2020 Elsevier Inc. All rights reserved.
Posted July 14, 2020.
Joyce Smith, BS, is a degreed laboratory technologist. She received her bachelor of arts with a major in Chemistry and a minor in Biology from the University of Saskatchewan and her internship through the University of Saskatchewan College of Medicine and the Royal University Hospital in Saskatoon, Saskatchewan. She currently resides in Bloomingdale, IL.
References:
- Maher BA, Ahmed IA, Karloukovski V, et al. Magnetite pollution nanoparticles in the human brain. Proc Natl Acad Sci U S A. 2016;113(39):10797-10801.
- Calderón-Garcidueñas L, González-Maciel A, Mukherjee PS, et al. Combustion- and friction-derived magnetic air pollution nanoparticles in human hearts. Environ Res. 2019;176:108567.
- Lelieveld J, Klingmüller K, Pozzer A, et al. Cardiovascular disease burden from ambient air pollution in Europe reassessed using novel hazard ratio functions. Eur Heart J. 2019;40(20):1590-1596.
- Pope CA, 3rd, Muhlestein JB, May HT, Renlund DG, Anderson JL, Horne BD. Ischemic heart disease events triggered by short-term exposure to fine particulate air pollution. Circulation. 2006;114(23):2443-2448.
- Gonet T, Maher BA. Airborne, Vehicle-Derived Fe-Bearing Nanoparticles in the Urban Environment: A Review. Environ Sci Technol. 2019;53(17):9970-9991.
- de Jesus AL, Rahman MM, Mazaheri M, et al. Ultrafine particles and PM(2.5) in the air of cities around the world: Are they representative of each other? Environ Int. 2019;129:118-135.
- Maher BA, González-Maciel A, Reynoso-Robles R, Torres-Jardón R, Calderón-Garcidueñas L. Iron-rich air pollution nanoparticles: An unrecognised environmental risk factor for myocardial mitochondrial dysfunction and cardiac oxidative stress. Environ Res. 2020;188:109816.
- Manickam V, Periyasamy M, Dhakshinamoorthy V, Panneerselvam L, Perumal E. Recurrent exposure to ferric oxide nanoparticles alters myocardial oxidative stress, apoptosis and necrotic markers in male mice. Chem Biol Interact. 2017;278:54-64.
- Nemmar A, Beegam S, Yuvaraju P, et al. Ultrasmall superparamagnetic iron oxide nanoparticles acutely promote thrombosis and cardiac oxidative stress and DNA damage in mice. Particle and fibre toxicology. 2016;13(1):22.
- Martelli A, Puccio H. Dysregulation of cellular iron metabolism in Friedreich ataxia: from primary iron-sulfur cluster deficit to mitochondrial iron accumulation. Front Pharmacol. 2014;5:130.