Effects Of Short-term Exposure Research Articles

Effects of short-term exposure to air pollution on hospital admissions for autism spectrum disorder in Korean school-aged children: a nationwide time-series study

ObjectivesThis study explored the effects of short-term exposure to air pollution on hospital admissions for autism spectrum disorder (ASD), a proxy for symptom aggravation, among Korean children aged 5–14 years.DesignTime-series...

Urban air pollution and emergency department visits for injury in Edmonton and Toronto, Canada

Air pollution is associated with a broad spectrum of health conditions. Among the reported associations are central nervous system effects, suggesting that air pollution may also affect human behavior and reaction time, which could in turn increase likelihood of injury. Injuries impose a significant public health and economic toll, but to our knowledge the relationship with air pollution has not been examined. This study investigated associations between air pollution and emergency department (ED) visits for injury and poisoning in two Canadian cities (Edmonton, Toronto). Daily concentrations of carbon monoxide, ozone, sulfur dioxide, nitrogen dioxide, and fine particulate matter (PM2.5), and two air quality indexes (AQHI, AQHIX; incorporating O3, NO2, and PM2.5), were considered. A time-stratified case-crossover design and conditional Poisson regression models were used to study short-term exposure effects (0 to 14 day lags). The analysis was done by sex, age group, and season. Significant positive associations were observed in both cities, albeit with some differences in the pattern of effects across strata. Relative risks (RR) and 95% confidence intervals (CI) for an interquartile range (IQR) increase of NO2 (IQR=13.0 ppb, Edmonton) in cold season (October-March) for male were RR=1.012 (95% CI: 1.005, 1.018), 1.025 (1.018, 1.031), 1.026 (1.020, 1.033), and 1.025 (1.019, 1.032), for lags from 0 to 3 days, respectively. The corresponding results in Toronto (IQR=8.8 ppb) were: 1.010 (1.004, 1.017), 1.007 (1.000, 1.013), 1.009 (1.003, 1.016), and 1.007 (1.000, 1.013). The data suggest a potential association between air pollution and increased number of ED visits for injury.

Acute ammonia stress-induced oxidative and heat shock responses modulated by transcription factors in Litopenaeus vannamei

The present study aimed to examine the effects of short-term exposure to ammonia on stress and oxidative responses in shrimp (Litopenaeus vannamei) and to determine whether the antioxidant system related to the regulatory role of transcription factors and stress proteins was activated. Shrimp were exposed ammonia-N at four concentrations: 0 (control), 5, 10, and 15 mg/L, for 48 h. The hepatopancreas was sampled to measure the levels of glutathione (GSH), malondialdehyde (MDA), nitric oxide (NO); the activities of superoxide dismutase (SOD), catalase (CAT), nitric oxide synthase (NOS); and the expression levels of GSH-px (encoding glutathione peroxidase), GST (encoding glutathione-S-transferase), HSP70 (encoding heat shock protein 70), HSP90 (encoding heat shock protein 90), p53, RELISH, and AKIRIN. We observed that exposure to a high ammonia content increased the abundance of oxidative factors (MDA, CAT, SOD, NOS, and NO), reduced the levels of GSH, and upregulated the mRNA expression levels of antioxidant genes (GSH-px and GST), stress-related genes (HSP70 and HSP90), and transcription factor genes (p53, RELISH, and AKIRIN). These results indicated that ammonia induced oxidative stress and inflammation. Both enzymatic and nonenzymatic antioxidant defense systems are involved, which might be regulated by HSPs, as well as certain transcription factors, such as p53 and nuclear factor kappa B (NF-κB), thus mounting an adaptive response to help rebalance redox homoeostasis.

