It is enlightening to determine the discrepancies and potential reasons for the degree of impact from the COVID-19 control measures on air quality as well as the associated health and economic impacts. Analysis of air quality, socio-economic factors, and meteorological data from 447 cities in 46 countries indicated that the COVID-19 control measures had significant impacts on the PM₂.₅ (particulate matter with an aerodynamic diameter less than 2.5 μm) concentrations in 20 (reduced PM₂.₅ concentrations of −7.4–29.1 μg m⁻³) of the selected 46 countries. In these 20 countries, the robustly distinguished changes in the PM₂.₅ concentrations caused by the control measures differed between the developed (95% confidence interval (CI): −2.7–5.5 μg m⁻³) and developing countries (95% CI: 8.3–23.2 μg m⁻³). As a result, the COVID-19 lockdown reduced death and hospital admissions change from the decreased PM₂.₅ concentrations by 7909 and 82,025 cases in the 12 developing countries, and by 78 and 1214 cases in the eight developed countries. The COVID-19 lockdown reduced the economic cost from the PM₂.₅ related health burden by 54.0 million dollars in the 12 developing countries and by 8.3 million dollars in the eight developed countries. The disparity was related to the different chemical compositions of PM₂.₅. In particular, the concentrations of primary PM₂.₅ (e.g., BC) in cities of developing countries were 3–45 times higher than those in developed countries, so the mass concentration of PM₂.₅ was more sensitive to the reduced local emissions in developing countries during the COVID-19 control period. The mass fractions of secondary PM₂.₅ in developed countries were generally higher than those in developing countries. As a result, these countries were more sensitive to the secondary atmospheric processing that may have been enhanced due to reduced local emissions.

A recently identified chemical, 2-((4-Methylpentan-2-yl)amino)-5-(phenylamino)cyclohexa-2,5-diene-1,4-dione (6PPD-quinone; 6PPD-Q), is a transformation product of an additive used in the manufacture of tire rubber and causes acute lethality in coho salmon (Oncorhynchus kisutch) in urban watersheds. Despite its potential presence and ecotoxicity in receiving waters worldwide, information on the occurrence and fate of 6PPD-Q is limited. Here, we investigated the concentrations of 6PPD-Q and its parent chemical, 6PPD, in road dust collected from arterial and residential roads in Tokyo, Japan from May to October 2021. 6PPD-Q concentrations were highest from May to June, when atmospheric ozone concentrations are the highest in Japan; a correlation between 6PPD-Q and photochemical oxidants, as an alternative to ozone, corroborated this finding. We also found that 6PPD-Q concentrations at photochemical oxidant concentrations ranging from 35 to 47 ppbv were higher in dust collected from roads with high traffic volumes (i.e., arterial roads; median: 8.6 μg/g-OC) than in dust collected from roads with lower traffic volumes (i.e., residential roads; median: 6.3 μg/g-OC), indicating that 6PPD-Q is generated from traffic-related sources. We also found that 6PPD-Q was leached from dust particles within a few hours, with a log partitioning coefficient between organic carbon and water (KOC) of 3.2–3.5. The present results will help to understand the environmental occurrence, fate, and behavior of 6PPD-Q.

Long-term exposure to PM₂.₅ has been linked to lung cancer incidence and mortality, but limited evidence existed for other cancers. This study aimed to assess the association between PM₂.₅ on cancer specific mortality. An ecological study based on the cancer mortality data collected from 5,565 Brazilian cities during 2010–2018 using a difference-in-differences approach with quasi-Poisson regression, was applied to examine PM₂.₅-cancer mortality associations. Globally gridded annual average surface PM₂.₅ concentration was extracted and linked with the residential municipality of participants in this study. Sex, age stratified and exposure-response estimations were also conducted. Totalling 1,768,668 adult cancer deaths records of about 208 million population living across 5,565 municipalities were included in this study. The average PM₂.₅ concentration was 7.63 μg/m³ (standard deviation 3.32) with range from 2.95 μg/m³ to 28.5 μg/m³. With each 10 μg/m³ increase in three-year-average (current year and previous two years) concentrations of PM₂.₅, the relative risks (RR) of cancer mortality were 1.16 (95% confidence interval [CI]: 1.11–1.20) for all-site cancers. The PM₂.₅ exposure was significantly associated with several cancer-specific mortalities including oral, nasopharynx, oesophagus, and stomach, colon rectum, liver, gallbladder, larynx, lung, bone, skin, female breast, cervix, prostate, brain and leukaemia. No safe level of PM₂.₅ exposure was observed in the exposure-response curve for all types of cancer. In conclusion, with nationwide cancer death records in Brazil, we found that long-term exposure to ambient PM₂.₅ increased risks of mortality for many cancer types. Even low level PM₂.₅ concentrations had significant impacts on cancer mortality.

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.

