Higher Exposure Concentrations Research Articles

How does the internal distribution of microplastics in Scylla serrata link with the antioxidant response in functional tissues?

Crabs can live in diverse lifestyles in both water and benthic environments, which are the basin of microplastics (MPs) inputs. Edible crabs with large consuming quantity, e.g., Scylla serrata were subjected to accumulate MPs in their tissues from surrounding environments and generate biological damages. However, no related research has been conducted. In order to accurately assess the potential risks to both crabs and humans consuming MPs contaminated crabs, S. serrata were exposed to different concentrations (2, 200 and 20,000 μg/L) of polyethylene (PE) microbeads (10–45 μm) for 3 days. The physiological conditions of crabs and a series of biological responses, including DNA damage, antioxidant enzymes activities and their corresponding gene expressions in functional tissues (gills and hepatopancreas) were investigated. PE-MPs accumulated in all tissues of crabs with concentration- and tissue-dependent manner, which was assumed to be via the internal distribution initialized by gills’ respiration, filtration and transportation. Significantly increased DNA damages were observed in both gills and hepatopancreas under exposures, however, the physiological conditions of crabs showed no dramatic alterations. Under low and middle concentration exposures, gills energetically activated the first line of antioxidant defense to against oxidative stress, e.g., superoxide dismutase (SOD) and catalase (CAT), but lipid peroxidation damage still occurred under high concentration exposure. In comparison, SOD and CAT composed antioxidant defense in hepatopancreas tended to collapse under severe MPs exposure and the defense mechanism attempted to switch to the secondary antioxidant response by compensatively stimulating the activities of glutathione S-transferase (GST), glutathione peroxidase (GPx) and the content of glutathione (GSH). The diverse antioxidant strategies in gills and hepatopancreas were proposed to be closely related to the accumulation capacity of tissues. The results confirmed the relation between PE-MPs exposure and antioxidant defense in S. serrata, and will help to clarify the biological toxicity and corresponding ecological risks.

Sub-chronic ammonia exposure induces hepatopancreatic damage, oxidative stress, and immune dysfunction in red swamp crayfish (Procambarus clarkii)

Ammonia, as one of the primary water pollutants in aquaculture, has been shown to induce a wide range of ecotoxicological effects on aquatic animals. In order to investigate the antioxidant and innate immune responses in crustaceans disrupted by ammonia, red swamp crayfish (Procambarus clarkii) were exposed to 0, 15, 30, and 50 mg/L total ammonia nitrogen for 30 d, the alterations of antioxidant responses as well as innate immunity were studied. The results showed that the severity of hepatopancreatic injury were aggravated by the increasing ammonia levels, which were mainly characterized by tubule lumen dilatation and vacuolization. The swollen mitochondria and disappeared mitochondria ridges suggested that oxidative stress induced by ammonia targets the mitochondria. Concurrently, enhanced MDA levels, and decreased GSH levels as well as the decreased transcription and activity of antioxidant enzymes, including SOD, CAT, and GPx were noticed, which suggested that high concentrations of ammonia exposure induce oxidative stress in P. clarkii. Furthermore, a significant decrease of the hemolymph ACP, AKP, and PO along with the significant downregulation of immune-related genes (ppo, hsp70, hsp90, alf1, ctl) jointly indicated that ammonia stress inhibited the innate immune function. Our findings demonstrated that sub-chronic ammonia stress induced hepatopancreatic injury and exert suppressive effects on the antioxidant capacity as well as innate immunity of P. clarkii. Our results provide a fundamental basis for the deleterious effects of ammonia stress on aquatic crustaceans.

