“…Many studies have shown that urban fine particulate matter (PM) has mutagenic and genotoxic activities in different short-term tests on bacteria and in vitro and in vivo human cells [ 1 , 2 , 3 , 4 , 5 , 6 ]. The genotoxic and mutagenic activity of PM varies according to its size and physical and chemical composition that depends mainly on local emissions [ 3 , 7 , 8 , 9 , 10 ].…”
The aim of this paper was to investigate the relationship between micronuclei and DNA damage in children’s buccal mucosa cells and the genotoxicity and mutagenicity of the different sized fractions of particulate matter as well as the concentration of PAHs (polycyclic aromatic hydrocarbons) and metals in particulate matter. Air particulate matter was collected by high volume samplers located near the schools attended by the children on the same days of biological samplings. The mutagenic activity was assessed in different cells in in vitro tests (Ames test on bacteria and comet test on leukocytes). Our study showed weak positive correlations between (a) the mutagenicity of the PM0.5 fraction and PAHs and (b) the micronuclei test of children’s buccal cells and PAHs detected in PM0.5 and PM0.5–3 fractions. A positive correlation was also found between in vitro comet test on leukocytes and PAHs in the PM3–10 fraction. No correlation was observed for metal concentrations in each PM fraction.
“…Many studies have shown that urban fine particulate matter (PM) has mutagenic and genotoxic activities in different short-term tests on bacteria and in vitro and in vivo human cells [ 1 , 2 , 3 , 4 , 5 , 6 ]. The genotoxic and mutagenic activity of PM varies according to its size and physical and chemical composition that depends mainly on local emissions [ 3 , 7 , 8 , 9 , 10 ].…”
The aim of this paper was to investigate the relationship between micronuclei and DNA damage in children’s buccal mucosa cells and the genotoxicity and mutagenicity of the different sized fractions of particulate matter as well as the concentration of PAHs (polycyclic aromatic hydrocarbons) and metals in particulate matter. Air particulate matter was collected by high volume samplers located near the schools attended by the children on the same days of biological samplings. The mutagenic activity was assessed in different cells in in vitro tests (Ames test on bacteria and comet test on leukocytes). Our study showed weak positive correlations between (a) the mutagenicity of the PM0.5 fraction and PAHs and (b) the micronuclei test of children’s buccal cells and PAHs detected in PM0.5 and PM0.5–3 fractions. A positive correlation was also found between in vitro comet test on leukocytes and PAHs in the PM3–10 fraction. No correlation was observed for metal concentrations in each PM fraction.
“… Figure 6 Effects of different compounds on NHBE cell death. The graph displays the cell death values of: cigarette mainstream smoke (CMS) 23 , E-liquid 23 , GO with chitosan (CHI) and hyaluronic acid (HA) 24 , cigarette smoke extract 25 , diesel exhaust particles (DEPs) 26 , Aspergillus fumigatus 27 , and particle matter (PM) (2.50–0.18 nm) 72 . Blue, red, or green lines represent the toxicity induced by GO, FLG, and sFLG.…”
Graphene and its derivative materials are manufactured by numerous companies and research laboratories, during which processes they can come into contact with their handlers' physiological barriers—for instance, their respiratory system. Despite their potential toxicity, these materials have even been used in face masks to prevent COVID-19 transmission. The increasingly widespread use of these materials requires the design and implementation of appropriate, versatile, and accurate toxicological screening methods to guarantee their safety. Murine models are adequate, though limited when exploring different doses and lengths of exposure—as this increases the number of animals required, contrary to the Three R's principle in animal experimentation. This article proposes an in vitro model using primary, non-transformed normal human bronchial epithelial (NHBE) cells as an alternative to the most widely used model to date, the human lung tumor cell line A549. The model has been tested with three graphene derivatives—graphene oxide (GO), few-layer graphene (FLG), and small FLG (sFLG). We observed a cytotoxic effect (necrosis and apoptosis) at early (6- and 24-h) exposures, which intensified after seven days of contact between cells and the graphene-related materials (GRMs)—with cell death reaching 90% after a 5 µg/mL dose. A549 cells are more resistant to necrosis and apoptosis, yielding values less than half of NHBE cells at low concentrations of GRMs (between 0.05 and 5 µg/mL). Indeed, GRM-induced cell death in NHBE cells is comparable to that induced by toxic compounds such as diesel exhaust particles on the same cell line. We propose NHBE as a suitable model to test GRM-induced toxicity, allowing refinement of the dose concentrations and exposure timings for better-designed in vivo mouse assays.
“…These particles generate cytotoxicity in a wide variety of cells, including NHBE [78, 79,80]. Remarkably, different studies show that exposure to even low doses of these toxic compounds have a detrimental effect on human health [22,24,25,70]. The results obtained in our study allow us to conclude that, for NHBE cells, a 5 µg/mL dose of GRMs (considered as low) generated toxicity after 24 hours of exposure, and a dose of 50 µg/mL was as toxic as higher doses of other, well-studied toxic nanoparticles.…”
Section: Discussionmentioning
confidence: 99%
“…In this work, we propose a model using primary normal human bronchial epithelial (NHBE) cells, which have been used previously to study particle-generated lung toxicity [22,24,25,70]. At present, the gold standard to study graphene-induced lung toxicity is the lung tumor cell line A549 [71,72].…”
Section: Discussionmentioning
confidence: 99%
“…Effects of different compounds on NHBE cell death. The graph displays the cell death values of: cigarette mainstream smoke (CMS) [22], E-liquid [22], GO with chitosan (CHI) and hyaluronic acid (HA) [23], cigarette smoke extract [24], diesel exhaust particles (DEPs) [25], Aspergillus fumigatus [26], and particle matter (PM) (2.50-0.18 nm) [70]. Blue, red, or green lines represent the toxicity induced by GO, FLG, and sFLG, respectively, as observed in our study.…”
Background
Graphene and its derivative materials are manufactured by numerous companies and research laboratories, during which processes they can come into contact with their handlers’ physiological barriers—for instance, their respiratory system. Despite their potential toxicity, these materials have even been used in face masks to prevent COVID-19 transmission. The increasingly widespread use of these materials requires the design and implementation of appropriate, versatile, and accurate toxicological screening methods to guarantee their safety. Murine models are adequate, though limited when exploring different doses and lengths of exposure—as this increases the number of animals required, contrary to the Three R’s principle in animal experimentation. This article proposes an in vitro model using primary, non-transformed normal human bronchial epithelial (NHBE) cells as an alternative to the most widely used model to date, the human lung tumor cell line A549. The model has been tested with three graphene derivatives—graphene oxide (GO), few-layer graphene (FLG), and small FLG (sFLG).
Results
We observed a cytotoxic effect (necrosis and apoptosis) at early (6- and 24-hour) exposures, which intensified after seven days of contact between cells and the graphene-related materials (GRMs)—with cell death reaching 90% after a 5 µg/mL dose. A549 cells are more resistant to necrosis and apoptosis, yielding values less than half those of NHBE cells at low concentrations of GRMs (between 0.05 and 5 µg/mL). Indeed, GRM-induced cell death in NHBE cells is comparable to that induced by toxic compounds such as diesel exhaust particles on the same cell line.
Conclusions
We propose NHBE as a suitable model to test GRM-induced toxicity, allowing refinement of the dose concentrations and exposure timings for better-designed in vivo mouse assays.
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