Previous studies have suggested a change of birth weight linked with elevated ambient air pollutant concentrations during the pregnancy. However, investigations of the influence of higher pollutant levels on birth weight change are limited. The goal of this study is to evaluate whether the air pollution of Ningbo is associated with birth weight, and which trimester could be a window period for maternal exposure to air pollution. A total of 170,008 live births were selected in the Ningbo city of Zhejiang, China, from 2015 to 2017. We estimated the association between the decreased birth weight and the increased air pollutant concentrations in the three trimesters and full gestation. The effects of interaction among pollutants were identified using a co-pollutant adjustment model. An interquartile range increases in PM2.5 (10.55 μg/m3), SO2(4.6 μg/m3), CO (125.59 μg/m3), and O3 (14.54 μg/m3) concentrations during the entire gestation were associated with 3.65 g (95% confidence interval: −6.02 g, −1.29 g), 5.02 g (−6.89 g, −3.14 g), 2.64 g (−4.65 g, −0.63 g) and 2.9 g (−4.8 g, 1 g) decreases, respectively, in birth weight. With each interquartile range increment in NO2 concentration was associated with an 8.05 g (6.24 g, 9.85 g) increase in birth weight. In the first trimester, only the PM2.5 exposure seemed to be associated with the greatest decline in birth weight. After adjustment for co-pollutant, both PM2.5 and SO2 were still associated with birth weight, except for CO for O3 adjustment, O3 for SO2 adjustment, and O3 for NO2 adjustment. Maternal exposure to air pollution may be associated with a decrease of birth weight, but the contribution of various pollutants is necessary to verify by future research.

A key action of current aquatic environmental sciences is the determination of concentration-response assessments to quantitatively measure the risk of pollutants, and fish lethal tests are still a regulatory requirement for assessing the environmental risk of both new and existing substances in the aquatic compartment. However, animal health and welfare aspects, as well as the time and resources required to support fish lethal testing, stimulate research for alternative in vitro methods, and cell-based assays are considered as one such alternative. The first goal of the present study was to compile existing fish short-term toxicity and cell toxicity data of pesticides through a scientific literature search, and relate in vivo and in vitro results to identify sensitive cell models, mammalian-, fish- or arthropod-derived. Discovering cell models which are sensitive is of great importance, since the risk of false negatives, believed to be the main limitation of cell-based assays as an alternative to fish tests, may decrease. As to the second goal, this study also determined and compared cell toxicity results for 12 pesticides using rat cardiomyoblast H9c2(2–1) cells with the corresponding fish LC₅₀,₉₆ₕ (50% lethal concentration at 96 h of exposure) values collected in literature. On the whole, the in vivo/in vitro ratio was obtained for 50 pesticides belonging to 23 groups, and presented only 27% of positive results, thus confirming the low sensitivity of cell-based assays in relation to fish lethal data for pesticides. In general, cell-based assays still do not seem to be an alternative to the regulatory short-term fish assay for pesticides, making further studies necessary.

Our world is awash with plastic. The massive increase in plastics production, combined with a shift to single-use, disposable plastics and widespread mismanagement of plastic waste, has created a huge “tragedy of the commons” (Hardin, 1968) in our oceans, seas and waterways. Plastics pollution is now a global externality that damages ecosystems, curtails biodiversity and ultimately has the potential to affect everyone on the planet. Although waste output is often modelled separately from environmental pollution in research, in the case of plastics, the waste problem has become one of global pollution. In this paper, we model the relationship between mismanaged plastic waste1 and income per capita for 151 countries, and for the first time find empirical support for the environmental Kuznets curve using plastics pollution data. Further, we find support for the hypothesis that a key instrument for reducing plastics pollution is investment in scientific and technological research. The paper concludes with a discussion of the results, limitations, and implications for future research and practice.

The effects of methylamine on human health have been debated for several years, but the exact adverse outcomes and definite signaling cascades have not been elucidated yet. Herein, a NF-κB signal pathway, a positive regulator of inflammation was identified as the main pathway of methylamine exposure induced adverse effects in bronchial airway cells (16HBE) for the first time. The results indicated that methylamine could stimulate the overproduction of reactive oxygen species (ROS) in cytoplasm and mitochondria of 16HBE cells. Moreover, ROS accelerate the translocation and phosphorylation of NF-κB in nucleic and promote the expression of inflammatory, such as IL-8 and IL-6. As a result, methylamine was found to be increased ROS-mediated NF-κB activation in cells, leading to the production of inflammatory cytokine. Furthermore, the results also showed that methylamine could affect the expression of cytokines related genes, p53, STAT3, Bcl2, c-myc, Cyclin D, Hes1, Mcl-1, TGF-β2. The breakdown of those cell proliferation and apoptosis related genes were leading to a common toxic mechanism of cell death. In summary, our work uncovers a mechanism by which methylamine can induce the formation of inflammation response and demonstrates potential inflammation and carcinogenesis in human airway cell upon the methylamine inhaled.

