The conventional risk factors for cardiovascular diseases (CVD) like hypertension,
dyslipidaemia, diabetes mellitus and smoking have largely overshadowed and perhaps
precluded any sincere efforts towards discovery of new risk factors. However, environmental
influences are waiting in the pipeline to be accounted for an increased chance of
development of cardiovascular diseases. Many large epidemiological studies have reported
a definite link between the exposure to fine air particles and an increase in cardiovascular
mortality1. Statistically significant correlations are now available for both short
and long term exposure and correlations with heart failure and arrhythmias1
2. As per the WHO around 7 million people died, one in eight of total global deaths,
as a result of air pollution exposure. Regionally, low- and middle-income countries
in the WHO South-East Asia and Western Pacific Regions had the largest air pollution-related
burden in 2012, with a total of 3.3 million deaths linked to indoor air pollution
and another 2.6 million to outdoor air pollution3. This finding more than doubles
the previous estimates and confirms that air pollution is now perhaps the world's
largest single environmental health risk4.
Long term effects
The Six Cities Study2, by Harvard environmental epidemiologists group, addressed this
vital issue. In this study, 8000 participants from six US cities with varying levels
of air pollution, were followed up for 14-16 yr and reported a 26 per cent increase
in all cause mortality (mostly cardiovascular) in the most heavily polluted city when
compared to the least polluted one. In another study, Pope et al
5 covering more than half a million people over 16 years noted that fine particulates
surprisingly were more strongly linked with cardiovascular deaths compared to respiratory
causes. The air pollutants like ozone, carbon monoxide, nitrogen oxides, sulphur dioxides
and lead also appear to have evident links with cardiovascular disease (CVD).
In another large study, The Women's Health Initiative Observational study6, database
of more than 65,000 post-menopausal women without prior CVD was studied for the relation
between long term exposure to air pollutants and the risk for a first cardiovascular
event. After correction for all confounding factors, it was concluded that for each
10 μg/m3 increase in pollution concentration, there were significant increases in
the risk of any cardiovascular event, death from CVD and of cerebrovascular events
(hazard ratios 1.24, 1.76 and 1.35 respectively)6. The American Health Association
(AHA) Scientific Statement (2004)7 has finally acknowledged that air pollutants pose
a “serious public health problem” for CVD.
Short-term effects: In addition to long-term risk, short-term exposure to air pollutants
(both ozone and fine particulate matter) has been associated with acute coronary ischaemic
events. In a study of 12,000 patients, a short-term increase in fine ambient particulate
matter had shown a positive correlation with an increase in acute ischaemic coronary
events2. In a systematic review and meta-analysis of data from 34 studies, carbon
monoxide, nitrogen dioxide, sulphur dioxide, and small particulate matter (<10 and
<2.5 microns) were all associated with an increased risk of myocardial infarction,
with the overall population attributable risk ranging from 1 to 5 per cent8.
Environmental noise like road or air traffic has also been correlated to an increased
risk of developing CVD9. This effect is hypothesized to be due to stress-related dysregulation
of the autonomic nervous system, leading to an increase in hypertension and subsequent
CVD.
Pathophysiological links: Numerous theories have been postulated to establish causal
association between environmental toxins and cardiovascular adverse events. A few
of these untoward effects may be mediated via atherosclerosis, vasoconstriction and
changes in heart rate variability, blood pressure, coagulation, abnormal platelet
activation, endothelial dysfunction with their consequent acute and chronic clinical
sequelae10
11.
Possible mechanisms by which fine particulate air pollution may increase the risk
of CVD include (i) an increase in mean resting arterial blood pressure through an
increase in sympathetic tone and/or the modulation of basal systemic vascular tone10;
(ii) an increase in the likelihood of intravascular thrombosis through transient increases
in plasma viscosity and impaired endothelial dysfunction11; and (iii) the initiation
and promotion of atherosclerosis12
13.
Preventive measures: The preceding facts and figures lead us to a sufficiently irrevocable
conclusive link between the environmental pollution - be it in the air we breathe,
food we eat, soil we grow, fuel we burn, noise we hear and even the stress we bear,
and cardiovascular disease progression. The evidences are sufficiently strong for
us to start taking preventive measures against this all pervasive hazard.
In the western and advanced nations, environmental cardiology appears to be increasingly
becoming a factor in research and public policy discussion. Strict implementations
of air quality regulation and pollution levels are possibly contributing to a meaningful
increase in life expectancy and reduction in cardiovascular mortality.
The obvious impediment in the developing countries is a lack of awareness coupled
with a non aggressive policy for the prevention of non communicable diseases. Some
of the suggestions mentioned below can help us progress in this direction:
(i)
Air pollution levels displays should be available in each city at crowded places,
to increase awareness.
(ii)
People should be discouraged to walk/exercise at places with high air pollution levels.
(iii)
The use of vehicle emanating fewer pollutants is already being encouraged by the Government.
It should be made mandatory and strictly enforced.
(iv)
Environmental factors should be referred to as reversible risk factors for atherosclerotic
coronary artery disease in the documents, textbooks and in a national health compendium.
(v)
Awareness of such a hazard should be prominently displayed at par with smoking and
tobacco in various Government sponsored advertisements.
(vi)
Posters and slides at places of entertainment like multiplexes and shopping malls
can support this message.
(vii)
Innovative catchy cartoons and drawings can be displayed at school fetes and functions.
(viii)
In any future environmental study, cardiovascular health should be included as an
endpoint.
(ix)
The drug industry should be advised to adopt this aspect as a thrust area for research
and innovation. Regional differences in disease patterns may be correlated and highlighted
to expose this insidious link.
Creating a heart healthy environment, being the result of a slow and collective process
without many immediate tangible benefits holds us back from working towards this goal
with a zest and zeal which it merits. However, knowledge, awareness and conviction
regarding its importance and utility and multiple benefits should be a sufficient
motivator for our present day thinkers and administrators.
To summarize, the environmental toxins are significantly contributing to the adverse
cardiovascular events. The gravity of this issue should be appreciated. The target
is to create a heart healthy environment for all.