Our results indicate that heavy metal concentrations in the feather, liver, and kidney are not spatially cross-autocorrelated but are statistically significantly correlated with some heavy metals in topsoil due to external and internal depositions. Further, multiple EF, Cod, and RI distributions for topsoil, along with the PRI of the feather, showed that adequate coverages for potential risk for birds were greater than 71.05% in the top 30% and 84.69% in the top 20% potential eco-risk priority area of heavy metals in bird liver and kidney. Hence, our proposed approach suggests that assessments of heavy metals in bird feathers and topsoils without bird organs can be utilized to identify spatially high-risk areas. The proposed approach could be improved by incorporating water and sediment samples to enhance the crowdsourcing and the species-specific data.Sulfometuron methyl (SM) is a widely used herbicide and thus leading to accumulation in the environment. The toxicity assessments of SM in model organisms are currently rare. In the present study, zebrafish were utilized for evaluating the detrimental effects of SM in aquatic vertebrates. Zebrafish embryos were exposed to 0, 10, 20, and 40 mg/L SM from 5.5 to 72 h post-fertilization (hpf), respectively. Consequently, SM exposure resulted in increasing the mortality rate and reducing hatching rate in larval zebrafish at 10, 20, and 40 mg/L SM-treated groups. The reduced numbers of immune cells (neutrophils and macrophages) were observed after SM exposure by a dose-dependent manner. The inflammatory responses (TLR4, MYD88, IL-1β, IL-6, IL-8, IFN-γ, IL-10, and TGF-β) were measured to estimate immune responses. Anti-inflammatory factors (IL-10 and TGF-β) were down-regulated in all the treated groups and significantly altered at 40 mg/L exposure group. Additionally, behavioral tests suggested that SM treatment significantly increased the total distance, average speed, and maximum acceleration of larval zebrafish during light-dark transition and subsequently enzymology test displayed the same trend to locomotor behaviors. The content significantly increased in oxidative stress, as reflected in ROS level in all the treated groups. The numbers of cell apoptosis were significantly increased at 20, and 40 mg/L and the highest concentration group induced the substantial increment (P less then 0.001) of apoptosis-related genes including p53, Bax/Bcl-2, caspase-9, and caspase-3. In summary, our results demonstrated that exposure to SM caused toxicity of development, immune system, locomotor behavior, oxidative stress, and cell apoptosis at the early developmental stages of zebrafish. Polychlorinated biphenyls (PCBs) are a large family of man-made organic, ubiquitous, and persistent contaminants with endocrine-disrupting properties. PCBs have been associated with numerous adverse health effects and were classified as carcinogenic to humans, but their long-term impact on mortality risk in the general population is unknown. To conduct a systematic review and meta-analysis in order to assess whether background exposure levels of PCBs increase all-cause and cancer- and cardiovascular-specific mortality risk in the general population. We searched the Pubmed, Web of Science, Cochrane Library, and Embase databases for eligible studies up to 1st of January, 2021. We included cohort and nested-case control studies comparing the lowest vs. https://www.selleckchem.com/products/tbopp.html the highest background exposure level of PCBs in the general population and reporting data for all-cause mortality and/or cancer-/cardiovascular-specific mortality. Studies reporting occupational and accidental exposures were excluded. Random-effects meta-anpecific mortality (SRR=1.38, 95% CI=1.14-1.66, n=3 studies, moderate certainty), while no association was found with cancer-specific mortality (SRR=1.07, 95% CI=0.72-1.59, n=5 studies, low certainty). Our meta-analysis suggests that background exposure to PCBs is associated with an increased risk of cardiovascular-specific mortality in the general population with a "moderate" level of evidence. These findings should be interpreted with caution given the small number of studies on mortality in the general population. Our meta-analysis suggests that background exposure to PCBs is associated with an increased risk of cardiovascular-specific mortality in the general population with a "moderate" level of evidence. These findings should be interpreted with caution given the small number of studies on mortality in the general population.Cancer occurrence and development are closely related to the environment. Aryl hydrocarbon receptor (AhR) is an important receptor mediating the toxic effects of many environmental compounds, and is also involved in regulating tumor cell migration. Glioblastoma is the most malignant glioma and exhibits high motility, but the effects of AhR on the migration of glioblastoma are still unclear. We aimed to understand the role of AhR in the migration of this type of tumor cell and to explore the underlying molecular mechanism. In cultured human neuroblastoma cells (U87), we found that AhR overexpression or knockdown increased or suppressed the migration ability of U87 cells, respectively. Furthermore, inhibition of basal activation of the AhR pathway suppressed migration ability, suggesting a positive correlation between endogenous activity of the AhR pathway and cell migration. When the AhR pathway was activated by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 6-formyl [3,2-b] carbazole (FICZ), the migration of U87 cells was inhibited by inducing the expression of a tumor suppressor, IL24, which is a downstream responsive gene of AhR activation. Moreover, a similar AhR-IL24-dependent mechanism for migration inhibition of TCDD was documented in a breast cancer cell line and a lung cancer cell line. This study demonstrated that AhR plays important roles in regulating the migration of glioblastoma, and the induction of the AhR-IL24 axis mediates the inhibition of migration in response to TCDD or FICZ treatment. Long-term exposure to PM has been linked to cancer incidence and mortality. However, it was unknown whether there was an association with cancer hospitalizations. Data on cancer hospitalizations and annual PM concentrations were collected from 1,814 Brazilian cities during 2002-2015. A difference-in-difference approach with quasi-Poisson regression was applied to examine State-specific associations. The State-specific associations were pooled at a national level using random-effect meta-analyses. PM attributable burden were estimated for cancer hospitalization admissions, inpatient days and costs. We included 5,102,358 cancer hospitalizations (53.8% female). The mean annual concentration of PM was 7.0μg/m (standard deviation 4.0μg/m ). With each 1μg/m increase in two-year-average (current year and previous one year) concentrations of PM , the relative risks (RR) of hospitalization were 1.04 (95% confidence interval [CI] 1.02 to 1.07) for all-site cancers from 2002 to 2015 without sex and age differences.