In China, PM₂.₅ pollution has caused extensive death and economic loss. Thus, an accurate assessment of the spatial distribution of these losses is crucial for delineating priority areas for air pollution control in China. In this study, we assessed the PM₂.₅ exposure-related health effects according to the integrated exposure risk function and non-linear power law (NLP) function in 338 prefecture-level cities in China by utilizing online monitoring data and the PM₂.₅ Hindcast Database (PHD). Our results revealed no significant difference between the monitoring data and PHD (p value = 0.66 > 0.05). The number of deaths caused by PM₂.₅-related Stroke (cerebrovascular disease), ischemic heart disease, chronic obstructive pulmonary disease, and lung cancer at the national level estimated through the NLP function was 0.27 million (95% CI: 0.06–0.50), 0.23 million (95% CI: 0.08–0.38), 0.31 million (95% CI: 0.04–0.57), and 0.31 million (95% CI: 0.16–0.40), respectively. The total economic cost at the national level in 2016 was approximately US$80.25 billion (95% CI: 24.46–132.25). Based on a comparison of Z statistics, we propose that the evaluation results obtained using the NLP function and monitoring data are accurate. Additionally, according to scenario simulations, Beijing, Chongqing, Tianjin, and other cities should be priority areas for PM₂.₅ pollution control to achieve considerable health benefits. Our statistics can help improve the accuracy of PM₂.₅-related health effect assessments in China.

Dinotefuran is a third-generation neonicotinoid pesticide and is increasingly used in agricultural production, which has adverse effects on nontarget organisms. However, the research on the impact of dinotefuran on nontarget organisms is still limited. Here the toxic effects of dinotefuran on an important economic species and a model lepidopteran insect, Bombyx mori, were investigated. Exposure to different doses of dinotefuran caused physiological disorders or death. Cytochrome P450, glutathione S-transferase, carboxylesterase, and UDP glycosyl-transferase activities were induced in the fat body at early stages after dinotefuran exposure. By contrast, only glutathione S-transferase activity was increased in the midgut. To overcome the lack of sensitivity of the biological assays at the individual organism level, RNA sequencing was performed to measure differential expressions of mRNA from silkworm larvae after dinotefuran exposure. Differential gene expression profiling revealed that various detoxification enzyme genes were significantly increased after dinotefuran exposure, which was consistent with the upregulation of the detoxifying enzyme. The global transcriptional pattern showed that the physiological responses induced by dinotefuran toxicity involved multiple cellular processes, including energy metabolism, oxidative stress, detoxification, and other fundamental physiological processes. Many metabolism processes, such as carbon metabolism, fatty acid biosynthesis, pyruvate metabolism, and the citrate cycle, were partially repressed in the midgut or fat body. Furthermore, dinotefuran significantly activated the MAPK/CREB, CncC/Keap1, PI3K/Akt, and Toll/IMD pathways. The links between physiological, biochemical toxicity and comparative transcriptomic analysis facilitated the systematic understanding of the integrated biological toxicity of dinotefuran. This study provides a holistic view of the toxicity and detoxification metabolism of dinotefuran in silkworm and other organisms.

The spread of SARS-CoV-2, the beta coronavirus responsible for the current pneumonia pandemic outbreak, has been speculated to be linked to short-term and long-term atmospheric pollutants exposure. The present work has been aimed at analyzing the atmospheric pollutants concentrations (PM₁₀, PM₂.₅, NO₂) and spatio-temporal distribution of cases and deaths (specifically incidence, mortality and lethality rates) across the whole Italian national territory, down to the level of each individual territorial area, with the goal of checking any potential short-term correlation between these two phenomena. The data analysis has been limited to the first quarter of 2020 to reduce the lockdown-dependent biased effects on the atmospheric pollutant levels as much as possible. The analysis looked at non-linear, monotonic correlations using the Spearman non-parametric correlation index. The statistical significance of the Spearman correlations has also been evaluated. The results of the statistical analysis suggest the hypothesis of a moderate-to-strong correlation between the number of days exceeding the annual regulatory limits of PM₁₀, PM₂.₅ and NO₂ atmospheric pollutants and COVID-19 incidence, mortality and lethality rates for all the 107 territorial areas in Italy. A weak-to-moderate correlation seems to exist when considering the 36 territorial areas in four of the most affected regions (Lombardy, Piedmont, Emilia-Romagna and Veneto). Overall, PM₁₀ and PM₂.₅ showed a higher non-linear correlation than NO₂ with incidence, mortality and lethality rates. As to particulate matters, PM₁₀ profile has been compared with the incidence rate variation that occurred in three of the most affected territorial areas in Northern Italy (i.e., Milan, Brescia, and Bergamo). All areas showed a similar PM₁₀ time trend but a different incidence rate variation, that was less severe in Milan compared with Brescia and Bergamo.

