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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (31 January 2020) | Viewed by 79431

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Special Issue Editor

Dr. Maurizio Gualtieri

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Guest Editor

ENEA Centro Ricerche Bologna; Via Martiri di Monte Sole, 4; 40129 Bologna BO, Italy
Interests: PM2.5; ultrafine particles; in vitro toxicology; inflammation; oxidative damage; ALI exposure

Special Issue Information

Dear Colleagues,

In the last decades, significant steps forward have been realized in the characterization of the mode of action of particulate matter (PM). Despite the information available on the toxicological effects of fine PM (PM2.5) on lung epithelial cells, there is still a significant lack of information on the effects of PM2.5 and ultrafine PM (UFP) on different tissues, first of all brain cells, and/or on exposing the in vitro models at the air liquid interface (ALI, micro cell cultures). In addition, growing interest is devoted to understanding the effects of PM and the UFP emitted by specific sources (such as diesel engines and biomass burning). Finally, interest in understanding the potential toxicological effects of indoor air pollution is gaining scientific attention in relation to the significant concentration of fine PM; UFP; and volatile organic compounds generated by specific sources, some of which include, for example, e-cigarettes and vaping cigarettes.

Papers submitted to this Special Issue must report high novelty results on the potential biological effects of PM and UFP. The identification of the molecular pathways activated by these particulates on cells that are representative of relevant target tissues is a reference topic. In addition, the application of innovative exposure systems; the use of 3D in vitro models; and the analysis of epigenetic modifications, metabolomics, and proteomics effects are also of interest, with a special emphasis on the modification, which may shed light on the mode of action of the effects fine and ultrafine particle on human health.

Dr. Maurizio Gualtieri
Guest Editor

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Keywords

Indoor and outdoor air pollution
Air liquid interface exposure
Combustion processes emission: biomass burning, vehicles emission, e-cigarette smoke, and indoor sources
Fine and ultrafine particulate matter
Inflammation
Oxidative stress
DNA damages
Epigenetic
Metabolomics
Proteomics

Published Papers (12 papers)

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Research

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14 pages, 1646 KiB

Open AccessArticle

Particulate Air Pollution, Clock Gene Methylation, and Stroke: Effects on Stroke Severity and Disability

by Laura Cantone, Eleonora Tobaldini, Chiara Favero, Benedetta Albetti, Roberto M. Sacco, Giuseppe Torgano, Luca Ferrari, Nicola Montano and Valentina Bollati

Int. J. Mol. Sci. 2020, 21(9), 3090; https://doi.org/10.3390/ijms21093090 - 27 Apr 2020

Cited by 16 | Viewed by 3166

Abstract

Circadian rhythm disturbances have been consistently associated with the development of several diseases, particularly cardiovascular diseases (CVDs). A central clock in the brain maintains the daily rhythm in accordance with the external environment. At the molecular level, the clock is maintained by “clock genes”, the regulation of which is mainly due to DNA methylation, a molecular mechanism of gene expression regulation, able to react to and be reprogrammed by environmental exposure such as exposure to particulate matter (PM). In 55 patients with a diagnosis of acute ischemic stroke, we showed that PM_2.5 exposure experienced before the event influenced clock genes methylation (i.e., circadian locomotor output cycles protein kaput CLOCK, period 2 PER2, cryprochrome 1 CRY1, Neuronal PAS Domain Protein 2 NPAS2), possibly modulating the patient prognosis after the event, as cryptochrome 1 CRY1 and period 1 PER1 methylation levels were associated with the Rankin score. Moreover, if PM_2.5 annual average was low, CRY1/CRY2 methylation levels were positively associated with the National Institutes of Health Stroke Scale (NIHSS) score, whereas they were negatively associated if PM_2.5 exposure was high. Whether epigenetic changes in clock genes need to be considered as a prognostic marker of stroke or rather a causal agent in stroke development remains to be determined. Further studies are needed to determine the role of clock gene methylation in regulating the response to and recovery after a stroke event. Full article

(This article belongs to the Special Issue Inhalation Toxicology and Biological Response)

