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@article{jairi:hal-04687711,

title = {Enhancing air pollution prediction: A neural transfer learning approach across different air pollutants},

author = {Idriss Jairi and Sarah Ben-Othman and Ludivine Canivet and Hayfa Zgaya-Biau},

url = {https://hal.science/hal-04687711},

doi = {10.1016/j.eti.2024.103793},

year  = {2024},

date = {2024-11-01},

urldate = {2024-11-01},

journal = {Environmental Technology and Innovation},

volume = {36},

pages = {103793},

publisher = {Elsevier},

note = {ACL},

keywords = {ER4},

pubstate = {published},

tppubtype = {article}

}

@article{jairi:hal-04763860,

title = {Enhancing particulate matter risk assessment with novel machine learning-driven toxicity threshold prediction},

author = {Idriss Jairi and Amelle Rekbi and Sarah Ben-Othman and Slim Hammadi and Ludivine Canivet and Hayfa Zgaya-Biau},

url = {https://hal.science/hal-04763860},

doi = {10.1016/j.engappai.2024.109531},

year  = {2024},

date = {2024-10-01},

urldate = {2024-10-01},

journal = {Engineering Applications of Artificial Intelligence},

volume = {139},

pages = {109531},

publisher = {Elsevier},

note = {ACL},

keywords = {ER4},

pubstate = {published},

tppubtype = {article}

}

@article{jairi:hal-04469637,

title = {Explainable based approach for the air quality classification on the granular computing rule extraction technique},

author = {Idriss Jairi and Sarah Ben-Othman and Ludivine Canivet and Hayfa Zgaya-Biau},

url = {https://hal.science/hal-04469637},

doi = {10.1016/j.engappai.2024.108096},

year  = {2024},

date = {2024-07-01},

urldate = {2024-07-01},

journal = {Engineering Applications of Artificial Intelligence},

volume = {133},

pages = {108096},

publisher = {Elsevier},

note = {ACL},

keywords = {ER4},

pubstate = {published},

tppubtype = {article}

}

@article{rorat:hal-03771752,

title = {Perspectives on particle-related health risk assessment},

author = {Agnieszka Rorat and Caroline Lanier and Hélène Gorge and Jean-Philippe Jaeg and Damien Cuny and Annabelle Deram and Ludivine Canivet},

url = {https://hal.archives-ouvertes.fr/hal-03771752},

doi = {10.1684/ers.2021.1571},

year  = {2021},

date = {2021-08-01},

urldate = {2021-08-01},

journal = {Environnement, Risques & Santé},

volume = {20},

number = {4},

pages = {389-394},

publisher = {John Libbey Eurotext},

note = {ACL},

keywords = {ER4},

pubstate = {published},

tppubtype = {article}

}

@article{Canivet2020,

title = {Toxicity of iron nanoparticles towards primary cultures of human bronchial epithelial cells},

author = {Ludivine Canivet and Franck-Olivier Denayer and Pierre Dubot and Guillaume Garcon and Jean-Marc Lo-Guidice},

year  = {2020},

date = {2020-01-01},

journal = {Journal of Applied Toxicology},

abstract = {Air pollution is a public health issue and the toxicity of ambient 

	particulate matter (PM) is well‐recognized. Although it does not 

	mostly contribute to the total mass of PM, increasing evidence indicates 

	that the ultrafine fraction has generally a greater toxicity than 

	the others do. A better knowledge of the underlying mechanisms involved 

	in the pathological disorders related to nanoparticles (NPs) remains 

	essential. Hence, the goal of this study was to determine better 

	whether the exposure to a relatively low dose of well‐characterized 

	iron‐rich NPs (Fe‐NPs) might alter some critical toxicological endpoints 

	in a relevant primary culture model of human bronchial epithelial 

	cells (HBECs). We sought to use Fe‐NPs representative of those frequently 

	found in the industrial smokes of metallurgical industries. After 

	having noticed the effective internalization of Fe‐NPs, oxidative, 

	inflammatory, DNA repair, and apoptotic endpoints were investigated 

	within HBECs, mainly through transcriptional screening. Taken together, 

	these results revealed that, despite it only produced relatively 

	low levels of reactive oxygen species without any significant oxidative 

	damage, low‐dose Fe‐NPs quickly significantly deregulated the transcription 

	of some target genes closely involved in the proinflammatory response. 

