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1.
Chemosphere ; 238: 124620, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31472354

RESUMO

Particulate toxic species, such as polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs), polycyclic aromatic hydrocarbons (PAHs) and heavy metals may have significant health risks. This study investigated characteristics, sources and health risks of all three classes of toxic species in PM2.5 (particles with aerodynamic diameter ≤2.5 µm) samples collected at an industrial area in Changzhou, a big city in the Yangtze Delta region of China. Fourteen heavy metals altogether constituted 2.87% of PM2.5 mass, with Fe, Al and Zn as the major elements. Principal component analysis (PCA) suggested that heavy metals came from four sources: vehicles, industry, crustal dust, mixed coal combustion and industrial process. The daily average concentration of 18 PAHs was 235.29 ng/m3, accounting for 0.21% of PM2.5 mass. The dominant PAHs were high molecular weight ones, contributing 73.5% to the total PAHs. Diagnostic analyses indicated that sources of PAHs included vehicle/coal combustion and petroleum emissions, wherein diesel emission played a more important role than gasoline emission. PCA showed that the largest contributor of PAHs was vehicle exhaust mixed with coal combustion, followed by three industry-related sources. Total concentration of 17 PCDD/Fs varied between 3.14 and 37.07 pg/m3, with an average of 14.58 pg/m3. The 10 PCDFs accounted for 70.5% of total concentration of 17 PCDD/Fs. Health risk assessments showed that the carcinogenic risk of heavy metals was acceptable, while risks from PAHs and PCDD/Fs cannot be ignored. Back trajectory analysis indicated that local/regional transported air masses from northern China was the major source areas of the toxic species.


Assuntos
Exposição por Inalação/efeitos adversos , Metais Pesados/análise , Neoplasias/induzido quimicamente , Material Particulado/efeitos adversos , Dibenzodioxinas Policloradas/análise , Hidrocarbonetos Policíclicos Aromáticos/análise , Medição de Risco/métodos , Adulto , Poluentes Atmosféricos/análise , Carcinógenos/análise , Criança , China , Monitoramento Ambiental , Feminino , Humanos , Indústrias , Exposição por Inalação/análise , Masculino , Material Particulado/administração & dosagem , Dibenzodioxinas Policloradas/efeitos adversos , Hidrocarbonetos Policíclicos Aromáticos/efeitos adversos , Estações do Ano , Emissões de Veículos/análise
3.
Chemosphere ; 233: 309-318, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31176132

RESUMO

Nasal epithelium provides a physical barrier to potentially harmful stimuli. Cilia, which is on the apical side of the human nasal epithelial cells (HNEpCs), plays a critical role in removing inhaled harmful matter. Ciliary beat frequency (CBF) and ciliary beat pattern (CBP) are the two important indicators for ciliary beat function. However, impacts of the fine particulate matter (PM2.5) on CBF and CBP are still unknown. We aimed to evaluate the impact of PM2.5 on the ciliary beat function of the HNEpCs and its potential mechanisms. After exposed to PM2.5 for 12 h, cilia of HNEpCs were in disordered arrangement. The ciliary coverage rate was decreased after PM2.5 exposure of a series of concentration, while the proportion of basal cells was continuously increased and could be observed on the apical side of the HNEpCs which is hardly be observed without PM2.5 exposure. PM2.5 increased the CBF after 12 h exposure, while 24 h exposure increased the CBF at the relative lower dosage groups and then made a decrease at relative higher dosage groups. CBF were classified into two different types, which had different changes following PM2.5 exposure. CBP showed significant changes characterized as the increased dyskinesia index. Total levels of cellular ATP and the mitochondrial membrane potential were decreased following 12 h exposure of PM2.5, while no change was found in O2 consumption. In conclusion, PM2.5 impact the ciliary beat function of HNEpCs, and the mitochondrial dysfunction might play an important role in it.