Spatial Distribution of PM10 and NO2 in Ambient Air Quality in Cape Town CBD, South Africa

Fixed air quality monitoring stations generally monitor the air quality in developing countries. However, this practice, in addition to being costly, inherently contains drawbacks associated with the inability to capture the spatial distribution of air pollutants. Against this limitation, it is necessary to employ flexible and dynamic monitoring techniques that are fundamental and influential in comprehending the spatial distribution of pollutants. Because of this, in recent times, the application of GIS as a monitoring technique has proved to be more efficient than using fixed monitoring stations. Therefore, to this end, the current study mapped the spatial distribution of PM10 and NO2 pollutants in Cape Town CBD using the GIS technique. Subsequently, the GIS monitoring technique revealed that both pollutants had high spatial distribution between 2017 and 2018, irrespective of the season. Furthermore, high exposure concentrations of PM10 were generally observed across the CBD in contrast to NO2 exposure levels, which were relatively low. To contextualize the findings, compared with other studies, the current research discovered that spatial distribution of air pollution is associated with meteorological conditions, such as wind speed and temperature, that traditional techniques of monitoring exposure can’t capture.

The short-term effects of air pollution exposure on preterm births in Chongqing, China: 2015–2020

Accumulating evidence suggested that the risk of preterm births (PTBs) following prenatal exposure to air pollution was inconclusive. The aim of this study is to investigate the relationship between air pollution exposure in the days before delivery and PTB and assess the threshold effect of short-term prenatal exposure to air pollution on PTB. This study collected data including meteorological factors, air pollutants, and information in Birth Certificate System from 9 districts during 2015–2020 in Chongqing, China. Generalized additive models (GAMs) with the distributed lag non-linear models were conducted to assess the acute impact of air pollutants on the daily counts of PTB, after controlling for potential confounding factors. We observed that PM2.5 was related to increased occurrence of PTB on lag 0–3 and lag 10–21 days, with the strongest on the first day (RR = 1.017, 95%CI: 1.000–1.034) and then decreasing. The thresholds of PM2.5 for lag 1–7 and 1–30 days were 100 μg/m3 and 50 μg/m3, respectively. The lag effect of PM10 on PTB was very similar to that of PM2.5. In addition, the lagged and cumulative exposure of SO2 and NO2 was also associated with the increased risk of PTB. The lag relative risk and cumulative relative risk of CO exposure were the strongest, with a maximum RR at lag 0 (RR = 1.044, 95%CI: 1.018, 1.069). Importantly, the exposure–response curve of CO showed that RR increased rapidly when the concentration exceeded 1000 μg/m3. This study indicated significant associations between air pollution and PTB. The relative risk decreases with day lag, while the cumulative effect increases. Thus, pregnant women should understand the risk of air pollution and try to avoid high concentration exposure.

Characterization of oxidative damage induced by nanoparticles via mechanism-driven machine learning approaches

The wide application of TiO2-based engineered nanoparticles (nTiO2) inevitably led to release into aquatic ecosystems. Importantly, increasing studies have emphasized the high risks of nTiO2 to coastal environments. Bivalves, the representative benthic filter feeders in coastal zones, acted as important roles to assess and monitor the toxic effects of nanoparticles. Oxidative damage was one of the main toxic mechanisms of nTiO2 on bivalves, but the experimental variables/nanomaterial characteristics were diverse and the toxicity mechanism was complex. Therefore, it was very necessary to develop machine learning model to characterize and predict the potential toxicity. In this study, thirty-six machine learning models were built by nanodescriptors combined with six machine learning algorithms. Among them, random forest (RF) – catalase (CAT), k-neighbors classifier (KNN) - glutathione peroxidase (GPx), neural networks - multilayer perceptron (ANN) – glutathione s-transferase (GST), random forest (RF) - malondialdehyde (MDA), random forest (RF) - reactive oxygen species (ROS), and extreme gradient boosting decision tree (XGB) - superoxide dismutase (SOD) models performed good with high accuracy and balanced accuracy for both training sets and external validation sets. Furthermore, the best model revealed the predominant factors (exposure concentration, exposure periods, and exposure matrix) influencing the oxidative stress induced by nTiO2. These results showed that high exposure concentrations and short exposure-intervals tended to cause oxidative damage to bivalves. In addition, gills and digestive glands could be vulnerable to nTiO2-induced oxidative damage as tissues/organs differences were the important factors controlling MDA activity. This study provided insights into important nano-features responsible for the different indicators of oxidative stress and thereby extended the application of machine learning approaches in toxicological assessment for nanoparticles.

