Air Pollution and Cardiovascular Episodes

The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 6 No. 2 • April–May 2003


Air Pollution and Cardiovascular Episodes: Possible Prevention by Fish Oil Supplements

As a result of immense expenditures, air pollution has been greatly decreased in the United States. Nevertheless, it is always possible to improve what has already been improved at great additional cost, and there are those who propose to spend lots of other people’s money to do it. We examine here the problems posed by air pollution to a particularly vulnerable population group and how those problems might be solved more cost-effectively with dietary n-3 fatty acids (omega-3 fatty acids, or fish oils).

A recent study1 reports that air pollution episodes have been associated with increased cardiovascular hospital admissions and mortality. The researchers tested the hypothesis that patients with a history of serious arrhythmia who had, as a result, implanted cardioverter defibrillators experience potentially life-threatening arrhythmias after such air pollution episodes. Their results indicated that elevated levels of nitrogen dioxide, carbon monoxide, black carbon, and fine-particle mass are associated with potentially life-threatening arrhythmias, leading to automatic therapeutic interventions by an implanted cardioverter defibrillator.

In a second paper,2 researchers studied the association between ambient pollution levels and cardiovascular function in 21 active Boston residents aged 53 to 87 years, observing each up to 12 times from June to September 1997. The protocol involved 25 minutes per week of continuous Holter ECG monitoring, including 5 minutes of rest, 5 minutes of standing, 5 minutes of exercise outdoors, 5 minutes of recovery, and 20 cycles of slow breathing. Heart-rate variability was assessed. Mean 4-hour PM(2.5) (particles with aerodynamic diameter less than or equal to 2.5 µm) ranged from 3 to 49 µg/m(3); one-hour ozone levels ranged from 1 to 77 ppb. The authors concluded that the particles and ozone exposure may decrease vagal (cholinergic) nerve tone, resulting in reduced heart-rate variability. Reduced heart-rate variability is a strong risk factor for potentially fatal cardiac arrhythmias.

There is a large and growing body of scientific literature showing that n-3 fatty acids (also called omega-3 fatty acids) from fish oils are effective in animal and human studies in combating arrhythmias and improving heart-rate variability.3-11 We would like to see a study similar to the one done in the paragraph above except that the participants would be supplemented with 1–2 g of EPA/DHA daily. It would be particularly interesting to see what the protective effective of EPA/DHA might be during periods of exceptionally bad pollution.

References

  1. Peters et al. Air pollution and incidence of cardiac arrhythmia. Epidemiology 11(1):11-17 (2000).
  2. Gold et al. Ambient pollution and heart rate variability. Circulation 101:1267-73 (2000).
  3. Siscovick et al. Dietary intake and cell membrane levels of long chain n-3 polyunsaturated fatty acids and the risk of primary cardiac arrest J Am Med Assoc 274:1363-7 (1995).
  4. Sellmayer et al. Am J Cardiol 76(12):974-7 (1995).
  5. Riemersma and Sargent. Dietary fish oil and ischaemic arrhythmias. J Int Med 225(Suppl 1):111-6 (1989).
  6. Christensen et al. Heart rate variability and fatty acid content of blood cell membranes: a dose-response study with n-3 fatty acids. Am J Clin Nutr 70:331-7 (1999).
  7. Leaf et al. n-3 Fatty acids in the prevention of cardiac arrhythmias. Lipids 34:S187-9 (1999).
  8. Christensen et al. n-3 Fatty acids and the risk of sudden cardiac death assessed by 24-hour heart rate variability. Lipids 34:S197 (1999).
  9. Albert et al. Blood levels of long-chain n-3 fatty acids and the risk of sudden death. N Engl J Med 346(15):1113-8 (2002).
  10. Jones and Lau. Effect of n-3 polyunsaturated fatty acids on risk reduction of sudden death. Nutr Rev 60(12):407-9 (2002).
  11. Sheard. Fish consumption and risk of sudden cardiac death. Nutr Rev 56(6):177-9 (1998).

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