”The most distant distance in the world is not life and death, but I hold your hand in the hazy day, but I can’t see your face ……” The dark killer of cardiovascular blood vessels Along with the successive haze, PM10 and PM2.5 are becoming familiar terms. PM10 and PM2.5 are solid and liquid suspended particles in the air with particle sizes below 10 microns and 2.5 microns, respectively. The former are partially blocked by the villi inside the nasal cavity or excreted through sputum, while others enter the upper respiratory tract. The latter is only one-tenth the size of a human hair in diameter and is not easily blocked. In contrast, PM2.5 is more harmful, and the human physiology determines that the human body has no protection against particles of this size. There is no doubt that the lungs are the first organ to be hit by haze. As early as 1989, an analysis by the Harvard School of Public Health of six U.S. cities from 1980-1981 showed that the proportion of children suffering from chronic cough, bronchitis and chest diseases was statistically correlated with the concentration of environmental pollutants such as PM2.5 and PM15 in the air. In recent years, studies have also found that PM2.5 increases the incidence of respiratory infections, tuberculosis, lung cancer, and other respiratory diseases. If haze is a positive blow to the lungs, it is a side attack to the cardiovascular system. PM2.5 is not only light in weight, but also stays in the atmosphere for a long time and can be transported far away by the atmospheric circulation. When it enters the lungs through the respiratory process, it can also be deposited in the alveoli, thus entering the blood, and “floating” to all parts of the body through the circulatory system. Domestic and international epidemiological surveys show that short-term exposure to PM2.5 can raise blood pressure, induce heart rate disorders, myocardial ischemia, myocardial infarction, heart failure and even sudden death. In contrast, long-term exposure increases the risk of cardiovascular events and death in the population. This is mainly due to the fact that PM2.5 entering the respiratory system causes oxidative stress in the lungs and the whole body, activates the coagulation system, promotes atherosclerosis, and leads to imbalance of the autonomic nervous system, which in turn causes a series of cardiovascular toxicity, mainly including oxidative stress injury and inflammation, vascular dysfunction, atherosclerosis, and imbalance of the autonomic nervous system. The cardiovascular toxicity of oxidative stress is particularly significant, with many precursors of cardiovascular disease, such as endothelial dysfunction, atheromatous plaque, and altered heart rate, being associated with them. Since the 1970s, when researchers in the Eskimo population found that their lower incidence of cardiovascular events may be associated with a diet rich in Omega-3 PUFA, numerous studies and large clinical trials have identified and confirmed the multiple cardiovascular protective effects of these substances. In the case of haze, based on the current research progress, Omega-3 PUFA may counteract its damage to the body mainly through hedging and antagonism. The protective effects of Omega-3 PUFA are pleiotropic, with varying degrees of alleviation and conservation of blood lipids, inflammation, coagulation and fibrinolytic system, blood pressure, atherosclerosis, vascular endothelial function and heart rate disorders. In view of this, Omega-3 PUFA has been approved by AHA (American Heart Association) Scientific Statement on Triglycerides and Cardiovascular Disease, European Society of Cardiology/European Society of Atherosclerosis, ESC/EAS (European Society of Cardiology/European Society of Atherosclerosis) Guidelines for the Management of Dyslipidemia, AHA/ACCF Guidelines for the Secondary Prevention of Cardiovascular Disease, NLA Patient-Centered Dyslipidemia Management Recommendations, International Atherosclerosis Society (IAS) Position Report Global Dyslipidemia Diagnosis and Treatment Recommendations, Chinese Adult Dyslipidemia Prevention and Treatment Guidelines and many other authoritative guidelines recommend for the prevention of cardiovascular events and dyslipidemia treatment. This shows that Omega-3 PUFA can effectively play its role in hedging against the cardiovascular toxicity of haze. In addition, the antagonistic effect of Omega-3 PUFA on haze toxicity is also an important defense force. As mentioned above, haze toxicity is mainly reflected in its ability to cause systemic oxidative stress in the body. Evidence shows that PM2.5 induces the production of reactive oxygen species (ROS, which can lead to oxidative stress) and NO in cardiovascular endothelial cells, as well as nuclear translocation of nuclear transcription factors. These are all pro-apoptotic factors, suggesting that PM2.5 can cause apoptosis in cardiovascular endothelial cells through the oxidative damage pathway, ultimately leading to the development of cardiovascular disease.