Assuntos
Mucosa Nasal/citologia , Mucosa Nasal/efeitos dos fármacos , Material Particulado/efeitos adversos , Trifosfato de Adenosina/metabolismo , Células Cultivadas , Cílios/efeitos dos fármacos , Exposição Ambiental/efeitos adversos , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/metabolismo , Humanos , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Material Particulado/administração & dosagem , Material Particulado/análise , Material Particulado/química
4.
J Biosci ; 44(2)2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31180054

RESUMO

This study was conducted to determine whether exposure to particulate matter 2.5 (PM2.5) affects the immune tolerance of neonatal mice via the regulation of PD-L1 expression. One-week-old BALB/c mice were exposed to PM2.5 for 8 days. From day 8 to day 18, the mice were treated with 5 µg house dust mite (HDM) (i. n.) every two days. Adenovirus-carried PD-L1 overexpression vectors were infected into mice via nasal inhalation 6 days after exposure to PM2.5. Airway hyperresponsiveness (AHR) was examined in mice 19 days after exposure to PM2.5, and the related parameters of airway inflammation were studied on day 22. Co-exposure to PM2.5 and HDM reduced PD-L1 expression but greatly increased infiltration of inflammatory cells, which was reversed by PD-L1 overexpression. Co-exposure to PM2.5 and HDM also elevated serum IL-4, IL-5 and IL-13 levels and reduced TGF-ß level. Exposure to PM2.5 alone slightly increased the numbers of dendritic cells (DCs) but reduced the numbers of antigen-presenting cells expressing PD-L1 and Treg cells. Therefore, early exposure to PM2.5 reduced PD-L1 expression in the lungs of neonatal mice, which interfered with immune tolerance establishment and subsequently resulted in allergic airway inflammation.


Assuntos
Antígeno B7-H1/imunologia , Células Dendríticas/efeitos dos fármacos , Tolerância Imunológica/efeitos dos fármacos , Pulmão/efeitos dos fármacos , Material Particulado/administração & dosagem , Hipersensibilidade Respiratória/imunologia , Adenoviridae/genética , Adenoviridae/imunologia , Administração por Inalação , Animais , Animais Recém-Nascidos , Antígeno B7-H1/antagonistas & inibidores , Antígeno B7-H1/genética , Células Dendríticas/imunologia , Células Dendríticas/patologia , Regulação da Expressão Gênica , Vetores Genéticos/administração & dosagem , Vetores Genéticos/química , Vetores Genéticos/imunologia , Interleucina-13/genética , Interleucina-13/imunologia , Interleucina-4/genética , Interleucina-4/imunologia , Interleucina-5/genética , Interleucina-5/imunologia , Pulmão/imunologia , Pulmão/patologia , Camundongos , Camundongos Endogâmicos BALB C , Pyroglyphidae/química , Pyroglyphidae/imunologia , Hipersensibilidade Respiratória/induzido quimicamente , Hipersensibilidade Respiratória/genética , Hipersensibilidade Respiratória/patologia , Transdução de Sinais , Linfócitos T Reguladores/efeitos dos fármacos , Linfócitos T Reguladores/imunologia , Linfócitos T Reguladores/patologia , Fator de Crescimento Transformador beta/genética , Fator de Crescimento Transformador beta/imunologia
5.
Artigo em Inglês | MEDLINE | ID: mdl-30987320

