In the previous publication “Can atmospheric pollution be considered a co-factor in extremely high level of SARS-CoV-2 lethality in Northern Italy?” Conticini et al. hypothesized that the surplus of lethality of the novel SARS-CoV-2 in Northern Italy may be at least in part explained by the evidence of highest pollution reported in this area, as both severe COVID-19 and smog exposure are correlated to an innate immune system hyper-activation with subsequent lung inflammation and injury. Since this hypothesis alone does not fully explain why specific subgroups of patients are at major risk, we hypothesized that obesity may be one of the links between COVID-19 severity and high level of air pollution. First, obesity is a predisposing factor for SARS-Cov-2 infection and worse COVID-19 outcomes, and unequivocal evidence demonstrated that fat mass excess is independently associated with several pulmonary diseases and lung inflammation. Moreover, it has been shown that obesity may intensify the detrimental effects of air pollution on the lungs, and this is not surprising if we consider that these conditions share an excessive activation of the immune system and a lung inflammatory infiltrate. Finally, fat mass excess has also been speculated to be itself a consequence of air pollutants exposure, which has been proved to induce metabolic disruption and weight gain in murine models. In conclusion, although many variables must be taken into account in the analysis of the pandemic, our observations suggest that obesity may act as effect modifier of smog-induced lung-injury, and the concomitant presence of these two factors could better explain the higher virulence, faster spread and greater mortality of SARS-CoV-2 in Northern Italy compared to the rest of the country.

Pharmaceuticals and personal care products (PPCPs) are a class of emerging contaminants commonly detected in environmental waters worldwide. Although reports about their detection in aquatic environments are increasing, limited studies show their effects on holometabolous insects. In this study, acute and chronic exposure to naproxen (0.02, 41, 82, 164, 382, 656, and 1312 mg L⁻¹) and propylparaben (0.02, 25, 50, 100, 250, 500, and 1000 mg L⁻¹) were evaluated in Aedes aegypti L. Acute exposure to naproxen (≥0.02 mg L⁻¹) and propylparaben (≥0.02 mg L⁻¹) reduced egg eclosion. Propylparaben (≥250 mg L⁻¹) caused significant larval mortality but naproxen did not even at the highest experimental concentration used. LC₅₀ for naproxen and propylparaben in larvae were 1100 mg L⁻¹ and 182.6 mg L⁻¹, respectively. Naproxen (≥0.02 mg L⁻¹) and propylparaben (≥0.02 mg L⁻¹) reduced pupation. Emergence was also reduced by naproxen (≥164 mg L⁻¹) and propylparaben (≥0.02 mg L⁻¹). The fecundity of females was significantly reduced due to chronic exposure to naproxen (≥0.02 mg L⁻¹). There was also a reduction in the fecundity of females due to chronic propylparaben exposure but it was statistically insignificant in the concentrations used. In the F1 generation eggs, only 100 mg L⁻¹ propylparaben reduced eclosion. Eclosion and larval survival were sensitive to acute exposure, particularly to propylparaben. The reduced pupation and emergence indicated a delay in the progression of the life cycle. Chronic exposure also indicated a reduction in fecundity. F1 eggs exhibited tolerance to the negative effect of subsequent exposure. Our findings suggest that propylparaben can affect Ae. aegypti more negatively than naproxen.

Fossil fuels still prevail over other energy sources in the world’s consumption energy matrix. Thus, oil transportation and operations over maritime routes have been in high demand for a long time. Although oil spill accidents caused by these activities have reduced significantly over the last few decades, they still cause great concern. From this perspective, this paper presents simulation analyses of oil spill case studies using TELEMAC-3D hydrodynamic model coupled with an oil model. Hence a location susceptible to such accidents was selected and three real oil spills were simulated, for each of which there were official technical monitoring reports available. The obtained results contribute to the knowledge of oil pollution susceptibility in environmentally sensitive areas, as well as provide information concerning oil slick behaviour. Additionally, similarities between the modelled results and the technical reports were confirmed. These findings are useful for contingency planning and responding to these probable accidents.

Microplastics (MPs) are new persistent organic pollutants derived from the degradation of plastics. They can accumulate along the food chain and enter the human body through oral administration, inhalation and dermal exposure. To identify the impact of Polystyrene (PS) MPs on the cardiovascular system and the underlying toxicological mechanism, 32 male Wister rats were divided into control group and three model groups, which were exposed to 0.5 μm PS MPs at 0.5, 5 and 50 mg/L for 90 days. Our results suggested that PS MPs exposure increased Troponin I and creatine kinase-MB (CK-MB) levels in serum, resulted in structure damage and apoptosis of myocardium, and led to collagen proliferation of heart. Moreover, PS MPs could induce oxidative stress and thus activate fibrosis-related Wnt/β-catenin signaling pathway. These results suggested that PS MPs could lead to cardiovascular toxicity by inducing cardiac fibrosis via activating Wnt/β-catenin pathway and myocardium apoptosis triggered by oxidative stress. The present study provided some novelty evidence to elucidate the potential mechanism of cardiovascular toxicity induced by PS MPs.