	Although this inflammatory process seemed to stay under control over 

	time in case of this acute scenario of exposure, the future study 

	of its evolution after a scenario of repeated exposure could be very 

	interesting to evaluate the toxicity of Fe‐NPs better.},

note = {ACL},

keywords = {ER4},

pubstate = {published},

tppubtype = {article}

}

@article{Platel2020,

title = {Study of in vitro and in vivo genotoxic effects of air pollution fine (PM2.5-0.18) and quasi-ultrafine (PM0.18) particles on lung models},

author = {Ane Platel and Killian Privat and Smail Talahari and Alexande Delobel and Gonzague Dourdin and Eulalie Gateau and Sophie Simar and Yara Saleh and Jules Sotty and Sébastien Antherieu and Ludivine Canivet and Laurent-Y. Alleman and Esperanza Perdrix and Guillaume Garçon and Franck-Olivier Denayer and Jean-Marc Lo-Guidice and Fabrice Nesslany},

year  = {2020},

date = {2020-01-01},

journal = {Science of the Total Environment},

volume = {711},

pages = {134666},

abstract = {Air pollution and particulate matter (PM) are classified as carcinogenic 

	to humans. Pollutants evidence for public health concern include 

	coarse (PM10) and fine (PM2.5) particles. However, ultrafine particles 

	(PM0.1) are assumed to be more toxic than larger particles, but data 

	are still needed to better understand their mechanism of action. 

	In this context, the aim of our work was to investigate the in vitro 

	and in vivo genotoxic potential of fine (PM2.5-018) and quasi ultra-fine 

	(PM0.18) particles from an urban-industrial area (Dunkirk, France) 

	by using comet, micronucleus and/or gene mutation assays. In vitro 

	assessment was performed with 2 lung immortalized cell lines (BEAS-2B 

	and NCI-H292) and primary normal human bronchial epithelial cells 

	(NHBE) grown at the air-liquid interface or in submerged conditions 

	(5 µg PM/cm2). For in vivo assessment, tests were performed after 

	acute (24 h, 100 µg PM/animal), subacute (1 month, 10 µg 

	PM/animal) and subchronic (3 months, 10 µg PM/animal) intranasal 

	exposure of BALB/c mice. In vitro, our results show that PM2.5-018 

	and PM0.18 induced primary DNA damage but no chromosomal aberrations 

	in immortalized cells. Negative results were noted in primary cells 

	for both endpoints. In vivo assays revealed that PM2.5-018 and PM0.18 

	induced no significant increases in DNA primary damage, chromosomal 

	aberrations or gene mutations, whatever the duration of exposure. 

	This investigation provides initial answers regarding the in vitro 

	and in vivo genotoxic mode of action of PM2.5-018 and PM0.18 at moderate 

	doses and highlights the need to develop standardized specific methodologies 

	for assessing the genotoxicity of PM. Moreover, other mechanisms 

	possibly implicated in pulmonary carcinogenesis, e.g. epigenetics, 

	should be investigated.},

note = {ACL},

keywords = {ER4},

pubstate = {published},

tppubtype = {article}

}

@conference{Rorat2020,

title = {Between physicochemical characterization of atmospheric particles and their impact on human health - challenges and perspectives (RECORD project)},

author = {Agnieszka Rorat and Caroline Lanier and Jean-Philippe Jaeg and Damien Cuny and Annabelle Deram and Ludivine Canivet},

year  = {2020},

date = {2020-01-01},

booktitle = {Atmso'Fair (Webinair), 23-24 juin 2020},

note = {ACTN},

keywords = {ER4},

pubstate = {published},

tppubtype = {conference}

}

@article{Sotty2020,

title = {Mitochondrial alterations triggered by repeated exposure to fine (pm2.5-0.18) and quasi-ultrafine (pm0.18) fractions of ambient particulate matter},

author = {Jules Sotty and Jérôme Kluza and Corentin De-Sousa and Sébastien Antherieu and Laurent Alleman and Ludivine Canivet and Esperanza Perdrix and Anne Loyens and Philippe Marchetti and Jean-Marc Lo-Guidice and Guillaume Garcon},

year  = {2020},

date = {2020-01-01},

journal = {Environment International},

volume = {142},

pages = {105830},

abstract = {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},

note = {ACL},

keywords = {ER4},

pubstate = {published},

tppubtype = {article}

}