Environmental Engineering Reference
In-Depth Information
vasorelaxation [40]. In long-term studies of nano-nickel hydroxide exposure, the research group
demonstrated the upregulation of genes associated with oxidative stress in heart tissue. Their work
suggests that at levels that are at least occupationally, if not environmentally, relevant, chronic
exposure to inhaled nano-NH signiicantly exacerbates atherosclerosis [41].
It is unlikely that all components of PM are equally toxic. Cohen et al. [11] reported that
candidates for especially active components of ambient PM are H + , ultraine number, and soluble
transition metals. While all three have some supporting toxicological evidence consistent with
known mechanisms of toxicity, only H + and UFPs have produced effects at exposure levels that
could occur in ambient air [2]. Perhaps the most likely candidate is a hybrid of H + and UFPs, that
is, acid-coated UFPs.
Chen et al. [42] exposed guinea pigs to varying amounts of sulfuric acid layered onto 10 8 ultra-
ine (90 nm) carbon core particles cm -3 , and to a constant (300 μg m -3 ) concentration of acid layered
onto 10 6 , 10 7 , or 10 8 particles cm -3 . Indicators of irritant potency on macrophages harvested from
the lungs of exposed animals clearly showed an increased response to a constant dose of acid when
it was divided into an increased number of particles, as well as a response to an increased dose of
acid at a constant number concentration. Oberdörster et al. [43] reported that nonreactive UFPs do
not appear to cause inlammation in young healthy rats.
Evidence, some of which was noted earlier, supports the hypothesis that the number of UFPs
that deposit per unit surface of the epithelial lining of the human respiratory system is an important
determining factor affecting lung injury [28,31,42,44-49], and that the resulting alveolar inlam-
mation is able to provoke attacks of acute respiratory illness in susceptible individuals [30]. In
particular, the work of Peters et al. [47] and Wichmann et al. [50] suggest that at ambient levels, the
number concentration of inhaled particles may be a signiicantly more important determinant of the
risk than inhaled mass measures. Very recent evidence has also shown that UFPs are associated
with human mortality [50].
8.6  EPIDEMIOLOGICAL STUDIES
Epidemiological research has determined that ambient ine particles (PM < 2.5 μm) are responsible
for much of the cardiac mortality and also for the lung cancer excess seen in the U.S. population
[51] but less evidence is available related to the risk from ambient UFPs (PM < 0.1 μm).
Although long-term animal exposures with concentrated ambient particles in this size range
demonstrate adverse effects on pulmonary and cardiac function, and toxicology has documented
potential mechanisms for cardiac and vascular damage, the risk to people from ambient UFPs is
still unclear.
A recent epidemiological study of the effects of ultraine ambient particles on cardiac function in
cyclists has demonstrated changes in heart rate variability [52].
A European “expert elicitation,” convened to quantitatively examine available data relating
concentration of ambient UFPs to human health, reported the “estimated percentage decrease in
all-cause mortality with a permanent 1000 particles/cm 3 decrease in UFP concentration ranged
between 0.1% and 1.2%, with a median of 0.30 However, there were substantial uncertainties [53].
The report suggests that although it is very unlikely that there is no effect, there is as yet insuficient
evidence to exclude the possibility.
8.7  SUMMARY
UFPs constitute the largest share of particles in the atmosphere by both number and surface
area. These particles, which are formed by condensation reactions of precursor atmospheric
gases and by nucleation of gas-phase species, range in size from approximately 1 to 150 nm.
Studies indicate that they are composed, in large part, of organic and elemental carbon, together
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