Chemical reactivities of ambient air samples in three Southern California communities

Abstract

The potential adverse health effects of PM2.5 and vapor samples from three communities that neighbor railyards, Commerce (CM), Long Beach (LB), and San Bernardino (SB), were assessed by determination of chemical reactivities attributed to the induction of oxidative stress by air pollutants. The assays used were dithiothreitol (DTT) and dihydrobenzoic acid (DHBA) based procedures for prooxidant content and a glyceraldehyde-3-phosphate dehydrogenase (GAPDH) assay for electrophiles. Prooxidants and electrophiles have been proposed as the reactive chemical species responsible for the induction of oxidative stress by air pollution mixtures. The PM2.5 samples from CM and LB sites showed seasonal differences in reactivities with higher levels in the winter whereas the SB sample differences were reversed. The reactivities in the vapor samples were all very similar, except for the summer SB samples, which contained higher levels of both prooxidants and electrophiles. The results suggest the observed reactivities reflect general geographical differences rather than direct effects of the railyards. Distributional differences in reactivities were also observed with PM2.5 fractions containing most of the prooxidants (74–81%) and the vapor phase most of the electrophiles (82–96%). The high levels of the vapor phase electrophiles and their potential for adverse biological effects point out the importance of the vapor phase in assessing the potential health effects of ambient air.

Chemical speciation, including polycyclic aromatic hydrocarbons (PAHs), and toxicity of particles emitted from meat cooking operations

“…The prooxidant content of the gas-phase samples was lower than that for the particlephase samples. This finding is in agreement with a previous study conducted on ambient air samples (Eiguren-Fernandez et al, 2015). The results reported here suggest that charbroiled cooking aerosols contain more redox-active constituents in the particle-phase than the gasphase of cooking emissions.…”

A Chemical Perspective of Pharmacology and Toxicology

“…We analyzed PM samples from three communities in the LA Basin: commerce in the midtown LA area; Long Beach, near the Port of LA; and San Bernardino in the eastern end of the LA Basin (approximately 60 miles east of LA) (68). Not surprisingly, San Bernardino had the highest levels of prooxidants and electrophiles, reflecting the increases in photochemical and atmospheric chemical transformations that convert aromatic hydrocarbons to quinones with the easterly movement of the air mass, an observation that we had made with phenanthrene, whose quinone concentration increased as the air mass moved from the western end of the LA Basin to the east (69).…”

In vitro Evaluation of Oxidative Stress Caused by Fine Particles (PM2.5) Exhausted from Heavy-Duty Vehicles Using Diesel/Biodiesel Blends under Real World Conditions

“…Oxidative stress is generally mediated by reactive oxygen species (ROS), such as hydroxyl radical (OH), hydrogen peroxide (HOOH), superoxide (O 2 -), organic hydroperoxides and other organic radical species. 1,6,16,[25][26][27][28] Although the actual mechanisms of how ROS damage cells are unknown, it is believed they trigger multiple biological signaling, which result in inflammation and other cellular distresses. 6,29,30 ROS may either be primarily transported on particles and/or be catalytically generated by other particle components through redox chemistry producing healthrelated issues.…”

“…Inhalation of diesel-emitted particles, mainly in the fine particulate fraction, is a matter of significant concern [1][2][3] since both environmental and occupational exposures to diesel exhaust particles (DEP) are considerable 1,2 and may lead to diverse health-related endpoints, such as cancer and pulmonary or respiratory disorders, [2][3][4][5][6][7] as well as morbidity and mortality. 8,9 When also considering premature deaths according to inhalation of fine particles in outdoor environments, there were 3.3 million deaths worldwide in 2010 and it is estimated to be more than 6.5 million premature deaths by 2050.…”

“…24,25 For instance, some transition metals (such as Fe and Cu) and organic species (e.g. polycyclic aromatic compounds and quinones or quinone-like compounds) as well as humic-like substances (HULIS), black and brown carbon (BC and BrC) within PM are known to increase the production of ROS either in vitro or in vivo, especially if they are present in fine and ultrafine size range, [4][5][6]24,[30][31][32][33][34][35] since they are able to go more profoundly in the respiratory system. Meanwhile, considering diesel/biodiesel blends exhausts are substantially composed by ever small size PM, such as nanoparticles and/or ultrafine particles rich in semi-volatile organic compounds and trace metals, 1,7,16 it is likely ROS may be contributing to the adverse health effects caused by DEP or even BEP.…”