Authors / Editors:
Health and Safety
Seaton et al (1995), described targeting UFP, diameter <.1 µm, as having the ability to create alveolar inflammation, exacerbate lung disease and increase blood coagulability (Seaton et al., 1995). Overall, these particles contribute very little to the total mass of PM, but they contribute to high number concentrations. Because of their small size, UFPs are able to penetrate and deposit via Brownian diffusion into the small airways (i.e. alveolar regions), and accumulate and under high exposure conditions potentially accumulate to high delivered concentrations. In addition, UFPs have the ability to cross the alveolar membranes, and directly influence the cardiovascular system, blood components, and lung receptor vitality (Nemmer et al., 2002). UFPs along with soluble constituents of PM2.5 (e.g. transition metals) may result in increased oxidation and inflammatory mechanisms within the lung and/or throughout the peripheral and systemic circulation. Because of their high surface area and numbers, there is additional evidence of the effects of UFP on changes in autonomic tone, which could contribute to vascular plaque instability leading to an increased risk of arrhythmias (Brooke et al., 2004).
Elevated exposures to UFP can result in damage to the alveoli resulting from chronic alveolar inflammation leading to decreased lung function, one of the major factors behind the development of adolescent non-atopic asthma. This condition is typically irreversible (Gauderman et al., 2004). Elderly and COPD patients are at a high risk for coronary heart disease (ischemia-decreased blood flow to the heart) and hypertension during episodes of elevated PM (Pope, 1999). Because PM exposure can trigger changes in pulmonary endothelial cells, (e.g. decreased endothelin-derived relaxation factor, such as nitric oxide (NO)), arterial constriction can occur through platelet aggregation and adhesion.