Effects Of Exposure Research Articles

Interactive effects of long-term exposure to PM10, NO2 and O3 on SARS-CoV-2 infection and severity: a population-based cohort study

Interactive effects of long-term exposure to PM10, NO2 and O3 on SARS-CoV-2 infection and severity: a population-based cohort study

Disparity in the effect of long-term exposure to air pollution on non-communicable disease burden across sub-populations in India

Disparity in the effect of long-term exposure to air pollution on non-communicable disease burden across sub-populations in India

The effects of adverse environmental exposures on risk for congenital Chagas transmission and adverse birth outcomes in Santa Cruz, Bolivia.

The effects of adverse environmental exposures on risk for congenital Chagas transmission and adverse birth outcomes in Santa Cruz, Bolivia.

Effect of prenatal exposure to organophosphates and pyrethroid pesticides on foetal growth

Effect of prenatal exposure to organophosphates and pyrethroid pesticides on foetal growth

Effects of combined exposure to railway vibration and noise on severe annoyance

Effects of combined exposure to railway vibration and noise on severe annoyance

Modeling time-varying dispersion to improve estimation of the short-term health effect of environmental exposure in a time-series design

Modeling time-varying dispersion to improve estimation of the short-term health effect of environmental exposure in a time-series design

The Joint Effects of Prenatal Pesticide Exposure and Psychosocial Stressors on Child Psychopathology in a South African Birth Cohort

The Joint Effects of Prenatal Pesticide Exposure and Psychosocial Stressors on Child Psychopathology in a South African Birth Cohort

The effect of low-level air pollution exposure on weight at birth

The effect of low-level air pollution exposure on weight at birth

Systematic review on health effects of long-term exposure to UFP

Systematic review on health effects of long-term exposure to UFP

Glyphosate Internal Doses of Exposure and Health Effects in Populations from an Agricultural Area of the Province of Cordoba (Argentina)

Glyphosate Internal Doses of Exposure and Health Effects in Populations from an Agricultural Area of the Province of Cordoba (Argentina)

Environmental noise exposure effect on cortisol levels in children from seven European birth cohorts: preliminary results

Environmental noise exposure effect on cortisol levels in children from seven European birth cohorts: preliminary results

Is greenspace in the eye of the beholder? Exploring perceived and objective greenspace exposure effects on mental health

Is greenspace in the eye of the beholder? Exploring perceived and objective greenspace exposure effects on mental health

Low doses of acetyl trihexyl citrate plasticizer promote adipogenesis in hepatocytes and mice.

Accumulating epidemiological evidence underscores the association between pervasive environmental factors and an increased risk of metabolic diseases. Environmental chemicals, recognized disruptors of endocrine and metabolic processes, may contribute to the global prevalence of metabolic disorders, including obesity. Acetyl tributyl citrate (ATHC), categorized as a citric acid ester plasticizer, serves as a substitute for di-(2-ethylhexyl) phthalate (DEHP) in various everyday products. Despite its widespread use and the increasing risk of exposure in humans and animals due to its high leakage rates, information regarding the safety of exposure to environmentally relevant doses of ATHC remains limited. This study aimed to investigate the potential impact of ATHC exposure on metabolic homeostasis. Both in vivo and in vitro exposure models were used to characterize the effects induced by ATHC exposure. C57BL/6J male mice were subjected to a diet containing ATHC for 12weeks, and metabolism-related parameters were monitored and analyzed throughout and after the exposure period. Results indicated that sub-chronic dietary exposure to ATHC induced an increase in body fat percentage, elevated serum lipid levels, and increased lipid content in the liver tissue of mice. Furthermore, the effect of ATHC exposure on murine hepatocytes were examined and results indicated that ATHC significantly augmented lipid levels in AML12 hepatocytes, disrupting energy homeostasis and altering the expression of genes associated with fatty acid synthesis, uptake, oxidation, and secretion pathways. Conclusively, both in vivo and in vitro results suggest that exposure to low levels of ATHC may be linked to an elevated risk of obesity and fatty liver in mice. The potential implications of ATHC on human health warrant comprehensive evaluation in future studies.

