Environmental determinants of cardiovascular disease, upsurge and neglected aspect: Dr Sushil

JAMMU : Dr. Sushil Sharma, Head of the Department of Cardiology at the GMCH, augmented his efforts to educate the public about the negative effects of cardiovascular diseases due to deteriorating air quality today by holding a day-long awareness cum screening camp at Raipur Domana. Participants of all ages and from all communi- ties were invited to attend.
Additionally, individuals with a high cardiac risk were urged to undergo addi- tional testing.
During his conversation with the patients, Dr. Sushil noted that over the last decade, a growing body of epidemiological and clinical evidence has increased con- cern about the possible neg- ative effects of ambient air pollution on health and its link to heart disease and stroke. Of special interest are several environmental air pollutants that include carbon monoxide, oxides of nitrogen, sulfur dioxide, ozone, lead, and particulate matter (“thoracic particles”
[PM10] <10 ?m in aerody- namic diameter, “fine parti- cles” [PM2.5] <2.5 ?m, and “coarse particles” [PM10 to 2.5]). These pollutants are associated with increased hospitalization and mortali- ty due to cardiovascular dis- ease, especially in persons with congestive heart fail- ure, frequent arrhythmias, or both. The well-estab- lished causal associations between active and passive smoking with heart disease and stroke support the plau- sibility of an adverse effect of PM on the cardiovascular system.
He further added that air pollution may accelerate the development of coronary
atherosclerosis and worsen its sequel. Some of these effects may occur over time, as with acceleration of the progression of atherosclero- sis, or rather abruptly, as with the triggering of an arrhythmia or myocardial infarction by acute inflam- matory responses, altered platelet adhesiveness, or perhaps vascular endothelial dysfunction. The putative biological mechanisms link- ing air pollution to heart dis- ease involve direct effects of pollutants on the cardiovas- cular system, blood, and lung receptors, and/or indi- rect effects mediated through pulmonary oxida- tive stress and inflammatory