Exposure to Volatile Organic Compounds in Paint Production Plants: Levels and Potential Human Health Risks.

A wide range of volatile organic solvents, including aliphatic and aromatic hydrocarbons, alcohols, and ketones, are used in the production of paints, and they comprise more than 30% of the ingredients of paints. The present study was designed to evaluate the occupational exposure to 15 volatile organic compounds (VOCs, including benzene, toluene, ethylbenzene, xylene, styrene, n-hexane, n-heptane, n-nonane, trichloroethylene, tetrachloroethylene, n-butyl acetate, n-octane, n-decane, dichlorofluoromethane, and acetone) in Iranian paint production factories and subsequently, the associated health risks. The samples were collected from the respiratory zone of workers using the NIOSH 1501 method, and their qualitative and quantitative characterization was performed using gas chromatography-mass spectrometry and gas chromatography-flame ionization detector, respectively. The individual concentrations of VOCs ranged from 23.76 ± 0.57 µg m-3 (acetone) to 92489.91 ± 0.65 µg m-3 (m,p-xylene). The predominant compounds were m,p-xylene (up to 92489.91 ± 0.65 µg m-3), ethylbenzene (up to 91188.95 ± 0.34 µg m-3), and toluene (up to 46088.84 ± 0.14 µg m-3). The non-cancer risks of benzene, n-nonane, trichloroethylene, tetrachloroethylene, xylene, and ethylbenzene surpassed the reference value in most of the sectors. In addition, total lifetime risks of cancer were in the range of 1.8 × 10-5-3.85 × 10-3, suggesting that there was a risk of carcinogenesis in all studied sections, mainly due to ethylbenzene and benzene. Considering their high exposure concentrations and their associated non-carcinogenic and carcinogenic risks, biological monitoring of workers and the use of technical and modern engineering control measures are recommended.

Metamifop as an estrogen-like chemical affects the pituitary-hypothalamic-gonadal (HPG) axis of female rice field eels (Monopterus albus).

Metamifop (MET) is a widely used herbicide. It is likely for it to enter water environment when utilized, thus potential impacts may be produced on aquatic animals. Little information is available about its effects on the endocrine system of fish to date. In the current study, female rice field eels (Monopterus albus) were exposed to different MET concentrations (0, 0.2, 0.4, 0.6, 0.8mgL -1) for 96h to examine the effect of MET on the hypothalamic-pituitary-gonadal (HPG) axis and sexual reversal. The results showed that high concentrations of MET exposure increased vitellogenin (VTG) levels in liver and plasma, but plasma sex hormone levels were not affected by MET exposure. MET exposure increased the expression of CYP19A1b and CYP17 that regulate sex hormone production in the brain, but the expression of genes (CYP19A1a, CYP17, FSHR, LHCGR, hsd11b2, 3β-HSD) associated with sex hormone secretion in the ovary and the estrogen receptor genes (esr1, esr2a, esr2b) in the liver were all suppressed. In addition, the expression of sex-related gene (Dmrt1) was suppressed. This study revealed for the first time that MET has estrogen-like effects and has a strong interference with the expression of HPG axis genes. MET did not show the ability to promote the sexual reversal in M. albus, on the contrary, the genes expression showed that the occurrence of male pathway was inhibited.

Sub-chronic exposure to waterborne extracellular microcystin-LR impairs calcium homeostasis in rainbow trout

