Triclosan (TCS) is widely applied in personal care products (PCPs) as an antimicrobial preservative. Due to its toxicity and potential risk to human health, TCS has attracted mounting concerns in recent years. However, biomonitoring of TCS in large human populations remains limited in China. In this study, 1163 adults in South China were recruited and urinary TCS concentrations were determined. TCS was detected in 99.5% of urine samples, indicating broad exposure in the study population. Urinary concentrations of TCS ranged from below the limit of detection (LOD) to 270 μg/L, with a median value of 3.67 μg/L. Urinary TCS concentrations from individuals were all lower than the Biomonitoring Equivalents reference dose, suggesting relatively low health risk in the participants. TCS concentrations did not differ significantly between sexes or education levels (p > 0.05). Nevertheless, marital status and age were found to be positively influence TCS levels (p < 0.001). After adjustment for body mass index (BMI), age was determined to be positively associated with TCS concentrations (p < 0.05), particularly in the age group from 31 to 51 years old. This study provides a baseline of urinary TCS exposure in South China general adult populations.

Studies on microplastic (MP) pollution in lakes are recent, although the problem of MP particles in the oceans was first discovered in the 1970s. The first study on lakes was published in 2011. Since then, to our knowledge, 98 lakes have been investigated worldwide. In recent years, studies on this topic have increased worldwide, particularly those focusing on urbanised lakes. Most of the plastic waste in the seas and oceans originates from the terrestrial environment and inland waters. Moreover, lakes are potential temporary or long-term MP accumulators, according to the residence time of water. They are also of high interest for biodiversity, ecology, and the economy. Lacustrine ecosystems may suffer the same fate as marine ecosystems, or even worse, owing to their greater exposure. With the significant focus on ocean and sea contamination, contamination of freshwater ecosystems and lakes is a new and rising topic. However, as a new field of research, several methodological issues have been raised. The team diversity worldwide has led to contrasting sampling techniques and materials, sample treatments, analyses, and presentation of results. Consequently, it is necessary to determine several consensuses between scientific teams in order to work together with accuracy, produce comparable results, speed up knowledge sharing and reduce the reproducibility crisis. This review focuses on (1) MP contamination in 98 worldwide lakes. We identify (2) the theoretical sources of MPs and provide (3) an estimate of MP pollution in different compartments of the lakes based on current state-of-the-art methods. In addition, we also report (4) the predominant MP size classes and polymer types. Finally, we suggest (5) several recommendations to build a consensus between all the working teams to facilitate decision-making by public authorities.

Numerous studies have established that acute or chronic exposure to environmental pollutants like particulate matter (PM) leads to the development of accelerated aging related pathologies including pulmonary and cardiovascular diseases, and thus air pollution is one of the major global threats to human health. Air pollutant particulate matter 2.5 (PM₂.₅)-induced cellular dysfunction impairs tissue homeostasis and causes vascular and cardiopulmonary damage. To test a hypothesis that elevated plasminogen activator inhibitor-1 (PAI-1) levels play a pivotal role in air pollutant-induced cardiopulmonary pathologies, we examined the efficacy of a drug-like novel inhibitor of PAI-1, TM5614, in treating PM₂.₅-induced vascular and cardiopulmonary pathologies. Results from biochemical, histological, and immunohistochemical studies revealed that PM₂.₅ increases the circulating levels of PAI-1 and thrombin and that TM5614 treatment completely abrogates these effects in plasma. PM₂.₅ significantly augments the levels of pro-inflammatory cytokine interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF), and this also can be reversed by TM5614, indicating its efficacy in amelioration of PM₂.₅-induced increases in inflammatory and pro-thrombotic factors. TM5614 reduces PM₂.₅-induced increased levels of inflammatory markers cluster of differentiation 107 b (Mac3) and phospho-signal transducer and activator of transcription-3 (pSTAT3), adhesion molecule vascular cell adhesion molecule 1 (VCAM1), and apoptotic marker cleaved caspase 3. Longer exposure to PM₂.₅ induces pulmonary and cardiac thrombosis, but TM5614 significantly ameliorates PM₂.₅-induced vascular thrombosis. TM5614 also reduces PM₂.₅-induced increased blood pressure and heart weight. In vitro cell culture studies revealed that PM₂.₅ induces the levels of PAI-1, type I collagen, fibronectin (Millipore), and sterol regulatory element binding protein-1 and 2 (SREBP-1 and SREBP-2), transcription factors that mediate profibrogenic signaling, in cardiac fibroblasts. TM5614 abrogated that stimulation, indicating that it may block PM₂.₅-induced PAI-1 and profibrogenic signaling through suppression of SREBP-1 and 2. Furthermore, TM5614 blocked PM₂.₅-mediated suppression of nuclear factor erythroid related factor 2 (Nrf2), a major antioxidant regulator, in cardiac fibroblasts. Pharmacological inhibition of PAI-1 with TM5614 is a promising therapeutic approach to control air pollutant PM₂.₅-induced cardiopulmonary and vascular pathologies.