There is now unequivocal evidence that sunscreen can severely affect marine ecosystems. However, so far, most studies have focused on the impact of single sunscreen ingredients rather than on the whole sunscreen products, which are released into the marine environment. In the present work, we investigated the ecological impact of six formulations, which represent the “new generation” organic UV filters such as diethylamino hydroxybenzoyl hexyl benzoate (DHHB), methylene bis-benzotriazolyl tetramethylbutylphenol (MBBT), ethylhexyl triazone (EHT), and bis-ethylhexyloxyphenol methoxyphenyl triazine (BEMT), which are progressively replacing the “old generation” organic UV filters (e.g., oxybenzone, octinoxate) banned in several countries of the world. The six formulations tested were characterized by a different combination of ingredients, on a model species particularly sensitive to environmental alterations: the sea urchin, Paracentrotus lividus. We investigated the sea urchin responses both in terms of gene expression and anomalies in embryonic development. We found that all sunscreen products containing only MBBT, DHHB, BEMT, and EHT as UV filters, are more eco-compatible than those also containing also ES, or other ingredients such as emollients and texturizing compounds, which may act synergistically causing molecular stress, morphological anomalies, and ultimately possible death. Overall, the results presented here provide new insights on the effects of sunscreen products based on “new generation” UV filters, and highlights the urgency of testing complete formulations, rather than just specific UV filters to ascertain the eco-compatibility of sunscreen products, to effectively minimize their impact on marine ecosystems.

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.

The outbreak of coronavirus (COVID-19) has forced China to lockdown many cities and restrict transportation, industrial, and social activities. This provides a great opportunity to look at the impacts of pandemic quarantine on air quality and premature death due to exposure to air pollution. In this study, we applied the difference-in-differences (DID) model to quantify the casual impacts of COVID-19 lockdown on air quality at 278 cities across China. A widely used exposure-response function was further utilized to estimate the short-term health impacts associated with changes in PM₂.₅ due to lockdown. Results show that lockdown has caused drastic reduction in air pollution level in terms of all criteria pollutants except ozone. On average, concentrations of PM₂.₅, PM₁₀, NO₂, SO₂ and CO are estimated to drop by 14.3 μg/m³, 22.2 μg/m³, 17.7 μg/m³, 2.9 μg/m³, and 0.18 mg/m³ as the result of lockdown. Cities with more confirmed cases of COVID-19 are related to stronger responses in air quality, despite that similar lockdown measures were implemented by the local governments. The improvement of air quality caused by COVID-19 lockdown in northern cities is found to be smaller than that of southern cities. Avoided premature death associated with PM₂.₅ exposures over the 278 cities was estimated to be 50.8 thousand. Our results re-emphasize the effectiveness of emission controls on air quality and associated health impacts. The high cost of lockdown, still high level of air pollution during lockdown and smaller effects in northern cities implies that source-specific mitigation policies are needed for continuous and sustainable reduction of air pollution.

We aimed to update the evidence-base of long-term noise exposures from road, rail, and aircraft traffic on both non-accidental and cardiovascular mortality.A systematic review and meta-analysis were conducted following PRISMA guidelines. The literature was searched using PubMed, Scopus, Web of Science, and EMBASE for the period between January 01, 2000 and October 05, 2020. 13 studies were selected for final review. The risk of bias and overall quality of evidence was evaluated using a pre-defined list of criteria. Risk estimates from each study were converted into per 10 dB higher of Ldₑₙ for each traffic source. Inverse-Variance heterogeneity (I-Vhet) meta-analysis was used to pool these individual risk estimates, along with assessment of heterogeneity and publication bias. Sensitivity analyses include using random-effect model and leave-one-out meta-analysis. Subgroup analyses by study design and noise exposure assessment were conducted to explore potential sources of heterogeneity.For road traffic, the pooled relative risk (RR) per 10 dB higher Ldₑₙ for mortality from non-accidental causes was 1.01 (95% CI: 0.98, 1.05) (5 studies, I² = 78%), CVD was 1.01 (95% CI: 0.98, 1.05) (5 studies, I² = 41%), ischemic heart disease (IHD) was 1.03 (95% CI: 0.99, 1.08) (7 studies, I² = 46%), and stroke was 1.05 (95% CI: 0.97, 1.14) (5 studies, I² = 62%). The overall quality of evidence for most meta-analyses was rated as very low to low, except for CVD or IHD mortality, for which the quality of evidence was rated as moderate. A possible threshold of 53 dB was visually suggested for CVD-related mortality from road traffic noise in the trend analysis. For aircraft noise, pooled estimates were based on fewer studies and varied by mortality outcomes.Evidence of long-term exposure to traffic noise on mortality remains weak except the association between road traffic noise and IHD mortality. High-quality longitudinal studies are required to better characterise mortality effects of traffic noise.

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.

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.