RESUMO

Exposure to particulate matter (PM) is leading to various respiratory health outcomes. Compared to coarse and fine particles, less is known about the effects of chronic exposure to ultrafine particles, despite their higher number and reactivity. In the present study, we performed a time-course experiment in mice to better analyze the lung impact of atmospheric ultrafine particles, with regard to the effects induced by fine particles collected on the same site. Trace element and PAH analysis demonstrated the almost similar chemical composition of both particle fractions. Mice were exposed intranasally to FF or UFP according to acute (10, 50 or 100 µg of PM) and repeated (10 µg of PM 3 times a week during 1 or 3 months) exposure protocols. More particle-laden macrophages and even greater chronic inflammation were observed in the UFP-exposed mice lungs. Histological analyses revealed that about 50% of lung tissues were damaged in mice exposed to UFP for three months versus only 35% in FF-exposed mice. These injuries were characterized by alveolar wall thickening, macrophage infiltrations, and cystic lesions. Taken together, these results strongly motivate the update of current regulations regarding ambient PM concentrations to include UFP and limit their emission.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Exposição Ambiental/efeitos adversos , Pulmão/efeitos dos fármacos , Pulmão/patologia , Material Particulado/efeitos adversos , Síndrome de Resposta Inflamatória Sistêmica/induzido quimicamente , Síndrome de Resposta Inflamatória Sistêmica/patologia , Poluentes Atmosféricos/análise , Animais , Modelos Animais de Doenças , Exposição Ambiental/análise , Pulmão/imunologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Tamanho da Partícula , Material Particulado/administração & dosagem , Fatores de Tempo
6.
Regul Toxicol Pharmacol ; 104: 59-73, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30872015

RESUMO

The biological activity induced by the extractable organic matter (EOM) of size-segregated airborne Particulate Matter (PM) from two urban sites, urban traffic (UT) and urban background (UB), was assessed by using bacterial assays. The Gram-negative Escherichia coli (E. coli) coliform bacterium was used to measure the intracellular formation of Reactive Oxygen Species (ROS) by employing the Nitroblue tetrazolium (NBT) reduction assay and the lipid peroxidation by malondialdehyde (MDA) measurement. To the best of our knowledge, this is the first study using E. coli for assessing the bioactivity of ambient air in term of oxidative mechanism studies. E. coli BL21 cells were further used for DNA damage assessment by employing the reporter (ß-galactosidase) gene expression assay. The bacterial strain S. typhimurium TA100 was used to assess the mutagenic potential of PM by employing the well-known mutation assay (Ames test). Four PM size fractions were assessed for bioactivity, specifically the quasi-ultrafine mode (<0.49 µm), the upper accumulation mode (0.49-0.97 µm), the upper fine mode (0.97-3 µm), and the coarse mode (>3.0 µm). The EOM of each PM sample included three organic fractions of successively increased polarity: the non-polar organic fraction (NPOF), the moderately polar organic fraction (MPOF), and the polar organic fraction (POF). The toxicological endpoints induced by each organic fraction were correlated with the concentrations of various organic chemical components determined in previous studies in an attempt to identify the chemical classes involved.


Assuntos
Dano ao DNA , Escherichia coli/efeitos dos fármacos , Compostos Orgânicos/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Material Particulado/toxicidade , Salmonella typhimurium/efeitos dos fármacos , Animais , Escherichia coli/genética , Escherichia coli/metabolismo , Testes de Mutagenicidade , Compostos Orgânicos/administração & dosagem , Material Particulado/administração & dosagem , Ratos , Ratos Sprague-Dawley , Espécies Reativas de Oxigênio/análise , Espécies Reativas de Oxigênio/metabolismo , Salmonella typhimurium/genética , Salmonella typhimurium/metabolismo
7.
Sci Total Environ ; 665: 606-616, 2019 May 15.
Artigo em Inglês | MEDLINE | ID: mdl-30776632

RESUMO

Plant response to microelements exposure can be modulated based on particle size. However, studies are lacking on the roles of particle size and specific microelements in mixed exposure systems designed for plant nutrition, rather than toxicology. Here, an addition-omission strategy was used to address particle-size and element-specific effects in soybean exposed to a mixture of nano and bulk scale oxide particles of Zn (2 mg Zn/kg), Cu (1 mg Cu/kg) and B (1 mg B/kg) in soil. Compared to the control, mixtures of oxide particles of both sizes significantly (p < 0.05) promoted grain yield and overall (shoot and grain) Zn accumulation, but suppressed overall P accumulation. However, the mixed nano-oxides, but not the mixed bulk-oxides, specifically stimulated shoot growth (47%), flower formation (63%), shoot biomass (34%), and shoot N (53%) and K (42%) accumulation. Compared by particle size, omission of individual elements from the mixtures evoked significant responses that were nano or bulk-specific, including shoot growth promotion (29%) by bulk-B; inhibition (51%) of flower formation by nano-Cu; stimulation (57%) of flower formation by bulk-B; grain yield suppression (40%) by nano-Zn; B uptake enhancement (34%) by bulk-Cu; P uptake stimulation by nano-Zn (14%) or bulk-B (21%); residual soil N (80%) and Zn (42%) enhancement by nano-Cu; and residual soil Cu enhancement by nano-Zn (72%) and nano-B (62%). Zn was responsible for driving the agronomic (biomass and grain yield) responses in this soil, with concurrent ramifications for environmental management (N and P) and human health (Zn nutrition). Overall, compared to bulk microelements, nanoscale microelements played a greater role in evoking plant responses.