Hydroquinone (HQ), one of the main metabolites of benzene, is a well-known human leukemogen. However, the specific mechanism of how benzene or HQ contributes to the development of leukemia is unknown. In a previous study, we demonstrated the upregulation of DNA methyltransferase (DNMT) expression in HQ-induced malignant transformed TK6 (HQ-TK6) cells. Here, we investigated whether a regulatory loop between the long noncoding RNA FAS-AS1 and DNMT3b exists in HQ-TK6 cells and benzene-exposed workers. We found that the expression of FAS-AS1 was downregulated in HQ-TK6 cells and workers exposed to benzene longer than 1.5 years via histone acetylation, and FAS-AS1 expression was negatively correlated with the time of benzene exposure. Restoration of FAS-AS1 in HQ-TK6 cells promoted apoptosis and inhibited tumorigenicity in female nude mice. Interestingly, treatment with a DNMT inhibitor (5-aza-2-deoxycytidine), histone deacetylase inhibitor (trichostatin A), or DNMT3b knockout led to increased FAS-AS1 through increased H3K27ac protein expression in HQ-TK6 cells, and DNMT3b knockout decreased H3K27ac and DNMT3b enrichment to the FAS-AS1 promoter region, which suggested that DNMT3b and/or histone acetylation involve FAS-AS1 expression. Importantly, restoration of FAS-AS1 resulted in reduced expression of DNMT3b and SIRT1 and increased expression of FAS in both HQ-TK6 cells and xenograft tissues. Moreover, the average DNMT3b expression in 17 paired workers exposed to benzene within 1.5 years was decreased, but that of the remaining 103 paired workers with longer exposure times was increased. Conversely, DNMT3b was negatively correlated with FAS-AS1 expression. Both FAS-AS1 and DNMT3b influenced the enrichment of H3K27ac in the FAS promoter region by regulating the expression of SIRT1, consequently upregulating FAS expression. Taken together, these observations demonstrate crosstalk between FAS-AS1 and DNMT3b via a mutual inhibition loop and indicate a new mechanism by which FAS-AS1 regulates the expression of FAS in benzene-related carcinogenesis.

Polycyclic Aromatic Hydrocarbons are strongly associated with agricultural, residential, transportation, and industrial activities. This study determined by GC-MS the concentration of 15 PAHs in soil and sediments at different sites from the Awotan-Asunle dumpsite area in the Southwestern region of Nigeria, which is one of the largest dumpsites in Africa. The sources of contamination, toxicity and associated risks for human health were also evaluated. Total PAHs concentrations were from 489 to 5616 μg kg⁻¹, and 642–2159 μg kg⁻¹, for soil and sediment, respectively. For soils, the highest values were observed for indeno[1,2,3-c,d]pyrene, coronene, and phenanthrene, while for sediments, the most abundant species were pyrene, fluoranthene and phenanthrene. Diagnostic ratios were used to determine the sources of PAHs and suggested that the compounds were mainly emitted from non-traffic sources. The total BaP-TEQ and BaP-MEQ for soils did not exceed the value recommended by the Canadian guideline since the country does not present guidelines. The analysis of incremental lifetime cancer risk was high mostly for dermal and ingestion exposures in the population. This study might provide valuable information regarding exposure to PAHs in soils of a Nigerian community.

Microplastics (MP) are omnipresent contaminants in the oceans, however little is known about the MP transfer between marine compartments and species. Three connected laboratory experiments using the filter-feeding mussel Mytilus galloprovincialis and the omnivorous polichaete Hediste diversicolor were conducted to evaluate whether the filtering action by mussels affects the vertical transfer of MP of different sizes (MPSMALL = 41 μm; MPLARGE = 129 μm) and densities (polyamide = 1.15 g cm⁻³; polypropylene = 0.92 g cm⁻³) across compartments and species with different feeding modes. Mussels significantly removed MP from the water column by incorporating them into biodeposits. This effect was particularly evident for the MPSMALL, whose deposition from the water column to the bottom was enhanced (about 15%) by the action of mussels. The incorporation of MP into faecal pellets increased the particles’ sinking velocity by about 3–4 orders of magnitude. Conversely, the MP presence significantly decreased the depositional velocities of faecal pellets, and the magnitude of this effect was greater with increasing MP size and decreasing density. The MP incorporation into mussels’ biodeposits also more than doubled the amount of MP uptake by H. diversicolor. We conclude that detrital pathways could be a transfer route of MP across marine compartments and food webs, potentially affecting the distribution of MP in sediments and creating hot-spots of bioavailable MP.

