Health & Environmental Research Online (HERO)


ISA-PM (current)


2,492 References Were Found:

The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

Titanium Dioxide Exposure Induces Acute Eosinophilic Lung Inflammation in Rabbits

Authors: Choi, GS; Oak, C; Chun, BK; Wilson, D; Jang, TW; Kim, HK; Jung, M; Tutkun, E; Park, EK (In Press) Industrial Health. HERO ID: 2337959

[Less] Titanium dioxide (TiO2) is increasingly widely used in industrial, commercial and home products. TiO2 . . . [More] Titanium dioxide (TiO2) is increasingly widely used in industrial, commercial and home products. TiO2 aggravates respiratory symptoms by induction of pulmonary inflammation although the mechanisms have not been well investigated. We aimed to investigate lung inflammation in rabbits after intratracheal instillation of P25 TiO2. One ml of 10, 50 and 250 µg of P25 TiO2 was instilled into one of the lungs of rabbits, chest computed-tomography was performed, and bronchoalveolar lavage (BAL) fluid was collected before, at 1 and 24hr after P25 TiO2 exposure. Changes in inflammatory cells in the BAL fluids were measured. Lung pathological assay was also carried out at 24hr after P25 TiO2 exposure. Ground glass opacities were noted in both lungs 1hr after P25 TiO2 and saline (control) instillation. Although the control lung showed complete resolution at 24hr, the lung exposed to P25 TiO2 showed persistent ground glass opacities at 24hr. The eosinophil counts in BAL fluid were significantly increased after P25 TiO2 exposure. P25 TiO2 induced a dose dependent increase of eosinophils in BAL fluid but no significant differences in neutrophil and lymphocyte cell counts were detected. The present findings suggest that P25 TiO2 induces lung inflammation in rabbits which is associated with eosinophilic inflammation.

The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

Air pollution-induced placental epigenetic alterations in early life: A candidate miRNA approach

Authors: Tsamou, M; Vrijens, K; Madhloum, N; Lefebvre, W; Vanpoucke, C; Nawrot, TS (In Press) Epigenetics. HERO ID: 3359719

[Less] Particulate matter (PM) exposure during in utero life may entail adverse health outcomes in later-life. . . . [More] Particulate matter (PM) exposure during in utero life may entail adverse health outcomes in later-life. Air pollution's adverse effects are known to alter gene expression profiles, which can be regulated by microRNAs (miRNAs). We investigate the potential influence of air pollution exposure in prenatal life on placental miRNA expression. Within the framework of the ENVIRONAGE birth cohort, we measured the expression of six candidate miRNAs in placental tissue from 210 mother-newborn pairs by qRT-PCR. Trimester-specific PM2.5 exposure levels were estimated for each mother's home address using a spatiotemporal model. Multiple regression models were used to study miRNA expression and in utero exposure to PM2.5 over various time windows during pregnancy. The placental expression of miR-21 (-33.7%, 95% CI: -53.2 to -6.2, P=0.022), miR-146a (-30.9%, 95% CI: -48.0 to -8.1, P=0.012) and miR-222 (-25.4%, 95% CI: -43.0 to -2.4, P=0.034) was inversely associated with PM2.5 exposure during the 2(nd) trimester of pregnancy, while placental expression of miR-20a and miR-21 was positively associated with 1(st) trimester exposure. Tumor suppressor phosphatase and tensin homolog (PTEN) was identified as a common target of the miRNAs significantly associated with PM exposure. Placental PTEN expression was strongly and positively associated (+59.6% per 5 μg/m³ increment, 95% CI: 26.9 to 100.7, P<0.0001) with 3(rd) trimester PM2.5 exposure. Further research is required to establish the role these early miRNA and mRNA expression changes might play in PM-induced health effects. We provide molecular evidence showing that in utero PM2.5 exposure affects miRNAs expression as well as its downstream target PTEN.

