Heart and Blood Vessels

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Updated May 25, 2017

Particulate pollution concentrations typical of the Wasatch Front increase mortality rates about 10% according to the formula recommended by the American Heart Association published in May, 2010.   A subsequent study suggests that number should be 14%.  That means between 1,000 and 2,000 Utahns die prematurely every year due to our air pollution.  A recent MIT study indicates that the annual number of premature deaths in the US due to air pollution is 210,000, and that the average premature death represents a loss of ten years of life.

  • The signature physiologic consequence of air pollution is the same as cigarette smoke: a low grade arterial inflammation, arteriole narrowing, and vascular prothrombotic changes.   As with cigarette smoke the effect can be almost immediate and chronic exposure to even low concentrations of pollution are associated with an acceleration of atherosclerosis and significant arteriole narrowing and stiffness.  Particulate pollution increases  blood levels of triglycerides and total serum cholesterol.  Breathing more ozone in childhood increases arterial wall thickness in young adults.
  • Simultaneously high concentrations of multiple pollutants have a synergistic effect on hospitalizations for cardiac disease.
  • Air pollution causes average blood pressure to increase within minutes.  All organs are affected.  Blood pressure rises are found in even in children.  Air pollution adversely affects the electrical activity of the heart, triggering arrhythmias and undoubtedly one of the reasons for higher rates of arrhythmias and sudden death.
  • Rates of heart attacks and strokes increase with air pollution and are the primary cause for increased community mortality rates.  Those rates increase within hours after exposure and stay elevated for as long as 30 days after the exposure has ended.  In fact, new studies indicate the increase in mortality risk persists for decades after exposure.
  • Mortality plotted against air pollution concentrations shows no safe threshold, even at low levels, well below EPA national ambient air quality standards (NAAQS).  Furthermore this curve is not linear.  The steepest part of the curve is at low doses, i.e. small air pollution reductions have even greater public health benefit when the concentrations are already low.  Risks for cardiopulmonary mortality are increased even at what are considered ‘background’ levels of particulate pollution compared to clean, filtered air.
  • Air pollution impairs exercise capability, even in the very fittest of individuals.  Even in young, healthy adults air pollution increases biomarkers of inflammation and thrombosis and increases blood pressure and heart rate.
  • Air pollution shortens life expectancy and accelerates the aging process. The residents of the average American city lose 1-3 years of life expectancy, in Northern China residents lose 5.5 years.
  • The increase in mortality risk persists for decades after exposure.
  • There are very likely genetic differences in human susceptibility to the arterial inflammation provoked by air pollution. Furthermore, the progression of inflammation and cardiovascular changes are more pronounced in those who are already at higher risk.
  • Pollution nanoparticles preferentially accumulate in inflamed and atherosclerotic lesions in the lining of blood vessels, a likely mechanism for their relationship to heart attacks and strokes.

 

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