The health risk of triadimefon (TF) to cardiovascular system of human is still unclear, especially to pesticide suicides population, occupational population (farmers, retailers and pharmaceutical workers), and special population (young children and infants, pregnant women, older people, and those with compromised immune systems) who are at a greater risk. Therefore, firstly we explored the toxic effects and possible mechanism of cardiovascular toxicity induced by TF using zebrafish model. Zebrafish at stage of 48 h post fertilization (hpf) exposed to TF for 24 h exhibited morphological malformations which were further confirmed by histopathologic examination, including pericardial edema, circulation abnormalities, serious venous thrombosis and increased distance between the sinus venosus (SV) and bulbus arteriosus (BA) regions of the heart. In addition to morphological changes, TF induced functional deficits in the heart of zebrafish, including bradycardia and a significant reduced cardiac output that became more serious at higher concentrations. To better understand the possible molecular mechanisms underlying cardiovascular toxicity in zebrafish, we investigated the transcriptional level of genes related to calcium signaling pathway and cardiac muscle contraction. Q-PCR (quantitative real-time polymerase chain reaction) results demonstrated that the expression level of genes related to ATPase (atp2a1l, atp1b2b, atp1a3b), calcium channel (cacna1ab, cacna1da) and cardiac troponin C (tnnc1a) were significantly decreased after TF exposure. For the first time, the present study revealed that TF exposure had observable morphological and functional negative impacts on cardiovascular system of zebrafish. Mechanistically, this toxicity might result from the pressure of down-regulation of genes associated with calcium signaling pathway and cardiac muscle contraction following TF exposure. These findings generated here can provide information for better pesticide poisoning treatments, occupational disease prevention, and providing theoretical foundation for risk management measures.

Studies have shown that residents living near rare earth mining areas have high concentrations of rare earth elements (REEs) in their hair. However, the adverse effects of REEs on human health have rarely been the focus of epidemiological studies. The goal of this study was to evaluate the relationship between REEs in hair and the risk of hypertension in housewives. We recruited 398 housewives in Shanxi Province, China, consisting of 163 women with hypertension (cases) and 235 healthy women without hypertension (controls). We analyzed 15 REEs (lanthanum (La), samarium (Sm), europium (Eu), gadolinium (Gd), terbium (Tb), dysprosium (Dy), holmium (Ho), erbium (Er), thulium (Tm), ytterbium (Yb), lutetium (Lu), Yttrium (Y), cerium (Ce), praseodymium (Pr), and neodymium (Nd)) and calcium (Ca) accumulated in housewives hair over a period of two years. The results revealed that, with the exception of Eu, concentrations of the REEs in hair were higher in the cases than in the controls. The univariate odds ratios (ORs) of the 14 REEs were >1, and four of the REEs (Dy, Tm, Yb, and Y) also had adjusted ORs > 1. The increasing dose-response trends of the four REEs further indicated the potential for increased hypertension risk. Moreover, the REEs were negatively correlated with Ca content in hair. These results might suggest an antagonistic effect of REEs on Ca in the human body. It was concluded that high intake of REEs might increase the risk of hypertension among housewives.

Plastic debris in marine environments and its impact on wildlife species is becoming a problem of increasing concern. In pinnipeds, entanglements commonly consist of loops around the neck of non-biodegradable materials from fishing gear or commercial packaging, known as “neck collars”. These entanglements can cause injuries, death by suffocation and starvation, and therefore they may add to the overall decrease in population. Our objective was to describe the entanglement of two species of otariids (Arctocephalus australis and Otaria flavescens) in the South West Atlantic Ocean. These two species have widely different population sizes and contrasting trends, being the O. flavescens population one order of magnitude lower in abundance with a negative population trend. A total number of 47 entangled individuals and the ingestion of a fishing sinker were recorded (A. australis: n = 26; O. flavescens: n = 22). For A. australis about 40% of the objects came from industrial fishing with which this species overlap their foraging areas, although also its lost or discarded gear can travel long distances. In O. flavescens 48% of observed injuries were very severe, which might indicate that they had been entangled for a long time. More than 60% of the objects came from artisanal and recreational fishing that operates within 5 nautical miles off the coast, which is probably related to coastal foraging habits of this species. Due to the frequent interaction between artisanal fisheries and O. flavescens, it is possible that entangled nets could be active gears. An important contribution to mitigate entanglements can be the development of education programs setting the scenario for effective communication, and exchange with involved fishermen to collect and recycle old fishing nets. Returning to natural fibers or replacement of the current materials used in fishing gear for biodegradable materials can also be a recommended mitigation measure.

