Air pollution causes atherosclerosis through inducing pathological changes in the blood (a new perspective)

Atherosclerosis has been correlated with air pollution. However, the air pollution's atherogenic mechanism is not clear yet. This hypothesis proposes an atherogenic mechanism for air pollution and claims that the air pollution changes the physiological properties of the blood and then these changes promote the formation of atherosclerotic plaques. The first atherogenic effect of air pollution is hypothesized to be the inactivation of alpha-1 antitrypsin molecules in plasma via oxidation. In the next step, oxidized alpha-1 antitrypsin attaches LDL and forms a complex in the blood stream of lungs. This complex goes through intima with the action of a mediator and when in the vascular wall it is catabolised 4 times more effectively than LDL alone. The result is the formation of foamy cells that characterize atherosclerosis. In this hypothesis, it is also reasoned that the mediator of the complex passage through the arterial walls is elastase. At the end, this hypothesis argues on the bases of its documents that the mean distribution of atherosclerosis in the body obeys a pattern of decreased intensity centrifugally from lungs.