In recent years, experimental studies have improved our understanding of the biological effects of atmospheric particles and helped us to explain epidemiologic observations. The deposit of particles in the respiratory system depends essentially on their size: the finest (d < 1 μm) particles can reach the alveolar region and persist in the lungs; the mechanisms of their action in this primary target organ have been elucidated in part. The particles induce oxidative stress that causes an inflammatory response, which may explain the pathophysiologic effects observed, especially the induction or aggravation of respiratory problems in sensitive populations. When, as is often the case, allergens are adsorbed onto the particle surface, patients with asthma may respond at lower levels of exposure to the allergens to which they are sensitized. Uncertainties, nonetheless, remain about the physicochemical properties responsible for these effects, in particular the respective roles of organic compounds, metals, surface reactivity, and particle size in the biological response. The still partial experimental data about these particles' systemic effects, especially cardiovascular, do not clarify either how they cross various barriers or the mechanisms by which they use inflammatory mediators generated in the lungs to exert more distant effects. The most recent studies stress the biological role of ultrafine (d < 0.1 μm) particles that can easily cross the epithelial barrier.
|Translated title of the contribution||Health impact of atmospheric particles: Toxicological aspects|
|Number of pages||11|
|Publication status||Published - 2005|
ASJC Scopus subject areas
- Atmospheric Science