Freshwater mussels are one of the most threatened taxonomic groups in the world, and many species are on the brink of local or global extinction. Human activities have altered mussel living conditions in a plethora of ways. One of the most destructive human-induced impacts on running waters is the catastrophic spill of harmful substances, which results in massive die-offs. Even though Finland is regarded as the world’s top country in terms of environmental regulation quality, riverine systems are not safe. In 2014, River Kokemäenjoki in western Finland experienced the worst NiSO4 spill in the country’s history, visibly affecting the mussel community – including protected Unio crassus – along the river. Because freshwater mussel toxicology is grossly understudied (particularly in Europe), any pollution –linked die-offs offer valuable opportunities to study the issue in natural environment. Here, we report the mussel investigations from 2014 and a follow-up study conducted in 2017 in order to assess the variation in species sensitivity on nickel pollution. In total, 104 sites were sampled, and over 20 000 mussels were identified and counted. Our results indicate that the most impacted species (i.e. that which experienced the highest spill-induced mortality) was Anodonta anatina (62%), followed by Unio pictorum (32%), U. crassus (24%) and Unio tumidus (9%). The underlying reason for the sensitivity of A. anatina is not resolved, hence more research is urgently needed. The low mortality among most of the species in 2017 highlights the temporal nature of the pollution impact and the recovery potential of the mussel community. However, the case is more complex with U. crassus population, which may be experiencing delayed impacts of the spill. Because nickel is one of the most commonly produced industrial metals in the world (hence the pollution incident risk is high) and River Kokemäenjoki hosts mussel community typical for European rivers, our results may benefit many researchers and stakeholders dealing with riverine environments.

On-road remote sensing technology measures the concentration ratios of pollutants over CO₂ in the exhaust plume in half a second when a vehicle passes by a measurement site, providing a rapid, non-intrusive and economic tool for vehicle emissions monitoring and control. A key assumption in such measurement is that the emission ratios are constant for a given plume. However, there is a lack of study on this assumption, whose validity could be affected by a number of factors, especially the engine operating conditions and turbulence. To guide the development of the next-generation remote sensing system, this study is conducted to investigate the effects of various factors on the emissions dispersion process in the vehicle near-wake region and their effects on remote sensing measurement. The emissions dispersion process is modelled using Large Eddy Simulation (LES). The studied factors include the height of the remote sensing beam, vehicle speed, acceleration and side wind. The results show that the measurable CO₂ and NO exhaust plumes are relatively short at 30 km/h cruising speed, indicating that a large percentage of remote sensing readings within the measurement duration (0.5 s) are below the sensor detection limit which would distort the derived emission ratio. In addition, the valid measurement region of NO/CO₂ emission ratio is even shorter than the measurable plume and is at the tailpipe height. The effect of vehicle speed (30–90 km/h) on the measurable plume length is insignificant. Under deceleration condition, the length of the valid NO/CO₂ measurement region is shorter than under cruising and acceleration conditions. Side winds from the far-tailpipe direction have a significant effect on remote sensing measurements. The implications of these findings are discussed and possible solutions to improve the accuracy of remote sensing measurement are proposed.

Perfluorooctanoic acid (PFOA) is a widely used synthetic industrial chemical which accumulates in ecosystems and organisms. Our study have investigated the neurobehavioral effects of PFOA and the alleviation effects of PFOA-induced neurotoxicity by blueberry anthocyanins (ANT) in Dugesia japonica. The planarians were exposed to PFOA and ANT for ten days. Researchs showed that exposure to PFOA affected locomotor behavior and ANT significantly alleviated the reduction in locomotion induced by PFOA. The regeneration of eyespots and auricles was suppressed by PFOA and was promoted by ANT. Following exposure to PFOA, acetylcholinesterase activity continually decreased and was unaffected in the ANT group, but was elevated after combined administration of PFOA and ANT. Oxidative DNA damage was found in planarians exposed to PFOA and was attenuated after administration of ANT by the alkaline comet assay. Concentrations of three neurotransmitters increased following exposure to PFOA and decreased after administration of ANT. Furthermore, ANT promoted and PFOA inhibited neuronal regeneration. DjotxA, DjotxB, DjFoxG, DjFoxD and Djnlg associated with neural processes were up-regulated following exposure to PFOA. Our findings indicate that PFOA is a neurotoxicant while ANT can attenuate these detrimental effects.