Assuntos
Produção Agrícola/métodos , Nanopartículas/administração & dosagem , Material Particulado/administração & dosagem , Soja/efeitos dos fármacos , Boro/administração & dosagem , Cobre/administração & dosagem , Nanopartículas Metálicas/administração & dosagem , Micronutrientes/administração & dosagem , Óxidos/administração & dosagem , Fenômenos Fisiológicos Vegetais/efeitos dos fármacos , Solo/química , Soja/fisiologia , Zinco/administração & dosagem
8.
Environ Geochem Health ; 41(3): 1445-1458, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30539333

RESUMO

Samples of PM2.5 were collected from an urban area close to a national highway in Agra, India and sequentially extracted into four different fractions: water soluble (F1), reducible (F2), oxidizable (F3) and residual fraction (F4) for chemical fractionation of arsenic (As), cadmium (Cd), cobalt (Co), chromium (Cr), nickel (Ni) and lead (Pb). The metals were analyzed by inductively coupled plasma optical emission spectroscopy in each fraction. The average mass concentration of PM2.5 was 93 ± 24 µg m-3.The total concentrations of Cr, Pb, Ni, Co, As and Cd in fine particle were 192 ± 54, 128 ± 25, 108 ± 34, 36 ± 6, 35 ± 5 and 8 ± 2 ng m-3, respectively. Results indicated that Cd and Co had the most bioavailability indexes. Risk Assessment Code and contamination factors were calculated to assess the environmental risk. The present study evaluated the potential Pb hazard to young children using the Integrated Exposure Uptake Biokinetic Model. From the model, the probability density of PbB (blood lead level) revealed that at the prevailing atmospheric concentration, 0.302 children are expected to have PbB concentrations exceeding 10 µg dL-1 and an estimated IQ (intelligence quotient) loss of 1.8 points. The predicted blood Pb levels belong to Group 3 (PbB < 5 µg dL-1). Based on the bioavailable fractions, carcinogenic and non-carcinogenic risks via inhalation exposure were assessed for infants, toddlers, children, males and females. The hazard index for potential toxic metals was 2.50, which was higher than the safe limit (1). However, the combined carcinogenic risk for infants, toddlers, children, males and females was marginally higher than the precautionary criterion (10-6).


Assuntos
Metais Pesados/toxicidade , Material Particulado/administração & dosagem , Material Particulado/análise , Arsênico/análise , Arsênico/química , Arsênico/toxicidade , Disponibilidade Biológica , Carcinógenos/toxicidade , Fracionamento Químico , Pré-Escolar , Monitoramento Ambiental/métodos , Feminino , Humanos , Índia , Lactente , Exposição por Inalação , Chumbo/sangue , Masculino , Metais Pesados/análise , Metais Pesados/química , Metais Pesados/farmacocinética , Material Particulado/toxicidade , Medição de Risco/métodos
9.
Inhal Toxicol ; 30(6): 239-246, 2018 05.
Artigo em Inglês | MEDLINE | ID: mdl-30249144