Effect of utilizing either a self-reported questionnaire or administrative data alone or in combination on the findings of a randomized controlled trial of the long-term effects of antenatal corticosteroids.

A combination of self-reported questionnaire and administrative data could potentially enhance ascertainment of outcomes and alleviate the limitations of both in follow up studies. However, it is uncertain how access to only one of these data sources to assess outcomes impact study findings. Therefore, this study aimed to determine whether the study findings would be altered if the outcomes were assessed by different data sources alone or in combination. At 50-year follow-up of participants in a randomized trial, we assessed the effect of antenatal betamethasone exposure on the diagnosis of diabetes, pre-diabetes, hyperlipidemia, hypertension, mental health disorders, and asthma using a self-reported questionnaire, administrative data, a combination of both, or any data source, with or without adjudication by an expert panel of five clinicians. Differences between relative risks derived from each data source were calculated using the Bland-Altman approach. There were 424 participants (46% of those eligible, aged 49 years, SD 1, 50% male). There were no differences in study outcomes between participants exposed to betamethasone and those exposed to placebo when the outcomes were assessed using different data sources. When compared to the study findings determined using adjudicated outcomes, the mean difference (limits of agreement) in relative risks derived from other data sources were: self-reported questionnaires 0.02 (-0.35 to 0.40), administrative data 0.06 (-0.32 to 0.44), both questionnaire and administrative data 0.01 (-0.41 to 0.43), and any data source, 0.01 (-0.08 to 0.10). Utilizing a self-reported questionnaire, administrative data, both questionnaire and administrative data, or any of these sources for assessing study outcomes had no impact on the study findings compared with when study outcomes were assessed using adjudicated outcomes.

Chronic Morphine Treatment Induces Sex- and Synapse-Specific Cellular Tolerance on Thalamo-Cortical Mu Opioid Receptor Signaling.

How cellular adaptations give rise to opioid analgesic tolerance to opioids like morphine is not well understood. For one, pain is a complex phenomenon comprised of both sensory and affective components, largely mediated through separate circuits. Glutamatergic projections from the medial thalamus (MThal) to the anterior cingulate cortex (ACC) are implicated in processing of affective pain, a relatively understudied component of the pain experience. The goal of this study was to determine the effects of chronic morphine exposure on mu-opioid receptor (MOR) signaling on MThal-ACC synaptic transmission within the excitatory and feedforward inhibitory pathways. Using whole-cell patch clamp electrophysiology and optogenetics to selectively target these projections, we measured morphine-mediated inhibition of optically evoked postsynaptic currents in ACC layer V pyramidal neurons in drug-naïve and chronically morphine treated mice. We found that that morphine perfusion inhibited the excitatory and feedforward inhibitory pathways similarly in females but caused greater inhibition of the inhibitory pathway in males. Chronic morphine treatment robustly attenuated morphine presynaptic inhibition within the inhibitory pathway in males, but not females, and mildly attenuated presynaptic inhibition within the excitatory pathway in both sexes. These effects were not observed in MOR phosphorylation-deficient mice. This study indicates that chronic morphine treatment induces cellular tolerance to morphine within a thalamo-cortical circuit relevant to pain and opioid analgesia. Furthermore, it suggests this tolerance may be driven by MOR phosphorylation. Overall, these findings improve our understanding of how chronic opioid exposure alters cellular signaling in ways that may contribute to opioid analgesic tolerance.

