Anthropogenic activities and the large volume of compounds released into the environment are sources of contamination for plants, animals, and humans. The herbicide monosodium methyl arsenate (MSMA) ranks among the best-selling agricultural pesticides in Brazil. It is classified as highly toxic, containing arsenic, which crosses the placenta, reaching the developing embryo. To assess the toxic effects of these chemicals, model organisms such as chicken embryos are used, as they share phylotypic features with human embryos in the early stages of development, allowing extrapolation between species. This study aimed to identify developmental alterations in chicken embryos induced by MSMA exposure after 3 and 7 days of incubation. The experiment involved three groups of fertilized eggs injected with 0.079, 0.79, and 7.9 μg mL[-1] of an MSMA solution, along with two control groups. We collected embryos to assess mortality rates, morphometric measurements, and morphological alterations. MSMA exposure was associated with embryo mortality, with a statistically significant increase in mortality observed in the MSMA II group after 7 days of incubation, and a non-significant tendency toward higher mortality in the remaining treated groups at the same period. Seven-day embryos exposed to MSMA exhibited significant reductions in embryo area and head, limb, and trunk length. Furthermore, MSMA exposure led to malformations in the cephalic region, neural tube, heart, optic vesicle, limbs, and beak, along with abnormal body curvature and body wall. These anomalies correspond to congenital disorders reported in humans, such as anencephaly, myelomeningocele, and skeletal malformations. These outcomes reveal the harmful effects of MSMA on chicken embryo development and suggest potential risks for human embryogenesis.

Accurate interpretation of gene expression in organisms exposed to emerging contaminants (ECs) requires reliable normalization using stable reference genes. In this study, six candidate housekeeping genes (EEF1A1, GAPDH, ACTB, TBP, RAG1, and PKM) were evaluated in fish (Labeo catla) liver under exposure to chlorpyrifos, triclosan, and oxytetracycline. Expression stability was assessed using geNorm, NormFinder, BestKeeper, and the ΔCt method, with RefFinder providing an integrated ranking. EEF1A1 consistently showed the highest stability, whereas PKM and RAG1 were the least reliable. Normalization of the xenobiotic response gene CYP1A1 with stable (EEF1A1) versus unstable (PKM, RAG1) genes revealed that inappropriate reference gene choice produced misleading expression profiles. These results highlight the critical importance of empirical reference gene validation for accurate qRT-PCR-based gene expression analysis, particularly in ecotoxicological studies involving exposure to complex mixtures of contaminants.

Terrestrial detritivores such as isopods and springtails play a vital role in cycling nutrients through soil ecosystems. Microplastics (MPs, < 5 mm) are increasingly recognized as contaminants of terrestrial soils, yet little is known about whether soil invertebrates themselves are impacted by consuming these plastics or if they can generate MPs from larger plastic debris. This study investigated the ability of three isopod species (Porcellio laevis, Porcellio scaber, and Porcellionides pruinosus) to fragment weathered low-density polyethylene into MPs and assessed the impact on isopod survival and growth. Weathered polyethylene fragments were provided to isopods and replaced weekly over a 28-day exposure; MPs generated in the sand substrate were recovered by hydrogen peroxide digestion, filtration, and microscopy, while survival and growth were also monitored throughout. All three species foraged on the fragments and produced MPs throughout the experiment (min.-max. values: P. laevis = 88.3-1676.0 μm; P. scaber = 82.5-940.4 μm; and P pruinosus = 75.0-823.1 μm). The mean size of MPs generated differed significantly among species and was positively correlated with isopod body size. Weekly MP production did not differ significantly among species, though P. scaber and P. pruinosus varied significantly across weeks; total MP production over the 28 days did not differ among species. No significant effects on isopod survival or growth were observed. These findings indicate that terrestrial isopods can generate substantial quantities of MPs from macroplastic debris without apparent adverse effects on their own survival or growth, underscoring their potential role as biotic generators of secondary MPs in terrestrial ecosystems.