RESUMO

Lots of epidemiological and experimental studies have found that ambient fine particulate matter (PM2.5) exposure is associated with the development of cardiopulmonary diseases, obesity and diabetes. This study focused on the effects of cumulative PM2.5 exposure on pulmonary and systemic inflammation and insulin resistance. Thirty-two 6-week-old male Balb/c mice were randomly divided into four groups (FA, PM, WEEK and DAY groups) and were continuously or intermittently exposed to concentrated PM2.5 or filtered air (FA) for four weeks using Shanghai Meteorological and Environmental Animal Exposure System ("Shanghai-METAS"). The levels of IL-6 and TNF-α in serum, bronchoalveolar lavage fluid (BALF), lung tissues and white adipose tissue (WAT) were measured. Meanwhile, the expression of NF-κB and phosphor-NF-κB in lung tissue was detected by Western blot. Glucose tolerance and insulin resistance were also determined at the end of exposure. The results found that the mice in PM group displayed moderate inflammatory cell infiltration in lung, whereas the mice in WEEK and DAY groups displayed slight inflammatory cell infiltration in lung. Compared with the mice in FA group, the mRNA expressions of IL-6 and TNF-α in lung tissue and WAT significantly increased in the mice of PM group. Importantly, IL-6 and TNF-α mRNA expressions in PM group were higher than those in WEEK and DAY groups. The protein expression of phospho-NF-κB in lung tissue showed that PM group showed the activation of NF-κB, which was higher than that in the WEEK and DAY groups. Meanwhile, the mice in PM group showed more severe glucose tolerance and insulin resistance than that in the WEEK and DAY groups. The results suggested that the reduction of PM2.5 cumulative exposure may alleviate pulmonary and adipose inflammation, insulin resistance and glucose tolerance impairment. The results provided a clue that the interruption of ambient PM2.5 exposures by systems such as indoor air purification could be of benefit to people's health.


Assuntos
Poluentes Atmosféricos/toxicidade , Resistência à Insulina , Lesão Pulmonar/induzido quimicamente , Material Particulado/toxicidade , Tecido Adiposo Branco/efeitos dos fármacos , Tecido Adiposo Branco/metabolismo , Animais , Glicemia/efeitos dos fármacos , Líquido da Lavagem Broncoalveolar/química , Relação Dose-Resposta a Droga , Interleucina-6/sangue , Interleucina-6/genética , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Pulmão/patologia , Lesão Pulmonar/metabolismo , Lesão Pulmonar/patologia , Masculino , Camundongos Endogâmicos BALB C , NF-kappa B/metabolismo , Material Particulado/administração & dosagem , Fator de Necrose Tumoral alfa/sangue , Fator de Necrose Tumoral alfa/genética
10.
Environ Sci Pollut Res Int ; 25(24): 23645-23656, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29978317

RESUMO

The paper presents an integrated methodology that combines experimental and modeling techniques and links exposure to airborne particulate matter (PM) with internal dose in the respiratory system and burden in adjacent tissues over a period of time. The methodology is used to estimate doses in the respiratory systems of elders that reside in 10 elderly care centers (ECCs) in the metropolitan area of Lisbon. Measurements of PM were performed in the ECCs and combined with a time-budget survey for the occupants. This information served as input to the first model that estimated particle doses in the different regions of the respiratory tract of the elderly, and then a second model was used to calculate particle build-up in the alveolar region, the interstitium and the hilar lymph nodes of the elders over a 5-year exposure period. It was found that in 5 years of continuous exposure to the average particle concentration measured over all ECCs, 258 mg of all particles are deposited on the surface of the alveoli of which 79.6% are cleared, 18.8% are retained in the alveolar region, 1.5% translocate to the hilar lymph nodes, and 0.1% are transferred to the interstitium.