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19 pages, 4763 KiB

Open AccessArticle

Waterpipe Tobacco Smoke Inhalation Triggers Thrombogenicity, Cardiac Inflammation and Oxidative Stress in Mice: Effects of Flavouring

by Abderrahim Nemmar, Suhail Al-Salam, Sumaya Beegam, Priya Yuvaraju, Nur Elena Zaaba, Javed Yasin and Badreldin H. Ali

Int. J. Mol. Sci. 2020, 21(4), 1291; https://doi.org/10.3390/ijms21041291 - 14 Feb 2020

Cited by 14 | Viewed by 2628

Abstract

The consumption of water-pipe smoking (WPS) has been promoted by the use of flavoured tobacco. However, little is known about the impact of flavouring on the cardiovascular toxicity induced by WPS inhalation. Here, we compared the cardiovascular effects and underlying mechanism of actions of plain (P) (unflavoured) versus apple-flavoured (AF) WPS (30 minutes/day, 5 days/week for 1 month) in mice. Control mice were exposed to air. Both P- and AF-WPS inhalation induced an increase in systolic blood pressure, thrombogenicity and plasma concentration of fibrinogen and von Willebrand factor. In heart homogenates, AF-WPS inhalation caused an increase of 8-isoprostane and a decrease in the levels of reduced glutathione (GSH) and superoxide dismutase (SOD). Nevertheless, P-WPS decreased only the activity of SOD. The concentrations of tumour necrosis factor α and interleukin 1β were increased only in heart homogenates of mice exposed to AF-WPS. Although both P- and AF-WPS increased the concentration of troponin I in heart homogenates and induced DNA damage, the concentration of cleaved caspase 3 was only increased in mice exposed to AF-WPS. Immunohistochemical analysis of the hearts showed that both P- and AF- WPS inhalation decreased the expression of SOD. Moreover, the expression of nuclear factor erythroid-derived 2-like 2 at nuclear level in the heart was higher in both AF-WPS and P-WPS compared with control group, and the effect observed in AF-WPS group was more significant than that seen in P-WPS group. Likewise, the concentration of heme oxygenase-1 was significantly increased in both P-WPS and AF-WPS groups compared with control group, and the effect seen in AF-group was higher than that observed in P-WPS group. In conclusion, our findings showed that both P- and AF-WPS induce thrombogenicity and cardiac injury, and that this toxicity is potentiated by the presence of flavouring. Full article

(This article belongs to the Special Issue Inhalation Toxicology and Biological Response)

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15 pages, 3256 KiB

Open AccessArticle

Airborne Particulate Matter (PM₁₀) Inhibits Apoptosis through PI3K/AKT/FoxO3a Pathway in Lung Epithelial Cells: The Role of a Second Oxidant Stimulus

by Claudia M. García-Cuellar, Yolanda I. Chirino, Rocío Morales-Bárcenas, Ernesto Soto-Reyes, Raúl Quintana-Belmares, Miguel Santibáñez-Andrade and Yesennia Sánchez-Pérez

Int. J. Mol. Sci. 2020, 21(2), 473; https://doi.org/10.3390/ijms21020473 - 11 Jan 2020

Cited by 9 | Viewed by 2819

Abstract

Outdoor particulate matter (PM₁₀) exposure is carcinogenic to humans. The cellular mechanism by which PM₁₀ is associated specifically with lung cancer includes oxidative stress and damage to proteins, lipids, and DNA in the absence of apoptosis, suggesting that PM₁₀ induces cellular survival. We aimed to evaluate the PI3K/AKT/FoxO3a pathway as a mechanism of cell survival in lung epithelial A549 cells exposed to PM₁₀ that were subsequently challenged with hydrogen peroxide (H₂O₂). Our results showed that pre-exposure to PM₁₀ followed by H₂O₂, as a second oxidant stimulus increased the phosphorylation rate of pAKT^Ser473, pAKT^Thr308, and pFoxO3a^Ser253 2.5-fold, 1.8-fold, and 1.2-fold, respectively. Levels of catalase and p27^kip1, which are targets of the PIK3/AKT/FoxO3a pathway, decreased 38.1% and 62.7%, respectively. None of these changes had an influence on apoptosis; however, the inhibition of PI3K using the LY294002 compound revealed that the PI3K/AKT/FoxO3a pathway was involved in apoptosis evasion. We conclude that nontoxic PM₁₀ exposure predisposes lung epithelial cell cultures to evade apoptosis through the PI3K/AKT/FoxO3a pathway when cells are treated with a second oxidant stimulus. Full article

