Environmental Engineering Reference
In-Depth Information
KEYWORDS
CAPs
Concentrated ambient air particulate matter
Cardiovascular effects
Cardiovascular system responses to inhaled particulate matter
PM Components
Chemical component masses within overall PM mass
Pulmonary effects
Pulmonary system responses to inhaled particulate matter
PM x
Particulate matter below cut-point x in aerodynamic diameter
Ultraine PM
PM with diameters below 0.1 μm, expressed as either mass or
number concentration
Fine PM
PM mass concentration with aerodynamic diameters below 2.5 μm
Accumulation mode PM
PM mass concentration with aerodynamic diameters between 0.1
and 2.5 μm
Coarse thoracic PM
PM mass concentration with aerodynamic diameters between 2.5
and 10 μm
14.1  INTRODUCTION
Studying the health effects of ambient air pollution has been a challenging endeavor for environ-
mental health scientists for many reasons. Epidemiologists have documented signiicant associations
between the routinely measured mass concentrations of particulate matter (PM) and excess mortality,
morbidity, lost function, and lost time at work or school, and these associations are stronger for PM 2.5 ,
that is, particles with aerodynamic diameters less than 2.5 μm, than those for PM in other particle size
ranges, or those for routinely measured pollutant gases (USEPA 2004, 2008). Although the relative
risks (RRs) for mortality and nonscheduled hospital admissions are relatively small, requiring sophis-
ticated mathematical models for analysis in epidemiological studies, the populations studied and the
populations at risk are quite large (Miller et al., 2007; Eftim et al., 2008; Schwartz et al., 2008; Pope
et al., 2009), resulting in large public health impacts (e.g., thousands of cases annually in the United
States). The bulk of this risk appears to be borne by the elderly, those in poor health, or both.
It seems highly unlikely that the health effects are caused by nonspeciic PM mass. Rather, it is
likely that some speciic chemical components within the PM mixtures are more potent than other
components. The situation is complicated by the fact that PM is present in the air over a broad range
of chemical compositions and particle sizes. Coarse dust particles with aerodynamic diameters above
10 μm do not normally penetrate beyond the larynx, have not been associated with health effects due
to ambient air pollution exposures, and are not routinely monitored. Particles with aerodynamic diam-
eters below 10 μm, known as PM 10 , can deposit along the conductive airways in the thorax, and nearly
all of those with aerodynamic diameters below 2.5 μm penetrate into the gas exchange region where
particle retention is much greater than for those that deposit on the conductive airways. A mucociliary
blanket covering the conductive airways facilitates fairly rapid particle removal to the gastrointestinal
tract. Furthermore, the smaller particles (PM 2.5 ) are chemically quite different from the larger ones.
The larger particles are mostly of mineral origin, while the PM 2.5 is composed largely of diesel engine
soot and particles formed by chemical transformations in the atmosphere from fossil fuel combus-
tion products (both solid and gaseous) and organic vapors. Most of these particles initially form as
ultraine PM (UFP), but rapidly aggregate into the accumulation mode, that is, PM in the 0.1-2.5 μm
size range. Suspicion concerning adverse health effects has centered on fossil fuel combustion prod-
ucts, including elemental and organic carbon (EC/OC) and on mineral ash in the form of inorganic
compounds containing metals within the PM 2.5 . A focus has often been on transition metals, such as
iron (Fe), vanadium (V), nickel (Ni), chromium (Cr), copper (Cu), and zinc (Zn), on the basis of their
ability to generate reactive oxygen species (ROS) in biological tissues. Most of the evidence pointing
to the biological effects of metals, as well as of EC and OC has come from studies involving exposures
of laboratory animals in vivo , or of cells in vitro .
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