ABSTRACT
Humans have been exposed to ultrafine particles in the atmosphere for centuries, from combustion as well as natural sources such as sea spray. Since the industrial revolution, the levels of ambient particles have increased significantly, and with the recent expansion of nanotechnology, we are likely to be exposed to manufactured as well as ambient nanoparticles. Organs such as the lungs are obvious targets for exposure to airborne agents via inhalation. The potential for nanoparticles to reach the brain and nervous systems seems, at first glance, to be unlikely, since they have well-developed barriers that are effective against many xenobiotics. However, very small agents and hydrophobic molecules can penetrate these barriers, to gain access to the elaborate networks of functional cells, the neurons and glia, within the nervous systems. Some agents can also take a direct route into the brain, from the olfactory epithelium in the nasal cavity, along the olfactory neurons and into the olfactory bulb. If they can cross synapses, access to distant structures within the brain is then plausible. There is the potential therefore for nanoparticles to access and affect the functions of the neurons within the central nervous system (CNS). Acute toxicity may be unlikely, except in extreme circumstances, but chronic toxicity might occur, and indeed, the etiology of many neurodegenerative diseases is considered to involve interaction between environmental agents, genetic factors, and aging (1). Furthermore, symptoms frequently only manifest themselves
when a large proportion of a particular population of neurons has been lost or is no longer functional; for example, the symptoms of Parkinson’s disease only become apparent when 60 to 80% of dopaminergic neurons in the motor coordination centers of the brain have died. Therefore, chronic exposure to even very low levels of nanoparticles might modulate neuronal function or induce cell death, and lead eventually to neurological problems.