(This article belongs to the Special Issue Inhalation Toxicology and Biological Response)

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17 pages, 3351 KiB

Open AccessArticle

Screening of Cellular Stress Responses Induced by Ambient Aerosol Ultrafine Particle Fraction PM0.5 in A549 Cells

by Pavlína Šimečková, Soňa Marvanová, Pavel Kulich, Lucie Králiková, Jiří Neča, Jiřina Procházková and Miroslav Machala

Int. J. Mol. Sci. 2019, 20(24), 6310; https://doi.org/10.3390/ijms20246310 - 13 Dec 2019

Cited by 4 | Viewed by 3221

Abstract

Effects of airborne particles on the expression status of markers of cellular toxic stress and on the release of eicosanoids, linked with inflammation and oxidative damage, remain poorly characterized. Therefore, we proposed a set of various methodological approaches in order to address complexity of PM0.5-induced toxicity. For this purpose, we used a well-characterized model of A549 pulmonary epithelial cells exposed to a non-cytotoxic concentration of ambient aerosol particle fraction PM0.5 for 24 h. Electron microscopy confirmed accumulation of PM0.5 within A549 cells, yet, autophagy was not induced. Expression profiles of various cellular stress response genes that have been previously shown to be involved in early stress responses, namely unfolded protein response, DNA damage response, and in aryl hydrocarbon receptor (AhR) and p53 signaling, were analyzed. This analysis revealed induction of GREM1, EGR1, CYP1A1, CDK1A, PUMA, NOXA and GDF15 and suppression of SOX9 in response to PM0.5 exposure. Analysis of eicosanoids showed no oxidative damage and only a weak anti-inflammatory response. In conclusion, this study helps to identify novel gene markers, GREM1, EGR1, GDF15 and SOX9, that may represent a valuable tool for routine testing of PM0.5-induced in vitro toxicity in lung epithelial cells. Full article

(This article belongs to the Special Issue Inhalation Toxicology and Biological Response)

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22 pages, 2977 KiB

Open AccessArticle

The Biological Effects of Complete Gasoline Engine Emissions Exposure in a 3D Human Airway Model (MucilAir^TM) and in Human Bronchial Epithelial Cells (BEAS-2B)

by Pavel Rossner, Jr., Tereza Cervena, Michal Vojtisek-Lom, Kristyna Vrbova, Antonin Ambroz, Zuzana Novakova, Fatima Elzeinova, Hasmik Margaryan, Vit Beranek, Martin Pechout, David Macoun, Jiri Klema, Andrea Rossnerova, Miroslav Ciganek and Jan Topinka

Int. J. Mol. Sci. 2019, 20(22), 5710; https://doi.org/10.3390/ijms20225710 - 14 Nov 2019

Cited by 16 | Viewed by 3526

Abstract

The biological effects induced by complete engine emissions in a 3D model of the human airway (MucilAir^TM) and in human bronchial epithelial cells (BEAS-2B) grown at the air–liquid interface were compared. The cells were exposed for one or five days to emissions generated by a Euro 5 direct injection spark ignition engine. The general condition of the cells was assessed by the measurement of transepithelial electrical resistance and mucin production. The cytotoxic effects were evaluated by adenylate kinase (AK) and lactate dehydrogenase (LDH) activity. Phosphorylation of histone H2AX was used to detect double-stranded DNA breaks. The expression of the selected 370 relevant genes was analyzed using next-generation sequencing. The exposure had minimal effects on integrity and AK leakage in both cell models. LDH activity and mucin production in BEAS-2B cells significantly increased after longer exposures; DNA breaks were also detected. The exposure affected CYP1A1 and HSPA5 expression in MucilAir^TM. There were no effects of this kind observed in BEAS-2B cells; in this system gene expression was rather affected by the time of treatment. The type of cell model was the most important factor modulating gene expression. In summary, the biological effects of complete emissions exposure were weak. In the specific conditions used in this study, the effects observed in BEAS-2B cells were induced by the exposure protocol rather than by emissions and thus this cell line seems to be less suitable for analyses of longer treatment than the 3D model. Full article