Fish mortality is associated with harmful algal blooms, although whether toxicity is related directly to the presence of cyanotoxins or the prevailing water chemistry remains unclear. Similarly, while planktivorous fish may be exposed to toxin through the diet, the hazard posed by waterborne extracellular toxin to carnivorous fish is less well understood. In this study rainbow trout (Oncorhynchus mykiss) were exposed for up to 28 d to waterborne microcystin-LR at nominal concentrations of 1.5 and 50 µg L−1 (measured values 2 and 49 µg L−1, respectively). The former represents the Canadian drinking water guideline, and the latter an elevated environmental level. This study hypothesised that waterborne toxin exposure would specifically impact gill function, and given the importance of this tissue in freshwater fish ion regulation, effects on plasma ions and branchial ion transporter activity would be observed. Microcystin-LR exposure resulted in a significant and persistent hypocalcaemia at the higher exposure concentration, but plasma sodium and branchial activities of the sodium/potassium ATPase, proton ATPase and calcium ATPase enzymes remained unaffected. An in vitro assessment failed to show any effect of microcystin-LR on branchial calcium ATPase activity even at exposure concentrations as high as 1000 µg L−1. A transient increase in hepatic alkaline phosphatase activity was also observed at 49 µg L−1, but there were no effects of toxin exposure on branchial or hepatic lactate dehydrogenase activity. These results suggest that microcystin-LR exposure does not have a general effect on ion regulation, but instead produces a novel and specific impact on calcium metabolism in rainbow trout, although the mechanism underlying this effect remains unknown.

Effects of short-term high-concentration exposure to PM2.5 on pulmonary tissue damage and repair ability as well as innate immune events

Short-term heavy air pollution still occurs frequently worldwide, especially during the winter heating period in some developing countries, which is usually accompanied by the temporary explosive growth of PM2.5. The pulmonary damage caused by PM2.5 exposure has been determined, but there have been few studies on the repair ability after the cessation of exposure and the important role of innate immune events. This study established a short-term (30 days) high-concentration (15 mg/kg body weight) PM2.5 exposure and recovery (15 days of exposure cessation) model by intratracheal instillation. The results showed that short-term PM2.5 exposure increased the content of collagen fiber in rat lung tissue, which was significantly repaired after recovery by 15 days of exposure cessation. Meanwhile, exposure to PM2.5 also caused changes in lung epithelial function, macrophage polarization and cell autophagy function. Most of these changes could be restored or reversed to a certain extent after recovery. However, there were also some biomarkers, including CLDN18.1, SP-A, SP-D, iNOS, CD206, Beclin1, p62 and LC3B, that were still significantly different between the exposure and control groups after recovery, suggesting that some toxic effects, especially epithelial function damage, were not completely repaired. In addition, there was a significant correlation between pulmonary fibrosis and innate immunity. The present study demonstrated that short-term high-concentration exposure to PM2.5 could cause temporary lung tissue damage and related innate immune events in rats, and the repair ability existed after the cessation of exposure, but part of the damage that required special attention still persisted.

Rhinological procedures result in minimal generation of aerosols.

COVID-19 and other respiratory infections spread through aerosols produced in respiratory activities and in certain surgical procedures considered as aerosol-generating procedures (AGP). Due to manipulation of the upper airway mucosa, rhinosurgery has been considered a particular risk for spread of respiratory infections. Our aim was to assess staff exposure to aerosols during common rhinosurgical procedures METHODS: Staff exposure to generated particle concentrations and size distributions between 0.3 μm and 10 μm were measured during rhinosurgery using an optical particle sizer without any additional collection methods. Similarly measured aerosol exposure during coughing (a commonly used risk reference for aerosol generation) and the operating room’s background concentration were chosen as reference values. Altogether 16 common rhinological surgeries (septoplasties and endoscopic sinus surgery) were measured. The use of suction produced significantly lower aerosol concentration compared to coughing. Low aerosol generation was observed during injection anaesthesia of the nasal mucosa. Instrument comparison revealed that the microdebrider produced fewer aerosols than cold dissection in particles of 1-5 μm and >5 μm. Common rhinosurgeries do not seem to generate as high aerosol concentration exposures as previously believed. Rather, the observed aerosol exposure is lower or similar to exposures during coughing. Therefore, the classification of common rhinosurgeries as AGPs should be re-assessed or possibly discarded.

Incident dementia and long-term exposure to constituents offine particle air pollution: A national cohort study in the United States.