Remediation of soil chromium (Cr) pollution is becoming more and more urgent. In this study, a multi-loaded nano-zero-valent iron (nZVI) material (CNH) was prepared by carboxymethyl cellulose (CMC) and humic acid (HA) as dispersant and support agent, respectively, and the remediation effect of CNH, HA and CN (CNH without HA) for Cr contaminated soil was investigated within 90 d cycle. After 7 d treatment of CNH, the HOAc-extractable Cr decreased significantly. After the 90 d remediation, the HOAc-extractable Cr decreased most in the treatment of 3% CNH, about 74.48% lower than control. All treatments eventually caused different decline of soil pH, with a range of 0.12–0.54, in which the CNH treatment group had the least depression. HA loading significantly weakened the toxicity of nZVI, resulting in the higher soil microbial quantity and enzyme activities compared with CN. Additionally, the improvement of soil microecology by CNH and HA was positively correlated with the ratio of application, while CN was negatively correlated (except FDA enzyme activity) with these indexes. These results emphasized the potential of the synthesized CNH as a promising material to remediate Cr contaminated soil. Furthermore, details of possible mechanistic insight into the Cr remediation were carefully discussed.

Ammonia (NH3) emission from agricultural sources has contributed significantly to air pollution, soil acidification, water eutrophication, biodiversity loss, and declining human health. Although there are numerous strategies for reducing NH3 emission from agricultural systems, the effectiveness of these measures is highly variable. Furthermore, the integrated assessment of measures to reduce NH3 emission both from livestock production and cropping systems based on animal and crop type is lacking. Therefore, we conducted a global meta-analysis and integrated assessment of measures to reduce NH3 emission from agricultural systems. Most of the studied mitigation strategies were effective in reducing NH3 emission. In the livestock production system, dietary additive, urease inhibitor (UI), manure acidification and deep manure placement have the highest mitigation potential relative to other mitigation strategies, with reduction ranges of 35.1–54.2%, 24.3–68.7%, 88.8–95.0%, and 93.8–99.7%, respectively, relative to the control, while manure storage management could significantly reduce NH3 emission by 70.0–82.1%. In the cropping system, fertilizer source, use of enhanced efficiency fertilizers, and method of field application are most effective for reducingNH3 emission. The use of ammonium nitrate, controlled release fertilizer (CRF), and deep placement of fertilizers could reduce NH3 emission by 88.3, 56.8, and 48.0%, respectively. Choosing a proper fertilizer is critical for decreasing NH3 emission from cropping systems. We conclude that carefully planned and adopted strategies suited for local conditions are promising for minimizing NH3 emission from agricultural systems on a global scale, while possible effects of those mitigation measures on the emission of greenhouse gases should be studied in the future.

Polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs) and new flame retardants (NFRs) are known thyroid hormone (TH) disruptors, but their disrupting mechanisms in humans are not completely understood. In this study, we aimed to explore the disrupting mechanisms of the aforementioned chemicals via examining TH-regulated proteins and gene expression in human serum. Adult participants from an e-waste dismantling (exposed group) and a control region (control group) in South China provided blood samples for the research. Some compounds of PCBs, PBDEs, and NFRs showed strong binding affinity to the thyroid-stimulating hormone (TSH), thyroglobulin, thyroxine-binding globulin (TBG), gene expression of TH receptor α (TRα) and β, and iodothyronine deiodinase I (ID1). The highly exposed individuals had lower levels of TBG, TSH, and expression of TRα, but higher expression of ID1 than those of the control group. The disruption of TH-regulated proteins and gene expression suggested the exertion of different and, at times, even contradictory effects on TH disruption. However, no statistically significant difference was found in the TH levels between the exposed and the control group, implying that the TH disruption induced by these chemicals depends on the combined influence of multiple mechanisms. Gene expression appears to be an effective approach for investigations of TH disruption and the potential health effects.