Personal PM2.5-bound PAH exposure and lung function in healthy office workers: A pilot study in Beijing and Baoding, China

The effect of short-term exposure to polycyclic aromatic hydrocarbons (PAHs) on the respiratory system among healthy residents is unclear. Beijing and Baoding are typical polluted cities in China, and there is little research on PAH exposure and its health effects at the individual level. Fourteen healthy female office workers were recruited in urban Beijing and Baoding, China, in 2019. The personal exposure to fine particulate matter (PM2.5)-bound PAHs and lung function were seasonally monitored. The relationships between PAH exposure and lung function were determined by a generalized mixed linear model. Subjects were exposed to high levels of PAH, in which the benzo[a]pyrene (BaP) level (1.26 ng/m3) was over than Chinese national indoor standard (1 ng/m3). All PAHs concentration was higher in winter than that in summer and autumn. Only benz[a]anthracene (BaA) and chrysene (Chr) exposure showed weak relations with decreased lung function, i.e., a 0.58% and 0.73% decrease in peak expiratory flow at lag 2 day, respectively (p < 0.05). PAHs may not be suitable exposure indicators for short-term change in lung function. Our findings highlight the importance of reducing PAH pollution for public respiratory health protection in heavy-polluted cities of China. This pilot study also provides experience on personal PAH assessment such as estimation of the number of repeated measurements required, which is helpful to determine the relationship between PAH exposure and health effect.

Exposure to amitriptyline induces persistent gut damages and dysbiosis of the gut microbiota in zebrafish (Danio rerio)

Amitriptyline (AMI), the most commonly prescribed tricyclic antidepressant, is widely detected in water environments. Exposure to AMI may lead to diverse adverse effects on aquatic organisms, but little is known about the effect of short-term exposure to AMI on the gut microbiota of aquatic organisms and their recovery characteristics. In the present study, adult zebrafish (Danio rerio) were exposed to AMI (0, 2.5, 10, and 40 μg/L) for seven days, and then allowed to recover in AMI-free culture water for 21 days. The exposure caused gut damages in all the AMI treated groups of zebrafish, which became more severe after recovery compared to the control group. AMI exposure also disturbed the microbiota of zebrafish guts and rearing water even after the 21-day recovery period. Furthermore, AMI exposure affected microbes involved in the substance and energy metabolic functions in zebrafish guts and tended to increase the abundance of microbial genera associated with opportunistic pathogens. In addition, the microbial predicted metabolic functions in AMI-exposed guts of zebrafish were significantly altered after the 21-day recovery period, explaining the persistent effects of short-term exposure to AMI. The results of this study suggest that acute exposure to AMI may have persistent impacts on the gut histomorphology and the gut microbiota in aquatic organisms.

Использование СВЧ излучения для предынкубационной стимуляции яиц сельскохозяйственной птицы

The article describes the effect of short-term exposure to an electromagnetic field (EMF) of microwave radiation at a frequency of 2.45 GHz on the rate of development of an embryo in an egg of an agricultural bird. To carry out the experiments, a laboratory microwave setup was developed for controlled and controlled impact on the object being processed. The dielectric characteristics of protein and yolk of fertilized and non-fertilized poultry eggs were measured and analyzed, on the basis of which computer electromagnetic modeling of a microwave chamber for a laboratory pre-incubation processing unit was carried out. The influence of the microwave field on the concentration of proteins in the eggs of poultry was experimentally tested depending on the time of exposure. Keywords: EMF MICROWAVE RADIATION, ENVIRONMENTALLY FRIENDLY STIMULATION OF DEVELOPMENT

Использование СВЧ излучения для предынкубационной стимуляции яиц сельскохозяйственной птицы

The article describes the effect of short-term exposure to an electromagnetic field (EMF) of microwave radiation at a frequency of 2.45 GHz on the rate of development of an embryo in an egg of an agricultural bird. To carry out the experiments, a laboratory microwave setup was developed for controlled and controlled impact on the object being processed. The dielectric characteristics of protein and yolk of fertilized and non-fertilized poultry eggs were measured and analyzed, on the basis of which computer electromagnetic modeling of a microwave chamber for a laboratory pre-incubation processing unit was carried out. The influence of the microwave field on the concentration of proteins in the eggs of poultry was experimentally tested depending on the time of exposure. Keywords: EMF MICROWAVE RADIATION, ENVIRONMENTALLY FRIENDLY STIMULATION OF DEVELOPMENT

Trehalose decreases mRNA and protein expressions of c-Jun and JunB in human cervical cancer HeLa cells.

