Comparison of trace elements in size-fractionated particles in two communities with contrasting socioeconomic status in Houston, TX.

Levels of ambient air pollutants, including particulate matter (PM), are often higher in low-socioeconomic status (SES) communities than in high-SES communities. Houston is the fourth largest city in the USA and is home to a large petrochemical industry, an active port, and congested roadways, which represent significant emission sources of air pollution in the region. To compare levels of air pollution between a low-SES and a high-SES community, we simultaneously collected a 7-day integrated size-fractionated PM between June 2013 and November 2013. We analyzed PM mass and elements for three particle size modes: quasi-ultrafine particles (quasi-UFP) (aerodynamic diameter <0.25 µm), accumulation mode particles (0.25-2.5 µm), and coarse mode particles (>2.5 µm). Concentrations of vanadium, nickel, manganese, and iron in the quasi-UFP mode were significantly higher in the low-SES community than in the high-SES community. In the accumulation and coarse modes, concentrations of crustal elements and barium were also significantly higher in the low-SES community compared to the high-SES community. These findings suggest that people living in the low-SES community may experience higher exposures to some toxic elements as compared to people in the high-SES community.

Metal enriched quasi-ultrafine particles from stainless steel gas metal arc welding induced genetic and epigenetic alterations in BEAS-2B cells.

Recent evidence has supported welding fume (WF)-derived ultrafine particles (UFP) could be the driving force of their adverse health effects. However, UFP have not yet been extensively studied and are currently not included in present air quality standards/guidelines. Here, attention was focused on the underlying genetic and epigenetic mechanisms by which the quasi-UFP (Q-UFP, i.e., ≤ 0.25 µm) of the WF emitted by gas metal arc welding-stainless steel (GMAW-SS) exert their toxicity in human bronchial epithelial BEAS-2B cells. The Q-UFP under study showed a monomodal size distribution in number centered on 104.4 ± 52.3 nm and a zeta potential of -13.8 ± 0.3 mV. They were enriched in Fe > Cr > Mn > Si, and displayed a relatively high intrinsic oxidative potential. Dose-dependent activation of nuclear factor erythroid 2-related factor 2 and nuclear factor-kappa B signaling pathway, glutathione alteration, and DNA, protein and lipid oxidative damage were reported in BEAS-2B cells acutely (1.5 and 9 µg/cm2, 24 h) or repeatedly (0.25 and 1.5 µg/cm2, 3 × 24 h) exposed to Q-UFP (p < 0.05). Alterations of the Histone H3 acetylation were reported for any exposure (p < 0.05). Differentially regulated miRNA and mRNA indicated the activation of some critical cell signaling pathways related to oxidative stress, inflammation, and cell cycle deregulation towards apoptosis. Taken together, these results highlighted the urgent need to better evaluate the respective toxicity of the different metals and to include the Q-UFP fraction of WF in current air quality standards/guidelines relevant to the occupational settings.

Quasi-ultrafine particles promote cell metastasis via HMGB1-mediated cancer cell adhesion.

With increasingly severe air pollution, the aggravated health risks of particulate matter, especially ultrafine particles, are emerging as an urgent and sensitive topic. Considering the heterogeneity and complexity of ultrafine particles, there is insufficient evidence about their toxic effects and possible molecular mechanisms. To address this question, we analyzed the emission characteristics of quasi-ultrafine particles collected during winter in a typical coal-burning city, Taiyuan, and confirmed their contribution to lung cancer cell adhesion and metastasis. For the specific mechanism, we revealed that the endocytosis of quasi-ultrafine particles stimulated the release of HMGB1, induced NFκB-facilitated proinflammatory cytokine production through the interaction of HMGB1 with RAGE, and resulted in cancer-endothelial cell adhesion. These findings remind us of the potential effects of anthropogenic quasi-ultrafine particle pollution and provide a theoretical reference for the mitigation of tumorigenesis in a severe particulate matter contaminated environment.

Toxicity of fine and quasi-ultrafine particles: Focus on the effects of organic extractable and non-extractable matter fractions.

