Risk assessments of the ecotoxicological effects insecticides impose on ectotherms have increasingly considered temperature. However, the changes toxicants induce in thermoregulatory behavioral traits may lead to a divergence of thermal selection and temperature-dependent changes of contaminant toxicity. This study demonstrated the interaction of behavioral thermoregulation and temperature-dependent toxicity of beta-cyfluthrin (BC) in the lizard Eremias argus. Based on the negative relationship between temperature and BC toxicity, seeking a warming environment was assumed to represent a self-rescue behavior (and vice versa). The results showed that BC-treated lizards (0–20 μg/g body weight (bw)) showed such self-rescue behavior, while lizards exposed to an extremely high BC dose (200 μg/g bw) sought a cooler environment. Biochemical assays showed that BC affected neurotransmitter systems, caused oxidative stress, and interfered with ion-transport in the central nervous system. Biomarkers of the cholinergic and glutamatergic system, ion-transport function, and oxidative stress were identified as potential biochemical variables related to thermoregulatory behavior. Apparently, seeking a warmer environment is a survival strategy with the aim to neutralize BC toxicity, while seeking a cooler environment aims to attenuate the harmful effects of metabolic and oxidative stress, and to decelerate internal BC diffusion. This phenomenon could be also explained by the concept of the “cooling trap”, i.e., a behavior where cooler temperatures are sought. This impairs survival after exposure to BC at it has a negative temperature coefficient, derived from a dysfunction of the central nervous system regarding thermoregulation caused by the high dosage of neurotoxicant and resulting temperature maladaptation. Implications of the interaction between thermoregulatory behavior and temperature-dependent toxicity are presented, which may aid further temperature-dependent risk assessments.

Urbanization alters land use, increasing the rate of greenhouse gas (GHG) emissions and hence atmospheric compositions. Nitrous oxide (N₂O) is a major GHG that contributes substantially to global warming. N₂O emissions are sensitive to changes in substrate availabilities, such as litter and N input, as well as micro-environmental factors caused by land-use change upon urbanization. However, the potential impacts of changing litter and N on soil N₂O emissions along urban-rural gradients is not well understood. Here, we conducted an in situ study over 19 months in Cinnamomum camphora plantations along an urban-rural gradient, to examine the effects of the urban-rural gradient, N and litter input on N₂O emissions from C. camphora plantation soils and the underlying mechanisms via N, litter and microbial communities. The results showed that urban soil N₂O emissions were 105% and 196% higher than those from suburban and rural soil, respectively, and co-occurred with a higher abundance of AOA, nirS and nirK genes. Litter removal increased cumulative N₂O emissions by 59.7%, 50.9% and 43.3% from urban, suburban and rural soils, respectively. Compared with litter kept treatment, increases in AOA and nirK abundance were observed in urban soil, and higher rural nirS abundance occurred following litter removal. Additionally, the relatively higher soil temperature and available N content in the urban soil increased N₂O emissions compared with the suburban and rural soil. Therefore, in addition to changes in microbial communities and abiotic environmental factors, litter kept in C. camphora plantations along an urban-rural gradient is also important in mitigating N₂O emissions, providing a potential strategy for the mitigation of N₂O emissions.

