The wetland ecosystem (WE) is subject to pollution by many anthropogenic activities, including domestic and industrial effluents. These effluents may contain toxic heavy metals that can interact within the aquatic ecosystem and have a capacity to disturb the metabolic activities, histological profile, and genetic structure and functions in aquatic species inhabiting the environment. The present study observed the karyological and histological alterations in gills of the freshwater fish, Mozambique tilapia, Oreochromis mossambicus in two different sublethal concentrations (1% and 3%) of heavy metals in 7, 15, and 30 days of experimental periods. The heavy metals induced various structural damages such as ring chromosome, sister chromatid exchange, acrocentric association region, condensed chromosomal morphology, heterochromatin region, and nucleolar organizer region in the chromosomes of O. mossambicus treated with 1% and 3% sublethal concentrations of water sample collected from Pallikaranai wetland ecosystem. Gills exposed to 1% and 3% effluent exhibited several variations in the respiratory surfaces of gill arches or lamellae in the light and scanning microscopical study. The gills exposed to 1% concentration for 30 days showed marked necrosis, and the secondary lamellae showed the lamellar membrane's dissolution. Exposure of gills to raw effluent in the field condition was observed in the presence of Cd, Pb, Cr, Cu, and Zn. Thus, this present study shows the environmental deterioration by heavy metal pollution on the structure of the gills in tilapia.

Microplastics and antibiotics widely coexist in the aquatic environment, especially in mariculture regions. However, antibiotics adsorbed on microplastics and their role in the colonization of microorganisms on microplastics are poorly understood. Therefore, in-situ aging experiments were conducted to investigate the impact of antibiotics and microplastics co-occurrence on microorganisms and assess their potential risks to human health. Results showed that antibiotics were adsorbed selectively on microplastics, with 29 investigated antibiotics (n = 40) detected in surrounding water but only 6 investigated antibiotics were adsorbed on microplastics. The concentration of antibiotics accumulated on microplastics was controlled by microplastic types and environmental conditions. For example, aged polypropylene (PP) had more developed pore structures resulting in higher adsorption of antibiotics than other microplastic types. High-throughput sequencing showed higher diversity and distinct composition of microorganisms attached to the microplastics than the surrounding water. Opportunistic pathogenic bacteria such as Mycobacterium possessed positive relationships with tetracycline and doxycycline on aged microplastics, which showed adsorbed antibiotics on aged microplastics could benefit some specific pathogens colonized on the microplastics and spread into unaffected ecosystems, marine organisms even humans. The health risk quotient (HQ) implied the potential human health risk of consuming commercial seafood polluted by antibiotics and microplastic loaded with antibiotics. This study revealed the interaction of antibiotics and microorganisms with aged microplastics in aquaculture systems, providing a novel insight into their synergistic effects on ecological and human health.

Urban runoff contains a range of organic micropollutants which, if not removed during wastewater treatment, pose a risk to aquatic environments. These mixtures are complex and often site-specific. Street drains provide an ideal sampling point given they collect the runoff from local and defined catchments. In this study, runoff was collected and sampled in five street drains located in a medium sized town in Germany. A specially constructed trap was used to collect the particulate and total water fractions of the runoff. In addition, passive samplers were deployed to determine the freely dissolved concentrations of selected compounds in the runoff. In sum, 187 polar organic micropollutants could be quantified using LC-HRMS. Thirty of these could only be detected by the use of passive samplers. Traffic derived pollutants such as corrosion inhibitors, rubber- and plastic additives, but also pollutants of industrial origin were strongly represented with sum median concentrations of 100 μg/kg dry weight (DW) in the sediment and 400 ng/L in the water fraction. Several of these substances are of concern due to their environmental persistence and mobility. Perfluorinated compounds and pesticides occurred at lower levels of several μg/kg DW sediment or ng/L water. A number of substances including pharmaceuticals, sweeteners and stimulants indicated domestic wastewater influences. Furthermore, a total of 62 parent and alkylated PAHs were quantified by GC-MS and contributed 30–70% to the sum concentrations of the micropollutants. Non-EPA PAHs dominated the carcinogenic PAH toxicity. The increased PAH alkylation indices (0.7–0.9) showed these primarily came from combustion sources. The runoff particles were additionally microscopically characterized, and correlations were found between the rubber particle counts and the PAH alkylation-index as well as the levels of 2-(methylthio)benzothiazole, a marker compound for tire leaching.