Increasing evidence suggests that trehalose, a non-reducing disaccharide, ameliorates disease phenotypes by activating autophagy in animal models of various human diseases, including neurodegenerative diseases. Multiple in vitro studies suggest that activation of transcription factor EB, a master regulator of lysosomal biogenesis and autophagy genes, is a major contributor to trehalose-induced autophagy at later stages of exposure. However, underlying causes of trehalose-induced autophagy possibly occur at the early stage of the exposure period. In this study, we investigated the effects of short-term exposure of HeLa cells to trehalose on several signal transduction pathways to elucidate the initial events involved in its beneficial effects. Phospho-protein array analysis revealed that trehalose decreases levels of phosphorylated c-Jun, a component of the transcription factor activator protein-1, after 6h. Trehalose also rapidly reduced mRNA expression levels of c-Jun and JunB, a member of the Jun family, within 1h, resulting in a subsequent decrease in their protein levels. Future studies, exploring the interplay between decreased c-Jun and JunB protein levels and beneficial effects of trehalose, may provide novel insights into the mechanisms of trehalose action.

Effect of short-term exposure to ambient nitrogen dioxide and particulate matter on repeated lung function measures in infancy: A South African birth cohort

BackgroundThe developing lung is highly susceptible to environmental toxicants, with both short- and long-term exposure to ambient air pollutants linked to early childhood effects. This study assessed the short-term exposure effects of nitrogen dioxide (NO2) and particulate matter (PM10) on lung function in infants aged 6 weeks, 6, 12 and 24 months, the early developmental phase of child growth. MethodsLung function was determined by multiple breath washout and tidal breathing measurement in non-sedated infants. Individual exposure to NO2 and PM10 was determined by hybrid land use regression and dispersion modelling, with two-week average estimates (preceding the test date). Linear mixed models were used to adjust for the repeated measures design and an age*exposure interaction was introduced to obtain effect estimates for each age group. ResultsThere were 165 infants that had lung function testing, with 82 of them having more than one test occasion. Exposure to PM10 (μg/m3) resulted in a decline in tidal volume at 6 weeks [-0.4 ml (−0.9; 0.0), p = 0.065], 6 months [-0.5 ml (−1.0; 0.0), p = 0.046] and 12 months [-0.3 ml (−0.7; 0.0), p = 0.045]. PM10 was related to an increase in respiratory rate and minute ventilation, while a decline was observed for functional residual capacity for the same age groups, though not statistically significant for these outcomes. Such associations were however less evident for exposure to NO2, with inconsistent changes observed across measurement parameters and age groups. ConclusionOur study suggests that PM10 results in acute lung function impairments among infants from a low-socioeconomic setting, while the association with NO2 is less convincing.

Associations between ambient temperature and risk of preterm birth in Sweden: A comparison of analytical approaches

