The epidemiological evidence supporting putative associations between air pollution and health-related outcomes continues to grow at an accelerated pace with a considerable heterogeneity and with varying consistency based on the outcomes assessed, the examined surveillance system, and the geographic region. We aimed to evaluate the strength of this evidence base, to identify robust associations as well as to evaluate effect variation. An overview of reviews (umbrella review) methodology was implemented. PubMed and Scopus were systematically screened (inception-3/2020) for systematic reviews and meta-analyses examining the association between air pollutants, including CO, NOX, NO₂, O₃, PM₁₀, PM₂.₅, and SO₂ and human health outcomes. The quality of systematic reviews was evaluated using AMSTAR. The strength of evidence was categorized as: strong, highly suggestive, suggestive, or weak. The criteria included statistical significance of the random-effects meta-analytical estimate and of the effect estimate of the largest study in a meta-analysis, heterogeneity between studies, 95% prediction intervals, and bias related to small study effects. Seventy-five systematic reviews of low to moderate methodological quality reported 548 meta-analyses on the associations between outdoor air quality and human health. Of these, 57% (N = 313) were not statistically significant. Strong evidence supported 13 associations (2%) between elevated PM₂.₅, PM₁₀, NO₂, and SO₂ concentrations and increased risk of cardiorespiratory or pregnancy/birth-related outcomes. Twenty-three (4%) highly suggestive associations were identified on elevated PM₂.₅, PM₁₀, O₃, NO₂, and SO₂ concentrations and increased risk of cardiorespiratory, kidney, autoimmune, neurodegenerative, cancer or pregnancy/birth-related outcomes. Sixty-seven (12%), and 132 (24%) meta-analyses were graded as suggestive, and weak, respectively. Despite the abundance of research on the association between outdoor air quality and human health, the meta-analyses of epidemiological studies in the field provide evidence to support robust associations only for cardiorespiratory or pregnancy/birth-related outcomes.

Metal-based nanoparticles (NPs) are considered detrimental to aquatic organisms due to their potential accumulation. However, little is known about the mechanisms underlying these effects and their species-specificity. Here we used stable silver (Ag) NPs (20 nm, from 10 to 500 μg/L) with a low dissolution rate (≤2.4%) to study the bioaccumulation and biological impacts in two freshwater gastropods: Lymnaea stagnalis and Planorbarius corneus. No mortality was detected during the experiments. Ag bioaccumulation showed a dose-related increase with an enhanced concentration in both species after 7d exposure. L. stagnalis displayed a higher accumulation for AgNPs than P. corneus (e.g., up to 18- and 15-fold in hepatopancreas and hemolymph, respectively) which could be due to the more active L. stagnalis having greater contact with suspended AgNPs. Furthermore, the hepatopancreas and stomach were preferred organs for bioaccumulation compared to the kidney, mantle and foot. Regarding biological responses, the hemolymph rather than hepatopancreas appeared more susceptible to oxidative stress elicited by AgNPs, as shown by significantly increasing lipid peroxidation (i.e., formation of malondialdehyde). Neurotoxicity was detected in L. stagnalis when exposed to high concentrations (500 μg/L). Comparison with impacts elicited by dissolved Ag revealed that the effects observed on AgNPs exposure were mainly attributable to NPs. These results highlighted the relationship between the physiological traits, bioaccumulation, and toxicity responses of these two species to AgNPs and demonstrated the necessity of species-specificity considerations when assessing the toxicity of NPs.

Ciprofloxacin (Cipro) is commonly detected in water worldwide, however, the ecotoxicological effects to aquatic biota is still not fully understood. In this study, using multiple biomarkers, it was investigated sublethal effects of short-term exposure to Cipro concentrations (1, 10 and 100 μg.L⁻¹) in the Neotropical catfish Rhamdia quelen compared to non-exposure treatment (Control). After 96 h of exposure, the fishes were anesthetized for blood collection to hematological and genotoxicity biomarkers analysis. After euthanasia, the brain and muscle were sampled for biochemical biomarkers analyses. Gills, liver and posterior kidney for genotoxicity, biochemical and histopathological biomarkers analysis and anterior intestine for histopathological biomarkers analysis. Genotoxicity was observed in all tissues, regardless of the Cipro concentrations. Hematological alterations, such as reduction of the number of erythrocytes and leucocytes, as well as in hematocrit concentration and histopathological damages, such as reduction of microridges in gill epithelium and necrosis in liver and posterior kidney, occurred mainly at 100 μg.L⁻¹. In addition, at 100 μg.L⁻¹, Cipro increased antioxidant system activity (Catalase in liver and posterior kidney). These results demonstrated that under short-term exposure, Cipro causes toxic effects in R. quelen that demands attention and surveillance of environmental aquatic concentrations of this antibiotic.

