ReviewAir pollutants: The key stages in the pathway towards the development of cardiovascular disorders
Introduction
Cardiovascular disorders are becoming a frequent event in modern societies owing to contemporary lifestyles in the developed world. The degree of environmental contamination with toxins and particularly airborne pollution, imposes stress on the heart which promotes the incidence of damaging cardiovascular events like arrhythmogenesis, myocardial infarction and cardiac hypertrophy. Air pollution is one such factor that promotes cardiac stress which leads to cardiovascular damage (Brook, 2008, Simkhovich et al., 2008). Various epidemiological and clinical studies have highlighted the deleterious effects of air pollution on heart disease (Hoek et al., 2002, Miller et al., 2007, Pope et al., 2004).
Air pollutants mainly include carbon mono-oxide, oxides of nitrogen, sulfur dioxide, ozone and particles composed of elemental carbon, organic carbon compounds, transition metals, metal oxides, acid concentrates, sulfates and nitrates (Routledge et al., 2003) (Table 1). Of these, particulate matter has become a major concern of cardiovascular research. There is substantial evidence that indicates the effect of ambient particulate matter on cardiovascular health.
Airborne particulate matter is a heterogeneous mixture of solid and liquid particles of varying size and chemical composition. In 1987, the regulatory focus was on particles that could readily penetrate and deposit in the tracheobronchial tree, or PM10 (PM with a median aerodynamic diameter of <10 μm). In 1997, the US EPA promulgated 24-h and annual average standards for PM2.5 (PM with median aerodynamic diameter <2.5 μm), comprising the size fraction that can reach the small airways and alveoli. The existing federal PM10 standards were retained, however, to address health effects that could be related to the “coarse fraction” (PM10–2.5; World Health Organization, 1987, World Health Organization, 2000). Particles of diameter less than PM10 are considered to have deleterious effects on health. However, ultra fine particles (UFP), which have diameter less than PM0.1 are an interesting area of research owing to their capability of penetrating deep into the lungs and may even pass directly into the circulatory system (Nemmar et al., 2001, Nemmar et al., 2002a). Such particles can thus have harmful effects on cardiovascular health. The present review will focus upon the various mechanisms that will explicate how air pollutants, especially ambient particulate matter is affecting the cardiovascular health and will throw light on various cardiovascular events which have been found to be influenced due to air pollution.
Section snippets
Mechanism
Various studies show that there is a link between the particulate air pollution and the deaths caused due to cardiovascular diseases such as myocardial infarction and arrhythmia. However any definite pathway that can explain the link between the two has not yet been determined. There are two possibilities that link air pollution to heart diseases. These involve the classical pathway that explains the indirect effects mediated through pulmonary oxidative stress and inflammatory responses and the
Linking air pollution to cardiovascular damage
Adverse effects of air pollution on cardiovascular health have been established through various studies. Exposure to air pollutants has resulted in an increased occurrence of various harmful events leading to cardiovascular morbidity. A few major events have been explained further.
Conclusion
The review provides some perspective on the extent of the involvement of air pollutants (especially particulate matter) in various cardiovascular events. The exact mechanisms involved are unknown for majority of events but these processes can be explored in terms of two major categories, i.e. direct translocation or via indirect secondary mediators. Inflammation proves to be the most common mediator of the adverse cardiovascular events of air pollution like thrombosis, vascular dysfunction,
Conflicts of interest
The authors declare that there are no conflicts of interest.
References (100)
- et al.
Effect of air-pollution control on death rates in Dublin, Ireland: an intervention study
Lancet
(2002) - et al.
Ultrafine (nanometre) particle mediated lung injury
J. Aerosol Sci.
(1998) - et al.
Effects of particulate air pollution on systolic blood pressure: a population-based approach
Environ. Res.
(2006) - et al.
Association between mortality and indicators of traffic-related air pollution in the Netherlands: a cohort study
Lancet
(2002) - et al.
Air pollution and hospitalization due to angina pectoris in Tehran, Iran: a time-series study
Environ. Res.
(2005) - et al.
Increased plasma viscosity during an air pollution episode: a link to mortality?
Lancet
(1997) - et al.
Heart rate variability associated with particulate air pollution
Am. Heart J.
(1999) - et al.
Particulate air pollution and acute health effects
Lancet
(1995) - et al.
Air pollution and cardiovascular injury: epidemiology, toxicology, and mechanisms
J. Am. Coll. Cardiol.
(2008) - et al.