BackgroundEvidence indicates that high temperatures are a risk factor for preterm birth. Increasing heat exposures due to climate change are therefore a concern for pregnant women. However, the large heterogeneity of study designs and statistical methods across previous studies complicate interpretation and comparisons. We investigated associations of short-term exposure to high ambient temperature with preterm birth in Sweden, applying three complementary analytical approaches. MethodsWe included 560,615 singleton live births between 2014 and 2019, identified in the Swedish Pregnancy Register. We estimated weekly mean temperatures at 1-km2 spatial resolution using a spatiotemporal machine learning methodology, and assigned them at the residential addresses of the study participants. The main outcomes of the study were gestational age in weeks and subcategories of preterm birth (<37 weeks): extremely preterm birth (<28 weeks), very preterm birth (from week 28 to <32), and moderately preterm birth (from week 32 to<37). Case-crossover, quantile regression and time-to-event analyses were applied to estimate the effects of short-term exposure to increased ambient temperature during the week before birth on preterm births. Furthermore, distributed lag nonlinear models (DLNM) were applied to identify susceptibility windows of exposures throughout pregnancy in relation to preterm birth. ResultsA total of 1924 births were extremely preterm (0.4%), 2636 very preterm (0.5%), and 23,664 moderately preterm (4.2%). Consistent across all three analytical approaches (case-crossover, quantile regression and time-to-event analyses), higher ambient temperature (95th vs 50th percentile) demonstrated increased risk of extremely preterm birth, but associations did not reach statistical significance. In DLNM models, we observed no evidence to suggest an increased effect of high temperature on preterm birth risk. Even so, a suggested trend was observed in both the quantile regression and time-to-event analyses of a higher risk of extremely preterm birth with higher temperature during the last week before birth. ConclusionsIn Sweden, with high quality data on exposure and outcome, a temperate climate and good quality ante-natal health care, we did not find an association between high ambient temperatures and preterm births. Results were consistent across three complementary analytical approaches.

Molecular, biochemical and behavioral responses of Daphnia magna under long-term exposure to polystyrene nanoplastics.

The presence and potential toxicity of nanoplastics (NPs) in aquatic ecosystems is an issue of growing concern. Although many studies have investigated the adverse effects of short-term exposure to high concentrations of NPs to aquatic organisms, the information on the consequences caused by the administration of low NPs concentrations over long-term exposure is limited. The present study aimed at investigating the effects induced by a long-term exposure (21-days) to two sub-lethal concentrations of polystyrene nanoplastics (PS-NPs; 0.05 and 0.5µg/mL) on Daphnia magna. A multi-level approach was performed to assess potential sub-individual (i.e., molecular and biochemical) and individual (i.e., behavioural) adverse effects. At molecular level, the modulation of the expression of genes involved in antioxidant defence, response to stressful conditions and specific physiological pathways was investigated. Oxidative stress (i.e., the amount of pro-oxidants, the activity of antioxidant and detoxifying enzymes and lipid peroxidation) and energetic (i.e., protein, carbohydrate, lipid and total caloric content) biomarkers were applied to assess effects at the biochemical level, while swimming activity was measured to monitor changes in individual behavior. Although the 21-days exposure to PS-NPs induced a slight modulation of gene involved in oxidative stress response, biochemical analyses showed that D. magna individuals did not experience an oxidative stress condition. Significant changes in energy reserves of individuals exposed for 21days to both the PS-NPs concentrations were observed, but no alterations of swimming activity occurred. Our results highlighted that the exposure to low concentrations of PS-NPs could pose a limited risk to D. magna individuals and suggested the importance of a multi-level approach to assess the risks of NPs on aquatic organisms.

Contributions of ambient temperature and relative humidity to the risk of tuberculosis admissions: A multicity study in Central China

BackgroundAs a communicable disease and major public health issue, many studies have quantified the associations between tuberculosis (TB) and meteorological factors with inconsistent results. The purpose of this multicenter study was to characterize the associations between ambient temperature, humidity and the risk of TB hospitalizations and to investigate potential heterogeneity. MethodData on daily hospitalizations for TB, meteorological factors and ambient air pollutants for 16 cities in Anhui Province were collected from 2015 to 2020. A distributed lag nonlinear model (DLNM) was performed to obtain the estimates of meteorological-TB relationships by cities. Then, we used the multivariate meta-regression model to pool the city-specific estimates with air pollution, demographic indicators, medical resource and latitude as potential modifiers to explore the sources of heterogeneity. Finally, we divided the whole province into three regions to validate the meteorological-TB relationships by regions. ResultsThe overall pooled temperature-TB association presented an approximate S-shaped curve, with relative risk (RR) peaking at 5 °C (RR = 1.536, 95% CI: 1.303–1.811) compared to the reference temperature (27 °C). Lag-response curve suggested that low temperature exposure increased the risk of TB hospitalizations at lag 0 and 1 day (lag0 day: RR = 1.136, 95% CI: 1.048–1.231, lag1 day: RR = 1.052, 95% CI: 1.023–1.082). However, the overall exposure-response curve between relative humidity and TB showed almost horizontal line with reference relative humidity to 78%. The residual heterogeneity ranged from 27.1% to 36.9%, with air pollution, latitude and medical resource explained the largest proportion. ConclusionWe found that low temperature exposure is associated with an acute increased risk of TB hospitalizations in Anhui Province. The association between temperature and TB admission varies depending on air pollution, latitude, and medical resources. Since the effect of short-term exposure to humidity is not significant, further studies are supposed to focus on the long-term effect of humidity.