Per- and polyfluoroalkyl substances (PFAS) are a large and diverse class of synthetic chemicals extensively used in industrial processes and consumer products. Human exposure to PFAS is widespread and occurs through multiple pathways, including drinking water, air, diet, household dust, textiles, cosmetics, and occupational contact, particularly with aqueous film-forming foams. Due to their extreme environmental persistence, bioaccumulative properties, and broad biological activity, PFAS are now recognized as a major public health concern. The kidney is a primary target organ for PFAS toxicity, as it plays a central role in PFAS filtration, active tubular reabsorption, and long-term retention. Many PFAS are inefficiently eliminated and accumulate in renal proximal tubular cells, resulting in sustained internal exposure and heightened susceptibility to renal injury. Consistent with this biological plausibility, growing epidemiological and experimental evidence links PFAS exposure to adverse kidney outcomes, including reduced glomerular filtration rate, chronic kidney disease, and nephrolithiasis. Emerging data further suggest an association between PFAS exposure and increased risk of renal malignancies, particularly renal cell carcinoma. This narrative review synthesizes and critically evaluates current evidence on PFAS-related kidney risks, spanning functional impairment, stone formation, chronic disease progression, and cancer development. Particular emphasis is placed on the cellular and molecular mechanisms underlying PFAS-induced nephrotoxicity, including altered renal transport, mitochondrial dysfunction, metabolic dysregulation, oxidative stress, inflammation, DNA damage, and epigenetic modifications. Finally, the review discusses potential preventive and therapeutic strategies, as well as regulatory implications for mitigating PFAS-associated kidney disease.

The increased use of agrochemicals to enhance crop production has had detrimental environmental effects including implication in the sharp decline of North American farmland-breeding birds. Here, using a combination of deep shotgun metatranscriptomics and pesticide exposure data, we sought to assess whether exposure to cotton (Gossypium spp.) production had a differential effect on ileum multi-kingdom microbial activity, metabolism, anti-microbial resistance, and virulence factors of sedentary northern mockingbirds (Mimus polyglottos) sampled from two cotton-producing areas (16 birds in total) and one uncultivated area (7 birds) in Texas, USA. Both Shannon Index values (Adj. r[2] = 0.174, F(1,21) = 5.633, p = 0.027) and a Mantel test (Spearman ρ = 0.184, p = 0.013) supported a relationship between metabolically active microbiota Bray-Curtis dissimilarities and differences in pesticide mixtures among study areas. Virulence factor richness (Adj. r[2] = 0.182, F(1,21) = 5.890, p = 0.024), Shannon Index (Adj. r[2] = 0.231, F(1,21) = 7.612, p = 0.012), and load (sum of virulence factor abundances; Adj. r[2] = 0.160, F(1,21) = 5.194, p = 0.033) were related to total pesticide load (total quantity of pesticides). We found no pesticide effects on expression of either antimicrobial resistance genes or metabolic pathways.

Natural radionuclides in cement and gypsum production materials pose significant risks of occupational radiation exposure that are not well documented in Iraqi Kurdistan. This study quantifies alpha and gamma radiation levels from naturally occurring radioactive materials, specifically [222]Rn, [238]U, [232]Th, and [40]K, in cement and gypsum samples from regional production facilities. Radionuclide activity concentrations were measured using alpha counting techniques and gamma spectrometry. The air concentrations of radon gas ranged from 76.14 to 285.98 Bq/m[3], with an average of 169.42 Bq/m[3]. Although the activity concentrations of gamma-emitting radionuclides were within internationally acceptable limits, they still contributed to cumulative radiation exposure. The risk of lung cancer was estimated for workers with occupational exposure durations of 5, 10, 20, and 30 years, considering both alpha particle exhalation and gamma radiation exposure. The results indicated an average lung cancer risk of 0.03% for individual workers, with a progressive increase corresponding to the duration of employment. For long-term exposure (30 years), this risk increased to between 0.029% and 0.04% per individual. While most radiological parameters fall within Health Canada Guidelines, the cumulative effects of radiation exposure suggest the need for strict radiation protection protocols. This research establishes essential baseline data for occupational health standards in the construction materials industry of Iraqi Kurdistan and highlights the importance of continuous radiological monitoring and safety measures for workers in cement and gypsum production facilities.

Paraquat (PQ) is a globally and widely used high-residue herbicide, also regarded as a potential environmental risk factor for neurodegenerative diseases (NDs). However, how PQ exerts neurotoxicity remains a mystery. The blood-brain barrier (BBB) plays a crucial role in communicating between the central nervous system (CNS) and the peripheral blood. In this article, the core genes, which were mainly based on the potential targets for PQ, MPTP, and Diquat chemicals from the CTD database, intersected with the potential targets related to the symptoms of NDs from databases GeneCards and OMIM. Then GO and KEGG enrichments revealed IL-17A was involved. After being treated with PQ, in vivo, C57BL/6J mice showed low mood and decreased learning and memory abilities. Pathologically, there were captured CD3 and its CD4/8 subsets, as well as IL-17A. Surprisingly, T cells in peripheral blood and spleen that responded to PQ gradually leaned towards Th17 cells and secreted IL-17A. Therefore, it is highly suspected that IL-17A plays a role in disrupting the BBB. In vitro, constructed with recombinant IL-17A, and single-PQ or mixtures (recombinant IL-17A and PQ) to bEnd.3 cells, which together showed that IL-17A is a helper for PQ to aggravately disrupt the BBB. In vivo, mice were treated with IL-17A neutralizing antibodies, which effectively inhibited the permeability damage of the BBB. And in the brain parenchyma, the expression of IL-17A also decreased. In summary, the first to respond to PQ were T cells in the peripheral blood, mainly secreting IL-17A, which also acted as a risk factor disrupting the BBB and assists PQ and other factors in infiltrating parenchyma.

