Personal P[M.Sub.2.5] Exposure and Markers of Oxidative Stress in Blood. (Research)

Article excerpt

Ambient particulate air pollution assessed as outdoor concentrations of particulate matter [less than or equal to] 2.5 [micro]m in diameter (P[M.sub.2.5]) in urban background has been associated with cardiovascular diseases at the population level. However, the significance of individual exposure and the involved mechanisms remain uncertain. We measured personal P[M.sub.2.5] and carbon black exposure in 50 students four times in 1 year and analyzed blood samples for markers of protein and lipid oxidation, for red blood cell (RBC) and platelet counts, and for concentrations of hemoglobin and fibrinogen. We analyzed protein oxidation in terms of [gamma]-glutamyl semialdehyde in hemoglobin (HBGGS) and 2-aminoadipic semialdehyde in hemoglobin (HBAAS) and plasma proteins (PLAAS), and lipid peroxidation was measured as malondialdehyde (MDA) in plasma. Median exposures were 16.1 [micro]g/[m.sup.3] for personal P[M.sub.2.5] exposure, 9.2 lag/[m.sup.3] for background P[M.sub.2.5] concentration, and 8.1 x [10.sup.-6]/m for personal carbon black exposure. Personal carbon black exposure and PLAAS concentration were positively associated (p < 0.01), whereas an association between personal P[M.sub.2.5] exposure and PLAAS was only of borderline significance (p = 0.061). A 3.7% increase in MDA concentrations per 10 [micro]g/[m.sup.3] increase in personal P[M.sub.2.5] exposure was found for women (p < 0.05), whereas there was no significant relationship for the men. Similarly, positive associations between personal P[M.sub.2.5] exposure and both RBC and hemoglobin concentrations were found only in women (p < 0.01). There were no significant relationships between background P[M.sub.2.5] concentration and any of the biomarkers. This suggests that exposure to particles in moderate concentrations can induce oxidative stress and increase RBCs in peripheral blood. Personal exposure appears more closely related to these biomarkers potentially related to cardiovascular disease than is ambient P[M.sub.2.5] background concentrations. Key words: carbon black, fibrinogen, hemoglobin, lipid peroxidation, particulate matter, platelets, protein oxidation, red blood cells. Environ Health Perspect 111:161-165 (2003). [Online 31 October 2002] doi:10.1289/ehp.5646 available via


Epidemiologic studies have shown that particulate air pollution in the urban environment is associated with an increased risk in human mortality and morbidity, especially that caused by cardiopulmonary diseases (Dockery et al. 1993; Peters et al. 2001; Pope et al. 2002). One of the proposed mechanisms is increased oxidative stress. This is assumed to be mediated partly by particle-induced inflammation in the lungs, causing macrophages to release reactive oxygen species (ROS), and partly by transition metals on the particle surface capable of generating ROS through the Fenton reaction (Donaldson et al. 1997; Li et al. 1997). The atherosclerotic process is thought to involve oxidation of low-density lipids, and a recent intervention study has shown that progression of arteriosclerosis can be reduced in heavily smoking men by supplementing with a combination of antioxidant vitamins C and E (Salonen et al. 2000). Long-term exposure to particles could thus possibly increase the risk of developing atherosclerotic plaques through increased oxidation of low-density lipids. Other possible mechanisms are short-term effects such as increased blood viscosity due to lung inflammation (Peters et al. 1997) or a direct effect of inhaled particles on the concentration of several hematologic parameters such as platelets and red blood cells (RBCs) (Salvi et al. 1999; Seaton et al. 1999). There is increasing evidence that abnormalities in blood rheology are related to various cardiovascular diseases (Koenig and Ernst 1992). A large epidemiologic study found blood viscosity to predict cardiovascular events as efficiently as low-density lipoproteins (LDL), cholesterol, and blood pressure (Lowe et al. …