Six ecotypes of Typha domingensis Pers. Jahlar (E₁), Sheikhupura (E₂), Sahianwala (E₃), Gatwala (E₄), Treemu (E₅) and Knotti (E₆) from different ecological regions were collected to evaluate the leaf anatomical and biochemical attributes under different levels of salinity and nickel stress viz; L₀ (control), L₁ (100 mM + 50 mg kg⁻¹), L₂ (200 mM + 100 mg kg⁻¹) and L₃ (300 mM + 150 mg kg⁻¹). Presence of salt and Ni in rooting medium consistently affected growth, anatomical and physio-biochemical attributes in all Typha ecotypes. Discrete anatomical modifications among ecotypes such as reduced leaf thickness, increased parenchyma area, metaxylem cell area, aerenchyma formation and improved metaxylem vessels were recorded with increasing dose of salt and Ni. The minimum anatomical damages were recorded in E₁ and E₆ ecotypes. In all ecotypes, progressive perturbations in ionic homeostasis (Na⁺, K⁺, Cl⁻, N) due to salt and metal toxicity were evident along with reduction in photosynthetic pigments. Maximum enhancement in Catalase (CAT), Superoxide dismutase (SOD), Peroxidase (POD) and modulated Malondialdehyde (MDA) activity was recorded in E₁ and E₆ as compared to other ecotypes. Accumulation of large amounts of metabolites such as total soluble sugars, total free amino acids content in Jahlar, Knotti, Treemu and Sahianawala ecotypes under different levels of salt and Ni prevented cellular damages in T. domingensis Pers. The correlation analysis exhibited a close relationship among different levels of salinity and Ni with various plant attributes. PCA-Biplot verified our correlational analysis among various attributes of Typha ecotypes. An obvious separation of Typha characters in response to different salinity and Ni levels was exhibited by PC1. We recommend that genetic potential of T. domingensis Pers. To grow under salt and Ni stresses must be investigated and used for phytoremediation and reclamation of contaminated soil.

Metal(loid)s (MLs) with natural or anthropogenic sources may cause adverse health effects in children. This study aimed to compare the childhood exposure to ΣMLs (essential, non-essential and toxic) in an industrial and an urban area in Southwest Iran using toenail tissue as a biomarker. The present study was carried out with school children in the age range of 7–12 years, who were living in an industrial area in the petrochemical and gas area (PGA) of the Central District of Asaluyeh County and in an urban area (UA) located in the Kaki District. A total of 270 boys and girls were recruited in January to April 2019. The ICP-MS was used for determination of the studied MLs. A multi-linear regression model was constructed to assess the effect of residence area on toenail ML levels. A significantly higher level of ΣMLs in toenail from the PGA was observed compared to the level in the UA (8.839 vs. 7.081 μg/g, β = -0.169 and p < 0.05). However, all of the 15 MLs studied were detected in the toenail samples from both study sites. Significant differences for the mean Cr (β = −0.563), Fe (β = −0.968), Mn (β = −0.501), Ni (β = −0.306), and Pb (β = −0.377) levels were found between toenail samples from the study areas (p < 0.05), with higher levels in the PGA. The results of this study suggest that children in industrial area are prone to a greater risk for ML exposures compared with those living in a non-industrial urban area.