The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

Quantifying population exposure to air pollution using individual mobility patterns inferred from mobile phone data

Authors: Nyhan, MM; Kloog, I; Britter, R; Ratti, C; Koutrakis, P (2018) HERO ID: 4543561

[Less] A critical question in environmental epidemiology is whether air pollution exposures of large populations . . . [More] A critical question in environmental epidemiology is whether air pollution exposures of large populations can be refined using individual mobile-device-based mobility patterns. Cellular network data has become an essential tool for understanding the movements of human populations. As such, through inferring the daily home and work locations of 407,435 mobile phone users whose positions are determined, we assess exposure to PM2.5. Spatiotemporal PM2.5 concentrations are predicted using an Aerosol Optical Depth- and Land Use Regression-combined model. Air pollution exposures of subjects are assigned considering modeled PM2.5 levels at both their home and work locations. These exposures are then compared to residence-only exposure metric, which does not consider daily mobility. In our study, we demonstrate that individual air pollution exposures can be quantified using mobile device data, for populations of unprecedented size. In examining mean annual PM2.5 exposures determined, bias for the residence-based exposures was 0.91, relative to the exposure metric considering the work location. Thus, we find that ignoring daily mobility potentially contributes to misclassification in health effect estimates. Our framework for understanding population exposure to environmental pollution could play a key role in prospective environmental epidemiological studies.

The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

Novel approach to study the cardiovascular effects and mechanism of action of urban particulate matter using lung epithelial-endothelial tetra-culture system

Authors: Kim, HR; Cho, HS; Shin, DY; Chung, KH (2017) Toxicology In Vitro 38:33-40. HERO ID: 3453674

[Less] In vitro models have become increasingly sophisticated, and their usefulness in supporting toxicity . . . [More] In vitro models have become increasingly sophisticated, and their usefulness in supporting toxicity testing is well established. The present study was designed to establish a novel in vitro model that mimics the cellular network surrounding airways and pulmonary blood vessels, to study the cardiovascular toxic effects of particulate matter (PM). Transwell culture method was used to develop a novel tetra-culture system consisting of tri-cultures (one lung epithelial and two immune cell lines) in the apical chamber and endothelial cells in the basolateral chamber. Tri-cultures were exposed to standard reference material (SRM) 1648a, an urban PM. SRM 1648a did not show cytotoxic effects; however, it increased IL-6 level in apical and basolateral chambers. The cells in the basolateral chamber showed increased monocyte adhesion. Furthermore, exposure of tri-cultured cells to SRM 1648a in the apical chamber induced ICAM-1 expression in endothelial cells in the basolateral chamber by activating the IL-6/STAT3 pathway. In conclusion, a tetra-culture system was established to facilitate the identification of cellular adhesion molecule expression induced by the interaction between pulmonary epithelial and endothelial cells. The tetra-culture system will contribute to elucidation of the relationships between inhalable PM and cardiovascular diseases.

The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

Developmental Toxicity of Nanoparticles on the Brain

Authors: Umezawa, M; Onoda, A; Takeda, K (2017) Yakugaku Zasshi 137:73-78. HERO ID: 3453686

[Less]  The toxicity of nanoparticles (nanotoxicology) is being investigated to understand both the health . . . [More]  The toxicity of nanoparticles (nanotoxicology) is being investigated to understand both the health impacts of atmospheric ultrafine particles-the size of which is a fraction (<0.1 μm aerodynamic diameter) of that of PM2.5 (<2.5 μm diameter)-and the safer use of engineered nanomaterials. Developmental toxicity of nanoparticles has been studied since their transfer from pregnant body to fetal circulation and offspring body was first reported. Here we reviewed the developmental toxicity of nanoparticles on the brain, one of the most important organs in maintenance of mental health and high quality of life. Recently the dose- and size-dependency of transplacental nanoparticle transfer to the fetus was reported. It is important to understand both the mechanism of direct effect of nanoparticles transferred to the fetus and offspring and the indirect effect mediated by induction of oxidative stress and inflammation in the pregnant body. Locomotor activity, learning and memory, motor coordination, and social behavior were reported as potential neurobehavioral targets of maternal nanoparticle exposure. Histopathologically, brain perivascular cells, including perivascular macrophages and surrounding astrocytes, have an important role in waste clearance from the brain parenchyma. They are potentially the most sensitive target of maternal exposure to low-dose nanoparticles. Further investigations will show the detailed mechanism of developmental toxicity of nanoparticles and preventive strategies against intended and unintended nanoparticle exposure. This knowledge will contribute to the safer design of nanoparticles through the development of sensitive and quantitative endpoints for prediction of their developmental toxicity.