Short-Term Exposure Effects of the Environmental Endocrine Disruptor Benzo(a)Pyrene on Thyroid Axis Function in Zebrafish.

Benzo(a)Pyrene (BaP) is one of the most widespread polycyclic aromatic hydrocarbons (PAHs) with endocrine disrupting properties and carcinogenic effects. In the present study, we tested the effect of BaP on thyroid development and function, using zebrafish as a model system. Zebrafish embryos were treated with 50 nM BaP from 2.5 to 72 h post fertilization (hpf) and compared to 1.2% DMSO controls. The expression profiles of markers of thyroid primordium specification, thyroid hormone (TH) synthesis, hypothalamus-pituitary-thyroid (HPT) axis, TH transport and metabolism, and TH action were analyzed in pools of treated and control embryos at different developmental stages. BaP treatment did not affect early markers of thyroid differentiation but resulted in a significant decrease of markers of TH synthesis (tg and nis) likely secondary to defective expression of the central stimulatory hormones of thyroid axis (trh, tshba) and of TH metabolism (dio2). Consequently, immunofluorescence of BaP treated larvae showed a low number of follicles immunoreactive to T4. In conclusion, our results revealed that the short-term exposure to BaP significantly affects thyroid function in zebrafish, but the primary toxic effects would be exerted at the hypothalamic-pituitary level thus creating a model of central hypothyroidism.

Association of short-term particulate matter exposure with suicide death among major depressive disorder patients: a time-stratified case-crossover analysis

There is growing evidence that suggests a potential association between particulate matter (PM) and suicide. However, it is unclear that PM exposure and suicide death among major depressive disorder (MDD) patients, a high-risk group for suicide. We aimed to assess the effect of short-term exposure to PM on the risk of suicide in MDD patients who are at high risk for suicide. We investigated the risk of suicide among 922,062 newly-diagnosed MDD patients from 2004 to 2017 within the Korean National Health Insurance Service (NHIS) database. We identified 3,051 suicide cases from January 1, 2015, to December 31, 2017, within the death statistics database of the Korean National Statistical Office. PMs with aerodynamic diameter less than 2.5 μm (PM2.5), less than 10 μm (PM10), and 2.5–10 μm (PM2.5–10) were considered, which were provided from the National Ambient Air Monitoring System in South Korea. Time-stratified case-crossover analysis was performed to investigate the association of particulate matter exposure to suicide events. The risk of suicide was significantly high upon the high level of exposure to PM2.5, PM2.5–10 (coarse particle) and PM10 on lag 1 (p for trend < 0.05). Short-term exposure to a high level of PM was associated with an elevated risk for suicide among MDD patients. There is a clear dose–response relationship between short-term PM exposures with suicide death among MDD patients. This result will be used as an essential basis for consideration when establishing an air pollution alarm system for reducing adverse health outcomes by PM.