Understanding the impact of increases in pCO₂ (OA) and extreme changes in temperature on marine organisms is critical to predicting how they will cope with climate change. We evaluated the effects of OA as well as warming and cooling trend temperature on early reproductive traits of Lessonia trabeculata, a bio-engineer kelp species. Sori discs were maintained for an exposure time (ET) of 3 (T3) and 7 (T7) days to one of two contrasting pCO₂ levels (450 and 1100 μatm). In addition, at each pCO₂ level, they were subjected to three temperature treatments: 15 °C (control), 10 °C (cool) and 19 °C (warm). Subsequently, we compared sorus photosynthetic performance (Fv/Fm), the number of meiospores released (MR) and their germination rate (GR) after 48 h of settlement, with values obtained from sori discs not exposed (DNE) to the treatments. The Fv/Fm measured for DNE was lower than at T3 and T7 at 10 and 15 °C but not at 19 °C. Regardless of temperature, we found no significant differences between MR measured at T0 and T3. MR at T7 was significantly lower at 19 °C than at 10 and 15 °C. We found only a significant reduction in MR in response to elevated pCO₂ at T3. The GR of meiospores released by DNE and then maintained for 48 h to 19 °C decreased significantly by ~33% when compared with those maintained for the same time at 10 and 15 °C. A similar, but more drastic reduction (~54%) in the GR was found in meiospores released by sori discs exposed for T3 and maintained for 48 h to 19 °C. We suggest that OA and warming trend will threaten the early establishment of this species with further consequences for the functioning of the associated ecosystem.

Lead (Pb) is a heavy metal that has been proven to be toxic to both animals and humans. Genom-wide DNA methylation in domestic dogs exposed to high levels of Pb in Kabwe, Zambia was analyzed in this study. Using next-generation sequencing on samples from 20 domestic dogs (mean blood Pb concentration: 43.6 μg/dL and 7.2 μg/dL in the high and low exposure groups), a digital restriction enzyme analysis of methylation was performed to identify the genomic locations of differentially methylated CpG sites. A validation study on an additional 20 dogs followed (blood Pb concentration: 4.9–29.7 μg/dL). The cluster analysis resolved two broad clusters indicating high and low Pb exposure. The study identified 827 (1.2%) CpG sites with differences in methylation (101 CpG sites were hypermethylated in the low exposure group and 726 were hypermethylated in the high exposure group). The sites corresponded to 26 genes with differentially methylated CpG sites at their promoter regions, including the NGF gene. The methylation of four CpG sites was validated using bisulfite pyrosequencing. The results indicate that aberrant hypermethylation is prevalent in dogs exposed to Pb. The altered DNA methylation of the genes identified in this study contributes to a greater understanding of the epigenetic changes caused by Pb exposure and highlights novel biomarker discoveries across species.

