Oxidative stress in ryegrass growing under different air pollution levels and its likely effects on pollen allergenicity

2019 ◽  
Vol 135 ◽  
pp. 331-340 ◽  
Author(s):  
Jose Antonio Lucas ◽  
Enrique Gutierrez-Albanchez ◽  
Teresa Alfaya ◽  
Francisco Feo-Brito ◽  
Francisco Javier Gutiérrez-Mañero
2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Mary Prunicki ◽  
Nicholas Cauwenberghs ◽  
Jennifer Arthur Ataam ◽  
Hesam Movassagh ◽  
Juyong Brian Kim ◽  
...  

Abstract Background Childhood exposure to air pollution contributes to cardiovascular disease in adulthood. Immune and oxidative stress disturbances might mediate the effects of air pollution on the cardiovascular system, but the underlying mechanisms are poorly understood in adolescents. Therefore, we aimed to identify immune biomarkers linking air pollution exposure and blood pressure levels in adolescents. Methods We randomly recruited 100 adolescents (mean age, 16 years) from Fresno, California. Using central-site data, spatial-temporal modeling, and distance weighting exposures to the participant’s home, we estimated average pollutant levels [particulate matter (PM), polyaromatic hydrocarbons (PAH), ozone (O3), carbon monoxide (CO) and nitrogen oxides (NOx)]. We collected blood samples and vital signs on health visits. Using proteomic platforms, we quantitated markers of inflammation, oxidative stress, coagulation, and endothelial function. Immune cellular characterization was performed via mass cytometry (CyTOF). We investigated associations between pollutant levels, cytokines, immune cell types, and blood pressure (BP) using partial least squares (PLS) and linear regression, while adjusting for important confounders. Results Using PLS, biomarkers explaining most of the variance in air pollution exposure included markers of oxidative stress (GDF-15 and myeloperoxidase), acute inflammation (C-reactive protein), hemostasis (ADAMTS, D-dimer) and immune cell types such as monocytes. Most of these biomarkers were independently associated with the air pollution levels in fully adjusted regression models. In CyTOF analyses, monocytes were enriched in participants with the highest versus the lowest PM2.5 exposure. In both PLS and linear regression, diastolic BP was independently associated with PM2.5, NO, NO2, CO and PAH456 pollution levels (P ≤ 0.009). Moreover, monocyte levels were independently related to both air pollution and diastolic BP levels (P ≤ 0.010). In in vitro cell assays, plasma of participants with high PM2.5 exposure induced endothelial dysfunction as evaluated by eNOS and ICAM-1 expression and tube formation. Conclusions For the first time in adolescents, we found that ambient air pollution levels were associated with oxidative stress, acute inflammation, altered hemostasis, endothelial dysfunction, monocyte enrichment and diastolic blood pressure. Our findings provide new insights on pollution-related immunological and cardiovascular disturbances and advocate preventative measures of air pollution exposure.


2020 ◽  
Vol 30 (Supplement_5) ◽  
Author(s):  
L Falcone ◽  
E Aruffo ◽  
P Di Carlo ◽  
P Del Boccio ◽  
M C Cufaro ◽  
...  