Entanglement of pinnipeds with plastic debris is an emerging conservation and animal welfare issue worldwide. However, the origins and long-term population level consequences of these entanglements are usually unknown. Plastic entanglement could produce a combination of wounds, asphyxiation, or inability to feed that results in the death of a certain percentage of individuals from the total population. In this research, we report on the consequent effect of plastic entanglement on population growth demographics in a South American fur seal (Arctocephalus australis australis) colony on Guafo Island, southern Chile. Using a stochastic matrix population model structured according to age and sex, and assuming an otherwise stable population, we explored population growth rates under five scenarios with differing rates of entanglement: A) a zero rate of plastic entanglement, B) entanglement rates (number of entangled individuals as a proportion of the total number of individuals) as observed in our study population (overall entanglement ratio of 1.2 × 10⁻³); and for the other scenarios, entanglement ratios as reported in the literature for other pinniped colonies around the world: C) 3.04 × 10⁻³, D) 4.42 × 10⁻², and E) 8.39 × 10⁻². Over the 30 years forecasting period and starting with a population size of ∼2950 individuals, the population growth rate was lower under all scenarios with rates of entanglement greater than zero (scenarios B-E). In comparison with scenario A, at the end of the 30-year period forecasted, we calculated a projected decrease in population size of between 20.34% (scenario B) and 91.38% (scenario E). These results suggest that even the lowest levels of entanglement in pinnipeds as reported in the literature might have significant effects over time on population-level dynamics. Our research offers potential insight when devising policy for the management and limitation of plastic pollution in the oceans, and indeed for the conservation and management policy of affected marine species. Furthermore, whilst there are some limitations to our methodology, it offers a straightforward and potentially useful approach for the standardized prediction of impacts at a population level of different rates of plastic pollution and entanglement and could be applied in distinct populations of the same species around the world.

In December 2019, a novel disease, coronavirus disease 19 (COVID-19), emerged in Wuhan, People’s Republic of China. COVID-19 is caused by a novel coronavirus (SARS-CoV-2) presumed to have jumped species from another mammal to humans. This virus has caused a rapidly spreading global pandemic. To date, over 300,000 cases of COVID-19 have been reported in England and over 40,000 patients have died. While progress has been achieved in managing this disease, the factors in addition to age that affect the severity and mortality of COVID-19 have not been clearly identified. Recent studies of COVID-19 in several countries identified links between air pollution and death rates. Here, we explored potential links between major fossil fuel-related air pollutants and SARS-CoV-2 mortality in England. We compared current SARS-CoV-2 cases and deaths from public databases to both regional and subregional air pollution data monitored at multiple sites across England. After controlling for population density, age and median income, we show positive relationships between air pollutant concentrations, particularly nitrogen oxides, and COVID-19 mortality and infectivity. Using detailed UK Biobank data, we further show that PM₂.₅ was a major contributor to COVID-19 cases in England, as an increase of 1 m³ in the long-term average of PM₂.₅ was associated with a 12% increase in COVID-19 cases. The relationship between air pollution and COVID-19 withstands variations in the temporal scale of assessments (single-year vs 5-year average) and remains significant after adjusting for socioeconomic, demographic and health-related variables. We conclude that a small increase in air pollution leads to a large increase in the COVID-19 infectivity and mortality rate in England. This study provides a framework to guide both health and emissions policies in countries affected by this pandemic.

Prorocentrum lima is a dinoflagellate that forms hazardous blooms and produces okadaic acid (OA), leading to adverse environmental consequences associated with the declines of zooplankton populations. However, little is known about the toxic effects and molecular mechanisms of P. lima or OA on zooplankton. Here, their toxic effects were investigated using the brine shrimp Artemia salina. Acute exposure of A. salina to P. lima resulted in lethality at concentrations 100-fold lower than densities observed during blooms. The first comprehensive results from global transcriptomic and metabolomic analyses in A. salina showed up-regulated mRNA expression of antioxidant enzymes and reduced non-enzyme antioxidants, indicating general detoxification responses to oxidative stress after exposure to P. lima. The significantly up-regulated mRNA expression of proteasome, spliceosome, and ribosome, as well as the increased fatty acid oxidation and oxidative phosphorylation suggested the proteolysis of damaged proteins and induction of energy expenditure. Exposure to OA increased catabolism of chitin, which may further disrupt the molting and reproduction activities of A. salina. Our data shed new insights on the molecular responses and toxicity mechanisms of A. salina to P. lima or OA. The simple zooplankton model integrated with omic methods provides a sensitive assessment approach for studying hazardous algae.