Cadmium (Cd) pollution is currently the most serious type of heavy metal pollution throughout the world. Previous studies have shown that Cd elevates the mortality of paddy field spiders, but the lethal mechanism remains to be explored profoundly. In the present study, we measured the activities of protective enzymes (acetylcholinesterase, glutathione peroxidase, phenol oxidase) and a heavy metal chelating protein (metallothionein) in the pond wolf spider Pardosa pseudoannulata after Cd exposure. The results indicated that Cd initially increased the enzyme activities and protein concentration of the spider after 10- and 20-day exposure before inhibiting them at 30-day exposure. Further analysis showed that the enzyme activities in the cephalothorax were inhibited to some extent. Since the cephalothorax region contains important venom glands, we performed transcriptome sequencing (RNA-seq) analysis of the venom glands collected from the spiders after long-term Cd exposure. RNA-seq yielded a total of 2826 differentially expressed genes (DEGs), and most of the DEGs were annotated into the process of protein synthesis, processing and degradation. Furthermore, a mass of genes involved in protein recognition and endoplasmic reticulum (ER) -associated protein degradation were down-regulated. The reduction of protease activities supports the view that protein synthesis and degradation in organelles and cytoplasm were dramatically inhibited. Collectively, our outcomes illustrate that Cd poses adverse effects on the expression of protective enzymes and protein, which potentially down-regulates the immune function in the venom glands of the spiders via the alteration of protein processing and degradation in the ER.

Elevated toxins in soybeans extensively threaten Asian residents and over one billion vegetarians worldwide. An integrated dataset of toxic trace metal(loid)s especially cadmium (Cd) analysis in soybean grain samples (n = 5217) from 12 countries/regions of origin was compiled for risk analysis. Worldwide grain Cd averaged 0.093 mg kg⁻¹, but mean values varied 16-fold between regions, with South China (0.32 mg kg⁻¹) > Argentina (0.15 mg kg⁻¹) = German (0.13 mg kg⁻¹) > Japan (0.11 mg kg⁻¹) > the United States (0.064 mg kg⁻¹) > Central-North China (0.020–0.60 mg kg⁻¹) ≥ Iran (0.042 mg kg⁻¹) = Brazil (0.023 mg kg⁻¹) = South Korea (0.020 mg kg⁻¹). Regression analysis suggested widespread contamination and acidic soil features significantly contributed the elevated food Cd contamination worldwide. Arsenic (As) and lead (Pb) are also of concern because excessive levels were often observed in grains. Given that soil Cd bioavailability is generally low in alkaline pH ranges, the feasibility of producing safe food from contaminated land was investigated by greenhouse experiments with one low-Cd soybean cultivar grown on 20 contaminated calcareous soils. Equilibrium-based approaches i.e., 0.01 M CaCl₂ and in-situ porewater extractions, and diffusion-based diffusive gradients in thin-films technique were used to determine the plant-available fractions of soil metal(loid)s to explain the bioaccumulation variation. The results suggested that soybean grains bioaccumulated mean 0.76 mg Cd kg⁻¹, ranging from 0.16 to 2.1 mg kg⁻¹, whereas As and Pb bioaccumulation was low. Cadmium accumulation was closely correlated with plant-available Cd fractions especially the 0.01 M CaCl₂-extractable Cd, but negatively correlated with soil pH. Even in the alkaline pH range, a slight decrease of soil pH would increase grain Cd significantly. Study region and those arable lands that have similar soil conditions are not recommended for growing soybean unless novel remediation strategies are developed.

Many environmental chemicals have been found to exert estrogenic effects in cells and experimental animals by activating nuclear receptors such as estrogen receptors and estrogen-related receptors. These compounds include bisphenols, pesticides, polybrominated diphenyl ethers (PBDEs), organophosphate flame retardants, phthalates and metalloestrogens. G protein-coupled estrogen receptor (GPER) exists widely in numerous cells/tissues of human and other vertebrates. A number of studies have demonstrated that GPER plays a vital role in mediating the estrogenic effects of environmental pollutants. Even at very low concentrations, these chemicals may activate GPER pathways, thus affect many aspects of cellular functions including proliferation, metastasis and apoptosis, resulting in cancer progression, cardiovascular disorders, and reproductive dysfunction. This review summarized the environmental occurrence and human exposure levels of these pollutants, and integrated current experimental evidence toward revealing the underlying mechanisms of pollutant-induced cellular dysfunction via GPER. The GPER mediated rapid non-genomic actions play an important role in the process leading to the adverse effects observed in experimental animals and even in human beings.