Effects of arsenic exposure on the PI3K/Akt/NF-κB signaling pathway in the hippocampus of offspring mice at different developmental stages

The primary purpose of present study was to explore the effects of arsenic exposure on the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/nuclear transcription factor-κB (NF-κB) signaling pathway in the hippocampus of offspring mice at different developmental stages. Sodium arsenite (NaAsO2) at doses of 0, 15, 30 or 60 mg/L administered to female mice and their pups. The nuclear translocation levels of NF-κB were assessed by EMSA. Real-time RT-PCR was used to measure Akt, NF-κB and PI3K mRNA levels. Protein expressions of PI3K, p-Akt, inhibitor kappa B kinase (IKK), p-NF-κB, protein kinase A (PKA), inhibitor kappa B (IκB), and cAMP response element-binding protein (CREB) were measured by Western blot. Results disclosed that exposure to 60 mg/L NaAsO2 could suppress NF-κB levels of nuclear translocation of postnatal day (PND) 20 and PND 40 mice. Arsenic downregulated the transcriptional and translational levels of PI3K, Akt and NF-κB. Additionally, protein expressions of p-IKK, p-IκB, PKA and p-CREB also reduced. Taken together, results of present study indicated that arsenic could downregulate the PI3K/Akt/NF-κB signaling pathway, particularly on PND 40, which might be involved in the cognitive impairments.

Evaluation of human vulnerability and toxic effects of chronic and acute occupational exposure to ammonia: A case study in an ice factory.

The hazardous material release has frequently occurred worldwide. As a respiratory stimulant and a toxic substance, ammonia has numerous adverse effects on human health. The purpose of this study was to evaluate the human vulnerability and toxic effects of both chronic and acute respiratory exposure to ammonia. This study was conducted in an ice factory. Ammonia reservoirs were selected as the danger center. The scenarios were evaluated from the perspective of the worst-case. The Emergency Response Planning Guidelines 1-3 was used to predict the dangerous concentrations in acute exposure. The probability of human vulnerability was estimated using the Probit model. PHAST 7.2 software was used to model consequences. As a measure of chronic exposure to ammonia, NMAM 6016 was used. A respiratory symptom questionnaire developed by the American Thoracic Society was used for collecting respiratory symptom histories. The ERPG3 level or concentration of 750 ppm was found at a distance of 617.71 and 411.01 meters from tanks, respectively, as a result of a rupture in reservoir 1 over a period of two halves of the year. It was found that the highest probit values for tank 2 at distances of zero, 25, 50, 75, 100, 125, and 150 meters were 9.55, 5.92, 5.47, 4.82, 4.23, 3.56 and 2.96, respectively. The prevalence of pulmonary symptoms, which include coughing, dyspnea, phlegm, and wheezing, was 28%, 19%, 15%, and 26% in the chronic exposure group. In the event that an ammonia reservoir ruptures catastrophically, it may cause human injury at ERPG-2 or ERPG-3 levels. Results revealed that exposure to this substance can impose many pulmonary symptoms on the respiratory system of workers in industries. In order to reduce the vulnerability of humans to potential release scenarios, control measures must be implemented. Also, preventive and mitigation measures can be designed to enhance safety and resilience against the release of hazardous materials.

Mitigating effects of selenium and zinc on oxidative stress and biochemical and histopathological changes in lung during prenatal and lactational exposure rats to barium chloride.

