Document Type

Thesis

Date of Degree Completion

Spring 2007

Degree Name

Bachelor of Science

Department

Biology

Committee Chair

Dr. Carin Thomas

Second Committee Member

Dr. Tom Cottrell

Third Committee Member

Andrew A. Piacsek

Abstract

Studies have shown that car exhaust particles increase cellular oxidative stress (Li, 2002), and people who live in highly polluted areas have shown a higher incidence of cardiovascular disease (Beck, 2005). Recently a theory has been developed that ultrafine particles (< 0.1 µm in diameter) contained in the atmospheric pollution are responsible for initiating the adverse effects of damage and disease (Li, 2003).

Ultrafine particles (UFP), which make up 72% of the particle concentration in the air (Beck, 2005), typically originate from sources involving combustion, such as cars, forest fires, volcanoes and industry (USDHHS, 1995). The small size and abundance of UFPs provide ample surface area with an increased absorption for damaging substances such as iron or reactive organic compounds (Beck, 2005; WHO, 2003). This was confirmed when lung cells exhibited oxidative stress due to an excess of free radicals during exposure to the particles (Oberdorster, 2001). The small size also enables inhaled particles to traverse the lungs and affect other parts of the body such as the cardiovascular system (Li, 2003, Oberdorster, 2001).

UFPs are small enough to cross the mitochondrial membrane (Fig. la) in lung cells while larger particles are collected in large cytoplasmic vacuoles (Fig. 1 b ). Once UFPs pass through the membrane the mitochondrial cristae begin to dissolve (Li, 2003), possibly inhibiting the membrane bound electron transport chain from carrying out energy production and cellular respiration. Despite its importance, the chemistry behind mitochondrial cristae deterioration has not been thoroughly investigated.

Comments

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