Growing evidence suggests that fine particulate matter (PM2.5) likely increases the risks of dementia, yet little is known about the relative contributions of different constituents. Here, we conducted a nationwide population-based cohort study (2000 to 2017) by integrating the Medicare Chronic Conditions Warehouse database and two independently sourced datasets of high-resolution PM2.5 major chemical composition, including black carbon (BC), organic matter (OM), nitrate (NO3-), sulfate (SO42-), ammonium (NH4+), and soil dust (DUST). To investigate the impact of long-term exposure to PM2.5 constituents on incident all-cause dementia and Alzheimer's disease (AD), hazard ratios for dementia and AD were estimated using Cox proportional hazards models, and penalized splines were used to evaluate potential nonlinear concentration-response (C-R) relationships. Results using two exposure datasets consistently indicated higher rates of incident dementia and AD for an increased exposure to PM2.5 and its major constituents. An interquartile range increase in PM2.5 mass was associated with a 6 to 7% increase in dementia incidence and a 9% increase in AD incidence. For different PM2.5 constituents, associations remained significant for BC, OM, SO42-, and NH4+ for both end points (even after adjustments of other constituents), among which BC and SO42- showed the strongest associations. All constituents had largely linear C-R relationships in the low exposure range, but most tailed off at higher exposure concentrations. Our findings suggest that long-term exposure to PM2.5 is significantly associated with higher rates of incident dementia and AD and that SO42-, BC, and OM related to traffic and fossil fuel combustion might drive the observed associations.

Effects on Growth of Juvenile Abalones Haliotis tuberculata Under Chronic Exposition to Metals Released from the Dissolution of an Aluminium-Based Galvanic Anode

In the marine environment, the galvanic anode cathodic protection system (GACP) undergoes oxidation and releases metals in the forms of ions or oxy-hydroxides into the environment. The objective of the present study was to investigate the toxicity of a cocktail of metals released from the dissolution of an aluminium-based galvanic anode (~ 95% Al, ~ 5% Zn) on the abalone Haliotis tuberculata. Juveniles were exposed for 16weeks (i.e. 12weeks of exposure and 4weeks of decontamination phase) and their growth, intake rate, conversion rate and metallic concentrations were monitored. A total of 6 conditions were tested: a control, 4 concentrations based on Al and a trophic control. Results showed that the mortality reached 57% for individuals exposed to 1125µg L-1 of Al, and the abalone growth significantly decreased for an Al concentration greater than 495µg L-1. At the highest exposure concentration, intake rate measurements revealed that the appetite of abalones was affected, supported by the large increase in the conversion rate which was indicative of a poor feed efficiency. The monitoring of metallic concentrations showed that H. tuberculata strongly bioconcentrated Al relative to zinc. The diet did not appear to be the primary pathway for metal entry. Concentrations that significantly impacted abalone growth and survival during the experiment were higher than those found in natural environment, but the bioconcentration of Al into the tissues of a primary consumer such as abalone may be a potential pathway for Al to enter food webs.

Comparative pulmonary and genotoxic responses to inhaled nickel subsulfide and nickel sulfate in F344 rats.

Inhalation studies with nickel (Ni) subsulfide (Ni3 S2 ) and Ni sulfate hexahydrate (NiSO4 ·6H2 O) investigated differences in mode of action that could explain why the former induced lung tumors in rats and the latter did not. Male rats were exposed to ≤0.22 mg Ni/m3 NiSO4 ·6H2 O or 0.44 mg Ni/m3 Ni3 S2 , 6 h/day, 5 days/week for 3 and 13 weeks; subsets of the rats exposed for 13 weeks were held for an additional 13 weeks. Analyses of bronchoalveolar lavage fluid, isolated cells, and whole lung tissue were conducted to compare the extent and persistence of any induced lung effects. Histological findings were qualitatively identical for both compounds and consistent with lesions reported in earlier studies. After 13 weeks of exposure, the incidence and severity of pulmonary inflammation and epithelial cell hyperplasia were greater among Ni3 S2 -exposed rats, whereas the reverse response was seen for apoptosis. Only Ni3 S2 exposure significantly increased epithelial and non-epithelial cell proliferation after 13 weeks of exposure. Both compounds induced DNA damage in isolated lung cells and DNA hypermethylation of whole lung tissue after 13 weeks of exposure at the highest exposure concentrations. Increases in cell proliferation, DNA damage, and tissue DNA hypermethylation did not persist during the 13-week recovery period. In summary, the highest concentrations of each compound produced marked pulmonary toxicity, but the lowest concentrations produced minimal or no effects. Differences in the proliferative and apoptotic responses between the two compounds may help explain differences in carcinogenicity, whereas the identification of no observed adverse effect concentrations (NOAECs) contributes to the risk characterization for inhalation exposure to nickel compounds.