(This article belongs to the Special Issue Inhalation Toxicology and Biological Response)

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21 pages, 1870 KiB

Open AccessArticle

Seasonal Variation in the Biological Effects of PM_2.5 from Greater Cairo

by Sara Marchetti, Salwa K. Hassan, Waleed H. Shetaya, Asmaa El-Mekawy, Elham F. Mohamed, Atef M. F. Mohammed, Ahmed A. El-Abssawy, Rossella Bengalli, Anita Colombo, Maurizio Gualtieri and Paride Mantecca

Int. J. Mol. Sci. 2019, 20(20), 4970; https://doi.org/10.3390/ijms20204970 - 09 Oct 2019

Cited by 19 | Viewed by 3260

Abstract

Greater Cairo (Egypt) is a megalopolis where the studies of the air pollution events are of extremely high relevance, for the geographical-climatological aspects, the anthropogenic emissions and the health impact. While preliminary studies on the particulate matter (PM) chemical composition in Greater Cairo have been performed, no data are yet available on the PM’s toxicity. In this work, the in vitro toxicity of the fine PM (PM_2.5) sampled in an urban area of Greater Cairo during 2017–2018 was studied. The PM_2.5 samples collected during spring, summer, autumn and winter were preliminary characterized to determine the concentrations of ionic species, elements and organic PM (Polycyclic Aromatic Hydrocarbons, PAHs). After particle extraction from filters, the cytotoxic and pro-inflammatory effects were evaluated in human lung A549 cells. The results showed that particles collected during the colder seasons mainly induced the xenobiotic metabolizing system and the consequent antioxidant and pro-inflammatory cytokine release responses. Biological events positively correlated to PAHs and metals representative of a combustion-derived pollution. PM_2.5 from the warmer seasons displayed a direct effect on cell cycle progression, suggesting possible genotoxic effects. In conclusion, a correlation between the biological effects and PM_2.5 physico-chemical properties in the area of study might be useful for planning future strategies aiming to improve air quality and lower health hazards. Full article

(This article belongs to the Special Issue Inhalation Toxicology and Biological Response)

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21 pages, 3926 KiB

Open AccessArticle

In Vivo Comparative Study on Acute and Sub-acute Biological Effects Induced by Ultrafine Particles of Different Anthropogenic Sources in BALB/c Mice

by Francesca Farina, Elena Lonati, Chiara Milani, Luca Massimino, Elisa Ballarini, Elisabetta Donzelli, Luca Crippa, Paola Marmiroli, Laura Botto, Paola Antonia Corsetto, Giulio Sancini, Alessandra Bulbarelli and Paola Palestini

Int. J. Mol. Sci. 2019, 20(11), 2805; https://doi.org/10.3390/ijms20112805 - 08 Jun 2019

Cited by 22 | Viewed by 3449

Abstract

Exposure to ultrafine particles (UFPs) leads to adverse effects on health caused by an unbalanced ratio between UFPs deposition and clearance efficacy. Since air pollution toxicity is first direct to cardiorespiratory system, we compared the acute and sub-acute effects of diesel exhaust particles (DEP) and biomass burning-derived particles (BB) on bronchoalveolar Lavage Fluid (BALf), lung and heart parenchyma. Markers of cytotoxicity, oxidative stress and inflammation were analysed in male BALB/c mice submitted to single and repeated intra-tracheal instillations of 50 μg UFPs. This in-vivo study showed the activation of inflammatory response (COX-2 and MPO) after exposure to UFPs, both in respiratory and cardiovascular systems. Exposure to DEP results also in pro- and anti-oxidant (HO-1, iNOS, Cyp1b1, Hsp70) protein levels increase, although, stress persist only in cardiac tissue under repeated instillations. Statistical correlations suggest that stress marker variation was probably due to soluble components and/or mediators translocation of from first deposition site. This mechanism, appears more important after repeated instillations, since inflammation and oxidative stress endure only in heart. In summary, chemical composition of UFPs influenced the activation of different responses mediated by their components or pro-inflammatory and pro-oxidative molecules, indicating DEP as the most damaging pollutant in the comparison. Full article