The effects of salinity on metal toxicity are complex: not only affecting metal bioaccumulation, but also altering the physiology and sensitivity of organisms. In this study, we used a toxicokinetic-toxicodynamic (TK-TD) model to separate and quantify the dual effects of salinity on copper (Cu) toxicity in a euryhaline clam Potamocorbula laevis. The toxicokinetics of Cu was determined using the stable isotope 65Cu as a tracer at concentrations (10–500 μg L−1) realistic to contaminated environments and at salinities ranging from 5 to 30. At low Cu concentrations (ca. 10 μg L−1), Cu bioaccumulation decreased monotonically with salinity, and the uptake rate constant (ku, 0.546 L g−1 h−1 to 0.213 L g−1 h−1) fitted well with an empirical equation, ku = 1/(1.35 + 0.116·Salinity), by treating salinity as a pseudo-competitor. The median lethal concentrations (LC50s) of Cu were 269, 224, and 192 μg L−1 at salinity 5, 15, and 30, respectively. At high Cu concentrations (ca. 500 μg L−1), elevating salinity were much less effective in decreasing Cu bioaccumulation; whereas Cu toxicity increased with salinity. The increased toxicity could be explained by the increases in Cu killing rates (kks), which were estimated to be 0.44–2.08 mg μg−1 h−1 and were presumably due to the osmotic stress caused by the deviation from the optimal salinity of the clams. The other toxicodynamic parameter, internal threshold concentration (CIT), ranged from 79 to 133 μg−1 g−1 and showed no clear trend with salinity.

Increasing trends of atmospheric nitrogen (N) deposition due to pollution and land-use changes are dramatically altering global biogeochemical cycles. Bryophytes, which are extremely vulnerable to N deposition, often play essential roles in these cycles by contributing to large nutrient pools in boreal and montane forest ecosystems. To interpret the sensitivity of epiphytic bryophytes for N deposition and to determine their critical load (CL) in a subtropical montane cloud forest, community-level, physiological and chemical responses of epiphytic bryophytes were tested in a 2-year field experiment of N additions. The results showed a significant decrease in the cover of the bryophyte communities at an N addition level of 7.4 kg ha−1 yr−1, which is consistent with declines in the biomass production, vitality, and net photosynthetic rate responses of two dominant bryophyte species. Given the background N deposition rate of 10.5 kg ha−1yr−1 for the study site, a CL of N deposition is therefore estimated as ca. 18 kg N ha−1 yr−1. A disordered cellular carbon (C) metabolism, including photosynthesis inhibition and ensuing chlorophyll degradation, due to the leakage of magnesium and potassium and corresponding downstream effects, along with direct toxic effects of excessive N additions is suggested as the main mechanism driving the decline of epiphytic bryophytes. Our results confirmed the process of C metabolism and the chemical stability of epiphytic bryophytes are strongly influenced by N addition levels; when coupled to the strong correlations found with the loss of bryophytes, this study provides important and timely evidence on the response mechanisms of bryophytes in an increasingly N-polluted world. In addition, this study underlines a general decline in community heterogeneity and biomass production of epiphytic bryophytes induced by increasing N deposition.