To date no study has been able to clearly attribute the observed toxicological effects of atmospheric particles (PM) to a specific class of components. The toxicity of both the organic extractable matter (OEM2.5-0.3) and non-extractable matter (NEM2.5-0.3) of fine particles (PM2.5-0.3) was compared to that of PM2.5-0.3 in its entirety on normal human epithelial bronchial BEAS-2B cells in culture. The specific effect of the quasi-ultrafine fraction (PM0.3) was assessed, by comparing the responses of cells exposed to the PM2.5-0.3 and PM0.3 organic extractable matter, OEM2.5-0.3 and OEM0.3 respectively. Chemically, PAH, O-PAH, and N-PAH were respectively 43, 17, and 4 times more concentrated in PM0.3 than in PM2.5-0.3, suggesting thereby a predominant influence of anthropogenic activities and combustion sources. BEAS-2B cells exposed to PM2.5-0.3, NEM2.5-0.3, EOM2.5-0.3 and OEM0.3 lead to different profiles of expression of selected genes and proteins involved in the metabolic activation of PAH, O-PAH, and N-PAH, and in the genotoxicity pathways. Specifically, OEM0.3 was the most inducer for phase I and phase II enzymes implicated in the metabolic activation of PAH (AHR, AHRR, ARNT, CYP1A1, CYP1B1, EPHX-1, GSTA-4) thereby producing the highest DNA damage, felt by ATR and, thereafter, a cascade of protein phosphorylation (CHK1/CHK2/MDM2) closely related to the cell cycle arrest (P21 and P53 induction). This study underlined the crucial role played by the organic chemicals present in PM0.3. These results should be considered in any future study looking for the main chemical determinants responsible for the toxicity of ambient fine PM.

Mitochondrial alterations triggered by repeated exposure to fine (PM2.5-0.18) and quasi-ultrafine (PM0.18) fractions of ambient particulate matter.

Nowadays ambient particulate matter (PM) levels still regularly exceed the guideline values established by World Health Organization in most urban areas. Numerous experimental studies have already demonstrated the airway toxicity of the fine fraction of PM (FP), mainly triggered by oxidative stress-induced airway inflammation. However, only few studies have actually paid close attention to the ultrafine fraction of PM (UFP), which is likely to be more easily internalized in cells and more biologically reactive. Mitochondria are major endogenous sources of reactive oxygen species (ROS) through oxidative metabolism, and coordinate many critical cellular signaling processes. Mitochondria have been often studied in the context of PM toxicity and generally associated with apoptosis activation. However, little is known about the underlying adaptation mechanisms that could occur following exposure at sub-apoptotic doses of ambient PM. Here, normal human bronchial epithelial BEAS-2B cells were acutely or repeatedly exposed to relatively low doses (5 µg.cm-2) of FP (PM2.5-0.18) or quasi-UFP (Q-UFP; PM0.18) to better access the critical changes in mitochondrial morphology, functions, and dynamics. No significant cytotoxicity nor increase of apoptotic events were reported for any exposure. Mitochondrial membrane potential (ΔΨm) and intracellular ATP content were also not significantly impaired. After cell exposure to sub-apoptotic doses of FP and notably Q-UFP, oxidative phosphorylation was increased as well as mitochondrial mass, resulting in increased production of mitochondrial superoxide anion. Given this oxidative boost, the NRF2-ARE signaling pathway was significantly activated. However, mitochondrial dynamic alterations in favor of accentuated fission process were observed, in particular after Q-UFP vs FP, and repeated vs acute exposure. Taken together, these results supported mitochondrial quality control and metabolism dysfunction as an early lung underlying mechanism of toxicity, thereby leading to accumulation of defective mitochondria and enhanced endogenous ROS generation. Therefore, these features might play a key role in maintaining PM-induced oxidative stress and inflammation within lung cells, which could dramatically contribute to the exacerbation of inflammatory chronic lung diseases. The prospective findings of this work could also offer new insights into the physiopathology of lung toxicity, arguably initiate and/or exacerbate by acutely and rather repeated exposure to ambient FP and mostly Q-UFP.

Micronucleus Frequency in Exfoliated Buccal Cells of Children Living in an Industrialized Area of Apulia (Italy).

Micronuclei (MN) are biomarkers of early biological effect often used for detecting DNA damage in human population exposed to genotoxic agents. The aim of this study was to evaluate the frequency of MN in exfoliated buccal cells of children living in an industrialized (impacted) area compared with that found in children living in a control area without significant anthropogenic impacts. A total of 462 6-8-year-old children (206 in the impacted area, 256 in the control area) attending primary school were enrolled. A questionnaire was administered to the parents of the recruited children to obtain information about personal data, lifestyles, and food habits of their children. Atmospheric particulate fractions were collected near the involved schools to assess the level of environmental exposure of the children. The presence of MN was highlighted in 68.4% of children living in the impacted area with a mean MN frequency of 0.66‱ ± 0.61‱. MN positivity and frequency were significantly lower in the control area (37.1% and 0.27‱ ± 0.43‱, respectively). The frequency of MN was positively associated with quasi-ultrafine particulate matter (PM0.5), traffic near the home, and consuming barbecued food; while adherence to the Mediterranean diet and practicing sport were negatively associated.

