According to World Health Organization (WHO), each year 7 million of people in the world die prematurely because of indoor and outdoor air pollutants. In recent years, ultrafine atmospheric particles (UFPs) are attracting more attention because of their health risks. Fine and ultrafine particles, due to their small size, can penetrate deeper and settle in the alveolar region of the lungs where they can translocate into the bloodstream through the capillary barrier and reach other organs. We want to better understand how the UFPs can affect our health and obtain an overview of the biological mechanisms induced. To do so, we tackled the matter with two different approaches, which are: a molecular one, using “omic” technologies, and an epidemiological one, focusing on the investigation of specific biomarkers. The molecular approach is to work with engineered nanoparticles (ENPs) as a manageable tool to study the mechanisms of toxicity of UFPs, given their similarities in size, metal content, induced biological effects and exposure pathways. We investigated the toxicity of Cadmium Sulfide Quantum Dots (CdS QDs), engineered nanoparticles, on two different cell lines representing different routes of exposure: HepG2 (liver hepatocellular carcinoma) and THP-1 (peripheral blood monocyte). Both cell lines were exposed for 24 hours to sub-toxic dose of CdS QDs, and subsequently the RNA sequencing and miRNome profiling were performed. Transcriptomic data and analysis of miRNAs-mRNAs interactions reveal for HepG2 the activation of the RAS and Calcium signalling pathways, while for THP-1 they point to JAK/STAT signalling and inflammatory pathways, leading to blockade of autophagic flux. In the second section an epidemiological approach was used. We developed a long-term investigation at population scale to assess the link between air pollutants (including UFPs) and inflammation and coagulation blood-biomarkers reflecting cardiovascular health. The air pollutants considered for this work were: PM(10; 2.5; coarse), NO(x; 2), O3 and ultrafine particles as PNC. The statistical method used for this analysis was "Multiple linear regression adjusting for confounders. The results exhibit a strong association between biomarkers of inflammation and coagulation with almost all the pollutants, in particular with UFPs since most inflammatory biomarkers show meaningful association. In conclusion, we observed adverse effects of nanoparticles at molecular level and in a short-term exposure, as well as at population-scale in long-term exposure. Moreover, this study highlighted the association among inflammation and coagulation blood-biomarker with PM and gaseous pollutant, linking it directly with the increasing risk of cardiovascular disease.
Contribution of applied biology to mitigation of urban air pollution and prevention of its effects on health and environment / Vogli, M.. - (2022).
Contribution of applied biology to mitigation of urban air pollution and prevention of its effects on health and environment
VOGLI, MEGI
2022-01-01
Abstract
According to World Health Organization (WHO), each year 7 million of people in the world die prematurely because of indoor and outdoor air pollutants. In recent years, ultrafine atmospheric particles (UFPs) are attracting more attention because of their health risks. Fine and ultrafine particles, due to their small size, can penetrate deeper and settle in the alveolar region of the lungs where they can translocate into the bloodstream through the capillary barrier and reach other organs. We want to better understand how the UFPs can affect our health and obtain an overview of the biological mechanisms induced. To do so, we tackled the matter with two different approaches, which are: a molecular one, using “omic” technologies, and an epidemiological one, focusing on the investigation of specific biomarkers. The molecular approach is to work with engineered nanoparticles (ENPs) as a manageable tool to study the mechanisms of toxicity of UFPs, given their similarities in size, metal content, induced biological effects and exposure pathways. We investigated the toxicity of Cadmium Sulfide Quantum Dots (CdS QDs), engineered nanoparticles, on two different cell lines representing different routes of exposure: HepG2 (liver hepatocellular carcinoma) and THP-1 (peripheral blood monocyte). Both cell lines were exposed for 24 hours to sub-toxic dose of CdS QDs, and subsequently the RNA sequencing and miRNome profiling were performed. Transcriptomic data and analysis of miRNAs-mRNAs interactions reveal for HepG2 the activation of the RAS and Calcium signalling pathways, while for THP-1 they point to JAK/STAT signalling and inflammatory pathways, leading to blockade of autophagic flux. In the second section an epidemiological approach was used. We developed a long-term investigation at population scale to assess the link between air pollutants (including UFPs) and inflammation and coagulation blood-biomarkers reflecting cardiovascular health. The air pollutants considered for this work were: PM(10; 2.5; coarse), NO(x; 2), O3 and ultrafine particles as PNC. The statistical method used for this analysis was "Multiple linear regression adjusting for confounders. The results exhibit a strong association between biomarkers of inflammation and coagulation with almost all the pollutants, in particular with UFPs since most inflammatory biomarkers show meaningful association. In conclusion, we observed adverse effects of nanoparticles at molecular level and in a short-term exposure, as well as at population-scale in long-term exposure. Moreover, this study highlighted the association among inflammation and coagulation blood-biomarker with PM and gaseous pollutant, linking it directly with the increasing risk of cardiovascular disease.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.