Pharmaceutical pollution of freshwater ecosystems is an emerging environmental and public-health issue in India. The high drug consumption in the country, along with the presence of concentrated manufacturing hubs, inadequate wastewater treatment, and weak monitoring systems, is leading to rising pollutant release. This review summarizes the existing evidence on pharmaceutical contaminants in Indian freshwaters with the focus on classes of pollutants, sources of contamination, environmental fate, toxicological pathways, ecological risks and remediation strategies. Antibiotics, non-steroidal anti-inflammatory drugs, stimulants and anticonvulsants are identified in the review as priority contaminant groups owing to their frequent detection, high use volume, environmental persistence and ecotoxicological relevance. These residues can enter freshwater systems through discharges from pharmaceutical manufacturing, hospital effluents, domestic wastewater, livestock runoff and agricultural pathways. Their persistence is due to their physicochemical properties, adsorption to sediment, incomplete biodegradation and limited removal in conventional wastewater treatment plants. Toxicological evidence points to risks of selection for antibiotic resistance, endocrine disruption, neurotoxicity, oxidative stress, reproductive impairment, genotoxicity and bioaccumulation in aquatic food webs. The review also covers microbial degradation, phytoremediation, constructed wetlands and advanced oxidation processes as remediation options and points out that the choice of technology should be context specific for industrial, municipal and natural water systems. This review offers a novel India-centric synthesis that links pharmaceutical production, consumption, environmental occurrence, ecological effects and remediation feasibility into an integrated framework for monitoring, policy reform and future research.

Brazilian social stingless bees are important pollinators and producers of honey, wax, royal jelly, propolis, and other products. These species are experiencing a population decline, attributed to different factors, such as the excessive use of pesticides. Biological control has been proposed as an alternative to chemical control, relying on the use of natural enemies to manage pests, including microorganisms such as entomopathogenic fungi. However, little is known about the effects of these agents on stingless bees. Therefore, this research evaluated the effect of the commercial bioproduct Metarhizium Oligos WP on the stingless bee Scaptotrigona depilis. After 5 and 10 days of exposure, the bees were cold-immobilized and then dissected in saline solution, and the midgut was collected for histological and ultrastructural analyses. Injured organs were analyzed semiquantitatively. Additionally, superoxide dismutase (SOD) and catalase (CAT) activities were determined to investigate the occurrence of oxidative stress. Behavioral assessments were also performed. Although there were no significant changes in SOD and CAT activities, oxidative stress may have been induced, possibly due to the accumulation of reactive oxygen species and free radicals generated during fungal infection. These effects are believed to be the cause of the observed alterations in midgut morphology, as well as physiological and behavioral changes, such as impaired locomotion. The findings demonstrate the negative impact of the bioproduct on S. depilis stingless bees and suggest it may affect their pollination potential.

Despite the widespread presence of cigarette butts in the environment, the potential toxicological effects posed by microplastics (MPs) derived from them remain poorly understood. In this study, we compared the effects of MPs from conventional cigarette butts (cellulose acetate) and heated tobacco devices (cellulose acetate and polylactic acid film), the latter being under-investigated. We also compared their effects before and after UV-accelerated aging. The most notable change in chemical properties of MPs following UV aging was a significant reduction in nicotine content, which fell below detection limits, while elemental composition remained largely unchanged. The surface of particles remained unchanged, but the size of heated tobacco devices cellulose acetate MPs also fragmented to smaller sizes. The effects were evaluated using Daphnia magna (48 h immobilization; 1, 10, 100 mg L[-1]), Lemna minor (168 h growth inhibition; 100 mg L[-1]), protozoan Tetrahymena thermophila (24 h, 100 mg L[-1]) and in vitro cytotoxicity test model using A549 human lung cells (24 h, 100 mg L[-1]). Toxicity tests revealed no significant effects of all types of MPs on any of used test models. UV-aging of MPs did not change the toxicological profile. Our findings showed that cigarette butt-derived MPs represent a complex mixture of polymers, residual nicotine, and metals. Comparing this research to previous studies suggests that MPs from different cigarette brands vary in chemical composition and toxicological potential.