Maternal exposure to polystyrene microplastics alters placental metabolism in mice.

The rapid growth in the worldwide use of plastics has resulted in a vast accumulation of microplastics in the air, soil and water. The impact of these microplastics on pregnancy and fetal development remains largely unknown. In pregnant mice, we recently demonstrated that exposure to micro- and nanoplastics throughout gestation resulted in significant fetal growth restriction. One possible explanation for reduced fetal growth is abnormal placental metabolism. To evaluate the effect of maternal exposure to microplastics on placental metabolism. In the present study, CD-1 pregnant mice were exposed to 5 μm polystyrene microplastics in filtered drinking water at one of four concentrations (0 ng/L (controls), 102 ng/L, 104 ng/L, 106 ng/L) throughout gestation (n = 7-11/group). At embryonic day 17.5, placental tissue samples were collected (n = 28-44/group). Metabolite profiles were determined using 1H high-resolution magic angle spinning magnetic resonance spectroscopy. The relative concentration of lysine (p = 0.003) and glucose (p < 0.0001) in the placenta were found to decrease with increasing microplastic concentrations, with a significant reduction at the highest exposure concentration. Multivariate analysis identified shifts in the metabolic profile with MP exposure and pathway analysis identified perturbations in the biotin metabolism, lysine degradation, and glycolysis/gluconeogenesis pathways. Maternal exposure to microplastics resulted in significant alterations in placental metabolism. This study highlights the potential impact of microplastic exposure on pregnancy outcomes and that efforts should be made to minimize exposure to plastics, particularly during pregnancy.

Joint Action Toxicity of Arsenic (As) and Lead (Pb) Mixtures in Developing Zebrafish.

Arsenic (As) and lead (Pb) are environmental pollutants found in common sites and linked to similar adverse health effects. Multiple studies have investigated the toxicity of each metal individually or in complex mixtures. Studies defining the joint interaction of a binary exposure to As and Pb, especially during the earliest stages of development, are limited and lack confirmation of the predicted mixture interaction. We hypothesized that a mixture of As (iAsIII) and Pb will have a concentration addition (CA) interaction informed by common pathways of toxicity of the two metals. To test this hypothesis, developing zebrafish (1-120 h post fertilization; hpf) were first exposed to a wide range of concentrations of As or Pb separately to determine 120 hpf lethal concentrations. These data were then used in the CA and independent action (IA) models to predict the type of mixture interaction from a co-exposure to As and Pb. Three titration mixture experiments were completed to test prediction of observed As and Pb mixture interaction by keeping the Pb concentration constant and varying As concentrations in each experiment. The prediction accuracy of the two models was then calculated using the prediction deviation ratio (PDR) and Chi-square test and regression modeling applied to determine type of interaction. Individual metal exposures determined As and Pb concentrations at which 25% (39.0 ppm Pb, 40.2 ppm As), 50% (73.8 ppm Pb, 55.4 ppm As), 75% (99.9 ppm Pb, 66.6 ppm As), and 100% (121.7 ppm Pb, 77.3 ppm As) lethality was observed at 120 hpf. These data were used to graph the predicted mixture interaction using the CA and IA models. The titration experiments provided experimental observational data to assess the prediction. PDR values showed the CA model approached 1, whereas all PDR values for the IA model had large deviations from predicted data. In addition, the Chi-square test showed most observed results were significantly different from the predictions, except in the first experiment (Pb LC25 held constant) with the CA model. Regression modeling for the IA model showed primarily a synergistic response among all exposure scenarios, whereas the CA model indicated additive response at lower exposure concentrations and synergism at higher exposure concentrations. The CA model was a better predictor of the Pb and As binary mixture interaction compared to the IA model and was able to delineate types of mixture interactions among different binary exposure scenarios.