Particulate air pollution induces progression of atherosclerosis
J. Am. Coll. Cardiol.
(2002)
Particulate matter initiates inflammatory cytokine release by activation of capsaicin and acid receptors in a human bronchial epithelial cell line
Toxicol. Appl. Pharmacol.
Life-threatening cardiovascular consequences of anger in patients with coronary heart disease
Cardiol. Clin.
Association between Ambient Particles and Daily Admissions for Cardiovascular Diseases
Ozone-induced airway inflammation in human subjects as determined by airway lavage and biopsy
Am. Rev. Respir. Dis.
Comparative respiratory effects of ozone and ambient oxidant pollution exposure during heavy exercise
J. Air Pollut. Control Assoc.
Exposure to particulate air pollution and risk of deep vein thrombosis
Arch. Intern. Med.
Air pollution and cardiovascular disease: a statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association
Circulation
Cardiovascular effects of air pollution
Clin. Sci.
Angiotensin II stimulates matrix metalloproteinase secretion in human vascular smooth muscle cells via nuclear factor-kappaB and activator protein 1 in a redoxsensitive manner
J. Vasc. Res.
“Normal” coronary angiography and vascular dysfunction: risk assessment strategies
PLoS Med.
Passive smoking and impaired endotheliumdependent arterial dilatation in healthy young adults
N. Engl. J. Med.
Particulate matter and heart rate variability among elderly retirees: the Baltimore 1998 PM study
J. Expo. Anal. Environ. Epidemiol.
Studies on the inflammatory potential of fine and ultrafine particles of carbon black, titanium dioxide and polystyrene/latex
Am. J. Respir. Crit. Care Med.
On-road exposure to highway aerosols. 2. Exposures of aged, compromised rats
Inhal. Toxicol.
Effects of aqueous extracts of PM(10) filters from the Utah valley on human airway epithelial cells
Am. J. Physiol.
Cardiac hypertrophy: the good, the bad, and the ugly
Annu. Rev. Physiol.
Interaction of alveolar macrophages and airway epithelial cells following exposure to particulate matter produces mediators that stimulate the bone marrow
Am. J. Respir. Cell Mol. Biol.
Mechanisms of thrombus formation
N. Engl. J. Med.
Retrieval analysis of clinical explanted vena cava filters
J. Biomed. Mater. Res. B: Appl. Biomater.
Concentrated ambient air particles induce mild pulmonary inflammation in healthy human volunteers
Am. J. Respir. Crit. Care Med.
Accumulation of iron in the rat lung after tracheal instillation of diesel particles
Toxicol. Pathol.
Mechanisms of morbidity and mortality from exposure to ambient air particles
Res. Rep. Health Eff. Inst.
Ambient pollution and heart rate variability
Circulation
Cardiac autonomic control mechanisms in power-frequency magnetic fields: a multistudy analysis
Environ. Health Perspect.
Rapid increases in the steady-state concentration of reactive oxygen species in the lungs and heart after particulate air pollution inhalation
Environ. Health Perspect.
Local intraluminal infusion of biodegradable polymeric nanoparticles: a novel approach for prolonged drug delivery after balloon angioplasty
Circulation
Irritative complaints, carboxyhemoglobin increase and minor ventilatory function changes due to exposure to chain-saw exhaust
Eur. J. Respir. Dis.
Prognostic value of coronary vascular endothelial dysfunction
Circulation
Does heavy physical exertion trigger myocardial infarction? A case-crossover analysis nested in a population-based case-referent study
Am. J. Epidemiol.
Carbon monoxide poisoning in children riding in the back of pickup trucks
JAMA
Residential exposure to traffic is associated with coronary atherosclerosis
Circulation
Effects of air pollution on blood pressure: a population-based approach
Am. J. Public Health
PM(10)-exposed macrophages stimulate a proinflammatory response in lung epithelial cells via TNF-alpha
Am. J. Physiol. Lung Cell. Mol. Physiol.
Oxidative stress: its role in air pollution and adverse health effects
Occup. Environ. Med.
Copper-dependent inflammation and nuclear factor-kappaB activation by particulate air pollution
Am. J. Respir. Cell Mol. Biol.
Interleukin 6 and haemostasis
Br. J. Haematol.
Translocation of ultrafine insoluble iridium particles from lung epithelium to extrapulmonary organs is size dependent but very low
J. Toxicol. Environ. Health A
Ambient air pollution and atherosclerosis in Los Angeles
Environ. Health Perspect.
Community air pollution
Daily variation of particulate air pollution and poor cardiac autonomic control in the elderly
Environ. Health Perspect.
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