Short-term effects of exposure to ambient PM1 on blood pressure in children and adolescents aged 9 to 18 years in Shandong Province, China

Limited evidence exists regarding the effect of exposure to ambient particle matters with aerodynamic diameter ≤1 μm (PM1) in a short-term on blood pressure (BP) in the pediatric population. This study aims to examine the association between short-term exposure to ambient PM1 on BP in children and adolescents. Population data were obtained from a large cross-sectional survey from 102 schools in Shandong Province, China. Daily air pollution data were collected, and individual exposure level was assigned based on coordinates of school addresses. Distributed lag non-linear models incorporated with a linear mixed model were used. A total of 35241 students aged 9–18 years were included in the study, and the mean values of PM1, particle matters with aerodynamic diameter ≤2.5 μm (PM2.5), and ≤10 μm (PM10) at the schools during the study period were 50.8 (SD = 7.2) μg/m3, 75.5 (SD = 14.7) μg/m3, and 138.9 (SD = 25.9) μg/m3, respectively. We found that per 10 μg/m3 increment in a cumulative exposure of PM1 at lag 0 and lag 1 day was significantly associated with a higher systolic BP (SBP, β = 1.46 mmHg), diastolic BP (DBP, β = 1.20 mmHg, 95% CI = 0.52 to 1.88), mean arterial pressure (MAP, β = 1.28 mmHg, 95% CI = 0.61 to 1.96), and pulse pressure (PP, β = 0.65 mmHg, 95% CI = 0.14 to 1.16), after adjusting for other air pollutants and individual covariates (including sex, age, BMI, residence, month of the survey, intake of eggs, intake of milk, physical activity, and screen time). The above associations were stronger in magnitude than for PM2.5- and PM10-related associations. The associations of PM1 with SBP, DBP, MAP, and PP were stronger among females, younger children, those overweight or obese, and those with insufficient physical activity levels. In conclusion, the susceptible window of short-term exposure to ambient PM1, PM2.5 and PM10 on BP levels for children and adolescents are lag 0 and lag 1 day, with PM1 exhibiting a stronger association. Future interventions should be conducted to reduce the impact of PM exposure, especially PM1, on health in children and adolescents.

Effect of Short-Term Exposure to Fine Particulate Matter and Particulate Matter Pollutants on Triggering Acute Myocardial Infarction and Acute Heart Failure

Long-term exposure to high concentrations of air pollution is known to lead to increased cardiovascular disease, but it remains unclear whether short-term exposure increases the incidence of acute myocardial infarction (AMI) and acute heart failure (AHF). A time-stratified case-crossover design was used, including data from the 2-year period (January 1, 2017 to December 31, 2018), from the National Health Insurance Academic Research Database of Taiwan. Air pollution data were obtained from the Air Quality Monitoring Station of the Environmental Protection Agency of the Executive Yuan. A generalized linear model was used for statistical analysis. In areas with a long-term moderate severity of air pollution, a 10 μg/m3 increase in fine particulate matter (PM2.5) and particulate matter (PM10) exposure in a short period of time coincided with an increase in AMI by 6.5% to 6.7% and 0.9% to 1.1%, respectively, and AHF by 6.1% to 6.4% and 0.9% to 1.0%, respectively. A long-term high severity of air pollution (PM2.5 and PM10) coincided with an increase in AMI by 7.9% to 8.8% and 4.4% to 4.9%, respectively, and AHF by 7.6% to 8.4% and 4.3% to 4.8%, respectively. In areas with a long-term moderate or high severity of air pollution, short-term exposure to high concentrations of PM2.5 and PM10 pollution is positively correlated with AMI and AHF.