Exposure to hypoxia has shown beneficial adjustments in different species, including silver catfish (Rhamdia quelen), especially in situations of aquatic contamination with pollutants such as manganese (Mn). Considering that hypoxia is seasonal in the natural aquatic environment, we decided to assess whether these adaptive mechanisms could be maintained when reoxygenation is established. Silver catfish acclimated to moderate hypoxia (∼3 mg L⁻¹, 41% O2 saturation) for 10 days and subsequently exposed to Mn (∼8.1 mg L⁻¹) for additional 10 days displayed lower (47%) Mn accumulation in the gills, and it was maintained (62.6%) after reoxygenation, in comparison to normoxia. Oxidative status in the gills allowed us to observe increased reactive species (RS) generation and protein carbonyl (PC) level together with decreased mitochondrial viability induced by Mn under normoxia. Inversely, while hypoxia per se was beneficial on RS generation and PC level, this acclimation was able to minimize Mn toxicity, as observed by the minor increase of RS generation and the minor reduction of mitochondrial viability, together with decreased PC level. Interestingly, after reoxygenation, part of the protective influences observed during hypoxia against Mn toxicity were maintained, as observed through a lower level of PC and higher mitochondrial viability in relation to the group exposed to Mn under normoxia. Only groups exposed to Mn under hypoxia showed increased activity of both catalase (CAT) and Na⁺/K⁺-ATPase in the gills, but, while CAT activity remained increased after reoxygenation, Na⁺/K⁺-ATPase activity was decreased by Mn, regardless of the oxygen level. Based on these outcomes, it is possible to propose that environment events of moderate hypoxia are able to generate rearrangements in the gills of silver catfish exposed to Mn, whose influence persists after water reoxygenation. These responses may be related to the adaptive development, reducing Mn toxicity to silver catfish.Moderate hypoxia generates rearrangements in the gills of Silver catfish, exerting beneficial and persistent protection against Mn toxicity.

Although several studies have estimated the effects of temperature on mortality and morbidity, little is known regarding the burden of out-of-hospital cardiac arrest (OHCA) attributable to solar radiation.We obtained data for all cases of OHCA and meteorological data reported between 2011 and 2014 in 3 Japanese prefectures: Hokkaido, Ibaraki, and Fukuoka. We first examined the relationship between daily solar radiation and OHCA risk for each prefecture using time-varying distributed lag non-linear models and then pooled the results in a multivariate random-effects meta-analysis. The attributable fractions of OHCA were calculated for low and high solar radiation, defined as solar radiation below and above the minimum morbidity solar radiation, respectively. The minimum morbidity solar radiation was defined as the specific solar radiation associated with the lowest morbidity risk.A total of 49,892 cases of OHCA occurred during the study period. The minimum morbidity solar radiation for each prefecture was the 100th percentile (72.5 MJ/m2) in Hokkaido, the 83rd percentile (59.7 MJ/m2) in Ibaraki, and the 70th percentile (53.8 MJ/m2) in Fukuoka. Overall, 20.00% (95% empirical confidence interval [eCI]: 10.97–27.04) of the OHCA cases were attributable to daily solar radiation. The attributable fraction for low solar radiation was 19.50% (95% eCI: 10.00–26.92), whereas that for high solar radiation was 0.50% (95% eCI: −0.07–1.01).Low solar radiation was associated with a substantial attributable risk for OHCA. Our findings suggest that public health efforts to reduce OHCA burden should consider the solar radiation level. Large prospective studies with longitudinal collection of individual data is required to more conclusively assess the impact of solar radiation on OHCA.

