Atherosclerosis is a chronic disease, characterized by chronic inflammation, endothelial dysfunction, and lipid deposition in the vessel. Although many major, well-identified risk factors for atherosclerosis [e.g., hyperlipidemia, hypertension, type 2 diabetes (T2D), smoking habit, and obesity] explain a lot about the risk, there is a considerable number of patients who develop atherosclerotic damage and undergo adverse events without presenting any of these established modifiable risk factors. This observation has stimulated an urgent need to expand knowledge towards the identification of additional, less established risk factors that may help in the assessment of risk and fill the gap of knowledge in the cardiovascular (CV) setting. Among them, the hypothesis of a possible relationship between viral infectious agents and atherosclerosis has risen since the early 1900s. However, there is still a great deal of debate regarding the onset and progression of CV disease in relation to the roles of the pathogens (as active inducers or bystanders), host genomic counterparts, and environmental triggers, affecting both virus abundance and the composition of viral communities. Accordingly, the aim of this review is to discuss the current state of knowledge on infectious agents in the atherosclerotic process, with particular focus on two environmental-related viruses, as examples of familiar (influenza) and unfamiliar [severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)] disease triggers.

Congenital heart defects (CHD) represent the most frequent congenital anomalies among newborns, as well as the leading cause of spontaneous abortion, stillbirth, neonatal and infant death. CHD have been recognized as multifactorial diseases, with environmental contaminants as potential contributors to the etiopathogenesis of CHD. Toxic elements, such as arsenic (As), cadmium (Cd), lead (Pb), and mercury (Hg) are known to be associated with adverse reproductive outcomes and certain congenital anomalies, however their association with the risk for CHD remains inconsistent. This review summarizes the updated evidence on the CHD-associated risk related to exposure to As, Cd, Hg, Pb during pregnancy, reporting the main findings from epidemiological and experimental studies and the underlying molecular mechanisms. Additionally, being diet the major source of these elements in the general population, after having identified the main vectors of toxic metals in food, possible remediation strategies to reduce diet-related risks are also described. Among these, a novel, consumer-centered approach in developing new foods is discussed, considering not only the nutritional characteristics of edible compounds foods are made up of, but also their organoleptic features, making the food even more appealing to the consumer. Overall, current data support the association of maternal exposure to As and Pb with increased risk for CHD, although significant associations have only been observed for total and/or specific subgroups. On the other hand, the evidence of association for Cd and Hg exposure in pregnancy with CHD in the offspring remains, yet, quite speculative. Further large prospective cohort studies and insights into the molecular and biomolecular processes of these relationships are warranted to further explore and/or verify these findings.