(This article belongs to the Special Issue Inhalation Toxicology and Biological Response)

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Review

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31 pages, 920 KiB

Open AccessReview

Inhalation Toxicology of Vaping Products and Implications for Pulmonary Health

by Hussein Traboulsi, Mathew Cherian, Mira Abou Rjeili, Matthew Preteroti, Jean Bourbeau, Benjamin M. Smith, David H. Eidelman and Carolyn J. Baglole

Int. J. Mol. Sci. 2020, 21(10), 3495; https://doi.org/10.3390/ijms21103495 - 15 May 2020

Cited by 60 | Viewed by 36896

Abstract

E-cigarettes have a liquid that may contain flavors, solvents, and nicotine. Heating this liquid generates an aerosol that is inhaled into the lungs in a process commonly referred to as vaping. E-cigarette devices can also contain cannabis-based products including tetrahydrocannabinol (THC), the psychoactive component of cannabis (marijuana). E-cigarette use has rapidly increased among current and former smokers as well as youth who have never smoked. The long-term health effects are unknown, and emerging preclinical and clinical studies suggest that e-cigarettes may not be harmless and can cause cellular alterations analogous to traditional tobacco smoke. Here, we review the historical context and the components of e-cigarettes and discuss toxicological similarities and differences between cigarette smoke and e-cigarette aerosol, with specific reference to adverse respiratory outcomes. Finally, we outline possible clinical disorders associated with vaping on pulmonary health and the recent escalation of acute lung injuries, which led to the declaration of the vaping product use-associated lung injury (EVALI) outbreak. It is clear there is much about vaping that is not understood. Consequently, until more is known about the health effects of vaping, individual factors that need to be taken into consideration include age, current and prior use of combustible tobacco products, and whether the user has preexisting lung conditions such as asthma and chronic obstructive pulmonary disease (COPD). Full article

(This article belongs to the Special Issue Inhalation Toxicology and Biological Response)

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16 pages, 782 KiB

Open AccessReview

Fifteen Years of Airborne Particulates in Vitro Toxicology in Milano: Lessons and Perspectives Learned

by Eleonora Marta Longhin, Paride Mantecca and Maurizio Gualtieri

Int. J. Mol. Sci. 2020, 21(7), 2489; https://doi.org/10.3390/ijms21072489 - 03 Apr 2020

Cited by 20 | Viewed by 3742

Abstract

Air pollution is one of the world’s leading environmental causes of death. The epidemiological relationship between outdoor air pollution and the onset of health diseases associated with death is now well established. Relevant toxicological proofs are now dissecting the molecular processes that cause inflammation, reactive species generation, and DNA damage. In addition, new data are pointing out the role of airborne particulates in the modulation of genes and microRNAs potentially involved in the onset of human diseases. In the present review we collect the relevant findings on airborne particulates of one of the biggest hot spots of air pollution in Europe (i.e., the Po Valley), in the largest urban area of this region, Milan. The different aerodynamic fractions are discussed separately with a specific focus on fine and ultrafine particles that are now the main focus of several studies. Results are compared with more recent international findings. Possible future perspectives of research are proposed to create a new discussion among scientists working on the toxicological effects of airborne particles. Full article

(This article belongs to the Special Issue Inhalation Toxicology and Biological Response)

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15 pages, 1838 KiB

Open AccessReview

Deciphering the Code between Air Pollution and Disease: The Effect of Particulate Matter on Cancer Hallmarks

by Miguel Santibáñez-Andrade, Yolanda I. Chirino, Imelda González-Ramírez, Yesennia Sánchez-Pérez and Claudia M. García-Cuellar

Int. J. Mol. Sci. 2020, 21(1), 136; https://doi.org/10.3390/ijms21010136 - 24 Dec 2019

