3. Psicología y salud
3.1. La Salud como Interdisciplina
As with sulphates, nitrates in PM are primarily formed secondarily in the atmosphere rather than being directly emitted. Nitrate in PM largely originates from nitrous oxide emissions, the l argest source of which is on-road vehicles. Generally, nitrate is <10-15% of the mass of PM (Harrison and Yin 2000, Reiss et al. 2007). The western US, with high traffic levels relative to fossil fuel -generated
171 electricity generation, is an exception, there nitrate levels in PM are comparable to or greater than sulphate levels (Harrison and Yin 2000, Reiss et al. 2007).
Not many studies have addressed the association between PM-nitrate and health outcomes. In two reviews of evidence published in 2007 (Reiss et al. 2007, Schlesinger 2007), a total of four separate epidemiological investigations were cited. Nitrate was significantly associated with all -cause mortality in the Netherlands (Hoek et al. 2000) and California (Lipfert et al. 2006, Ostro et al. 2007) and, cardiovascular mortality in California (Fairley 1999). However, in another US study, nitrate was not significantly associated with all-cause mortality in Atlanta in people ≥65 years of age (Klemm et al. 2004). The study of Hoek et al measured aerosol nitrate rather than nitrate as a component of a PM size fraction, therefore it is not possible to directly compare the strength of the association of nitrate with that of PM mass (mortality risk estimates were marginally higher for nitrate than for PM10). Of the other studies with significant mortality associations, one study found a stronger association with PM2.5-nitrate than with total PM2.5 (Lipfert et al. 2006). In the other two studies (Fairley 1999, Ostro et al. 2007), the association between PM2.5-nitrate and mortality was the same or weaker than the association for total PM2.5 mass.
Since those reviews, source apportionment studies from the US have found that PM2.5-nitrate was not associated with daily all-cause and cardiovascular mortality or, hospital emergency department presentations for cardiorespiratory disease (Ito et al. 2006, Sarnat et al. 2008). In contrast, a source apportionment study from Barcelona found that PM2.5-nitrate was positively associated with cardiovascular mortality and to a greater extent than was total PM2.5 mass (Ostro et al. 2011). An analysis of a data set of 12.5 million Medicare enrolees (≥ 65 years of age) found that long -term exposure to increased PM2.5-nitrate (a one-standard deviation increase in the 7-year average) was associated with a 1.2% increase in mortality (Chung et al. 2015). In that study, increased long-term PM2.5-sulphate was associated with a decrease in mortality.
An examination of the effects of various components of PM2.5 on cardiovascular mortality and hospitalisations in New York found that PM2.5-nitrate was associated with cardiovascular hospitalisations but not mortality, while total PM2.5 mass was associated with both outcomes (Ito et al. 2011). In another study of 25 US communities, PM2.5-nitrate was not associated with all-cause mortality (Franklin et al. 2008). In London, PM2.5-nitrate was positively associated with daily respiratory, but not all-cause or cardiovascular mortality (Atkinson et al. 2010). Cardiovascular and respiratory hospitalisations for persons 65 years or older in 106 US counties were not associated with PM2.5-nitrate, although for cardiovascular hospitalisations the positive risk estimate was greater than for the majority of the other 19 constituents of PM2.5 that were measured (Bell et al. 2009). In an analysis which utilised US Medicare billing claims in order to determine hospital admissions for a population of 12 million people from 119 US counties, it was demonstrated that hospital admissions for cardiovascular disease, but not respiratory disease, were positively associated with PM2.5-nitrate (Levy et al. 2012). In a meta-analysis of estimates of effect from four time-series studies, a 10 µg/m3 increase in PM2.5-nitrate was associated with a non-statistically significant 2.7% increase in all-cause mortality (Levy et al. 2012). Long-term exposure to PM2.5-nitrate has been associated with all-cause and cardiorespiratory mortality in female teachers in California, but not to a greater extent than was long-term exposure to total PM2.5 (Ostro et al. 2010).
172 There have been few toxicological studies on which to evaluate the health effects of PM-nitrate. Generally toxicological studies have involved exposure to nitrated compounds rather than nitrate bound to PM, with mixed results (Schlesinger 2007).
In summary, the evidence base for health impacts associated with exposure to PM-nitrate is limited. As with sulphate, the evidence is difficult to interpret because PM2.5-nitrate concentrations are highly correlated with total PM2.5 mass, making it difficult to determine whether nitrate or whole particle mass is responsible for observed health outcomes. There is more evidence linking PM- nitrate with cardiovascular than respiratory outcomes.
7.5 Summary
Epidemiological studies that portray regional heterogeneity in the health effects of exposure to PM and, toxicological studies that demonstrate compositional variability in PM toxicity, strongly suggest that particle composition influences the health effects of PM. Thus it is not solely the mass concentration of ambient PM that determines the biological (and consequently health) response to exposure. It is unlikely that any single chemical component of PM is responsible for all adverse health outcomes. Rather, an array of elements/compounds may be associated with specific outcomes. Most of the evidence linking compositional elements of PM with health effects is inconsistent and conflicting. Although there are constituent candidates for causing adverse health effects (e.g. the transition metals vanadium and nickel), there is presently insufficient evidence to infer that a particular particle (or population of particles) will have a greater impact on health than other particles on the basis of composition alone.
Some metals in PM, such as vanadium and nickel, are associated with adverse health effects but due to the complexity of PM composition it is not known whether it is specifically the metals in ambient PM which are responsible for adverse health outcomes.
There are biologically plausible mechanisms for the adverse health effects associated with the inhalation of transition metals.
Organic compounds in PM, particularly those emitted during the process of fossil fuel combustion, are likely to cause health effects, however it is presently unclear what the health impacts of the inhalation of organic compounds in ambient PM are.
Health outcomes have been associated with both sulphate and nitrate in PM but there is no clear evidence that the presence of these constituents increases the toxicity of ambient PM over and above total PM2.5 mass.
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