The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

Diesel Exhaust Particles Enhance MUC4 Expression in NCI-H292 Cells and Nasal Epithelial Cells via the p38/CREB Pathway

Authors: Park, IH; Kang, JH; Kim, JA; Shin, JM; Lee, HM (2017) International Archives of Allergy and Immunology 171:209-216. HERO ID: 3453688

[Less] BACKGROUND: Diesel exhaust particles (DEPs), the major contributors to air pollution, . . . [More] BACKGROUND: Diesel exhaust particles (DEPs), the major contributors to air pollution, induce inflammatory responses in the nasal epithelium. Overproduction of airway mucins is an important pathogenic finding in inflammatory airway diseases.

OBJECTIVE: The aims of the present study were to determine the effect of DEPs on the expression of the mucin gene MUC4 and to investigate the underlying mechanism of DEP-induced MUC4 expression in NCI-H292 cells and primary nasal epithelial cells (PNECs).

METHODS: NCI-H292 cells were stimulated for 24 h with DEPs. Messenger RNA (mRNA) and protein expression of MUC4 was determined by real-time reverse transcription (RT) polymerase chain reaction (PCR) and Western blotting. NCI-H292 cells were exposed to 3 mitogen-activated protein kinase inhibitors (U0126, SB203580, and SP600125) and a CREB (cAMP response element-binding protein) inhibitor prior to stimulation with DEPs, and MUC4 expression was examined by RT-PCR and Western blotting. PNECs were pretreated with a p38 inhibitor and CREB inhibitor prior to stimulation with DEPs, and MUC4 expression was then determined by RT-PCR and/or Western blotting.

RESULTS: DEPs significantly increased the expression of MUC4 mRNA and protein. MUC4 mRNA and protein expression was inhibited by pretreatment with p38 and CREB inhibitors in NCI-H292 stimulated with DEPs. p38 and CREB inhibitors also blocked the expression of MUC4 mRNA and protein in DEP-stimulated PNECs.

CONCLUSIONS: We demonstrated that DEPs stimulated the expression of MUC4 via the p38/CREB pathway in NCI-H292 cells and PNECs. The results of the present study pave the way for further studies on the role of MUC4 in DEP-induced hypersecretion in airway epithelium.

The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

Statins reduce the burden of ambient particulate matter and inflammatory cells within the lung tissues of smokers with and without COPD

Authors: Hiraiwa, K; Miller, S; Ngan, DA; Vasilescu, DM; Hackett, TL; Kinose, D; Cheng, JC; van Eeden, SF (2017) European Respiratory Journal 49. [Letter] HERO ID: 3453691


The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

Urban fine particulate matter exposure causes male reproductive injury through destroying blood-testis barrier (BTB) integrity

Authors: Cao, XN; Shen, LJ; Wu, SD; Yan, C; Zhou, Y; Xiong, G; Wang, YC; Liu, Y; Liu, B; Tang, XL; Guo, M; Liu, DY; Long, CL; Sun, M; He, DW; Lin, T; Wei, GH (2017) Toxicology Letters 266:1-12. HERO ID: 3455300

[Less] Blood-testis barrier (BTB) provides a suitable microenvironment for germ cells that is required for . . . [More] Blood-testis barrier (BTB) provides a suitable microenvironment for germ cells that is required for spermatogenesis. Exposure to particulate matter (PM) is recognized to occasion male reproductive impairment, but the mechanism of which remains unclear. Male Sprague-Dawley (SD) rats were used to establish animal models with PM2.5 exposure concentration of 0, 10, and 20mg/kg.b.w. once a day for four weeks. Success rate of mating, sperm quality, epididymal morphology, expressions of spermatogenesis markers, superoxide dismutases (SOD) activity and expression in testicular tissues, and expressions of BTB junction proteins were detected. In addition, in vitro experiments were also performed. After PM2.5 treatment, reactive oxygen species (ROS) production and apoptosis of Sertoli cells were analyzed. Our results indicated that after PM2.5 exposure male rats presented inferior uberty and sperm quality, with decreased expressions of spermatogenesis markers, escalated SOD activity and expression levels, and reduced expressions of tight junction, adherens junction, and gap junction proteins in testicular tissues. Meantime, PM2.5-treated Sertoli cells displayed increased SOD production and apoptosis. PM2.5 exposure engenders male reproductive function injury through breaking BTB integrity.