Tissue distribution of legacy and emerging per-and polyfluoroalkyl substances (PFASs) in several kinds of edible fishes collected from Meiliang bay of Taihu Lake, China were investigated and the related human health risks were assessed. Perfluorooctanesulfonate (PFOS), perfluorooctanesulfonamide (PFOSA) and 6:2 fluorotelomer phosphate diester (6:2 diPAP) were the most abundant legacy perfluoroalkyl acid (PFAA), PFOS related precursor (PreFOS), and the emerging PFASs in all fish tissues, respectively. Similar to the legacy PFAAs, 6:2 diPAP and 6:6 perfluorophosphinate (6:6 PFPiA) had the highest levels in the fish liver, whereas the highest level of PFOSA was in kidney, which might be due to its intensive transformation in fish liver. The concentrations of PFASs were generally positively correlated with the trophic levels. The profiles of PFASs were significantly different among bitterling, crucian and other fish, which might be related to their different metabolic capacities. Bioaccumulation factors (BAFs) of PreFOSs, 6:2 diPAP, and 6:6 PFPiA were lower than those of PFAAs with the same number of perfluorinated carbons. The calculated hazard ratios (HR) of PFOS (Range: 0.0100–0.655) and perfluorooctanoic acid (PFOA) (<0.00200) in all fish muscles were less than 1.0. However, the HR of the ∑PFASs in crucian muscle was 1.04, which implied that frequent consumption of crucian collected from Meiliang Bay might pose potential risks to human health.

The objective of this study was to validate the hypothesis that increased serum concentrations of perfluoroalkyl substances (PFASs) cause kidney damage. A causal interpretative study was designed using the US 2003–2018 National Health and Nutrition Examination Survey (NHANES) datasets.Three statistical models, including multivariable linear regression, generalized additive model, and regression discontinuity model (RDM), were applied to the US 2003–2018 NHANES datasets to evaluate the causal relationship between the four PFAS agents and estimated glomerular filtration rate (eGFR). Directed acyclic graphs were plotted for a more valid causal inference.In the RDM, when the natural logarithm of each PFAS agent increases by 1 ng/mL after each cut-off value, eGFR decreased 4.63 mL/min/1.73 m² for perfluorooctanoic acid, 3.42 mL/min/1.73 m² for perfluorooctane sulfonic acid, 2.37 mL/min/1.73 m² for perfluorohexane sulfonic acid, and 2.87 mL/min/1.73 m² for perfluorononanoic acid. The possibility of reverse causation that increased serum PFAS concentration is the consequence of reduced eGFR, not the cause, was low, and an additional adjustment of potential confounders was not needed.This study contributes to the understanding of PFAS-induced kidney damage. Further longitudinal epidemiological and toxicological studies are recommended.

Cadmium (Cd), as an environmental pollutant, can lead to nephrotoxicity. However, its nephrotoxicological mechanisms have not been fully elucidated. In this study, Cd (1.5 mg/kg body weight, gavaged for 4 weeks) was found to induce the renal damage in mice, based on indicators including Cd concentration, kidney index, serum creatinine and blood urea nitrogen levels, pro-inflammatory cytokines and their mRNA expressions, levels of Bcl-2, Bax and caspase9, and histopathological changes of the kidneys. Furthermore, Cd-caused detrimental changes through inducing inflammation and apoptosis via the miR-34a/Sirt1/p53 axis. This is the first report on the role of miR-34a/Sirt1/p53 axis in regulating Cd-caused apoptosis and nephrotoxicity in mice. The findings obtained in this study provide new insights into miRNA-based regulation of heavy metal induced-nephrotoxicity.

The Wood mouse (Apodemus sylvaticus) is a widespread mammalian species that acts as a reservoir host for multiple infections, including zoonotic diseases. Exposure to immunotoxins, like for instance trace metals, may reduce the ability of the host to mount proper responses to pathogens, potentially increasing the transmission and prevalence of infections. Antibody-mediated responses are crucial in preventing and limiting infections, and the quantification of the primary antibody response is considered a sensitive predictor of immunosuppression. The current study aims to investigate effects of cadmium exposure on the antibody-mediated responses of wood mice inhabiting polluted and non-polluted areas in the Netherlands. Wood mice were captured alive at different locations and immunized to sheep red blood cells (SRBC) to induce a primary antibody response. SRBC-specific antibody-producing cells, or plaque forming cells (PFC), were quantified and related to kidney cadmium levels. Differential circulating main leukocyte populations were also characterised. Cadmium concentrations in mice kidneys differed between mice captured at different locations, and increased with individual body mass, likely associated with age-related time of exposure. Effect of cadmium was apparent on the percentages of B cell counts in blood. Because of potential natural immune heterogeneity between wild rodent populations, mice immune responses were analysed and compared grouped by captured locations. Capture location had significant effect on the total counts of white blood cells. Increasing cadmium exposure in wood mice captured from polluted sites was associated with a decrease of splenic PFC counts. This field research shows that wood mice antibody responses can be impaired by cadmium exposure, even at low environmental levels, by affecting B cell functioning mainly. Impaired B cell function can make exposed mice more susceptible to infections, potentially increasing the reservoir function of their populations. It also shows that immunomodulatory effects in the field should be assessed site specifically.

