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      World Heart Day - creating heart healthy environments

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          Abstract

          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.

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          Most cited references 9

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          Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults.

          Time-series, cross-sectional, and prospective cohort studies have observed associations between mortality and particulate air pollution but have been limited by ecologic design or small number of subjects or study areas. The present study evaluates effects of particulate air pollution on mortality using data from a large cohort drawn from many study areas. We linked ambient air pollution data from 151 U.S. metropolitan areas in 1980 with individual risk factor on 552,138 adults who resided in these areas when enrolled in a prospective study in 1982. Deaths were ascertained through December, 1989. Exposure to sulfate and fine particulate air pollution, which is primarily from fossil fuel combustion, was estimated from national data bases. The relationships of air pollution to all-cause, lung cancer, and cardiopulmonary mortality was examined using multivariate analysis which controlled for smoking, education, and other risk factors. Although small compared with cigarette smoking, an association between mortality and particulate air pollution was observed. Adjusted relative risk ratios (and 95% confidence intervals) of all-cause mortality for the most polluted areas compared with the least polluted equaled 1.15 (1.09 to 1.22) and 1.17 (1.09 to 1.26) when using sulfate and fine particulate measures respectively. Particulate air pollution was associated with cardiopulmonary and lung cancer mortality but not with mortality due to other causes. Increased mortality is associated with sulfate and fine particulate air pollution at levels commonly found in U.S. cities. The increase in risk is not attributable to tobacco smoking, although other unmeasured correlates of pollution cannot be excluded with certainty.
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            Inhalation of fine particulate air pollution and ozone causes acute arterial vasoconstriction in healthy adults.

            Fine particulate air pollution and ozone are associated with increased cardiovascular events. To help explain the mechanism behind these observations, we investigated the effect of air pollution exposure on vascular function. Twenty-five healthy adults underwent a randomized, double-blind, crossover study comparing the vascular response to the 2-hour inhalation of approximately 150 microg/m(3) of concentrated ambient fine particles (CAP) plus ozone (120 ppb) versus the response to the inhalation of filtered air. High-resolution vascular ultrasonography was used to measure alterations in brachial artery diameter, endothelial-dependent flow-mediated dilatation (FMD) and endothelial-independent nitroglycerin-mediated dilatation (NMD). Exposure to CAP plus ozone caused a significant brachial artery vasoconstriction compared with filtered air inhalation (-0.09+/-0.15 mm versus +0.01+/-0.18 mm, P=0.03). There were no significant differences in FMD (+0.29+/-4.11% versus -0.03+/-6.63%, P=0.88), NMD (+3.87+/-5.43% versus +3.46+/-7.92%, P=0.83), or blood pressure responses between exposures. Short-term inhalation of fine particulate air pollution and ozone at concentrations that occur in the urban environment causes acute conduit artery vasoconstriction.
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              Exposure assessment for estimation of the global burden of disease attributable to outdoor air pollution.

              Ambient air pollution is associated with numerous adverse health impacts. Previous assessments of global attributable disease burden have been limited to urban areas or by coarse spatial resolution of concentration estimates. Recent developments in remote sensing, global chemical-transport models, and improvements in coverage of surface measurements facilitate virtually complete spatially resolved global air pollutant concentration estimates. We combined these data to generate global estimates of long-term average ambient concentrations of fine particles (PM(2.5)) and ozone at 0.1° × 0.1° spatial resolution for 1990 and 2005. In 2005, 89% of the world's population lived in areas where the World Health Organization Air Quality Guideline of 10 μg/m(3) PM(2.5) (annual average) was exceeded. Globally, 32% of the population lived in areas exceeding the WHO Level 1 Interim Target of 35 μg/m(3), driven by high proportions in East (76%) and South (26%) Asia. The highest seasonal ozone levels were found in North and Latin America, Europe, South and East Asia, and parts of Africa. Between 1990 and 2005 a 6% increase in global population-weighted PM(2.5) and a 1% decrease in global population-weighted ozone concentrations was apparent, highlighted by increased concentrations in East, South, and Southeast Asia and decreases in North America and Europe. Combined with spatially resolved population distributions, these estimates expand the evaluation of the global health burden associated with outdoor air pollution.
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                Author and article information

                Journal
                Indian J Med Res
                Indian J. Med. Res
                IJMR
                The Indian Journal of Medical Research
                Medknow Publications & Media Pvt Ltd (India )
                0971-5916
                0975-9174
                September 2014
                : 140
                : 3
                : 327-329
                Affiliations
                [1 ]Sahara Hospital, Former Head Department of Cardiology Sanjay Gandhi Postgraduate Institute of Medical, India
                [2 ]Department of Cardiology, King Geroge's Medical University, Lucknow 226 003, India
                [3 ]Professor Emeritus, King Geroge's Medical University, Lucknow 226 003, India
                Author notes
                [* ] For correspondence: sinha.nakul@ 123456gmail.com

                This editorial is published on the occasion of World Heart Day - September 28, 2014.

                Article
                IJMR-140-327
                4248375
                25366196
                Copyright: © Indian Journal of Medical Research

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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