Estuaries are subject to intense human use globally, with impacts from multiple stressors, such as metal contaminants. A key challenge is extending beyond traditional monitoring approaches to understand effects to biota and system function. To explore the metabolic effects of complex metal contaminants to sediment dwelling (benthic) fauna, we apply a multiple-lines-of-evidence approach, coupling environmental monitoring, benthic sampling, total metals analysis and targeted metabolomics.We characterise metabolic signatures of metal exposure in three benthic invertebrate taxa, which differed in distribution across sites and severity of metal exposure: sipunculid (very high), amphipod (high), maldanid polychaete (moderate). We observed sediment and tissue metal loads far exceeding sediment guidelines where toxicity-related adverse effects may be expected, for metals including, As, Cd, Pb, Zn and Hg.Change in site- and taxa-specific metabolite profiles was highly correlated with natural environmental drivers (sediment total organic carbon and water temperature). At the most metal influenced sites, metabolite variation was also correlated with sediment metal loads. Using supervised multivariate regression, taxa-specific metabolic signatures of increased exposure and possibility of toxic effects were characterised against multiple reference sites. Metabolic signatures varied according to each taxon and degree of metal exposure, but primarily indicated altered cysteine and methionine metabolism, metal-binding and elimination (lysosomal) activity, coupled to change in complex biosynthesis pathways, responses to oxidative stress, and cellular damage.This novel multiple-lines-of-evidence approach combining metabolomics with traditional environmental monitoring, enabled detection and characterisation of chronic metal exposure effects in situ in multiple invertebrate taxa. With capacity for application to rapid and effective monitoring of non-model species in complex environments, these approaches are critical for improved assessment and management of systems that are increasingly subject to anthropogenic drivers of change.

Indoor air pollution has aroused increasing concerns due to its significant adverse health impacts. Indoor PM₂.₅ exposure assessments often rely on PM₂.₅ concentration measured at a single height, which overlooks the vertical variation of PM₂.₅ concentrations accompanied by various indoor activities. In this study, we characterize the vertical profile of PM₂.₅ concentration by monitoring PM₂.₅ concentration at eight different heights in the kitchen and the bedroom, respectively, using low-cost sensors with high temporal resolution. The localized enhancement of PM₂.₅ concentration in elevated heights in the kitchen during cooking was observed on clean and polluted days, showing dominating contribution from cooking activities. The source contribution from cooking and outdoor penetration was semi-quantified using regression models. Stratified source contribution from cooking activities was evident in the kitchen during the cooking period. The contribution in elevated heights (above 170 cm) almost tripled the contrition in bottom layers (below 140 cm). In contrast, little vertical variation was observed during other times of the day in the kitchen or the bedroom. The exposure level calculated using the multi-height measurement in this study is consistently higher than the exposure level estimated from the single-height (at 110 cm) measurement. A more significant discrepancy existed for the cookers (17.8%) than the non-cookers (13.5%). By profiling the vertical gradient of PM₂.₅ concentration, we show the necessity to conduct multi-height measurements or proper breathing-height measurements to obtain unbiased concentration information for source apportionment and exposure assessment. In particular, the multi-height measuring scheme will be crucial to inform household cooking emission regulations.

Experimental studies have suggested perfluoroalkyl substances (PFASs) as mammary toxicants, but few studies evaluated the prospective associations of PFASs with breast cancer risk. We performed a case-cohort study within the Dongfeng-Tongji cohort, including incident breast cancer cases (n = 226) and a random sub-cohort (n = 990). Baseline plasma concentrations of four perfluorinated carboxylic acids (PFCAs) [perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), and perfluoroheptanoic acid (PFHpA)] and two perfluorinated sulfonic acids (PFSAs) [perfluorooctane sulfonic acid (PFOS) and perfluorohexane sulfonic acid (PFHxS)] were measured. Barlow-weighted Cox regression models revealed that each 1-unit increase in ln-transformed PFOA and PFHpA was associated with a separate 35% and 20% elevated incident risk of breast cancer [HR(95%CI) = 1.35(1.03, 1.78) and 1.20(1.02, 1.40), respectively], which were also significant among postmenopausal females [HR(95%CI) = 1.34(1.01, 1.77) and 1.23 (1.02, 1.48), respectively]. Quantile g-computation analysis observed a 19% increased incident risk of breast cancer along with each simultaneous quartile increase in all ln-transformed PFCA concentrations [HR(95%CI) = 1.19(1.01, 1.41)], with PFOA accounting for 56% of the positive effect. Our findings firstly revealed the impact of short-chain PFHpA on increased incident risk of breast cancer, suggested exposure to PFASs as a risk factor for breast cancer, and shed light on breast cancer prevention by regulating PFASs as a chemical class.

