|
INQUINAMENTO ATMOSFERICO E RISCHIO CARDIOVASCOLARE
Commento: Domenico Sommariva - Divisione di Medicina Interna 1, Ospedale G. Salvini, Garbagnate Milanese
Particulate
air pollution as a risk factor for ST-segment depression in patients with
coronary artery disease BACKGROUND:
The association of particulate matter (PM) with cardiovascular morbidity
and mortality is well documented. PM-induced ischemia is considered a
potential mechanism linking PM to adverse cardiovascular outcomes. METHODS
AND RESULTS: In a repeated-measures study including 5979 observations
on 48 patients 43 to 75 years of age, we investigated associations of
ambient pollution with ST-segment level changes averaged over half-hour
periods measured in the modified V(5) position by 24-hour Holter ECG monitoring.
Each patient was observed up to 4 times within 1 year after a percutaneous
intervention for myocardial infarction, acute coronary syndrome without
infarction, or stable coronary artery disease without acute coronary syndrome.
Elevation in fine particles (PM(2.5)) and black carbon levels predicted
depression of half-hour-averaged ST-segment levels. An interquartile increase
in the previous 24-hour mean black carbon level was associated with a
1.50-fold increased risk of ST-segment depression > or =0.1 mm (95%
CI, 1.19 to 1.89) and a -0.031-mm (95% CI, -0.042 to -0.019) decrease
in half-hour-averaged ST-segment level (continuous outcome). Effects were
greatest within the first month after hospitalization and for patients
with myocardial infarction during hospitalization or with diabetes. CONCLUSIONS:
ST-segment depression is associated with increased exposure to PM(2.5)
and black carbon in cardiac patients. The risk of pollution-associated
ST-segment depression may be greatest in those with myocardial injury
in the first month after the cardiac event. Cardiovascular
Effects of Air Pollution Air pollution is a heterogeneous mixture of gases, liquids and PM (particulate matter). In the modern urban world, PM is principally derived from fossil fuel combustion with individual constituents varying in size from a few nanometres to 10 microm in diameter. In addition to the ambient concentration, the pollution source and chemical composition may play roles in determining the biological toxicity and subsequent health effects. Nevertheless, studies from across the world have consistently shown that both short- and long-term exposures to PM are associated with a host of cardiovascular diseases, including myocardial ischaemia and infarctions, heart failure, arrhythmias, strokes and increased cardiovascular mortality. Evidence from cellular/toxicological experiments, controlled animal and human exposures and human panel studies have demonstrated several mechanisms by which particle exposure may both trigger acute events as well as prompt the chronic development of cardiovascular diseases. PM inhaled into the pulmonary tree may instigate remote cardiovascular health effects via three general pathways: instigation of systemic inflammation and/or oxidative stress, alterations in autonomic balance, and potentially by direct actions upon the vasculature of particle constituents capable of reaching the systemic circulation. In turn, these responses have been shown to trigger acute arterial vasoconstriction, endothelial dysfunction, arrhythmias and pro-coagulant/thrombotic actions. Finally, long-term exposure has been shown to enhance the chronic genesis of atherosclerosis. Although the risk to one individual at any single time point is small, given the prodigious number of people continuously exposed, PM air pollution imparts a tremendous burden to the global public health, ranking it as the 13th leading cause of morality (approx. 800,000 annual deaths).
Both
long-term and short-term exposure to air pollution is associated with
a marked increase in cardiovascular morbidity and mortality because of
the coronary syndrome and its complications. The exact molecular mechanism
that is responsible for these acute and chronic effects is not elucidated
yet. Potential pathophysiological pathways, however, include vascular
dysfunction, inflammation, and oxidative stress and altered cardiac autonomic
dysfunction. Actually, the cardiovascular risk assessment for individual
patients with regard to air pollution is still complicated. To support
decision-making in clinic, we propose a risk model, named 'CardioVascular
and AIR pollution' risk table, composed of acknowledged factors in the
relationship of cardiovascular disease and air pollution. Air
pollution is increasingly recognized as an important and modifiable determinant
of cardiovascular disease in urban communities. Acute exposure has been
linked to a range of adverse cardiovascular events including hospital
admissions with angina, myocardial infarction, and heart failure. Long-term
exposure increases an individual's lifetime risk of death from coronary
heart disease. The main arbiter of these adverse health effects seems
to be combustion-derived nanoparticles that incorporate reactive organic
and transition metal components. Inhalation of this particulate matter
leads to pulmonary inflammation with secondary systemic effects or, after
translocation from the lung into the circulation, to direct toxic cardiovascular
effects. Through the induction of cellular oxidative stress and proinflammatory
pathways, particulate matter augments the development and progression
of atherosclerosis via detrimental effects on platelets, vascular tissue,
and the myocardium. These effects seem to underpin the atherothrombotic
consequences of acute and chronic exposure to air pollution. An increased
understanding of the mediators and mechanisms of these processes is necessary
if we are to develop strategies to protect individuals at risk and reduce
the effect of air pollution on cardiovascular disease. Exposure
to particulate air pollution and risk of deep vein thrombosis BACKGROUND:
Particulate air pollution has been linked to heart disease and stroke,
possibly resulting from enhanced coagulation and arterial thrombosis.