Investigating environmental pollution is important to understand its impact on endangered species such as green turtles (Chelonia mydas). In this study, we investigated the accumulation and potential toxicity of selected persistent organic pollutants (POPs) and naturally occurring MeO-PBDEs in liver, fat, kidney and muscle of turtles (n = 30) of different gender, size, year of death, location and health status. Overall, POP concentrations were low and accumulation was highest in liver and lowest in fat which is likely due to the poor health of several animals, causing a remobilization of lipids and associated compounds. PCBs and p,p’-DDE dominated the POP profiles, and relatively high MeO-PBDE concentrations (2′-MeO-BDE 68 up to 192 ng/g lw, 6-MeO-BDE 47 up to 79 ng/g lw) were detected in all tissues. Only few influences of factors such as age, gender and location were found. While concentrations were low compared to other marine wildlife, biological toxicity equivalences obtained by screening the tissue extracts using the micro-EROD assay ranged from 2.8 to 356 pg/g and the highest values were observed in muscle, followed by kidney and liver. This emphazises that pollutant mixtures found in the turtles have the potential to cause dioxin-like effects in these animals and that dioxin-like compounds should not be overlooked in future studies.

Bifenazate is a novel acaricide for selective foliar spraying and is widely used to control mites in agricultural production. However, its toxicity to aquatic organisms is unknown. Here, a zebrafish model was used to study bifenazate toxicity to aquatic organisms. Exposure to bifenazate was found to cause severe cardiotoxicity in zebrafish embryos, along with disorders in the gene expression related to heart development. Bifenazate also caused oxidative stress. Cardiotoxicity caused by bifenazate was partially rescued by astaxanthin (an antioxidant), accompanied by cardiac genes and oxidative stress-related indicators becoming normalized. Our results showed that exposure to bifenazate can significantly change the ATPase activity and gene expression levels of the calcium signaling pathway. These led to heart failure, in which the blood accumulated outside the heart without entering it, eventually leading to death. The results indicated that bifenazate exposure caused cardiotoxicity in zebrafish embryos through the induction of oxidative stress and inhibition of the calcium signaling pathway.

Owing to environmental health concerns, a number of per- and polyfluoroalkyl substances (PFAS) have been phased-out, and increasingly replaced by various chemical analogs. Most prominent among these replacements are numerous perfluoroether carboxylic acids (PFECA). Toxicity, and environmental health concerns associated with these next-generation PFAS, however, remains largely unstudied. The zebrafish embryo was employed, in the present study, as a toxicological model system to investigate toxicity of a representative sample of PFECA, alongside perfluorooctanoic acid (PFOA) as one of the most widely used, and best studied, of the “legacy” PFAS. In addition, high-resolution magic angle spin (HRMAS) NMR was utilized for metabolic profiling of intact zebrafish embryos in order to characterize metabolic pathways associated with toxicity of PFAS. Acute embryotoxicity (i.e., lethality), along with impaired development, and variable effects on locomotory behavior, were observed for all PFAS in the zebrafish model. Median lethal concentration (LC₅₀) was significantly correlated with alkyl chain-length, and toxic concentrations were quantitatively similar to those reported previously for PFAS. Metabolic profiling of zebrafish embryos exposed to selected PFAS, specifically including PFOA and two representative PFECA (i.e., GenX and PFO3TDA), enabled elaboration of an integrated model of the metabolic pathways associated with toxicity of these representative PFAS. Alterations of metabolic profiles suggested targeting of hepatocytes (i.e., hepatotoxicity), as well as apparent modulation of neural metabolites, and moreover, were consistent with a previously proposed role of mitochondrial disruption and peroxisome proliferator-activated receptor (PPAR) activation as reflected by dysfunctions of carbohydrate, lipid and amino acid metabolism, and consistent with a previously proposed contribution of PFAS to metabolic syndrome. Taken together, it was generally concluded that toxicity of PFECA is quantitatively and qualitatively similar to PFOA, and these analogs, likewise, represent potential concerns as environmental toxicants.

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.