Journal of ISSN: 2373-4396JCCR

Cardiology & Current Research
Volume 7 Issue 3 - 2016
Environment and Cardiovascular Disease
Aurelio Leone1,2,3*
1Fellow of the American Society of Hypertension (FASH), USA
2Fellow of the Royal Society for Promotion of Health (FRSPH), UK
3Editor-in-Chief of the Journal of Cardiology&Current Research, USA
Received: November 22, 2016 | Published: December 06, 2016
*Corresponding author: Aurelio Leone, Fellow of the Royal Society for Promotion of Health, Via Provinciale 27, 19030 Castelnuovo Magra (SP), Italy, Tel: +393472272215; Email:
Citation: Leone A (2016) Environment and Cardiovascular Disease. J Cardiol Curr Res 7(3): 00251. DOI: 10.15406/jccr.2016.07.00251


Recent studies describe a clear role of the environment to determining development and the impairment of cardiovascular disease, primarily hypertension and ischemic heart disease [1-3]. My previous papers [4,5] emphasized the evidence that the environment according to its specific characteristics is a factor that could influence either positively or adversely cardiovascular system of all individuals, primarily the older population because of some altered physiological responses to harmful stimuli.

An environment may be commonly defined as a complex structure where individuals with similar and, otherwise, different lifestyle play their activity, particularly modifying and organizing various events strongly related to their living habit. This factor often changes the natural course of the environment itself [4]. Therefore, the natural environment, which should be not influenced by human activity, really does not exist, and a correct lifestyle is fundamental to prevent a large number of diseases by reducing morbidity and mortality of living subjects through the control of several pollutants, primarily industrial and smoking toxics [5-7]. There is no doubt that the characteristics of an environment have been and are continuously changed by the human progress, which usually walks in an opposite way to that the natural environment should need.

A large number of factors, primarily derived from chemical industries pollute the atmosphere and, so doing, adversely influence individuals’ health including heart and blood vessel welfare. Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function [8]. Cigarette smoking, one of the powerful air pollutant, exerts harmful effects on the cardiovascular system by those chemical compounds given out to the atmosphere [9].

It is worth noting that an environment is structurally formed by outdoor and indoor spaces and, therefore, the pollution depends on its characteristics. When the spaces are widely ventilated, evidence indicates a lower pollutant concentration. Geographically, unhealthy climates have been demonstrated to determine a higher rate of infectious heart disease [10]. Tropical and subtropical regions around a circled area involving American, Asian, Australian and African continents as well as the Pacific and Indian oceans show cardiovascular alterations primarily due to Protozoa and Metazoa, with a significant major rate compared to what observed in other geographical areas, where ischemic heart disease, hypertension and heart disorders due to metabolic factors are prevailing [11]. Thus, this is an evident proof associated with the role of the environment.

When individuals’ habit is associated with some specific characteristics of the environment, the health status undoubtedly meets outcomes able to further impair cardiovascular system. The effects of always increasing cardiovascular risk factors may be clearly explained in this way. Cardiovascular disease may be considered as a condition able to change the lifestyle of the individuals and environment characteristics being, in its turn, strongly influenced by these factors. A topic to be taken into account is the relationship between environment and some genetic factors for the cardiovascular disease.

A large number of cardiovascular disease has been documented to have a complex multifactorial etiology. Neither genetic nor environmental agents acting independently may cause disease. An individual’s genetic makeup or, conversely, exposures to adverse environments cannot predict with certainty the onset, progression, or severity of disease. Cardiovascular disease may develop as the result of interactions between the “initial” conditions, which characterize the genotype, and exposures to environmental agents acting for a long time in a polluted atmosphere [12]. Therefore, a correct lifestyle should be fundamental to prevent those cardiovascular disorders mainly influenced by ambient pollutants with possible and significant reduction in mortality, morbidity and disability of living subjects [13]. Thus, changes in lifestyle could be carried out with the purpose to reduce the incidence of cardiovascular fatal and non-fatal events.


In conclusion, from these short observations a basic question arises: Is the natural environment able to influence adversely the cardiovascular system or, on the contrary, are the current progresses due to industrial and manufactured products responsible of the environmental changes and, then, cardiovascular alterations? Epidemiological reports clearly support the second hypothesis unless for some geographical areas, as aforesaid, where the environment may directly harm cardiovascular system, primarily by infectious agents living in these regions.


  1. Leone A (2003) Relationship between cigarette smoking and other coronary risk factors in atherosclerosis: risk of cardiovascular disease and preventive measures. Curr Pharm Des 9(29): 2417-2423.
  2. Glantz SA, Parmley WW (1985) Passive smoking and heart disease. JAMA 273(13): 1047-1053.
  3. O’Toole TE, Conklin DJ, Bhatnagar A (2008) Environmental risk factors for heart disease. Rev Environ Health 23(3): 167-202.
  4. Leone A (2015) “The Old Man and the Sea”: Elderly and Environment in Cardiovascular Physiopathology. J Cardiol Curr Res 4(3): 00143.
  5. Leone A, Landini L, Centaro E (2014) Blood pressure at Sea level and Mountains in winter and summer holiday people. JCH 8(4): e48.
  6. Briggs D (2003) Environmental pollution and the global burden of disease. Br Med Bull 68(1): 1-24.
  7. Leone A (2005) Biochemical markers of cardiovascular damage from tobacco smoke. Curr Pharm Des 11(17): 2199-2208.
  8. Pope AC, Burnett RT, Thurston GD, Thun M, Calle EE, et al. (2004) Cardiovascular mortality and long-term exposure to particulate air pollution. Epidemiological evidence of general pathophysiological pathways of disease. Circulation 109(1): 71-77.
  9. Leone A (2015) Toxics of tobacco smoke and cardiovascular system: From functional to cellular damage. Curr Pharm Des 21(30): 4370-4379.
  10. Leone A (2011) Passive smoking and infectious disease: a serious hazard for cardiovascular system. Imnt J Clin Med 2: 550-555.
  11. Lakka HA, Laaksonen DE, Lakka TA, Niskanen LK, Kumpusalo E, et al. (2002) The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. JAMA 288(21): 2709-2716.
  12. Sing CF, Stengard JH, Kardia SLR (2003) Genes, environment, and cardiovascular disease. Arterioscler Thromb Vasc Biol 23: 1190-1196.
  13. Wald NJ, Hackshaw AK (1996) Cigarette smoking: an epidemiological overview. Br Med Bull 52(1): 3-11.
© 2014-2018 MedCrave Group, All rights reserved. No part of this content may be reproduced or transmitted in any form or by any means as per the standard guidelines of fair use.
Creative Commons License Open Access by MedCrave Group is licensed under a Creative Commons Attribution 4.0 International License.
Based on a work at
Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version | Opera |Privacy Policy