Health Effects of Ambient Ultrafine Particles - Aerosols: Measurement, Dosimetry, and Health Effects - page 211

TABLE 8.2
Toxic Effects of Ultraine Particles

Inhalation Exposure Result

High concentration metal or polymer fume
(occupational exposures)

Fever, diffusion impairment, respiratory symptoms

Aggregated ultraines (TiO 2 , carbon black, diesel soot) Epithelial cell proliferation, occlusion of inter-alveolar pores,

impairment of alveolar macrophages, chronic pulmonary
inlammation, pulmonary ibrosis, induction of lung tumors

11 nm CuO at 10 9 /cm 3 60 min (hamsters) [54] Fourfold increase in pulmonary resistance. Particles dispersed

throughout lung (interstitium, alveolar capillaries, pulmonary
lymphatics)

Telon (PTFE) fume (26 nm) 10 6 /cm 3 , 10-30 min [33] Highly inlammatory/mortality

Oxidative stress in lung

TiO 2 1000 μg/m 3 , 7 h [55]

PTFE fumes, whole body inhalation, 1, 2.5, or 5 × 10 5
particles/cm 3 , 18 nm, rat, 15 min, analysis 4 h
postexposure [56]

Increased PMN, mRNA of MnSOD, and MT, IL-1α, IL-1β,
IL-6, MIP-2, TNF-α mRNA of MT and IL-6 expressed around
all airways and interstitial regions; PMN expressed IL-6, MT,
TNF-α; AM and epithelial cells were actively involved

PTFE fumes, whole body inhalation, 1, 2.5, or
5.3 × 10 5 particles/cm 3 , 18 nm, mice, C57BL/6J, 8
weeks and 8 months old, mice 30 min exposure
analysis 6 h following exposure [57]

Increased PMN, lymphocytes, and protein levels in old mice
over young mice; increased TNF-α mRNA in old mice over
young mice; no difference in LDH and β-glucuronidase

CdO fumes, 8 nm, rats and mice, 1-3 h [58] Mice created more metallothionein than rats, which may be

protective of tumor formation

Source: Adapted from U.S. EPA, Air quality for particulate matter, Vols. I, II, III, EPA/600/P-95/001aF, EPA/600/
P-95/001bF, EPA/600/P-95/001cF, 1996.

with very high eficiency in lungs. Additionally, it has been demonstrated that UFPs are more
rapidly transferred to the interstitium than are ine particles of the same composition, and exhibit a
greater accumulation in the regional lymph nodes and a greater retention in the lung [33,34]. Thus,
UFPs may penetrate the epithelium better and they may be less effectively cleared by macrophages,
and the nonphagocytosed particles may penetrate the interstitium in a few hours. Those with low
solubility appear to be signiicantly more inlammatory in the lung than are larger-sized particles of
the same composition [35].
In addition to lung injury, evidence has accumulated that adverse cardiac effects result from
inhalation of PM 2.5, the ine particle fraction of ambient air. In the laboratory, single exposures
of mice to concentrated PM 2.5 were shown to increase the frequency of cardiac arrhythmias in
aged male rats [36]. Long-term exposure demonstrated adverse effects on cardiac function such as
changes in heart rate variability and exacerbation of atherosclerosis in susceptible mice [37]. Most
studies have focused on PM 2.5, but cardiac effects associated with the ultraine fraction have been
demonstrated [38].
The potential for inhaled nanoparticles to become widely distributed in the body was
demonstrated by [39] who reported dose-dependent pulmonary inlammatory responses to
inhaled nickel hydroxide nanoparticles. The particles were approximately 40 nm in diameter and
composed of agglomerates of 5 nm primary particles. Using both short- and long-term inhalation
exposures, they found a clearance half-time of approximately 1 day for the nickel. This rapid
clearance contrasts with that measured for larger nickel-containing particles and may demonstrate
the increased solubility of nanoparticles due to their large surface area. Short-term exposure in
mice has also been shown to induce acute endothelial disruption and alter vasoconstriction and