Investigating environmental pollution is important to understand its impact on endangered species such as green turtles (Chelonia mydas). In this study, we investigated the accumulation and potential toxicity of selected persistent organic pollutants (POPs) and naturally occurring MeO-PBDEs in liver, fat, kidney and muscle of turtles (n = 30) of different gender, size, year of death, location and health status. Overall, POP concentrations were low and accumulation was highest in liver and lowest in fat which is likely due to the poor health of several animals, causing a remobilization of lipids and associated compounds. PCBs and p,p’-DDE dominated the POP profiles, and relatively high MeO-PBDE concentrations (2′-MeO-BDE 68 up to 192 ng/g lw, 6-MeO-BDE 47 up to 79 ng/g lw) were detected in all tissues. Only few influences of factors such as age, gender and location were found. While concentrations were low compared to other marine wildlife, biological toxicity equivalences obtained by screening the tissue extracts using the micro-EROD assay ranged from 2.8 to 356 pg/g and the highest values were observed in muscle, followed by kidney and liver. This emphazises that pollutant mixtures found in the turtles have the potential to cause dioxin-like effects in these animals and that dioxin-like compounds should not be overlooked in future studies.

Environmental lead exposure has been linked with reduced kidney function. However, evidence about its role in diabetic kidney damage, especially when considering the nutritional status of vitamin D, is sparse. In this observational study, we investigated the association between low-level lead exposure and urinary albumin-to-creatinine ratio (UACR) and assessed potential impact of vitamin D among 4033 diabetic patients in Shanghai, China. Whole blood lead was measured by graphite furnace atomic absorption spectrometry. Serum 25-hydroxyvitamin D [25(OH)D] was tested using a chemiluminescence immunoassay. The associations of blood lead with UACR and albuminuria, defined as UACR ≥30 mg/g, according to 25(OH)D levels were analyzed using linear and Poisson regression models. A doubling of blood lead level was associated with a 10.7% higher UACR (95% CI, 6.19%–15.5%) in diabetic patients with 25(OH)D < 50 nmol/L, whereas the association was attenuated toward null (2.03%; 95% CI, −5.18% to 9.78%) in those with 25(OH)D ≥ 50 nmol/L. Similarly, the risk ratios of prevalent albuminuria per doubling of blood lead level between the two groups were 1.09 (95% CI, 1.03–1.15) and 0.99 (95% CI, 0.86–1.14), respectively. Joint analysis demonstrated that a combination of high blood lead and low 25(OH)D corresponded to significantly higher UACR. Among diabetic patients with 25(OH)D < 50 nmol/L, the increment of UACR relative to blood lead was more remarkable in those with reduced estimated glomerular filtration rate (<60 mL/min/1.73 m²). These results suggested that higher blood lead levels were associated with increased urinary albumin excretion in diabetic patients with vitamin D deficiency. Further prospective studies are needed to validate our findings and to determine whether vitamin D supplementation yields a benefit.

As ubiquitous, persistent organic pollutants, polycyclic aromatic hydrocarbons (PAHs) have adverse impacts on human health. Phenanthrene (Phe) is one of the most abundant PAHs in the environment. However, the long-term effects of exposure to environmental level of Phe on the kidneys and the potential mechanisms are unclear. T helper (Th) cells, a subtype of CD4⁺ T cells that play a central role in the renal immune microenvironment. In this study, male mice were chronically exposed to 5, 50, and 500 ng/kg bw Phe every other day for total 210 days. Those results indicated that environmental Phe exposure caused kidney hypertrophy, injury and fibrosis in the mice. Chronic, long-term environmental level of Phe exposure did not significantly alter the innate immune response but induced adaptive immune response changes (Th1/Th2 related cytokines release), causing a type 1 immune response in the 5 ng/kg bw Phe group and a type 2 immune response in the high dose groups (50 and 500 ng/kg bw). This study provides novel insights into the roles of adaptive immune response in long-term PAH exposure-induced chronic kidney injury and fibrosis, which is beneficial for further understanding the potential health hazards of PAHs and providing new avenues for immune intervention strategies to alleviate PAHs toxicity.