|Before the Air Pollution Control Act of 1955, air pollution was not considered a national environmental problem. (Photo credit: Wikipedia)|
While many factors contribute to setting and progression of atherosclerosis; key contributors are smoking, sedentary lifestyle, unhealthy diet, alcohol ingestion, diabetes and age related hormonal changes.
The study finds association of particulate matter (PM) of diameter less than 2.5 micrometer that is about 30 times less than the diameter of a hair, in a concentration of 2.5 microgram/cubic meter with increased in risk of getting cardiovascular disease.
Particulate matter in the atmosphere is characterized by size/diameter (does not include gaseous air pollutants):
· <10 µm (thoracic particles [PM10]),
· < 2.5 um (fine particles [PM 2.5]) – come primarily from burning of fossil fuels in traffic, by industry and in power generation.
· <0.1 µm (ultra fine particles, UFP),
· 2.0-10 µm (coarse particles [PM 2.5-10])
In metropolitan population that is typically exposed to the high level of air pollution, they studied the Intima (Inner Cellular Layer) Media (Middle Layer) Thickness [IMT] that is an indicator of atherosclerosis.
They measured the IMT of an artery in neck, the carotid over the period of time to register the changes.
Higher long-term residential concentrations of PM2.5 experience a faster rate of IMT progression as compared to other people within the same metropolitan area.
|Stages of endothelial dysfunction in atheroscerosis (Photo credit: Wikipedia)|
Improvements in air quality over the duration of the study were similarly associated with changes in IMT progression, with greater reductions in PM2.5 showing slower IMT progression.
These findings suggest that higher long-term PM2.5 exposures may be associated with an acceleration of vascular pathologies over time.
While, there is no clear-cut explanation for association of air pollution with progression of atherosclerosis,it has been proposed that several factors are generated in the tissue of lungs in response to the particulate matter may have key roles to play.
Human alveolar macrophages exposed to PM10 in vitro produce tumor necrosis factor-alpha (TNF-alpha) in a dose-dependent manner, as well as several other cytokines, including interleukin (IL)-1-beta, IL-6 and granulocyte-macrophage colony–stimulating factor. Bronchial epithelial cells exposed to PM10 produce IL-8 and TNF-alpha.
Tumor necrosis factor-alpha and IL-1-beta are known to up-regulate the secretion of monocyte chemoattractant protein-1 (MCP-1) to endothelial cells and promote the accumulation of monocytes and T lymphocytes in atherosclerotic lesions.
In addition, TNF-alpha activates arterial endothelium to increase l-selectin–dependent monocyte adhesion, which is a key pathogenic event in atherosclerogenesis.
Interleukin-6 activates the hematopoietic system to release leukocytes and platelets into the circulation and stimulates the production of acute-phase proteins, such as fibrinogen and C-reactive protein.
The interaction between PMNs and the endothelium causes the release of functionally active MCP-1, which assists in the recruitment of both monocytes and T lymphocytes into atherosclerotic lesions.
It is postulated that the leukocytosis, high levels of C-reactive protein and fibrinogen that have been implicated in the pathogenesis of atherosclerosis and induction of acute coronary events can be initiated by cytokines released by alveolar macrophages when they phagocytose atmospheric particulates deposited in the lung.