Whether particulate air pollution exposure is related to venous thrombosis
is unknown. METHODS: We examined the association of exposure to particulate
matter of less than 10 microm in aerodynamic diameter (PM10) with deep
vein thrombosis (DVT) risk in 870 patients and 1210 controls from the
Lombardy region in Italy, who were examined between 1995 and 2005. We
estimated exposure to PM10 in the year before DVT diagnosis (cases) or
examination (controls) through area-specific mean levels obtained from
ambient monitors. RESULTS: Higher mean PM10 level in the year before the
examination was associated with shortened prothrombin time (PT) in DVT
cases (standardized regression coefficient [beta] = -0.12; 95% confidence
interval [CI], -0.23 to 0.00) (P = .04) and controls (beta = -0.06; 95%
CI, -0.11 to 0.00) (P = .04). Each increase of 10 microg/m3 in PM10 was
associated with a 70% increase in DVT risk (odds ratio [OR], 1.70; 95%
CI, 1.30 to 2.23) (P < .001) in models adjusting for clinical and environmental
covariates. The exposure-response relationship was approximately linear
over the observed PM10 range. The association between PM10 level and DVT
risk was weaker in women (OR, 1.40; 95% CI, 1.02 to 1.92) (P = .02 for
the interaction between PM10 and sex), particularly in those using oral
contraceptives or hormone therapy (OR, 0.97; 95% CI, 0.58 to 1.61) (P
= .048 for the interaction between PM10 level and hormone use). CONCLUSIONS:
Long-term exposure to particulate air pollution is associated with altered
coagulation function and DVT risk. Other risk factors for DVT may modulate
the effect of particulate air pollution. Air
pollution exposure as an emerging risk factor for cardiovascular disease:
a literature review Several
epidemiological studies have demonstrated a consistent statistical association
between cardiovascular disease and air pollution exposure. In this review
we describe the nature of the most common ambient-air pollutants (either
gaseous or particulate of different size); then, we examine the pathophysiological
pathways linking the air pollutants with their cardiovascular effects
(arterial vasoconstriction, systemic inflammatory response, enhanced thrombosis,
a propensity for arrhythmia). A comprehensive review of the literature
on air pollution and the rate of hospital admission, morbidity, and mortality
due to cardiovascular reasons are also provided. In the last section,
we review the most recent studies that have outlined the correlation between
the onset of acute myocardial infarction and the level of outdoor air
pollution. In conclusion, scientific evidence is growing in support of
the hypothesis that ambient air pollution acts as a risk factor for cardiovascular
disease, and may trigger the onset of acute myocardial infarction. Recent epidemiological findings have suggested that urban atmospheric pollution may have adverse effects on the cardiovascular system as well as on the respiratory system. We carried out an exhaustive search of published studies investigating links between coronary heart disease and urban atmospheric pollution. The review was conducted on cited articles published between 1994 and 2005 and whose main objective was to measure the risk of ischaemic heart diseases related to urban pollution. Of the 236 references identified, 46 epidemiological studies were selected for analysis on the basis of pre-defined criteria. The studies were analysed according to short-term effects (time series and case-crossover designs) and long-term effects (case-control and cohort studies). A link between coronary heart disease and at least one of the pollutants studied (PM10, O3, NOx, CO, SO2) emerged in 40 publications. Particulate matter, nitrogen oxides, and carbon monoxide were the pollutants most often linked with coronary heart disease. The association was inconstant for O3. Although the mean mortality or morbidity risk related to urban atmospheric pollution is low compared with that associated with other better-known risk factors, its impact on health is nevertheless major because of the large number of people who are exposed. This exhaustive review supports the possibility that urban pollution is indeed an environmental cardiovascular risk factor and should be considered as such by the cardiologists.
|