Rice growing in flooded paddy soil often accumulates considerable levels of inorganic and organic arsenic (As) species, which may cause toxicity to plants and/or pose a risk to human health. The bioavailability and toxicity of As in soil depends on its chemical species, which undergo multiple transformations driven primarily by soil microbes. However, the role of endophytes inside rice roots in As species transformation remains largely unknown. We quantified the abundances of microbial functional genes involved in As transformation in the endosphere and rhizosphere of rice roots growing in three paddy soils in a pot experiment. We also isolated 46 different bacterial endophytes and tested their abilities to transform various As species. The absolute abundances of the arsenate reductase gene arsC and the dissimilatory arsenate reductase gene arrA in the endosphere were comparable to those in the rhizosphere, whereas the absolute abundances of the arsenite methylation gene arsM and arsenite oxidation gene aioA in the endosphere were lower. After normalization based on the bacterial 16S rRNA gene, all four As transformation genes showed higher relative abundances in the endosphere than in the rhizosphere. Consistent with the functional gene data, all of the 30 aerobic endophytic isolates were able to reduce arsenate, but only 3 strains could oxidize arsenite. Among the 16 anaerobic endophytic isolates, 4 strains belonging to Desulfovibrio, Terrisporobacter or Clostridium could methylate arsenite and/or methylarsenite. Six strains of aerobic endophytes could demethylate methylarsenite, among which three strains also could reduce and demethylate methylarsenate. None of the isolates could demethylate dimethylarsenate. These results suggest that diverse endophytes living inside rice roots could participate in As species transformation and affect As accumulation and species distribution in rice plants.

This study assessed the dermal exposure of population to polycyclic aromatic hydrocarbons (PAHs) in a South China city. Skin wipe samples of the face, hand, forearm, and shank were collected from 120 volunteers (50% male and 50% female) belonging to different age groups (preschooler, thresholder, middle-aged, and elderly). Concentrations of PAHs in the skin wipe samples varied from 18 to 27000 ng/m² in the order of face > hand > forearm > shank, regardless of age and gender. The PAH concentrations of bare skin locations were significantly higher in females than in males, while no significant differences were observed for clothing-covered skin locations between genders. The PAH concentrations for faces were significantly higher in the elderly compared to the other groups. The PAH composition was distinct between the four age groups. The dermal exposure levels of total PAHs and total BaP equivalent concentration (BaPₑq) varied from 25.6 to 620 and 0.093–37.4 ng/kg body weight/d, respectively. The dermal exposure levels of total PAHs were significantly higher in females than in males in all age groups except for the middle-aged group. The hand-mouth exposure doses were significantly higher in the preschoolers than in the other age groups. The values of the carcinogenic risk caused by dermal PAH exposure were between 3.5 × 10⁻⁶ and 1.4 × 10⁻³ with 29% of the population (35/120) having risk values exceeding significant levels (1 × 10⁻⁴). The thresholder group exhibited the highest risk for PAH dermal exposure among all groups of the population. This study provides a comprehensive evaluation of the age- and gender-related risk of PAH through dermal exposure.

RNA N⁶-methyladenosine (m⁶A) modification regulates the cell stress response and homeostasis, but whether titanium dioxide nanoparticle (nTiO₂)-induced acute pulmonary injury is associated with the m⁶A epitranscriptome and the underlying mechanisms remain unclear. Here, the potential association between m⁶A modification and the bioeffects of several engineered nanoparticles (nTiO₂, nAg, nZnO, nFe₂O₃, and nCuO) were verified thorough in vitro experiments. nFe₂O₃, nZnO, and nTiO₂ exposure significantly increased the global m⁶A level in A549 cells. Our study further revealed that nTiO₂ can induce m⁶A-mediated acute pulmonary injury. Mechanistically, nTiO₂ exposure promoted methyltransferase-like 3 (METTL3)-mediated m⁶A signal activation and thus mediated the inflammatory response and IL-8 release through the degeneration of anti-Mullerian hormone (AMH) and Mucin5B (MUC5B) mRNAs in a YTH m⁶A RNA-binding protein 2 (YTHDF2)-dependent manner. Moreover, nTiO₂ exposure stabilized METTL3 protein by the lipid reactive oxygen species (ROS)-activated ERK1/2 pathway. The scavenging of ROS with ferrostatin-1 (Fer-1) alleviates the ERK1/2 activation, m⁶A upregulation, and the inflammatory response caused by nTiO₂ both in vitro and in vivo. In conclusion, our study demonstrates that m⁶A is a potential intervention target for alleviating the adverse effects of nTiO₂-induced acute pulmonary injury in vitro and in vivo, which has far-reaching implications for protecting human health and improving the sustainability of nanotechnology.

Although an association between urinary phthalate (PAE) metabolites and respiratory symptoms and diseases has been reported, knowledge regarding its effect on pulmonary function is limited, especially in adolescents. Using cross-sectional data from 1389 adolescents (aged 10–19 years) in the 2007–2012 National Health and Nutrition Examination Survey, the association of mixed urinary PAE metabolites with pulmonary function was evaluated using the weighted quantile sum. Moreover, multivariate linear regression was performed to investigate associations between each urinary PAE metabolite and pulmonary function indicators and to estimate the interaction effects between urinary PAE metabolites and demographic characteristics. We found that mixed urinary PAE metabolites were negatively associated with forced expiratory volume at the 1 s (FEV1, p < 0.001) and forced vital capacity (FVC, p = 0.008) levels. In individual PAE metabolite analyses, mono (carboxynonyl) pthalate (MCNP), mono-n-butyl pthalate (MnBP), mono-isobutyl pthalate (MiBP), mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP) and mono-benzyl phthalate (MBzP) correlated negatively with both FVC and FEV1 values (Holm-Bonferroni corrected p < 0.05). Mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) was negatively associated with the FVC value. Significant interactions between sex and urinary MnBP or MBzP levels for the risk of FEV1 decrease in girls were found (p = 0.005), as was a significant interaction between sex and urinary MBzP level for the risk of FVC decline. Our findings suggest that higher PAE exposure is associated with respiratory dysfunction; the association is more pronounced among girls.