Polybrominated diphenyl ethers (PBDEs) and heavy metals are two key groups of electric and electronic equipment contaminants. Despite their co-occurrence in aquatic environments, their combined effects remain largely unknown, particularly under a chronic exposure regime. In the present study, adult zebrafish (Danio rerio) were exposed to environmentally relevant concentrations of BDE-209 and lead (Pb), or their binary mixtures, for 3 months. After chronic parental exposure, increased transfer of BDE-209 and Pb to the offspring eggs was activated in the coexposure groups, with BDE-197 being the predominant PBDE congener, indicating the dynamic metabolism of BDE-209 in parental zebrafish. In the presence of Pb, culturing the eggs in clean water until 5 days post-fertilization (dpf) further accelerated the debromination of BDE-209 towards BDE-197 in the offspring, caused by the preferential removal of bromine atoms at meta positions. BDE-209 and Pb combinations induced reproductive and thyroid endocrine disruption in adults, which resulted in an imbalanced deposition of hormones in the eggs. However, compared with single chemical exposure, the larval offspring at 5 dpf from the coexposure groups had reversed the adverse influences from maternal origin. In addition, the interaction between BDE-209 and Pb led to transgenerational developmental neurotoxicity in the larval offspring, where inhibited neuronal growth and neurotransmitter signaling, disorganized muscular assembly, and impaired visual function contributed to the observed neurobehavioral deficits. Overall, depending on specific biological events, the complex interaction between BDE-209 and Pb under chronic exposure resulted in significant alterations in their environmental fate and toxicological actions, thus complicating the accurate evaluation of ecological risks and constituting an unquantified threat to environmental safety.

To investigate particulate matter (PM2.5)-induced damage to human corneal epithelial cells (HCECs) and to determine the underlying mechanisms.HCECs were exposed to PM2.5 at a series of concentrations for various periods. Cell viability was measured by using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell proliferation was evaluated via 5-ethynyl-2’-deoxyuridine (EdU) analysis, while autophagy was determined by immunofluorescence and Western blot.PM2.5-induced cell damage of HCECs occurred in a time- and dose-dependent manner. Decreased cell viability and proliferation as well as increased apoptosis were observed in HCECs after PM2.5 exposure for 24 h. Autophagy in HCECs was slightly inhibited in the early stage (before 4 h) of exposure but significantly activated in the late stage (after 24 h), as evidenced by a decrease in the former and increase in the latter of the expression of the autophagy-associated markers LC3B, ATG5, and BECN1. Interestingly, rapamycin, an autophagy activator, attenuated early-stage but aggravated late-stage PM2.5-induced cell damage, suggesting that the role of autophagy in HCECs may change over time during PM2.5 exposure. In addition, in the early stage, the expression of LC3B and ATG5 increased in cells co-treated with rapamycin and PM2.5 compared to rapamycin-only or PM2.5-only treated cells, suggesting that autophagy may benefit cell viability after PM2.5 exposure.The results indicate the potential role of autophagy in the treatment of PM2.5-induced ocular corneal diseases and provide direct evidence for the cytotoxicity, possibly involving an autophagic process, of PM2.5 in HCECs.

The continuous accumulation of microplastics in the environment poses ecological threats and has been an increasing problem worldwide. In this study, eight bacterial strains were isolated from mangrove sediment in Peninsular Malaysia to mitigate the environmental impact of microplastics and develop a clean-up option. The bacterial isolates were screened for their potential to degrade UV-treated microplastics from polyethylene (PE), polyethylene terephthalate (PET), polypropylene (PP), and polystyrene (PS). Only two isolates, namely, Bacillus cereus and Bacillus gottheilii, grew on a synthetic medium containing different microplastic polymers as the sole carbon source. A shake flask experiment was carried out to further evaluate the biodegradability potential of the isolates. Degradation was monitored by recording the weight loss of microplastics and the growth pattern of the isolates in the mineral medium. The biodegradation extent was validated by assessment of the morphological and structural changes through scanning electron microscopy and Fourier transform infrared spectroscopy analyses. The calculated weight loss percentages of the microplastic particles by B. cereus after 40 days were 1.6%, 6.6%, and 7.4% for PE, PET, and PS, respectively. B. gottheilii recorded weight loss percentages of 6.2%, 3.0%, 3.6%, and 5.8% for PE, PET, PP, and PS, respectively. The designated isolates degraded the microplastic material and exhibited potential for remediation of microplastic-contaminated environment. Biodegradation tests must be conducted to characterize the varied responses of microbes toward pollutants, such as microplastics. Hence, a novel approach for biodegradation of microplastics must be developed to help mitigate the environmental impact of plastics and microplastic polymers.