Effects of short-term exposure to the heavy metal, nickel chloride (Nicl2) on gill histology and osmoregulation components of the gray mullet, Mugil cephalus

The gray mullet, Mugil cephalus is an inshore and bottom-feeding fish species of Oman sea. Therefore, the gray mullet may be more exposed to heavy metal contamination, as the toxic impacts of heavy metals mullet has been reported in various studies. This study was conducted to evaluate the toxic effects of the heavy metal, nickel (as NiCl2) on osmoregulation of the gray mullet by measuring blood biochemicals, hormones, minerals and gill histology. Fish (10 fish/tank) were experimentally exposed to NiCl2 at three environmentally relevant concentrations of 5, 10 and 15 μg/l for 96 h. Then, fish were challenged with seawater (35 mg/l) for a period of 120 min. The samples (blood and gill tissue) were collected After 96 exposure to NiCl2 and during salinity challenge (30, 60 and 120 min post challenge). The plasma levels of cortisol and glucose significantly increased in NiCl2−exposed fish. In addition, cortisol increased in all experimental groups 30 min after salinity challenge and then returned gradually to the same levels as the control at 120 min post salinity challenge (PSC). The triiodothyronine (T3) and thyroxine (T4) levels significantly decreased in response to 10 and 15 μg/l NiCl2. In all groups, the thyroid hormones significantly elevated at 30 min PSC. After 30 min PSC, T3 levels in all NiCl2−exposed fish and T4 in the treatment, 10 μg/l NiCl2 remained unchanged throughout the salinity challenge. In the treatment, 5 μg/l NiCl2, T4 levels were recovered at 120 min PSC and reached the same levels as the control. Exposure of fish to high concentrations of NiCl2 and salinity stress increased the lactate levels. However, lactate levels in 5 and 10 μg/l NiCl2 groups were recovered at 120 min PSC and reached the same levels as the control. Furthermore, plasma protein increased in response to 10 and 15 μg/l NiCl2. At 30 PSC, the protein levels decreased in control and 5 μg/l NiCl2 group, while it remained unchanged in fish exposed to 10 and 15 μg/l NiCl2 throughout the salinity challenge. Exposure of fish to NiCl2 disrupted the electrolyte (Na+, Cl−) balance both before and after salinity challenge, which may be due to gill lesions induced by the heavy metal and following alternations in gill permeability. However, fish in 5 μg/l NiCl2 re-established the ionic balance in the blood at the end of salinity challenge period. The malondialdehyde (MDA) levels significantly increased in response to 10 and 15 μg/l NiCl2. The MDA levels returned to the same levels as the control group at 120 min PSC. The results of the present study showed that nickel-induced toxicity (especially at high concentrations) can reduce the osmoregulation capabilities of mullet. However, fish are able to recover from the toxic effects over time, if contamination be eliminated.

Short-term effects of exposure to ambient PM1, PM2.5, and PM10 on ischemic and hemorrhagic stroke incidence in Shandong Province, China

BackgroundShort-term exposure to ambient PM2.5 and PM10 is associated with increased risk of mortality and hospital admissions for stroke. However, there is less evidence regarding the effect of exposure to PM1 on stroke incidence. We estimated the incidence risk of stroke and the attributable fractions related to short-term exposure to ambient PM1, PM2.5 and PM10 in China. MethodsCounty-specific incidence of stroke was obtained from health statistics in years 2014–2019. We linked county-level mean daily concentrations of PM1, PM2.5 and PM10 with stroke incidence. We used the time stratified case-crossover design to estimate the associations between stroke incidence and exposure to PM1, PM2.5 and PM10. We also estimated the disease burden fractions attributable to PM1, PM2.5, and PM10. ResultsThe study included a total of 2,193,954 stroke, from which 1,861,331 were ischemic and 332,623 were hemorrhagic stroke. PM1, PM2.5, and PM10 levels were associated with increased risks of total stroke and ischemic stroke at when assessing the associations in exposure at lag0−4 days. The increase of 10 μg/m3 in PM1, PM2.5, and PM10 was associated with total stroke, and the relative risks were 1.012 (95% confidence interval: 1.008, 1.015), 1.006 (1.004, 1.007) and 1.003 (1.002, 1.004), while the associations with ischemic stroke were 1.013 (1.010, 1.017), 1.006 (1.005, 1.008) and 1.003 (1.002, 1.004), respectively. There was no significant association between PM and risk of hemorrhagic stroke. The attributable fractions of total stroke were 6.9% (5.1%, 8.5%), 5.6% (4.2%, 6.8%) and 5.6% (3.9%, 7.1%) for PM1, PM2.5, and PM10, respectively. ConclusionsPM1 showed a stronger association with stroke, with a larger attributable fraction of outcomes, than PM2.5 and PM10. Clean air policies should target the whole scope of PM, including PM1.