The current study investigated seasonal fluctuations in diversity of fish and heavy metal concentrations in coastal areas, as well as the possible human health risks associated by the heavy metals (Mercury, Lead, Chromium, Cadmium, Copper and Zinc). From five different locations across the coastal area, 44 finfish species from 11 orders and 33 families were collected. Four finfish species such as Mugil cephalus, Lates calcarifer, Etroplus suratensis, and Chanos chanos were used to estimate and assess the heavy metal concentrations based on abundance and distribution across coastal area. Results revealed that the metal concentration in these fish species, water, and sediment were all found to be significantly comparable. During the southwest monsoon season, the highest concentrations of metals were found in Chanos chanos, Mugil cephalus, and Lates calcarifer. A hazard index and a target hazard quotient were calculated to determine the human-related health risk. Except for Hg and Cd in children, the anthropological health hazard assessment revealed that most element exposure doses are safe for both children and adults.

Contamination of heavy metals is a serious threat, which causes threats to the environment. Our study aimed to determine the role of endophytic bacteria in Cd phytoremediation and heavy metal ATPase gene expression. Cadmium (Cd) resistant endophytic bacteria were isolated from Solanum nigrum on LB agar plates, contaminated with 0–30 mg/L Cd. The phosphate solubilization and indole-3-acetic acid (IAA) production of endophytes were estimated by growing them on Pikovskaya agar medium and GC-MS analysis, respectively. An experiment in a pot was performed to evaluate the effects of bacteria on rice plants contaminated with 5–25 mg/L of Cd. Expression of Cd response genes was quantified through qRT–PCR and Cd translocation from one part to another part of the plant was measured through the ICP. BLAST alignment of 16 S-rDNA gene sequences confirmed the bacterial isolates as Serratia sp. AI001 and Klebsiella sp. Strain AI002. Both strains tolerated Cd up to 25 mg/L and produced 27–30 μg/mL of IAA. Inoculation of AI001 and AI002 improved plant growth dynamics (i.e., plant length, biomass, chlorophyll contents), relieved electrolyte leakage, and improved reduced glutathione significantly (P < 0.05). The inoculation of AI001 and AI002 significantly (P < 0.05) induced the expression of heavy metal ATPase genes ie., “HMA2, HMA3, and HMA4” and Cd translocation compared to uninoculated plants. Both AI001 and AI002 exhibited very prominent plant-growth-promoting and Cd phytoremediation properties. The results revealed that isolates also contributed a lot to the expression of rice plant heavy metal ATPase genes and in the Cd translocation in the plant.

Particulate matter with a diameter of less than 2.5 μm or PM2.5 is recognized worldwide as a cause of public health problems, mainly associated with respiratory and cardiovascular diseases. There is accumulating evidence to show that exposure to PM2.5 has a crucial causative role in various neurological disorders, the main ones being dementia and Alzheimer's disease (AD). PM2.5 can activate glial and microglial activity, resulting in neuroinflammation, increased intracellular ROS production, and ultimately neuronal apoptosis. PM2.5 also causes the alteration of neuronal morphology and synaptic changes and increases AD biomarkers, including amyloid-beta and hyperphosphorylated-tau, as well as raising the levels of enzymes involved in the amyloidogenic pathway. Clinical trials have highlighted the correlation between exposure to PM2.5, dementia, and AD diagnosis. This correlation is also displayed by concordant evidence from animal models, as indicated by increased AD biomarkers in cerebrospinal fluid and markers of vascular injury. Blood-brain barrier disruption is another aggravated phenomenon demonstrated in people at risk who are exposed to PM2.5. This review summarizes and discusses studies from in vitro, in vivo, and clinical studies on causative relationships of PM2.5 exposure to AD-related neuropathology. Conflicting data are also examined in order to determine the actual association between ambient air pollution and neurodegenerative diseases.

