Particles in our environment
Since several decades, it is known that smoke and dust from industry or traffic constitutes health risks to the affected population. Particularly, an increased risk to develop lung cancer exists for dust-burdened people. By technical improvements, the more coarse dust fractions (> PM10, PM10) were efficiently reduced and this concerns particles which reach only the upper bronchial tubes. By contrast, the size fraction that can reach the small airways and alveoli (fine particles: PM2.5, ultra fine particles: PM0.1, and nanoparticles) displays a minor reduction. The concentration of ultra fine particles rather increased in the inhaled air because they are now less efficiently scavenged by larger particles.
In addition to the well-known soot particles (range about 20 to 150 nm), a new class of nanoparticles with extremely small diameters between 2 and 6 nm and with a different chemical composition was detected only recently (see below). Definitely, these particles play a role in flames as soot precursors and, under conditions of incomplete conversion, they may be emitted together with soot. At present it is not clear whether these particles obey conventional laws of aerosol dynamics. In this case they would be scavenged by larger particles, especially soot. There are, however, experimental findings suggesting a nanoparticle lifetime sufficient for their release into the atmosphere. In fact, they were discovered as immissions in early rain fractions.
Inhaled particles from the environment increase the risk for humans to develop respiratory or cardiovascular diseases. A large number of studies has correlated acute airway symptoms in a susceptible person subgroup (asthma, allergy patients, very young and old people) and an increased mortality with increased concentrations of airborne particles in ambient air. E.g. the improvement of the air quality in the 1990s resulted in a decrease in the prevalence of non-allergic infectious diseases, but in an increase in the prevalence of asthma, bronchial hyperactivity, hay fever and specific sensibilisation against aeroallergens. On the basis of epidemiologic studies, there is little doubt that a higher particle concentration in the inhaled air is related to an increased incidence of respiratory and cardiovascular diseases (atherosclerosis, ventricular arrhythmias, sudden death, myocardial infarction and stroke). The mechanisms of these particle effects are largely unknown; several studies have shown changes in the systolic blood pressure, the heart rate, the plasma viscosity, the fibrinogen concentration and the amount of C-reactive protein, an acute phase protein, depending on the particle concentration. A possible influence of the particles on the autonomous control of the heart becomes apparent by the modified heart rate variability and the heart rate under particle exposition. Strong air pollution such as in Mexico City is proposed as risk factor for neurological diseases (Alzheimer, Parkinson). Extrapolated to the total population, diseases initiated by particulate air pollution produce a huge economic damage. The results of long lasting environmental-epidemiologic research are even more remarkable at first sight, as the air in many large cities is perceived much cleaner than some decades ago. In the face of these facts, the ultra fine aerosol particles, mostly emitted by motor vehicles, represent an up-to-date field of research.
Health hazards by nanoparticles
Several research results suggest that the emission of ultra fine particles increases if the mass emission of soot is reduced. Concomitantly, an inverse dependency of health effects on particle size has been shown. In the context of this workshop, nanoparticles are clusters with typical particle diameters of 2 to 6 nm and a mass of about 1000 to 20000 atomic mass units, generated during combustion processes. They are emitted in flame and motor exhaust together with soot and can reach mass flow rates comparable to those of soot, but their particle numbers are several magnitudes higher due to their smaller volume. About ninety percent of the exhaust particles of combustion engines have been classified as nanoparticles under certain combustion conditions.
The potential for health hazards by nanoparticles is in their composition and in their high number concentration, their water solubility and their very small size. This allows nanoparticles to be incorporated by unspecific mechanisms in addition to the conventional alveoli pathway. They may be transported through the whole body and may thus affect the cardiovascular function, a mechanism which could endorse the results of epidemiologic studies.
Recent investigations in rats have shown that nanoparticles can advance, possibly via the olfactory nerve and/or the blood circulation, in the brain and cause inflammation or degeneration. The nanoparticles consist of polycyclic aromatic hydrocarbons (PAHs) in very open structures. Consequently, on a mass basis they show a larger surface and a higher oxidative capacity than larger particles. Nanoparticles can be carcinogenic and mutagenic due to their toxic ingredients. In present-day legislation, limit values for the particle output directly at the exhaust pipe (emission) or for the particle concentration in the atmosphere (immission) are based on the mass rendering nanoparticles virtually meaningless. In the meantime, there is increasing evidence that health effects are more related to number concentrations of particles or to their surfaces rather than to the particle mass.
On cellular and molecular level, the mode of action of the particles is under investigation. The increase of the oxidative stress in the cell is discussed as a mechanism of action, which can in turn result in the release of inflammatory mediators (e.g. IL-8). These mediators can stimulate inflammatory processes in many organs (lung, heart, brain, vascular endothelium). A latent systemic inflammation can be associated with changes in the coagulation factors and could be responsible, besides atherosclerotic vascular changes, for an increased occurrence of myocardial infarction and strokes. Degeneration, e.g. neurodegeneration, is considered as late sequelae of the inflammatory processes.
Since the toxicity of these particles remains unexplained and since technical devices for their reduction are not investigated as well, a concerted action of toxicologists, molecular biologists, combustion engineers and measurement engineers is required to minimize possible health effects for humans and animals. Especially the enlightenment of the molecular mechanisms of the toxic effects of nanoparticles could allow a realistic assessment of the nanoparticle toxicity.