Fine particulate matter (PM2.5) is a recognized cardiovascular toxicant, yet the exposure duration at which mitochondrial stress responses transition from adaptive to persistently injurious remains poorly defined. Here, we identified a duration-dependent transition in mitochondrial responses under the present exposure conditions. Female Wistar rats were exposed to PM2.5 (250 μg/m[3], 3 h/day) for 1, 7, 14, or 21 days, followed by integrated evaluation of cardiac mitochondrial bioenergetics, redox balance, quality control pathways, and ex vivo cardiac function, with washout validation. Short-term exposure (1-7 days) elicited transient mitochondrial oxidative stress and activation of adaptive quality control responses without impairing respiratory efficiency, electron transport chain activity, ATP production, or cardiac performance; these changes returned to values comparable to controls after a 24-h pollutant-free washout under the present experimental conditions. Under the exposure conditions employed, sustained mitochondrial dysfunction first became evident after 14 days of repeated exposure, characterized by coordinated suppression of mitochondrial respiration, ETC complex activities, and ATP synthesis, accompanied by mitochondrial DNA depletion, impaired biogenesis and quality control signaling, sustained oxidative stress, and intramitochondrial metal accumulation. Notably, mitochondrial and cardiac functional deficits induced after ≥ 14 days persisted despite washout, indicating that these deficits were not restored within the 24-h recovery period examined, rather than reflecting delayed recovery within this window. Collectively, these findings define a duration-dependent temporal toxicity progression at which repeated PM2.5 exposure shifts cardiac mitochondria from transient, recoverable stress responses to persistent bioenergetic impairment under the present experimental conditions providing a mechanistic basis for exposure-duration-informed cardiovascular hazard characterization.

Bisphenol A (BPA), a prevalent endocrine disruptor and component of synthetic resins, has recently gained attention for its nephrotoxic potential. Experimental evidence demonstrates that BPA induces kidney injury through oxidative stress, inflammation, and apoptosis. BPA exposure leads to excessive production of reactive oxygen species, increased lipid peroxidation, and decreased levels of key antioxidant enzymes such as superoxide dismutase, catalase, and glutathione, resulting in redox imbalance. Concurrently, BPA activates inflammatory cytokines, including IL-1β, IL-6, and TNF-α, as well as the NF-κB signaling pathway, which contribute to renal inflammation and tissue injury. Histopathological analyses consistently reveal glomerular congestion, tubular degeneration, and necrosis. In vitro studies further demonstrate reduced renal cell viability and enhanced apoptosis mediated by the activation of PI3K/AKT, Bcl2/Bax-caspase, and AMPK/mTOR signaling pathways. Collectively, these findings highlight BPA's ability to cause both structural and functional damage to the kidney through oxidative and inflammatory cascades. Despite advances in understanding BPA-induced nephrotoxicity, translating experimental findings to human health remains challenging due to interspecies variations, differing exposure routes, and inconsistent epidemiological data. Moreover, growing evidence suggests that BPA substitutes, such as bisphenol F and bisphenol S, possess similar endocrine-disrupting and nephrotoxic effects, raising further safety concerns. Future research should focus on elucidating mechanisms underlying BPA-induced cell cycle arrest, its long-term effects on renal repair, and susceptibility factors such as genetic and sex-specific differences. Addressing these gaps is essential for improving risk assessment and guiding regulatory measures to mitigate BPA-related kidney dysfunction.

Antibiotics are a common contaminant of freshwaters, yet surprisingly understudied compared to other classes of drugs. Even trace concentrations of antibiotics can alter the gut microbiome, in turn affecting multiple systems including physiology, biochemistry, and behavior. Concurrently, climate change is leading to higher average temperatures and more frequent temperature spikes. The microbiome of poikilotherms is also highly sensitive to temperature. Little is known of how these two stressors interact. In this study we investigated the effects of amoxicillin, an antibiotic that is widely used in human and veterinary medicine, on the swimming behavior and predatory avoidance responses of zebrafish at two temperatures, 28°C (normal) and 32°C (heat-stressed). Additionally, we investigated the effects of the two stressors on the gut microbiome and heat shock protein expression. Both temperature and amoxicillin affected key behaviors including boldness, sociability, and swimming speed, with fish exposed to low-dose amoxicillin having higher swimming velocity suggesting a possible hormesis response. Amoxicillin exposure also increased fish boldness, while temperature had the opposite effect. A high temperature also reduced fish sociability. Both stressors also altered zebrafish responses to a conspecific alarm cue and induced heat shock protein gene expression. Heat stress and amoxicillin both altered the fish gut microbiome at the genus level with heat stress alone increasing several genera (e.g., Nordella, Nocardia, Reyranella), while heat stress plus high amoxicillin (20 μg/L) further increased others (e.g., Bradyrhizobium, Legionella, Xanthobacter). Overall alpha diversity (Shannon) changed little, but community composition (ANOSIM) shifted most clearly under high amoxicillin and under heat combined with amoxicillin, indicating dose- and temperature-dependent restructuring of the gut microbiome. Overall, the microbiome is emerging as an important regulator of physiology and behavior that is vulnerable to multiple stressors.