Rice consumption is the major pathway for human methylmercury (MeHg) exposure in inland China, especially in mercury (Hg) contaminated regions. MeHg production, a microbially driven process, depends on both the chemical speciation of inorganic divalent mercury, Hg(II), that determines Hg bioavailability for methylation. Studies have shown that Hg(II) speciation in contaminated paddy soils is mostly controlled by natural organic matter and sulfide levels, which are typically thought to limit Hg mobility and bioavailability. Yet, high levels of MeHg are found in rice, calling for reconsideration of the nature of Hg species bioavailable to methylators in paddy soils. Here, we conducted incubation experiments using a multi-isotope tracer technique including ¹⁹⁸Hg(NO₃)₂, natural organic matter bond Hg(II) (NOM-¹⁹⁹Hg(II)), ferrous sulfide sorbed Hg(II) (≡FeS-²⁰⁰Hg(II)), and nanoparticulate mercuric sulfide (nano-²⁰²HgS), to investigate the relative importance of geochemically diverse yet relevant Hg(II) species on Hg methylation in paddy soils across a Hg concentration gradient. We show that methylation rates for all Hg(II) species tested decreased with increasing Hg concentrations, and that methylation rates using NOM-¹⁹⁹Hg(II) and nano-²⁰²HgS as substrates were similar or greater than rates obtained using the labile ¹⁹⁸Hg(NO₃)₂ substrate. ≡FeS-²⁰⁰Hg(II) yielded the lowest methylation rate in all sites, and thus the formation of FeS is likely a sink for labile ¹⁹⁸Hg(NO₃)₂ in sulfide-rich paddy soils. Moreover, the variability in the methylation data for a given site (1 to 5-fold variation depending on the Hg species) was smaller than what was observed across the Hg concentration gradient (10³–10⁴ fold variation between sites). These findings emphasize that at broad spatial scales, site-specific characteristics, such as microbial community structure, need to be taken into consideration, alongside the nature of the Hg substrate available for methylation, to determine net MeHg production. This study highlights the importance of developing site-specific strategies for remediating Hg pollution.

Excessive exposure to light at night (LAN) has become a serious public health concern. However, little is known about the impact of indoor LAN exposure on blood pressure, particularly among young adults. We aimed to investigate the effects of bedroom individual-level LAN exposure in real-world environment on blood pressure and hypertension among vulnerable young adults, and to evaluate the possible buffering effect of physical activity. In this cross-sectional study, a total of 400 healthy young adults aged 16–22 years were included. Bedroom LAN exposure was recorded at 1-min intervals for two consecutive nights using a TES-1339 R illuminance meter. Blood pressure was measured three times (8–11 a.m. in the physical examination day) in the seated position using an Omron HEM-7121 digital sphygmomanometer. A wrist-worn triaxial accelerometer (ActiGraph GT3X-BT) was used to assess physical activity for seven consecutive days. Each 1 lx increase of bedroom LAN intensity was associated with 0.55 mmHg-increase in SBP (95% CI: 0.15, 0.95), 0.30 mmHg-increase in DBP (95% CI: 0.06, 0.54), and 0.38 mmHg-increase in MAP (95% CI: 0.12, 0.65). Higher levels of LAN exposure were associated with increased risk of hypertension (LAN ≥ 3lx vs. LAN < 3lx: OR = 3.30, 95%CI = 1.19–9.19; LAN ≥ 5lx vs. LAN < 5lx: OR = 3.87, 95%CI = 1.37–10.98). However, these detrimental effects of bedroom LAN exposure on blood pressure and hypertension were not observed among young adults with high MVPA (≥2 h/day) level. MVPA can alleviate negative effects of bedroom LAN exposure on blood pressure and hypertension. Maintaining bedroom settings darkness at night may be an important strategy for reducing the risk of hypertension. Furthermore, for individuals living with high levels of indoor LAN exposure, regular physical activity may be a good option for preventing cardiovascular disease and hypertension.