Short-term effect of fine particulate matter (PM2.5) on daily mortality due to diseases of the circulatory system in Madrid (Spain)
Introduction
Airborne particulate matter (PM) is extremely complex air pollutant: whereas, coarse ambient particulate matter having an aerodynamic diameter ≤ 10 μm (PM10) tends to be largely made up of components of a natural type, i.e., basically primary pollutants, the composition of fine ambient particulate matter having an aerodynamic diameter ≤ 2.5 μm (PM2.5) tends to be more toxic, since its main source is anthropogenic, being fundamentally made up of secondary particles. Indeed, this is why the World Health Organisation (WHO) recommends using PM2.5 rather than PM10 concentrations as air quality indicators (WHO, 2006).
Motor vehicle traffic, which has increased exponentially in recent years, is the principal cause of high pollutant levels (Ballester and Peiro, 2008). Specifically, in densely populated urban areas such as Madrid, vehicle emissions contribute up to 85% in terms of PM2.5 levels (Madrid City Council/Ayuntamiento de Madrid, 2006), due in particular to the high percentage of diesel vehicles, which emit up to six times more particles than do gasoline-driven vehicles (Spanish Observatory for Sustainability/Observatorio de la Sostenibilidad en España (OSE), (2007)). Traffic intensity and proximity to main thoroughfares are two important predictors of differences in particle concentrations inside a city (Briggs et al., 1997, Hoek et al., 2002).
In Spain, PM levels can be influenced by atmospheric conditions, owing to the country's lower degree of precipitation and wind action compared to its more northern European neighbours (Rodríguez et al., 2002a, Rodríguez et al., 2002b), and to inflows of airborne particles (Saharan dust) from North Africa in the case of PM10 (Rodríguez et al., 2001, Artiñano et al., 2004, Escudero et al., 2005) (the substantially lower proportion of mineral material means that intrusions of Saharan dust do not tend to affect PM2.5 levels) (Querol et al., 2004, Salvador et al., 2004, Pérez et al., 2008).
The most important effects of air pollution on human health have been associated with PM. Not only does it lead to an increase in mortality (Dockery et al., 1993, Peters et al., 2000, Pope et al., 2002, Jerrett et al., 2005, Yorifuji et al., 2005, Ballester et al., 2008) and the number of hospital admissions due to different causes (Halonen et al., 2009, Linares & Díaz, 2010a, Linares & Díaz, 2010b), but the amount of Quality Adjusted Life Years (QALYs) lost as a consequence of exposure to such particles is estimated by the WHO at 6.4 million years (Cohen et al., 2005).
Two factors other than concentration influence the effects that particles have on human health. These are: their size, as it this determines the degree of penetration into the respiratory system; and their composition, since it has been observed that, in areas where alkalis are more abundant, particles tend to have a more toxic effect than when they are essentially made up of acid components (Brauer et al., 1995), with particulate matter containing aluminium, arsenic, sulphates, silicon and nickel being associated with greater increases in mortality (Zeller et al., 2006).
A number of studies link exposure to PM2.5 to increased mortality (Dockery et al., 1993, Pope et al., 2002, Jerrett et al., 2005, Yorifuji et al., 2005, Halonen et al., 2009). Chronic exposure to PM2.5 raises the risk of respiratory and cardiovascular diseases, and of tumours of the respiratory tract. As with the effects of pollution in general, the most sensitive population segments are children, the elder patients and patients with chronic diseases, whether a respiratory (asthma and bronchitis) or cardiac (ischemic heart disease and arrhythmias), as well as persons with cardiovascular risk factors (mainly diabetes, hypertension, dyslipidemia and smoking).
It is easy to understand the pathophysiology of the association between PM2.5 and diseases of the respiratory tract (fundamentally, asthma, chronic obstructive pulmonary disease, respiratory infections and respiratory failure), as these pollutants enter the body via the respiratory tract.
