Oxidative stress and systemic inflammation as modifiers of cardiac autonomic responses to particulate air pollution

Abstract

Background The role of oxidative stress and systemic inflammation on the association between personal exposures to ambient fine particulate matter ≤ 2.5 μm in diameter (PM2.5) and cardiac autonomic dysfunction, indicated by reduction in heart rate variability (HRV), has not been examined. Methods We performed a repeated measures study on community adults in a densely populated inner city neighborhood in Boston, Massachusetts. Continuous ambulatory electrocardiogram (ECG) monitoring and personal exposure to PM2.5 were measured for up to two consecutive days. Peripheral blood and spot urine samples were collected at 12-hour intervals for the measurements of markers of inflammation including C-reactive protein (CRP), fibrinogen, white blood cell (WBC) and platelet counts as well as for the analysis of urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG), a marker of oxidative DNA damage. Results After adjusting for confounders, we found a pronounced decrease in nighttime standard deviation of normal-to normal intervals (SDNN): an interquartile range (IQR) increase in PM2.5 (13.6 μg/m3) was associated with an 8.4% decrease in SDNN (95% CI: −11.3 to −5.5). Compared with the lower eightieth percentile, significantly greater PM2.5 associated nighttime SDNN reductions were observed among subjects in the upper twentieth percentile of 8-OHdG by −25.3%, CRP by −24.9%, fibrinogen by −28.7%, WBC by −23.4%, and platelet counts by −24.0% (all P < 0.0001; all Pinteraction <0.01). Conclusions These data suggest that oxidative stress and systemic inflammation exacerbate the adverse effects of PM2.5 on the cardiac autonomic function even at ambient levels of exposure.

Amelioration of particulate matter-induced oxidative damage by vitamin c and quercetin in human bronchial epithelial cells

“…Our results also indicated that PM 2.5 exposure may stimulate the inflammation-associated cytokine activation to trigger inflammatory damage. Similarly, numerous studies have revealed that acute pro-inflammatory cytokines had been associated with cell damage-caused by PM 2.5 (Corsini et al, 2013;Lee et al, 2014). In our previous study, we have observed exposure to Taiyuan winter PM 2.5 also induced the cellular oxidative heart damage, and uncovered filter-derived quartz debris did not cause bias in our experimental outcomes (Li et al, 2015).…”

Particulate Matter Exposure and Stress Hormone Levels

“…These biomarkers reflect DNA oxidative damage (8-hydroxy-2-deoxyguansine), lipid peroxidation (malondialdehyde and iso-prostaglandin F2α), or antioxidant potential (superoxide dismutase), which have been examined extensively in previous studies on PM 2.5 . 5,[22][23][24][25][26] In addition, we measured 6 serum biomarkers of systemic inflammation (soluble CD40 ligand, high-sensitivity C-reactive protein, interleukin-1β, interleukin-6, tumor necrosis factor-α, and intercellular adhesion molecule-1) and 3 hormones (insulin, corticotropin-releasing hormone [CRH], and adrenocorticotropic hormone [ACTH]). We then calculated homeostatic model assessment of insulin resistance as an indicator of insulin resistance using the following formula: homeostatic model assessment of insulin resistance=fasting glucose (mg/ dL)×insulin (mU/L)/405.…”

Mitochondrial damage: An important mechanism of ambient PM2.5 exposure-induced acute heart injury in rats

“…These ultra-structural damage results implied that PM 2.5 exposure induced strong structural mitochondrial changes, subsequently having influences upon the function of gas exchange and lead to mitochondrial damage. As is reported in the literatures, the mitochondrial number increase may be to enhance cardiac mitochondrial energy production [30], 13 whereas swelling, cristae disorder and mitochondrial vacuolation account for the pathological changes of heart mitochondria [20]. Besides, Marchini et al (2013) reported that an acute PM exposure could produce significant mitochondrial dysfunction accompanied by the decreased cardiac oxygen consumption, succinate dehydrogenase activity and mitochondrial membrane potential as well as impaired oxidative phosphorylation [31].…”

“…Importantly, it is observed that oxidative stress, calcium homeostasis imbalance and inflammation have close relationships with dysfunctional mitochondria in a wide range of heart diseases [12,13,44]. First, the mitochondrion is a major source of ROS production.…”

“…Additionally, increasing evidences indicate that the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), oxidative stress, calcium homeostasis imbalance and inflammatory responses are involved in PM-related cardiovascular disease [12][13]. However, there has been only limited data on the detailed mechanisms of PM 2.5 -induced heart acute injury associated with mitochondrial fusion/fission balance, oxidative stress and inflammation so far.…”