NewsCarcinogenicity of diesel-engine and gasoline-engine exhausts and some nitroarenes
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Formation of nitrated naphthalene in the sulfate radical oxidation process in the presence of nitrite
2024, Water ResearchPolycyclic aromatic hydrocarbons (PAHs) have become a global environmental concern due to their potential hazardous implication for human health. In this study, we found that sulfate radical (SO4•−) could effectively degrade naphthalene (NAP), a representative PAH in groundwaters, generating 1-naphthol. This intermediate underwent further degradation, yielding ring-opening products including phthalic acid and salicylic acid. However, the presence of nitrite (NO2−), a prevalent ion in subsurface environments, was observed to compete with NAP for SO4•−, thus slowing down the NAP degradation. The reaction between NO2− and SO4•− generated a nitrogen dioxide radical (NO2•). Concurrently, in-situ formed 1-naphthol underwent further oxidization to the 1-naphthoxyl radical by SO4•−. The coupling of 1-naphthoxyl radicals with NO2• gave rise to a series of nitrated NAP, namely 2-nitro-1-naphthol, 4-nitro-1-naphthol, and 2,4-dinitro-1-naphthol. In addition, the in-situ formed phthalic acid and salicylic acid also underwent nitration, generating nitrophenolic products, although this pathway appeared less prominent than the nitration of 1-naphthol. When 10 μΜ NAP was subjected to heat activated peroxydisulfate oxidation in the presence of 10 μΜ NO2−, the total yield of nitrated products reached 0.730 μΜ in 120 min. Overall, the presence of NO2− dramatically altered the behavior of NAP degradation by SO4•− oxidation and contributed to the formation of toxic nitrated products. These findings raise awareness of the potential environmental risks associated with the application of SO4•−-based oxidation processes for the remediation of PAHs-polluted sites in presence of NO2−.
Influence of oil extraction on concentration distributions, migration, secondary formation and carcinogenic risk of NPAHs and OPAHs in air and soil in an oilfield development area in China
2024, Science of the Total EnvironmentOil extraction leads to environmental pollution from the oilfields and dweller activities, however, knowledge of the concentration distributions, migration, secondary formation and toxicity of nitrated/oxygenated polycyclic aromatic hydrocarbons (N/OPAHs) in oilfield regions is limited. In this research, atmospheric and soil samples in 7 different location types in an important oil industrial base in China were gathered. The ΣNPAHs and ΣOPAHs in the air ranged from 0.05 to 2.47 ng/m3 and 0.14–22.72 ng/m3, respectively, and in soil ranged from 0.22 to 17.81 ng/g and 9.69–66.86 ng/g, respectively. Both NPAHs and OPAHs in the atmosphere exhibited higher concentrations during winter. The atmospheric NPAH concentrations decreased exponentially with distance from urban area especially in the summer, revealing the impact of vehicles on the air in the Yellow River Delta area. High NPAH and OPAH concentrations were found only in soil near oil extraction facilities, indicating that the impact of oil extraction is limited to the soil near the extraction facilities. The air-soil exchanges of N/OPAHs were assessed through fugacity fraction analysis, and NPAHs were in the equilibrium-deposition state and OPAHs were in the net-deposition state in the winter. Higher incremental lifetime cancer risk (ILCR) occurred at the urban, industrial, and oilfield sites in the atmospheric samples, and the soil samples had the largest ILCR values in the oilfield sites. However, ILCR values for both air and soil did not exceed the threshold of 10−6.
ALKBH5 SUMOylation-mediated FBXW7 m6A modification regulates alveolar cells senescence during 1-nitropyrene-induced pulmonary fibrosis
2024, Journal of Hazardous MaterialsOur previous study revealed that 1-nitropyrene (1-NP) exposure evoked pulmonary fibrosis in mice. However, the exact mechanism remained elusive. We found that 1-NP induced telomere damage and cellular senescence in mice lungs, and two alveolar epithelial cells lines. 1-NP downregulated telomere repeat binding factor 2 (TRF2), and upregulated FBXW7. Mechanistically, 1-NP-caused TRF2 ubiquitination and proteasomal degradation depended on E3 ubiquitin ligase activity of FBXW7. Moreover, 1-NP upregulated FBXW7 m6A modification via an ALKBH5-YTHDF1-dependent manner. Further analysis suggested 1-NP promoted ALKBH5 SUMOylation and subsequent proteasomal degradation. Additionally, 1-NP evoked mitochondrial reactive oxygen species (mtROS) overproduction. Mito-TEMPO, a mitochondrial-targeted antioxidant, mitigated 1-NP-caused mtROS overproduction, ALKBH5 SUMOylation, FBXW7 m6A modification, TRF2 degradation, cellular senescence, and pulmonary fibrosis. Taken together, mtROS-initiated ALKBH5 SUMOylation and subsequent FBXW7 m6A modification is indispensable for TRF2 degradation and cellular senescence in alveolar epithelial cells during 1-NP-induced pulmonary fibrosis. Our study provides target intervention measures towards 1-NP-evoked pulmonary fibrosis.
Dose-response-relationship between occupational exposure to diesel engine emissions and lung cancer risk: A systematic review and meta-analysis
2024, International Journal of Hygiene and Environmental HealthIn 2012, the International Agency for Research on Cancer (IARC) concluded that diesel engine emissions (DEE) emissions cause cancer in humans. However, there is still controversy surrounding this conclusion, due to several studies since the IARC decision citing a lack of evidence of a dose-response relationship.