Abstract Background Reactive oxygen species (ROS) and oxidative stress in the respiratory system are involved in lung inflammation and tumorigenesis. Ozone (O3) is one of the main components of air pollution in urban areas able to act as strong pro-oxidant agent, however its effects on human health is still poorly investigated. In this study the effect of O3 has been evaluated in THP-1 monocytes differentiated into macrophages with PMA and in HBEpC (primary human bronchial epithelial) cells, two model systems for in vitro studies and translational research. Methods Cell viability, ROS and pro-inflammatory cytokines like interleukin-8(IL-8) and tumor necrosis factor(TNF-α) have been tested in the above-mentioned cell lines not exposed to any kind of pollution (basal condition-b.c.) or exposed to O3 at a concentration of 120 ppb. In HBEpC a labelfree shotgun proteomics analysis has been also performed in the same conditions. Results Ozone significantly increased the production of IL-8 and TNF-α in THP-1 whereas no changes were shown in HBEpC. In both cell lines lipopolysaccharide(LPS) caused an increase of IL-8 and TNF-α production in b.c. and O3 treatment potentiated this effect. Ozone exposure increased ROS formation in a time dependent manner in both cell lines and in THP-1 cells a decrease in catalase activity was also shown. Finally, according to these data, functional proteomics analysis revealed that in HBEpC exposure to O3 many differential proteins are related to oxidative stress and inflammation. Conclusions Our results indicate that O3, at levels that can be reached in urban areas, causes an increase of pro-inflammatory agents either per se or potentiating the effect of immune response stimulators in cell models of human macrophages and human airway epithelial cells. Interestingly, the proteomic analysis showed that besides the dysregulated proteins, O3 induced the expression of AKR1D1 and AKR1B10, proteins recognized to play a significant role in cancer development. Key messages This study adds new pieces of information on the association between O3 exposure and detrimental effects on respiratory system. This study suggests the need for further research on the mechanisms involved and for a continued monitoring/re-evaluation of air pollution standards aimed at safeguarding human health.


1998 ◽  
Vol 12 (4) ◽  
pp. 900-905 ◽  
Author(s):  
B. Forsberg ◽  
N. Stjernberg ◽  
R. Linné ◽  
B. Segerstedt ◽  
S. Wall

2021 ◽  
Vol 195 ◽  
pp. 110870
Author(s):  
Jennifer K. Mann ◽  
Liza Lutzker ◽  
Stephanie M. Holm ◽  
Helene G. Margolis ◽  
Andreas M. Neophytou ◽  
...  

2021 ◽  
Author(s):  
Hannah Marley ◽  
Kim Dirks ◽  
Andrew Neverman ◽  
Ian McKendry ◽  
Jennifer Salmond

<p><span><span>A brown air pollution haze that forms over some international cities during the winter has been found to be associated with negative health outcomes and high surface air pollution levels. Previous research has demonstrated a well-established link between the structure of the atmospheric boundary layer (ABL) and surface air quality; however, the degree to which the structure of the ABL influences for formation of local-</span></span><span><span>scale</span></span><span><span> brown haze is unknown. Using continuous ceilometer data covering seven consecutive winters, we investigate the influence of the structure of the ABL in relation to surface air pollution and brown haze formation over an urban area of complex coastal terrain in the Southern Hemisphere city of Auckland, New Zealand. Our results suggest the depth and evolution of the ABL has a strong influence on severe brown haze formation. When days with severe brown haze are compared with those when brown haze is expected but not observed (based on favorable meteorology and high surface air pollution levels), days with severe brown haze are found to coincide with significantly shallower daytime convective boundary layers (~ 48% lower), and the nights preceding brown haze formation are found to have significantly shallower nocturnal boundary layers (~ 28% lower). On severe brown haze days the growth rate during the morning transition phase from a nocturnal boundary layer to a convective daytime boundary layer is found to be significantly reduced (70 m h</span></span><sup><span><span>-1</span></span></sup><span><span>) compared to days on which brown haze is expected but not observed (170 m h</span></span><sup><span><span>-1</span></span></sup><span><span>). Compared with moderate brown haze, severe brown haze conditions are found to be associated with a significantly higher proportion of days with a distinct residual layer present in the ceilometer profiles, suggesting the entrainment of residual layer pollutants may contribute to the severity of the haze. This study illustrates the complex interaction between the ABL structure, air pollution, and the presence of brown haze, and demonstrates the utility of a ceilometer instrument in understanding and predicting the occurrence of brown haze events. </span></span></p>


Author(s):  
Gennaro Liccardi ◽  
Matteo Martini ◽  
Maria Beatrice Bilò ◽  
Manlio Milanese ◽  
Paola Rogliani

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