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Tim Kelleher

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Increasing Evidence Suggests Air Pollution is Arrhythmogenic

The impact of air pollution on cardiac health is the subject of research recently published in The Lancet,1 aiming to estimate the burden of disease generated worldwide by exposure to second-hand smoke. This was calculated from disease-specific relative risk estimates and area-specific estimates of the proportion of people exposed, by comparative risk-assessment methods, with data from 192 countries during 2004.

The findings estimate that 603,000 deaths were attributable to the effects of passive smoking in 2004, of which 379,000 were from ischaemic heart disease.  The report also revealed that ischaemic heart disease accounted for the largest disease burden attributable to second-hand smoke in adults, advising that “substantial health gains could be made by extending effective public health and clinical interventions to reduce passive smoking worldwide”.

pollution2A recent study[2] from a research team led by Dr. Gopal Sivagangabalan of the Toronto General Hospital also suggests that the effects of air pollution on cardiac rhythm and its link to arrhythmia mortality may be under-recognised. The research examines changes in the repolarisation parameters of healthy individuals exposed to concentrated ambient particles (CAP) and/or ozone (O3), illuminating the role air pollutants may play in urban arrhythmogenesis.

The study enrolled 25 healthy individuals (18 to 50 years of age), allowing for carefully controlled exposure to air pollution with the hypothesis that specific exposures would increase ECG-derived measures of spatial dispersion of repolarisation.  Results showed measurable alteration in cardiac electrophysiological properties in the cohort of healthy volunteers, while exposed to levels of pollution commonly encountered across the developed and developing world.

The changes in repolarisation dynamics are said to pose a risk to those with preexisting heart disease and baseline abnormalities of repolarisation, especially during periods of acute or prolonged exposure. Exposure-induced changes were most pronounced when breathing in both CAP and O3.

The authors emphasise that deriving such data from healthy subjects raises the possibility of pollution-induced changes posing an even greater risk to the increasing number of people who are living with structural cardiac disease.  Sivagangabalan et al call for more research concerning the pro-arrhythmic role of pollutants, with concurrent physician awareness and participation in global efforts to increase education, as well as reducing pollutant emissions.

The researchers claim added weight for their results by the thoroughness of their methods, the precise exposure levels of all subjects being fully characterised – “a feature that is lacking in most observational and epidemiologic studies on the cardiovascular effects of air pollution where central site monitoring data are usually used to estimate personal exposures” [2] (p.202).

Rachel Lambert, MD, Yale School of Medicine gives further credence to the findings in her accompanying editorial[3]: “This study adds significantly to our understanding of the pathophysiological links between air pollution and ventricular arrhythmias and sudden death.  Future studies can focus further on populations at risk as well as other indices of repolarization heterogeneity to confirm these mechanistic pathways”.

However, she also advises a balanced approach to the data: “Although exciting, these findings should be considered hypothesis generating.  The increases in mortality and arrhythmia due to air pollution predominantly occur in those with underlying heart disease, and whether these findings in normal volunteers can be extrapolated to those populations is unknown.  It is likely, however, that structural abnormalities leading to baseline repolarization heterogeneity would magnify the effects seen”.

References

  1. Öberg, Mattias, et al, Worldwide burden of diseases from exposure to second-hand smoke: a retrospective analysis of data from 192 countries, (The Lancet, Vol. 377; Iss.9760; 139-146)
  2. Sivagangabalan et al, The Effect of Air Pollution on Spatial Dispersion of Myocardial Repolarization in Healthy Human Volunteers, (Journal of the American College of Cardiology, 2011; 57; 198-206)
  3. Lampert, Rachel MD, Air Pollution and Repolarization Heterogeneity: More Impetus for Alternative Energy, (Journal of the American College of Cardiology, 2011; 57; 207-209)

Published on: January 13, 2011

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