Through a systematic review, we aimed to evaluate all evidence on the association between occupational DEE and lung cancer to investigate whether there is an increased risk of lung cancer for workers exposed to DEE and if so, to describe the dose-response relationship.
We registered the review protocol with PROSPERO and searched for observational studies in relevant literature databases. Two independent reviewers screened the studies’ titles/abstracts and full texts, and extracted and assessed their quality. Studies with no direct DEE measurement but with information on length of exposure for high-risk occupations were assigned exposure values based on the DEE Job-Exposure-Matrix (DEE-JEM). After assessing quality and informativeness, we selected appropriate studies for the dose-response meta-analysis.
Sixty-five reports (from thirty-seven studies) were included in the review; one had a low risk of bias (RoB) (RR per 10 μg/m3-years: 1.014 [95%CI 1.007–1.021]). There was an increased, statistically significant risk of lung cancer with increasing DEE exposure for all studies (RR per 10 μg/m3-years = 1.013 [95%CI 1.004–1.021]) as well as for studies with a low RoB in the exposure category (RR per 10 μg/m3-years = 1.008 [95% CI1.001–1.015]). We obtained a doubling dose of 555 μg/m3-years for all studies and 880 μg/m3-years for studies with high quality in the exposure assessment.
We found a linear positive dose-response relationship for studies with high quality in the exposure domain, even though all studies had an overall high risk of bias. Current threshold levels for DEE exposure at the workplace should be reconsidered.
Épidémiologie du cancer du poumon en France
2023, Revue des Maladies Respiratoires ActualitesAvec près de 50 000 nouveaux cas et 30 000 décès par an en France, le cancer bronchopulmonaire est le 3e cancer le plus fréquent et la 1re cause de mortalité par cancer. Tandis que les taux d’incidence et de mortalité chez les hommes se sont stabilisés, ils connaissent une augmentation préoccupante chez les femmes, en lien direct avec l’évolution du tabagisme féminin. La survie à 5 ans des cancers bronchopulmonaires a connu une progression importante, passant de 9 % en 1990 à 20 % pour les personnes diag nostiquées entre 2010 et 2015. Si le tabagisme est effectivement le principal facteur de risque du cancer bronchopulmonaire, responsable de 81 % des cas, les facteurs de risque et expositions responsables de cancers bronchopulmonaires sont multiples, tels que l’alimentation faible en fruits < 300 g/jour (10 % des cas), les expositions professionnelles (16,6 % des cas), et les expositions environnementales, notamment le radon (près de 10 %) et la pollution de l’air (3,6 %). La part des expositions environnementales étant probablement sous-estimée. De façon combinée, près de 90 % des cas de cancer broncho-pulmonaire sont ainsi attribuables à des facteurs modifiables et offrent de nombreux leviers pour les politiques de prévention.
1877-1203/© 2023 SPLF. Publié par Elsevier Masson SAS. Tous droits réservés.
With almost 50,000 new cases and 30,000 deaths per year in France, lung cancer is the 3rd most common cancer and the 1st cause of cancer-related death. While incidence and mortality rates in men have stabilized, they are demonstrating an alarming growth in women, linked to the increase in female tobacco consumption. The 5-year survival rate for lung cancers has increased considerably, from 9% in 1990 to 20% for people diagnosed between 2010 and 2015. While smoking is indeed the main risk factor for lung cancer, responsible for 81% of cases, the risk factors and exposures are numerous, such as a diet low in fruit <300g/day (10% of cases), occupational exposures (16% of cases), and environmental exposures, such as radon (almost 10% of cases) and outdoor air pollution (3.6% of cases). The proportion of environmental exposures being probably underestimated. Combined, close to 90% of lung cancer cases are attributable to modifiable factors, offering numerous levers for prevention policies.
1877-1203/© 2023 SPLF. Published by Elsevier Masson SAS. All rights reserved.
Diesel exhaust particles exposure induces liver dysfunction: Exploring predictive potential of human circulating microRNAs signature relevant to liver injury risk
2023, Journal of Hazardous MaterialsDiesel exhaust particles (DEP) pollution should be taken seriously because it is an extensive environmental and occupational health concern. Exploring early effect biomarkers is crucial for monitoring and managing DEP-associated health risk assessment. Here, we found that serum levels of 67 miRNAs were dysregulated in DEP exposure group. Notably, 20 miRNAs were identified as each having a significant dose-response relationship with the internal exposure level of DEP. Further, we revealed that the DEP exposure could affect the liver function of subjects and that 7 miRNAs (including the well-known liver injury indicator, miR-122–5p) could serve as the novel epigenetic-biomarkers (epi-biomarkers) to reflect the liver-specific response to the DEP exposure. Importantly, an unprecedented prediction model using these 7 miRNAs was established for the assessment of DEP-induced liver injury risk. Finally, bioinformatic analysis indicated that the unique set of miRNA panel in serum might also contribute to the molecular mechanism of DEP exposure-induced liver damage. These results broaden our understanding of the adverse health outcomes of DEP exposure. Noteworthy, we believe this study could shed light on roles and functions of epigenetic biomarkers from environmental exposure to health outcomes by revealing the full chain of exposure-miRNAs-molecular pathways-disease evidence.