The Effect of Short-Term Exposure to Cadmium on the Expression of Vascular Endothelial Barrier Antigen in the Developing Rat Forebrain and Cerebellum: A Computerized Quantitative Immunofluorescent Study.

Clinical and laboratory studies have shown that environmental exposure to cadmium produces damage to several organs, including bones, lungs, and kidneys. The involvement of cadmium in central nervous system (CNS) disorders has also been widely reported, but the precise pathophysiological mechanism is not yet fully understood. Children who were exposed to cadmium during pregnancy are known to suffer from developmental delays, learning difficulties, attention deficit hyperactivity disorder (ADHD), and other cognitive and neurobehavioral deficits. Results from numerous studies suggest that dysfunction of the blood-brain barrier (BBB) structures is an important step in the neurotoxicity of cadmium. A rat-specific BBB marker protein, the endothelial barrier antigen (EBA), has been previously isolated and classified by Sternberger and others. The mouse IgG1 clone, anti-endothelial barrier antigen (anti-EBA), detects a protein triplet (23.5kDa, 25 kDa, and 30kDa) localized to the luminal surface of central and peripheral nervous system (CNS and PNS) vascular endothelial cells with selective permeability barrier functions. This marker has been widely used for characterizing BBB alterations under demyelinating, inflammatory, and other CNS pathologies. Many studies have been published using the rat model system for studying the neurotoxic effect of acute and chronic exposure to cadmium.We applied the indirect immunofluorescent techniques using the anti-EBA antibody in conjunction with the Olympus cellSens computerized image analysis to detect and quantify the surface areas of BBB-competent microvessel profiles in paraformaldehyde-fixed, paraffin-embedded brains of term-delivered young rats after intraperitoneal injection of a single dose of cadmium chloride. We detected a statistically significant reduction in EBA-positive microvessel surface areas in the forebrain (t = 5.86, df = 1789, p-value < 0.001) and cerebellum (t=73.40, df=1337, p < 0.001) of cadmium-treated rats compared to the normal controls. Thus, this study supports the hypothesis that the EBA is a sensitive and measurable indicator for quantitative assessment of the impact of cadmium exposure in the developing rat brain.

Effects of short-term exposure to tralopyril on physiological indexes and endocrine function in turbot (Scophthalmus maximus).

Tralopyril is an emerging marine antifouling agent with potential toxic effects on non-target aquatic organisms. To evaluate the toxicity of tralopyril, to turbot (Scophthalmus maximus), we assessed biomarkers, including oxidative stress, neurotoxicity, and osmotic homeostasis regulation enzymes, after a 7-day exposure to tralopyril (5μg/L, 15μg/L, 30μg/L). Superoxide dismutase activity was significantly decreased at 30μg/L, and Ca2+-Mg2+-ATPase activity in the gills was significantly increased at 15μg/L and 30μg/L. No statistically significant differences in the responses of acetylcholinesterase and nitric oxide were detected. In addition, 15μg/L and 30μg/L tralopyril induced hyperthyroidism, reflected by significantly increased of T3 levels. The expression levels of hypothalamus-pituitary-thyroid axis-related genes were also upregulated. The molecular docking results showed that the thyroid system disruption was not caused by competitive binding to the receptor. In addition, the integrated biomarker response index showed that 15μg/L tralopyril had the greatest effect on turbot. In general, tralopyril caused oxidative damage, affected energy metabolism, and interfered with the endocrine system. These findings could provide reference data for assessing the ecological risk of tralopyril in marine environments.