Incident Dementia and Long‐Term Exposure to Constituents of U.S. Fine Particle Air Pollution: A National Cohort Study

AbstractBackgroundGrowing evidence suggests that PM2.5 likely increases the risks of neurological disorders, yet little is known about the relative contributions of different constituents. Understanding constituent‐specific effects are critical to targeting emission reductions of specific sources with the greatest health protection.MethodWe conducted a nationwide population‐based cohort study (2000‐2017), by integrating the Medicare Chronic Conditions Warehouse database and two sets of high‐resolution, multiple‐species, air pollution datasets to investigate the impact of long‐term exposure to PM2.5 constituents on incident dementia and Alzheimer’s disease (AD). and home health‐care claims. Hazard ratios for dementia and AD were estimated using single‐ and multi‐constituent Cox proportional hazards models, and penalized splines were used to evaluate potential nonlinear concentration‐response relationships.ResultsOf the 18.5 million dementia and 19.2 million AD individuals within these cohorts, 31.5% and 14.6% developed dementia and AD events, respectively. From the single‐pollutant models, an interquartile range (IQR) increase in PM2.5 mass was associated with an increase in dementia incidence ranging between 6‐7% using two exposure datasets. For different PM2.5 constituents, associations remained significant in black carbon (BC), organic matter (OM), sulfate (SO4 2−), and ammonium (NH4 +). Incident dementia was observed to have the strongest association with increases in exposure to SO4 2− and BC (10‐11% increase and 4‐6% per IQR increase, respectively). Effect estimates for AD were even larger. For both endpoints, all constituents had largely linear concentration‐response relationships in the low exposure range, but most tailed off at high exposure concentrations, particularly for AD.ConclusionOur study suggests that long‐term exposure to PM2.5 is significantly associated with increased incident dementia and AD, and that the different PM2.5 constituents may elicit differential neurotoxicity. Reduction of PM2.5 emissions, especially for the main sources of BC and SO4 2−, may reduce the burden of dementia or AD in the aging US population.

Detoxification effects of ascorbic acid on the oxidative stress, neurotoxicity, and metallothionein (MT) gene expression in juvenile rockfish, Sebastes schlegelii by the dietary chromium exposure

Juvenile rockfish Sebastes schlegelii (mean length 10.8 ± 1.4 cm, and mean weight 31.7 ± 3.6 g) were exposed for 4 weeks with the different levels of dietary chromium (Cr6+) at 0, 120 and 240 mg/L and ascorbic acids (AsA) at 100, 200 and 400 mg/L. Superoxide dismutase (SOD) activity, glutathione S-transferase (GST) activity, and glutathione (GSH) level of liver and gill were evaluated as antioxidant response indicators for the 4 weeks exposure. The SOD and GST activity of liver and gill were substantially increased by the high concentrations of dietary Cr exposure, whereas a significant decrease was observed in the GSH levels of liver and gill. Metallothionein (MT) gene in liver was significant stimulated in the response to the dietary Cr exposure. In neurotoxicity, AChE activity was considerably inhibited in brain and muscle tissues by dietary Cr exposure. The high levels of AsA supplementation were highly effective to attenuate the alterations in the antioxidant responses, MT gene expression, and AChE activity by the dietary Cr exposure.

Chromium Induced Developments of Diseases and their Inhibitions by Cargos

The exposure of hexavalent chromium (Cr-VI) mainly through the inhalation, skin contact or oral administration by the environmental chromium industrial processes causes the major toxicity-induced health hazardous mortality throughout the world. Though reduced chromium (Cr-III), as an essential micronutrient, is utilized to maintain the normal blood glucose, lipid and protein profiles through the metabolism in the body to activate the action of the hormones such as insulin, the high concentration exposures of Cr-VI and Cr-III cause oxidative stress-induced DNA oxidation and adducts, DNA strand breaks and mutations, DNA-protein cross-links, membrane-lipid peroxidation and reduced/altered antioxidant/immune response activities, leading to cellular damage-related various diseases and the development of malignant cancer.&#x0D; Applications of different cargos may inhibit Cr-VI or its intermediates-induced cytotoxicity, immunotoxicity, or genotoxicity through chromium-chelating and scavenging free radical reactive species, restoring antioxidant and immune response activities or arresting disease-oriented signal transductions or other pathways at cellular and molecular levels. This review mainly demonstrates the development of various diseases by chromium exposure and their inhibitions by cargos.