Although less studied and not as well understood, much progress has been made in recent years in explaining the pathophysiological mechanisms through which PM2.5 causes damage to the circulatory system (Brook, 2008). The salient aspects of current knowledge could be summarised as follows: the presence of PM2.5 in pulmonary alveoli induces a local inflammatory process, which, coupled with an increase in oxidative stress, has systemic repercussions, through the release into the blood stream of inflammatory mediators (Peters et al., 1997, Danesh et al., 1998, Utell et al., 2002), specifically cytokines (such as tumour necrosis factor α (TNF-α)), C-reactive protein (CRP) (Brook et al., 2003, Pope et al., 2004, Zeka et al., 2006) and leukocytes (Peters et al., 2001, van Eeden et al., 2001) and pro-thrombotic factors (fibrinogen (Schwartz, 2001, Ghio et al., 2003, Zeka et al., 2006) and platelets), thereby also causing a reduction in platelet stability. The result of these processes (pro-inflammatory and pro-thrombotic) is twofold: among patients with atheromatous plaques there is a risk, which may be more or less acute, of peripheral thrombosis, both arterial (including coronary arteries) and venous, with the additional possibility of erosion and even fragmentation of the atheromatous plaque (Nemmar et al., 2002, Zeller et al., 2006); and in the long term, chronic exposure to PM2.5 is associated with acceleration of the process of atherosclerosis (Suwa et al., 2002, Routledge et al., 2003, Brook et al., 2004, Kunzli et al., 2005, Miller et al., 2007, Zeka et al., 2006, Kunzli et al., 2010). Furthermore, these particles act on the autonomic nervous system, stimulating the sympathetic and inhibiting the parasympathetic branch. It has thus been shown, in healthy subjects (Brook et al., 2002, Urch et al., 2005) as well as those with cardiovascular diseases (Zanobetti et al., 2004), that PM2.5 acts on vascular tone, causing vasoconstriction. This, in turn, leads to an increase in arterial blood pressure, which, together with greater plasma viscosity, may trigger ischemic episodes (Peters et al., 1997, Wellenius et al., 2003). Via the same mechanism, PM2.5 has also been associated with a greater susceptibility to cardiac arrhythmias (Hoek et al., 2001).
As can be seen, elevated PM2.5 levels may be potentially associated with short-, medium- and long-term mortality due to cardiovascular diseases, such as ischemic heart disease, arrhythmias, peripheral vascular disease or cerebrovascular accident.
Prevailing European legislation governing air pollution is based on Community Directive 2008/50/EC (European Parliament and Council, 2008). Somewhat surprisingly, this new Directive lowers the PM2.5 requirements envisaged under earlier enactments, allowing higher limits than those recommended by the WHO in its guideline values for the protection of health (WHO, 2006). Whereas the latter organisation recommended mean maximum values of 25 μg/m3 (daily/24 h) and 10 μg/m3 (annual), the new Directive phases in higher values in two stages, namely: Stage I, a mean maximum annual value of 25 μg/m3 (deadline to achieve this goal: 2015); and Stage II, a mean maximum annual value of 20 μg/m3 (deadline to achieve this goal: 2020), though it indicates that this latter value will be revised in 2013 taking into account any new evidence on its effects on human health, experience gained in Stage I, and technical viability.
There are few European cities in which studies have been conducted linking PM2.5 to mortality. In Madrid, there are data on PM10 (Boldo et al., 2006), and insofar as PM2.5 is concerned, there is evidence of association between its levels and hospital admissions (Linares & Díaz, 2010a, Linares & Díaz, 2010b) and short-term mortality among the elderly (persons aged over 75 years) (Jiménez et al., 2009), but there are no studies that associate these concentrations with short-term mortality in the general population, let alone short-term mortality due to circulatory diseases. Similarly, there are no such studies for other Spanish cities. Accordingly, our study sought to analyse and quantify the short-term impact of PM2.5 on daily overall circulatory mortality in Madrid.
Section snippets
Materials and methods
A longitudinal ecological time-series study was conducted. The study population was made up of all persons residing in Madrid, regardless of age, who died as a result of diseases of the circulatory system (International Classification of Diseases-10th revision (ICD-10): I00–I99) during the period 1 January 2003 to 31 December 2005.
Results
Table 1 shows the descriptive statistics of our study variables. The mean number of daily all-cause circulatory deaths (ICD-10: I00–I99) was 18.65 (standard deviation (SD): 5.41); of the total of 20,445 deaths caused by diseases of the circulatory system, 20.75% (4243 deaths) were due to AMI, 11.82% (2417 deaths) were due to other ischemic heart diseases and 23.16% (4735 deaths) were due to cerebrovascular diseases. These three specific causes were observed to be jointly responsible for 55.73%
Discussion
During the study period, daily mean PM2.5 concentrations in Madrid ranged from 5 μg/m3 (minimum) to 71 μg/m3 (maximum), with an overall mean of 19.16 μg/m3 (SD: 8.64), indicating that in the city of Madrid the mean annual level recommended by the WHO (10 μg/m3) was practically doubled (WHO, 2006). Furthermore, the 25-μg/m3 limit set by the WHO as the maximum mean daily concentration was exceeded on 20.42% of the total of 1038 days in this period for which there were PM2.5 records (212, i.e., 1 out
Conclusion
- 1.
PM2.5 concentrations are an important risk factor for daily circulatory-cause mortality in Madrid. The results of our study not only confirm a statistically significant association between daily mean PM2.5 concentrations and short-term overall circulatory and AMI mortality in the city of Madrid, but also quantify this association, with the AR% for increases of 10 μg/m3 being considerable.
- 2.
PM2.5 is a better indicator of urban air pollution levels than PM10. PM2.5 concentrations should be used as
Acknowledgement
This study was funded by the Carlos III Institute of Health (SEPY Project 1453/07).
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