Human Toxicology and Effects of Nanoparticles - Environmental and Human Health Impacts of Nanotechnology - page 355

Understanding hazard Understanding exposure
Understanding risk

Manage hazard Manage exposure

Manage risk

Maximise potential of nanotechnology
with minimum risk

Figure 9.3 Understanding hazard and exposure allows risk to be understood, which in turn
allows hazard, exposure and therefore risk to be managed. If risk can be managed then the
new technologies and industries using nanoparticles can reach their full potential with
minimum risk.

9.2 Ultrafi ne Particle Toxicology

9.2.1 Air Pollution

In the mid 1990s evidence accumulated to support the suggestion that ambient
air particulate pollution was associated with increased ill health and deaths due
to both respiratory and cardiovascular diseases (Dockery et al. , 1993 ; Schwartz,
1994). Ambient air particulate pollution is monitored in many cities around
the world as PM 10 (approximately defi ned as particles collected through a fi lter
collecting 10 µ m diameter particles with an effi ciency of 50%) and consists of par-

ticles of 10 m represents the largest

particles that can be inhaled into the human respiratory system. These particles
include carbonaceous particles (contaminated with metals and organic material),
coarse wind blown dust and soluble secondary particles made by photochemical
reactions as well as organic particles such as pollen (Donaldson et al. , 2003 ) (for a
more detailed description of the composition of PM 10 see Chapter 5). In fact, in
towns and cities a large majority of the particles in PM 10 are carbonaceous particles
derived from traffi c and other combustion processes; these particles are below
100 nm in diameter and in the past have been termed ultrafi ne particles (Stone et
al. , 2000a ; Donaldson et al. , 2005 ). Seaton et al. (1995) published the ' Ultrafi ne
hypothesis' in the Lancet. This paper suggested that it was the ultrafi ne particles
in PM 10 which are responsible for driving the adverse cardiovascular health effects
caused by this pollutant. This hypothesis was based upon the observations by
Oberdorster's group that ultrafi ne TiO 2 induced a greater infl ammatory response
in the rat lung than larger respirable TiO 2 particles (Ferin et al. , 1990 ; Oberdoerster
et al. , 1990 ). Seaton et al. , (1995) therefore hypothesised that the ultrafi ne particles
in PM 10 induce an infl ammatory response, that in susceptible individuals led to an
exacerbation of their pre-existing cardiovascular disease symptoms, generating an
increase in hospital admissions and deaths.

µ m diameter and smaller. The fi gure of 10 µ