Toxicological appraisal of the chemical fractions of ambient fine (PM2.5-0.3) and quasi-ultrafine (PM0.3) particles in human bronchial epithelial BEAS-2B cells.

New toxicological research is still urgently needed to improve the current knowledge about the induction of some underlying mechanisms of toxicity by the different chemical fractions of ambient particulate matter (PM). This in vitro study sought also to better evaluate and compare the respective toxicities of fine particles (PM2.5-0.3) and their inorganic and organic chemical fractions, and the respective toxicities of the organic chemical fractions of PM2.5-0.3 and quasi-ultrafine particles (PM0.3). Human bronchial epithelial BEAS-2B cells were also exposed for 6-48 h to relatively low doses of PM2.5-0.3 and their organic extractable (OEM2.5-0.3) and non-extractable (NEM2.5-0.3) fractions, and the organic extractable fraction (OEM0.3) of PM0.3. We reported that not only PM2.5-0.3, but also, to a lesser extent, its inorganic chemical fraction, NEM2.5-0.3, and organic chemical fraction, OEM2.5-0.3, were able to significantly induce ROS overproduction and oxidative damage notwithstanding the early activation of NRF2 signaling pathway. Moreover, for any exposure, inflammatory and apoptotic events were noticed. Similar results were observed in BEAS-2B cells exposed to OEM0.3, rich of polycyclic aromatic hydrocarbons and their nitrated and oxygenated derivatives. In BEAS-2B cells exposed for 24 and 48 h to OEM2.5-0.3 and OEM0.3, to a higher extent, there was an alteration of the levels of some critical proteins even though crucial for the autophagy rather than a real reduction of autophagy. It is noteworthy that the toxicological effects were equal or mostly higher in BEAS-2B cells exposed for 6 and/or 24 h to PM2.5-0.3 from those exposed to NEM2.5-0.3 or OEM2.5-0.3, and in BEAS-2B cells exposed for 6 and/or mostly 24 h to OEM0.3 from those exposed to OEM2.5-0.3. Taken together, these results revealed the higher potentials for toxicity, closely linked to their respective physical and chemical characteristics, of PM2.5-0.3 vs NEM2.5-0.3 and/or OEM2.5-0.3, and OEM0.3 vs OEM2.5-0.3.

Indoor-outdoor association of particulate matter and bounded elemental composition within coarse, quasi-accumulation and quasi-ultrafine ranges in residential areas of northern India.

Attempts have been made to comprehend size distribution pattern of Particulate Matter (PM) and associated elemental concentration within coarse (2.5-10µm), quasi-accumulation (q-Acc) (0.25-2.5µm) and quasi-ultrafine (q-UF) (<0.25µm) ranges at indoors and outdoors of residential homes of Agra. Overall, the average mass concentrations of PM10 and PM2.5 in indoors were found to be 263.24±59.24 and 212.01±38.06µgm-3 while in outdoors the concentrations accounted to 194.28±15.25 and 152.88±16.31µgm-3 respectively; exceeding WHO standards. In view of geographical variation, significantly higher (t=2.461; P=0.044) PM mass was found in outdoor samples of roadside location when compared to homes located far away from busy traffic; whereas indoor concentration exhibited non-significant relationship (t=1.887; P=0.095) between the two categorized homes. Findings of size partitioning trend through deployment of Sioutas Cascade Impactor evidenced presence of high proportion of PM and elemental concentrations within q-Acc and q-UF modes with their distribution pattern and probable emission sources conferred upon. Absence of modal peak in coarse range indicated predominance of anthropogenic emissions with presumed wash-out of coarse particles during frequent precipitation coincidental with sampling event. Seeming modal shifts for some elements (K, Cd, Zn) from q-Acc to q-UF were perceived during infiltration process. Presence of high traffic emission in homes near busy road stemmed the shifting of particles (Cu, K, Co, Zn) towards finer size (preferably q-UF mode) thus exposing residents to adverse health effects through their penetration (Finf=0.14) into indoor environment. Flat slopes (0.11) and poor correlation (8.4%) for metals in coarser range obtained through regression model hypothesized their high deposition velocities and low penetration efficiency. Our findings suggest enhanced resident exposure to fine particles (81%) especially q-UF range (37%) through indoor and outdoor (through infiltration) sources along with complexity of size distribution of airborne particles that prerequisites surplus consideration to achieve a healthier environment within residential area.