Selenium (Se) and zinc (Zn) are essential trace elements with antioxidant properties, and their supplementation has been shown to be protective against the toxicity of various environmental and dietary substances. The aim of this study was to investigate the potential protective effect of selenium and zinc as adjuvants against barium (Ba) toxicity in lactating rats and their offspring. The pregnant rats were divided into six groups: the first as control; group 2 received barium (67ppm) in the drinking water; group 3 had combined Ba + Se (0.5mg/kg) in the diet; group 4 received Zn (50mg/kg bw) by gavage together with Ba; groups 5 and 6, positive controls, were treated with selenium (0.5mg/kg) and zinc (50mg/kg bw), respectively. MDA, H2O2, AOPP, CAT, GPx, and SOD levels were measured and lung histopathology was performed. Our results showed that barium administration caused lung damage as evidenced by an increase in MDA, H2O2, and AOPP levels and a decrease in the activities of CAT, GPx, and SOD in mothers and their offspring. A decrease in lung GSH, NPSH, and MT levels was also observed. Supplementation of Ba-treated rats with Se and/or Zn significantly improved the pulmonary antioxidant status of mothers and their offspring. Histopathological examinations were also consistent with the results of biochemical parameters, suggesting the beneficial role of Se and Zn supplementation, as evidenced by less accumulation of collagen fibers as studied by hematoxylin and eosin (H&E) and Masson's trichrome staining. In conclusion, we demonstrate the adverse effects of maternal barium exposure during pregnancy and on neonatal lung health and the protective effects of selenium and zinc in preventing the adverse effects of barium exposure.

Identification of the effects of alkalinity exposure on the gills of oriental river prawns, Macrobrachium nipponense

Macrobrachium nipponense is an important commercial freshwater species in China. However, the ability of alkali tolerance of M. nipponense is insufficient to culture in the major saline-alkali water source in China. Thus, it is urgently needed to perform the genetic improvement of alkali tolerance in this species. In the present study, we aimed to analyse the effects of alkali treatment on gills in this species after 96 h alkalinity exposure under the alkali concentrations of 0 mmol/L, 4 mmol/L, 8 mmol/L, and 12 mmol/L through performing the histological observations, measurement of antioxidant enzymes, metabolic profiling analysis, and transcriptome profiling analysis. The results of the present study revealed that alkali treatment stimulated the contents of malondialdehyde, glutathione, glutathione peroxidase in gills, indicating these antioxidant enzymes plays essential roles in the protection of body from the damage, caused by the alkali treatment. In addition, high concentration of alkali treatment (> 8 mmol/L) resulted in the damage of gill membrane and haemolymph vessel, affecting the normal respiratory function of gill. Metabolic profiling analysis revealed that Metabolic pathways, Biosynthesis of secondary metabolites, Biosynthesis of plant secondary metabolites, Microbial metabolism in diverse environments, Biosynthesis of amino acids were identified as the main enriched metabolic pathways of differentially expressed metabolites, which are consistent with the previous publications, treated by the various environmental factors. Transcriptome profiling analyses revealed that the alkali concentration of 12 mmol/L has more regulatory effects on the changes of gene expression than the other alkali concentrations. KEGG analysis revealed that Phagosome, Lysosome, Glycolysis/Gluconeogenesis, Purine Metabolism, Amino sugar and nucleotide sugar metabolism, and Endocytosis were identified as the main enriched metabolic pathways in the present study, predicting these metabolic pathways may be involved in the adaption of alkali treatment in M. nipponense. Phagosome, Lysosome, Purine Metabolism, and Endocytosis are immune-related metabolic pathways, while Glycolysis/Gluconeogenesis, and Amino sugar and nucleotide sugar metabolism are energy metabolism-related metabolic pathways. Quantitative PCR analyses of differentially expressed genes (DEGs) verified the accuracy of the RNA-Seq. Alkali treatment significantly stimulated the expressions of DEGs from the metabolic pathways of Phagosome and Lysosome, suggesting Phagosome and Lysosome play essential roles in the regulation of alkali tolerance in this species, as well as the genes from these metabolic pathways. The present study identified the effects of alkali treatment on gills, providing valuable evidences for the genetic improvement of alkali tolerance in M. nipponense.

The Effect of Short-Term Exposure to Lower Body Positive Pressure on Motor Signal Processing, Reaction Times, and Cardiovascular Parameters in Healthy Volunteers Using Medical Anti-shock Trousers

The Effect of Short-Term Exposure to Lower Body Positive Pressure on Motor Signal Processing, Reaction Times, and Cardiovascular Parameters in Healthy Volunteers Using Medical Anti-shock Trousers