This study assessed the contamination levels, bioaccessibility, and potential health risks of As, Cd, Cu, Pb, and Zn in sediments from three dry riverbeds (El Beal-EB, Las Matildes-LM, and Ponce-PN) impacted by historical mining activities in the Cartagena-La Unión Mining District. Sediment samples (20 samples from EB, 13 samples from LM, and 19 samples from PN) were collected and analyzed for total and bioaccessible metal(loid) concentrations, and physicochemical properties. Spatial distribution for the contamination factor (Cf), pollution load index (PLI), and correlation analyses were employed to evaluate sediment pollution status. Bioaccessibility was determined using the Solubility Bioaccessibility Research Consortium (SBRC) method. Human health risks were assessed using hazard quotients (HQ) and carcinogenic risk (CR) for children, considering total (scenario 1) and bioaccessible (scenario 2) concentrations. The PLI indicated severe contamination, with maximum values of 66, 78, and 80 for EB, LM, and PN, respectively. Bioaccessible fractions varied widely across all metals and sites, ranging from 0.04% for As to 98.4% for Cd in Las Matildes; in El Beal, Pb bioaccessibility varied between 22.0% and 92.1%, while in Ponce, Pb bioaccessibility ranged from 5.6% to 96.3%. In addition, PN exhibited that pH and inorganic carbon collectively govern metal(loid) bioaccessibility, with strongly acidic conditions enhancing the solubility of Cd, Pb, and Zn. The correlations between total and bioaccessible metal(loid) concentrations were strong and significant in EB-PN, but no correlation in LM was found, emphasizing the importance of site-specific geochemical factors in assessing human health risks. Health risk assessments revealed that total Pb concentration posed the highest non-carcinogenic risk (non-carcinogenic risk was considered significant when HQ > 1), with HQ reaching a mean value of 2.43 in LM and 1.09 in EB. However, when non-carcinogenic risk was evaluated via bioaccessible fraction, mean HQ values decreased by 58% for Pb, remained above the safety threshold (HQ > 1) in specific samples. Additionally, total As concentrations contributed to carcinogenic risk, with values exceeding the threshold (CR > 10[-5]) across the riverbeds. However, when bioaccessible concentrations were considered, carcinogenic risk was substantially reduced (CR < 10[-5]), indicating no significant carcinogenic risk. This study highlights the importance of considering bioaccessibility in risk assessment studies of mining-impacted areas.

Thiram is an agricultural fungicide known to disrupt cellular calcium homeostasis by inducing endoplasmic reticulum (ER) stress and mitochondrial calcium overload in hepatic and growth plate (GP) tissues. Current study investigated thiram-induced alterations at mitochondria-associated membranes (MAMs) and their impact on inter-organ calcium signaling. Following thiram exposure in chickens, hepatic ER stress markers GRP78 and CHOP, along with key calcium-transfer proteins mediating ER-mitochondrial coupling, including inositol 1,4,5-trisphosphate receptor 1 (IP3R1) and voltage-dependent anion channel 1 (VDAC1), were significantly upregulated. Importantly, hepatic ER stress driven hyperactivation of IP3R1/VDAC1 signaling was accompanied by parallel calcium dysregulation and mitochondrial stress responses in the tibial growth plate, providing direct evidence that liver ER stress acts upstream of skeletal calcium imbalance. These findings establish a previously unrecognized liver-bone axis in which thiram-induced hepatic ER stress propagates calcium signaling disturbances to the growth plate, thereby disrupting chondrocyte calcium homeostasis and bone development. Collectively, this study elucidates a mechanistic framework linking MAM-mediated calcium-transfer, ER stress, and cross-organ communication, offering new insights into how toxicant-induced hepatic stress orchestrates systemic calcium metabolism and skeletal pathology.