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Cardiopulmonary diseases mortality

There are statistically significant associations between combustion-derived particles and elevations in mortality and morbidity, particularly among elderly persons with cardiopulmonary disease. The mechanism(s) by which these particles exert their effect is unknown, but may also involve generation of oxidants from transition metals present on these particles. Additionally, the size and acidity of PM 10 may contribute to its toxicity, as may organic or biological compounds found on the surface of these particles. [Pg.459]

An understanding of the mechanisms whereby inhaled particles cause acute morbidity and mortality has not yet been realized. Epidemiological evidence suggests that cardiopulmonary disease is a primary predecessor of these outcomes (8). Many of these studies have further suggested the importance of investigating fine and ultrafine particles as the primary particulate culprits. [Pg.593]

To date, increased pulmonary inflammation and decrements in pulmonary function have been clearly associated with C APs exposure in animals with cardiopulmonary disease. Normal animals are also not immune to the effects of inhaled particulate matter these animals have exhibited significant, albeit less severe, lung injury following particle exposure. The future of these studies lies in the investigation of the signaling pathways that are responsible for the sudden mortality observed. Given these data, it is clear that these pathways should be further delineated to develop potential measures to prevent sudden mortality and morbidity in exposed populations. [Pg.594]

Particulate matter air pollution is especially harmful to people with lung disease such as asthma and chronic obstructive pulmonary disease (COPD), which includes chronic bronchitis and emphysema, as well as people with heart disease. Exposure to particulate air pollution can trigger asthma attacks and cause wheezing, coughing, and respiratory irritation in individuals with sensitive airways. It was estimated in one major study that the excess risk of total mortality is 6.2% per each increase in 10pgPM2.s/m and 9.3% for cardiopulmonary mortality. ... [Pg.554]

Table 1 reviews examples of three types of studies (1) multi-city studies, such as the Six Cities and ACS studies (2) multi-county studies and (3) studies of a particular location, in this case the Atlanta area (chosen because of the wealth of studies in this area). Health outcomes examined are restricted to all-cause and cardiopulmonary mortality, and cardiovascular disease hospital or emergency department admissions, in order to retain focus. Although additional studies could be included, these studies were chosen because, in concert, they are among the best to illustrate with the least amount of complexity how epidemiology studies with some similarities can reach different conclusions about which pollutants are harmful. In particular, the multi-county and Atlanta studies were chosen because they monitored for many types of PM2 5. Table 1 generally does not include factor analyses (such as those of Mar et al. [2(X)0, 2006]), because (as discussed in Sect. 1.4) such analyses typically come to inconsistent conclusions, because of varying inputs and methodological factors. [Pg.576]

Table 1 Multi-city studies, multi-county studies, studies in Atlanta area varying conclusions regarding which particle components are associated with allcause mortality, cardiopulmonary mortality, or emergency department visits for cardio-vascular disease... [Pg.577]

Increases in the concentration of fine particles in the air are associated with increases in mortality. The excess deaths are predominantly from respiratory causes, but deaths from cardiovascular causes are affected as well. This association has been observed in many cities worldwide and perhaps most remarkably, remains strong at low particle concentrations previously thought to be without adverse health effects. The mechanisms by which particulate pollution induces health effects at such low mass concentrations remain unclear. Determining the biological mechanisms involved has been identified as a high-priority research need in the United States (1) and other countries. As suggested by the word cardiopulmonary this chapter will explore hypotheses and evidence linking particle exposure with both respiratory and cardiac dysfunction and disease. [Pg.653]


See other pages where Cardiopulmonary diseases mortality is mentioned: [Pg.4954]    [Pg.2251]    [Pg.428]    [Pg.206]    [Pg.415]    [Pg.155]    [Pg.41]    [Pg.449]    [Pg.593]    [Pg.629]    [Pg.211]    [Pg.37]    [Pg.171]    [Pg.123]    [Pg.128]    [Pg.169]    [Pg.594]    [Pg.476]    [Pg.581]    [Pg.449]    [Pg.577]    [Pg.603]   
See also in sourсe #XX -- [ Pg.538 ]




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