The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

Particulate matter exposure induces the autophagy of macrophages via oxidative stress-mediated PI3K/AKT/mTOR pathway

Authors: Su, R; Jin, X; Zhang, W; Li, Z; Liu, X; Ren, J (2017) Chemosphere 167:444-453. HERO ID: 3455355

[Less] Many epidemiological investigations have consistently demonstrated the immunotoxicity of fine particulate . . . [More] Many epidemiological investigations have consistently demonstrated the immunotoxicity of fine particulate matter (PM2.5), but the underlying molecular mechanism remains unclear and needs to be elucidated. In this work, the immune cells, including pulmonary macrophages of SD rats and Raw264.7 cells, were applied to further investigate the effect of PM2.5 on cell autophagy of macrophages, thus clarified the possible molecular mechanism of immunotoxicity caused by PM2.5. SD rats were exposed to summer (0.2, 0.6, 1.5 mg kg(-1) b.w.) and winter (0.3, 1.5, 2.7 mg kg(-1) b.w.) PM2.5 adopting the intratracheal instillation method. The exposure was performed one time every 3 days and continued for 2 months. The data showed that PM2.5 exposure decreased numbers of immune cells in pulmonary macrophages of SD rats. In addition, PM2.5 could induce the cell autophagy through the increased LC3 and decreased p62 mRNA and protein levels of pulmonary macrophages in SD rats and Raw264.7 cells in a concentration-dependent manner. Strikingly, PM2.5-induced oxidative stress was observed. However, NAC supplement (the ROS inhibitor) significantly reversed PM2.5-caused effects. Additionally, the PI3K/AKT/mTOR pathway was activated in PM2.5-treated cells and NAC had an important inhibitory effect. These results demonstrated that PM2.5 exposures induced autophagy of pulmonary macrophages via the oxidative stress-mediated PI3K/AKT/mTOR pathway, which may contribute to explain the molecular mechanism of immunotoxicity caused by PM2.5 and provide the theoretical foundation for environment toxicology of PM2.5.

The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

Histone deacetylases 3 deletion restrains PM2.5-induced mice lung injury by regulating NF-κB and TGF-β/Smad2/3 signaling pathways

Authors: Gu, LZ; Sun, H; Chen, JH (2017) Biomedicine & Pharmacotherapy 85:756-762. HERO ID: 3455494

[Less] Acute lung injury (ALI) as a serious disease with high mortality has been emphasized as a threat to . . . [More] Acute lung injury (ALI) as a serious disease with high mortality has been emphasized as a threat to human health and life. Accumulating studies demonstrated that PM2.5 plays a significant role in metabolic and lung diseases. Histone deacetylases 3 (HDAC3) is an important regulator in control of gene transcription, required in up-regulation of inflammation-related signaling, and has been known as a key hotpot in treating a lot of chronic inflammatory diseases. TGF-β/Smad signaling pathway has been proven to be of significance in fibrosis development. Our results found that PM2.5 induced lung function injury in WT mice with a inflammatory responses through the activation of TGF-β/Smad signaling pathways, resulting in lung injury. Of note, HDAC3-deficient mice after PM2.5 administration further promoted TGF-β/Smad signaling pathways activation. In addition, TLR4, p-NF-κB and p-IκBα indicated that HDAC3 knockout mice have a higher inflammation-related signals expression in lung tissue than WT mice after PM2.5 administration, resulting in pro-inflammatory cytokines releasing. Moreover, in vitro experiment of lung epithelial cells challenged with PM2.5, further indicated that TGF-β/Smad2/3 was involved in fibrosis development, leading to inflammation response. Also, the activation of TLR4/NF-κB could be observed in PM2.5-induced lung epithelial cells, leading to inflammation infiltration. These results indicate a new therapeutic target to protect against lung injury caused by PM2.5.