Air pollution is one of the main environmental risk factors for health worldwide. According to the World Health Organization, exposure to air pollutants is associated with millions of premature deaths every year, many of them related to cardiovascular diseases. Despite this evidence, the specific mechanisms by which pollution affects the heart, particularly regarding the development of severe arrhythmias, were not fully understood.

A study led by the Cardiovascular Diseases Group at the Vall d’Hebron Research Institute (VHIR), part of the CIBER of Cardiovascular Diseases (CIBERCV), with the participation of the Pharmacokinetic Nanoparticles Group at VHIR, affiliated with the CIBER of Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), provides new experimental evidence that helps fill this knowledge gap.

The research, published in the journal Particle and Fiber Toxicology, shows that continuous exposure to diesel particles, an everyday component of urban pollution, significantly increases the risk of developing ventricular arrhythmias, a type of heart rhythm disorder that can have very serious consequences, including sudden death.

“What we show in this work is a direct causal relationship between diesel particle pollution and the onset of ventricular arrhythmias,” explains Antonio Rodríguez Sinovas, principal investigator of the Cardiovascular Diseases Research Group at VHIR. “Unlike previous studies, here we are not only talking about statistical associations, but about a direct effect observed in a controlled experimental model.”

The study was conducted by a multidisciplinary team of researchers from VHIR, the Institut de Recerca Sant Pau, the Institute of Biomedical Research of Barcelona (IIBB-CSIC), and the Autonomous University of Madrid, all of them integrated into CIBERCV.

An experimental model to understand the real effects of pollution

To accurately analyze the effects of pollution on the heart, researchers used an animal model that allowed them to reproduce a three-week exposure to pollutant particles. Over this period, rats were repeatedly exposed to diesel particles through a procedure that simulates inhalation.*

At the end of this period, researchers studied the electrical function of the heart using advanced electrophysiological techniques. The results showed a clear increase in both the incidence and duration of sustained ventricular arrhythmias, which are the most severe forms of arrhythmia. In addition, electrocardiograms from exposed animals showed alterations associated with a higher arrhythmic risk. These data indicate that pollution not only triggers arrhythmic episodes, but also modifies the heart in a way that makes it more vulnerable to them.

“A particularly relevant aspect is that these changes are observed in hearts that were previously healthy,” highlights Ignacio Ferreira González, head of the Cardiology Service at Vall d'Hebron University Hospital head of the Cardiovascular Diseases Group at VHIR. “This indicates that pollution can act as a trigger of disease, not only as an aggravating factor in people with pre-existing conditions.”

Oxidative stress and inflammation: the origin of the problem

The study delves deeper into the biological mechanisms responsible for these effects. Researchers detected a sustained increase in oxidative stress in the heart, a process that occurs when there is an excess of reactive oxygen molecules capable of damaging cells. This oxidative stress was associated with an exaggerated and persistent inflammatory response.

As a consequence, cardiac tissue developed fibrosis, that is, an excessive accumulation of rigid scar tissue that interferes with the proper propagation of electrical impulses in the heart. This combination of structural and molecular changes creates what researchers refer to as an “arrhythmic substrate,” which facilitates the appearance of severe arrhythmias.

“Oxidative stress acts as a central mechanism linking pollution to cardiac damage,” notes Rodríguez Sinovas. “When this process is sustained over time, the heart enters a state of greater electrical fragility.”

According to Ferreira González, these results help explain why episodes of high pollution are also associated, in humans, with increased hospital admissions and cardiovascular mortality. “This study allows us to propose a mechanism for the clinical observations we have been seeing for years,” he adds.

Antioxidant nanoparticles as a potential protective strategy

One of the most innovative aspects of the study is the analysis of a potential strategy to reduce the harmful effects of pollution on the heart. Researchers treated a group of animals exposed to diesel particles with cerium oxide nanoparticles (CeO₂NP), a compound with very powerful antioxidant properties capable of neutralizing the molecules responsible for cellular damage.

This treatment significantly reduced oxidative stress and inflammation, decreased myocardial fibrosis, and normalized electrocardiogram alterations. As a result, both the incidence and severity of ventricular arrhythmias were markedly reduced.

“These nanoparticles show that if we intervene in oxidative stress, we can reverse many of the effects of pollution,” explains Rodríguez Sinovas. “We are still far from a clinical application, but this opens up a very promising line of research.”

Ferreira González emphasizes that these results should not be interpreted as an alternative to reducing pollution. “The absolute priority must be to reduce emissions and improve air quality. At the same time, it is important to explore strategies that may help protect the most vulnerable people while this global goal has not yet been achieved.”

*Institutional statement on research animals