DCOIT (4,5-dichloro-2-n-octyl-4-isothiazolin-3-one) is the main component of SeaNine-211, a new antifouling agent that replaces tributyltin to prevent the growth of undesirable organisms on ships. There have been some studies on the toxicity of DCOIT, but the mechanism of DCOIT’s toxicity to crustaceans still requires elucidation. This study examined the chronic toxicity (4 weeks) of 0, 3, 15, and 30 μg/L DCOIT to the Pacific white shrimp (Litopenaeus vannamei) from the aspects of growth and physiological and histological changes in the hepatopancreas and gills. A transcriptomic analysis was performed on the hepatopancreas to reveal the underlying mechanism of DCOIT in shrimp. The exposure to 30 μg/L DCOIT significantly reduced the survival and weight gain of L. vannamei. High Na⁺/K⁺-ATPase activity and melanin deposition were found in the gills after 4 weeks of 15 μg/L or 30 μg/L DCOIT exposure. The highest concentration of DCOIT (30 μg/L) induced changes in hepatopancreatic morphology and metabolism, including high anaerobic respiration and the accumulation of triglycerides. Compared with the exposure to 3 μg/L DCOIT, shrimp exposed to 15 μg/L DCOIT showed more differentially expressed genes (DEGs) than those in the control, and these DEGs were involved in biological processes such as starch and sucrose metabolism and choline metabolism in cancer. The findings of this study indicate that L. vannamei is sensitive to the antifouling agent DCOIT and that DCOIT can induce altered gene expression at a concentration of 15 μg/L and can interfere with shrimp metabolism, growth and survival at 30 μg/L.

The adsorption of polycyclic aromatic hydrocarbons (PAHs) by components such as elemental carbon (EC), total organic carbon (TOC), and particles is different, and EC and PAHs are good materials for reconstructing historical human activity patterns and pollution conditions. In this study, the effects of EC (soot and char), TOC and particles of different grain size on PAHs in surface sediments were quantitatively analysed, and their historical concentrations in a sediment core from western Taihu Lake were reconstructed. The contents of soot, TOC, clay, EC and char explained 57.2%, 27.6%, 26.0%, 24.0% and 16.4%, respectively, of the PAH concentrations in surface sediments. The correlation between the soot and PAH levels was significantly higher than that between the char, TOC, and clay contents and PAH levels, and PAHs were mainly affected by the local economic development and human activity, as indicated by metrics of population, highway mileage, coal burning, and industrial output. With the development of the economy of the Taihu Lake Basin, the composition of PAHs in the sediments has changed: the proportion of low-molecular-weight PAHs decreased from 42.4% to 17.5%, and that of high-molecular-weight PAHs increased from 58.7% to 82.5%. The concentration of PAHs in pore water from Taihu Lake over the past 100 years was reconstructed and ranged from 43.1 to 961.2 μg L−1, with an average of 180.7 μg L−1. After China's reform and opening up, the concentrations of various PAHs in Taihu Lake changed from safe to chronic pollution levels. The ratios of lead (Pb) isotopes and the diagnostic ratios of PAHs showed that the main sources of PAHs in western Taihu Lake sediments were human activities such as coal and petroleum combustion.

Diesel exhaust (DE) contributes to air pollution, an important risk factor for cardiovascular diseases. However, the mechanisms by which DE exposure induces cardiovascular dysfunction remain unknown and there is still debate on the contribution of the primary particulate matter (PM) fraction compared to the gaseous phase. Although the mitochondria play a key role in the events leading to cardiovascular diseases, their role in DE-induced cardiovascular effects has not been investigated. The aim of this study was to highlight cardiac and mitochondrial events that could be disrupted following acute and/or repeated DE exposures and the contribution of gaseous pollutants to these effects. To address this question, Wistar rats were exposed to DE generated under strictly controlled and characterized conditions and extracted upstream or downstream of the diesel particulate filter (DPF). Evaluation of the cardiac function after acute DE exposure showed a disturbance in echocardiographic parameters, which persisted and worsened after repeated exposures. The presence of the DPF did not modify the cardiovascular dysfunction revealing an important implication of the gas phase in this response. Surprisingly, redox parameters were not altered by DE exposures while an alteration in mitochondrial oxidative capacity was observed. Exploration of the mitochondrial function demonstrated a more specific alteration in complex I of the respiratory chain after repeated exposures, which was further confirmed by transcriptional analysis of left ventricular (LV) tissue. In conclusion, this work provides new insights into cardiovascular effects induced by DE, demonstrating a cardiac mitochondrial impairment associated with the gaseous phase. These effects suggest deleterious consequences in terms of cardiac function for vulnerable populations with underlying energy deficit such as patients with heart failure or the elderly.