Cited by 37 | Viewed by 6941

Abstract

Air pollution has been recognized as a global health problem, causing around 7 million deaths worldwide and representing one of the highest environmental crises that we are now facing. Close to 30% of new lung cancer cases are associated with air pollution, and the impact is more evident in major cities. In this review, we summarize and discuss the evidence regarding the effect of particulate matter (PM) and its impact in carcinogenesis, considering the “hallmarks of cancer” described by Hanahan and Weinberg in 2000 and 2011 as a guide to describing the findings that support the impact of particulate matter during the cancer continuum. Full article

(This article belongs to the Special Issue Inhalation Toxicology and Biological Response)

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16 pages, 1421 KiB

Open AccessReview

Ultrafine Particles from Residential Biomass Combustion: A Review on Experimental Data and Toxicological Response

by Emanuela Corsini, Marina Marinovich and Roberta Vecchi

Int. J. Mol. Sci. 2019, 20(20), 4992; https://doi.org/10.3390/ijms20204992 - 09 Oct 2019

Cited by 28 | Viewed by 4228

Abstract

Biomass burning is considered an important source of indoor and outdoor air pollutants worldwide. Due to competitive costs and climate change sustainability compared to fossil fuels, biomass combustion for residential heating is increasing and expected to become the major source of primary particulate matter emission over the next 5–15 years. The understanding of health effects and measures necessary to reduce biomass emissions of harmful compounds is mandatory to protect public health. The intent of this review is to report available data on ultrafine particles (UFPs, i.e., particles with diameter smaller than 100 nm) emitted by residential biomass combustion and their effects on human health (in vitro and in vivo studies). Indeed, as far as we know, papers focusing specifically on UFPs originating from residential biomass combustion and their impact on human health are still lacking. Full article

(This article belongs to the Special Issue Inhalation Toxicology and Biological Response)

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21 pages, 2067 KiB

Open AccessReview

Oxidative Potential Versus Biological Effects: A Review on the Relevance of Cell-Free/Abiotic Assays as Predictors of Toxicity from Airborne Particulate Matter

by Johan Øvrevik

Int. J. Mol. Sci. 2019, 20(19), 4772; https://doi.org/10.3390/ijms20194772 - 26 Sep 2019

Cited by 78 | Viewed by 4490

Abstract

Background and Objectives: The oxidative potential (OP) of particulate matter (PM) in cell-free/abiotic systems have been suggested as a possible measure of their biological reactivity and a relevant exposure metric for ambient air PM in epidemiological studies. The present review examined whether the OP of particles correlate with their biological effects, to determine the relevance of these cell-free assays as predictors of particle toxicity. Methods: PubMed, Google Scholar and Web of Science databases were searched to identify relevant studies published up to May 2019. The main inclusion criteria used for the selection of studies were that they should contain (1) multiple PM types or samples, (2) assessment of oxidative potential in cell-free systems and (3) assessment of biological effects in cells, animals or humans. Results: In total, 50 independent studies were identified assessing both OP and biological effects of ambient air PM or combustion particles such as diesel exhaust and wood smoke particles: 32 in vitro or in vivo studies exploring effects in cells or animals, and 18 clinical or epidemiological studies exploring effects in humans. Of these, 29 studies assessed the association between OP and biological effects by statistical analysis: 10 studies reported that at least one OP measure was statistically significantly associated with all endpoints examined, 12 studies reported that at least one OP measure was significantly associated with at least one effect outcome, while seven studies reported no significant correlation/association between any OP measures and any biological effects. The overall assessment revealed considerable variability in reported association between individual OP assays and specific outcomes, but evidence of positive association between intracellular ROS, oxidative damage and antioxidant response in vitro, and between OP assessed by the dithiothreitol (DDT) assay and asthma/wheeze in humans. There was little support for consistent association between OP and any other outcome assessed, either due to repeated lack of statistical association, variability in reported findings or limited numbers of available studies. Conclusions: Current assays for OP in cell-free/abiotic systems appear to have limited value in predicting PM toxicity. Clarifying the underlying causes may be important for further advancement in the field. Full article

(This article belongs to the Special Issue Inhalation Toxicology and Biological Response)

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