Biochar particles are extensively used in soil remediation and interact with microplastics (MPs), especially metal oxide-modified biochar may have stronger interactions with MPs. The mechanism of interactions between humic acid (HA) and different valence cations is different and the co-effect on the transport of MPs is not clear. In this study, the co-effects of HA and cations (Na⁺, Ca²⁺) on the transport and retention of MPs in saturated porous media with peanut shell biochar (PSB) and MgO-modified PSB (MgO-PSB) were systematically investigated. Breakthrough curves (BTCs) of MPs were fitted by the two-site kinetic retention model for analysis. In the absence of HA, the addition of PSB and MgO-PSB significantly hindered the transport of MPs in saturated porous media, and the retention of MPs increased from 34.2% to 59.1% and 75.5%, respectively. In Na⁺ solutions, the HA concentration played a dominant role in controlling MPs transport, compared to the minor role of Na⁺. The transport capacity of MPs always increased gradually with the increase of HA concentration. Whereas, in Ca²⁺ solutions, Ca²⁺ concentrations had a stronger effect than HA. The transport ability of MPs was instead greater than that in Na⁺ solutions as the HA concentration increased at low ionic strength (1 mM). However, the transport capacity of MPs was significantly reduced with increasing HA concentrations at higher ionic strength (10, 100 mM). The two-site kinetic retention model indicated that chemical attachment and physical straining are the main mechanisms of MPs retention in the saturated porous media.

The massive use of plastic has contributed to huge quantities of hazardous refuse at a global scale and represents one of the most prominent issues of the Anthropocene. Microplastics (MPs) have been detected in almost all environments and pose a potential threat to a variety of plant and animal species. Many studies have reported a variety of effects, from negligible to detrimental, of MPs to aquatic organisms. Conversely, much less is known about their effect on terrestrial biota, and particularly on animal behavior and cognition. We assessed the oral toxicity of polyethylene (PE) MPs at three different concentrations (0.5, 5, and 50 mg L⁻¹), and at different timescales (1 day and 7 days of exposure) and tested for their effects on survival, food intake, sucrose responsiveness, habituation to sucrose and appetitive olfactory learning and memory in the honey bee Apis mellifera. We found that workers were not completely unaffected by acute and prolonged ingestion of this polymer. A significant effect of PE on bee mortality was found for the highest concentration but not for lower ones. PE affected feeding behavior in a concentration-dependent manner, with bees consuming more food than controls when exposed to low concentration PE. Regarding our behavioral and cognitive experiments, the high concentration PE was found to affect only bees’ ability to respond consistently to sucrose but not sucrose sensitivity, habituation to sucrose or learning and memory abilities, even for prolonged exposure to PE. While these last results may look somewhat encouraging, we discussed why caution is warranted before ruling out the possibility that PE particles at environmental concentrations are harmful to honey bees.

Air pollution consists of a multi-faceted mix of gases and ambient particulate matter (PM) with diverse organic and non-organic chemical components that contribute to increasing morbidity and mortality worldwide. In particular, epidemiological and clinical studies indicate that respiratory health is adversely affected by exposure to air pollution by both causing and worsening (exacerbating) diseases such as chronic obstructive pulmonary disease (COPD), asthma, interstitial pulmonary fibrosis and lung cancer. The molecular mechanisms of air pollution-induced pulmonary toxicity have been evaluated with regards to different types of PM of various sizes and concentrations with single and multiple exposures over different time periods. These data provide a plausible interrelationship between cellular toxicity and the activation of multiple biological processes including proinflammatory responses, oxidative stress, mitochondrial oxidative damage, autophagy, apoptosis, cell genotoxicity, cellular senescence and epithelial-mesenchymal transition. However, these molecular changes have been studied predominantly in cell lines rather than in primary bronchial or nasal cells from healthy subjects or those isolated from patients with airways disease. In addition, they have been conducted under different cell culture conditions and generally in submerged culture rather than the more relevant air-liquid interface culture and with a variety of air pollutant exposure protocols. Cell types may respond differentially to pollution delivered as an aerosol rather than being bathed in media containing agglomerations of particles. As a result, the actual pathophysiological pathways activated by different PMs in primary cells from the airways of healthy and asthmatic subjects remains unclear. This review summarises the literature on the different methodologies utilised in studying the impact of submicron-sized pollutants on cells derived from the respiratory tract with an emphasis on data obtained from primary human cell. We highlight the critical underlying molecular mechanisms that may be important in driving disease processes in response to air pollution in vivo.