Acute deltamethrin exposure induces oxidative stress, triggers endoplasmic reticulum stress, and impairs hypoxic resistance of crucian carp

Deltamethrin (Del) has been widely used for effectively controlling ectoparasites of crucian carp and was also strictly prohibited in a hypoxic environment. A previous study indicated that Del exposure causes gill injury in Carassius auratus, which is associated with oxidative stress and endoplasmic reticulum stress (ER stress), but the precise mechanism is not well understood. Here, crucian carp were exposed to Del (0.61, 1.22, 2.44, 4.88 μg/L) for 24 h and then subjected to acute hypoxia challenge (1.0 mg/L) for 24 h. The results revealed that acute exposure to Del notably increased MDA content but markedly decreased CAT activities. Moreover, the T-AOC and SOD activities first increased and then decreased in the 4.88 μg/L Del group. Likewise, the mRNA levels of Nrf2 signaling and its target genes (ho-1, mt, sod, cat, and gpx1) were significantly downregulated in the high concentration exposure groups, while the mRNA levels of keap1 showed the opposite change trend. Meanwhile, Del exposure evoked the PERK-ATF4-CHOP and IRE1 signaling pathways and triggered ER stress in a dose-dependent manner in crucian carp. Importantly, we found that Del exposure significantly decreased the survival rate of crucian carp after hypoxia challenge by reducing oxygen uptake, modifying energy metabolism, and promoting lactate accumulation. Additionally, Del exposure aggravated gill damage and apoptosis under hypoxic stress, which was confirmed by histological assays. Collectively, we inferred that acute exposure to deltamethrin induces oxidative stress and ER stress and impairs hypoxic resistance of crucian carp.

Evaluation of Three Low-Cost Particulate Matter (PM2.5) Sensors for Ambient and High Exposure Conditions in Arba Minch, Ethiopia

The burden of disease from ambient and indoor air pollution is highest in low-income countries, while their resources for monitoring air pollutants are the lowest. PM2.5 is the primary indicator of air pollution. Reference monitors of PM2.5 are expensive, but there is an increased use of low-cost sensors (LCS). Three LCS, the UCB-PATS+ (PATS), Airvisual Pro (IQAV) and Sensirion SPS30 (SPSA) are being used in Arba Minch, Ethiopia, but their quality has not yet been evaluated under circumstances common to low-income countries, and the variety of metrics used in evaluation studies make comparisons difficult. This study aims to evaluate the three LCS under circumstances encountered in Arba Minch, with metrics commonly used and officially prescribed. Measurements were conducted with the LCS at 2 ambient and 4 high exposure (kitchen) concentrations, and at four of those locations with the gravimetric reference method as well. The quality of the three LCS was evaluated within identical, with reference, and between different types, with commonly reported (regression slope and R2) and officially prescribed (Pearson correlation, bias, accuracy, expanded uncertainty) metrics. The SPSA has low within variation in both ambient and high-exposure situations, meets official requirements compared to the reference, and shows a stable bias across different time and concentration levels. The IQAV and PATS within variations are not up to official standards but show strong linear associations. The IQAVs as a group, and PATSs individually, meet official reference requirements at daily level. Between comparison reveals that all LCS show strong linear associations even at 10-minute average level. For SPSA the association is similar across all ranges, and for the others the association is strong when different ranges are taken into account. Generally, all LCS are a good alternative for expensive reference methods. The strong linear associations suggest the possibility of correcting LCS measurement data based on other studies’ results and based on other LCS, across different concentration ranges. Projects with a budget of $600 can already supply 10 measurement locations. Higher-budget projects can contribute to the quality of low-budget projects when they do not only use expensive monitors, but also LCS at the same location.