Assuntos
Aerossóis/efeitos adversos , Poluição do Ar em Ambientes Fechados/efeitos adversos , Exposição Ambiental/análise , Casas de Saúde , Material Particulado/efeitos adversos , Aerossóis/administração & dosagem , Aerossóis/farmacocinética , Idoso de 80 Anos ou mais , Poluição do Ar em Ambientes Fechados/análise , Exposição Ambiental/efeitos adversos , Feminino , Humanos , Pulmão/efeitos dos fármacos , Linfonodos/efeitos dos fármacos , Masculino , Modelos Teóricos , Material Particulado/administração & dosagem , Material Particulado/análise , Material Particulado/farmacocinética , Portugal , Alvéolos Pulmonares/efeitos dos fármacos
11.
Biosci Rep ; 38(5)2018 10 31.
Artigo em Inglês | MEDLINE | ID: mdl-29899163

RESUMO

To investigate the effect of stimulation of human bronchial epithelial cells (HBECs) by arterial traffic ambient PM2.5 (TAPM2.5) and wood smoke PM2.5 (WSPM2.5) on the expression of long non-coding RNAs (lncRNAs) in order to find new therapeutic targets for treatment of chronic obstructive pulmonary disease (COPD). HBECs were exposed to TAPM2.5 and WSPM2.5 at a series of concentrations. The microarray analysis was used to detect the lncRNA and mRNA expression profiles. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and gene ontology (GO) enrichment were conducted to analyze the differentially expressed lncRNAs and mRNAs. Quantitative real-time PCR (qRT-PCR) was performed to confirm the differential expression of lncRNAs. Western blot was performed to study the expression of autophagy and apoptosis-associated proteins. Flow cytometry was used to detect the apoptotic cells. The results indicated that fine particulate matter (PM2.5)-induced cell damage of HBECs occurred in a dose-dependent manner. The microarray analysis indicated that treatment with TAPM2.5 and WSPM2.5 led to the alteration of lncRNA and mRNA expression profiles. LncRNA maternally expressed gene 3 (MEG3) was significantly up-regulated in HBECs after PM2.5 treatment. The results of Western blot showed that PM2.5 induced cell apoptosis and autophagy by up-regulating apoptosis-associated gene, caspase-3, and down-regulating autophagy-associated markers, Bcl-2 and LC3 expression. In addition, we demonstrated that TAPM2.5 and WSPM2.5 accelerated apoptosis of human bronchial (HBE) cells, silencing of MEG3 suppressed apoptosis and autophagy of HBE cells. These findings suggested that the lncRNA MEG3 mediates PM2.5-induced cell apoptosis and autophagy, and probably through regulating the expression of p53.


Assuntos
Brônquios/citologia , Células Epiteliais/efeitos dos fármacos , Material Particulado/toxicidade , RNA Longo não Codificante , Apoptose/efeitos dos fármacos , Apoptose/genética , Autofagia/efeitos dos fármacos , Autofagia/genética , Brônquios/efeitos dos fármacos , Células Cultivadas , Relação Dose-Resposta a Droga , Células Epiteliais/fisiologia , Perfilação da Expressão Gênica , Regulação da Expressão Gênica/efeitos dos fármacos , Ontologia Genética , Inativação Gênica , Humanos , Material Particulado/administração & dosagem , RNA Longo não Codificante/genética , RNA Mensageiro , Fumaça/efeitos adversos
12.
Neurotoxicology ; 67: 234-244, 2018 07.
Artigo em Inglês | MEDLINE | ID: mdl-29920326

RESUMO

Hyperoxia during treatment for prematurity may enhance susceptibility to other risk factors for adverse brain development, such as air pollution exposure, as both of these risk factors have been linked to a variety of adverse neurodevelopmental outcomes. This study investigated the combined effects of neonatal hyperoxia followed by inhalation of concentrated ambient ultrafine particles (CAPS, <100 nm in aerodynamic diameter) on learning. C57BL/6 J mice were birthed into 60% oxygen until postnatal day (PND) 4 and subsequently exposed to filtered air or to CAPS using the Harvard University Concentrated Ambient Particle System (HUCAPS) from PND 4-7 and 10-13. Behavior was assessed on a fixed interval (FI) schedule of reinforcement in which reward is available only after a fixed interval of time elapses, as well as expected reductions in behavior during an extinction procedure when reward was withheld. Both produce highly comparable behavioral performance across species. Performance measures included rate of responding, response accuracy, and temporal control (quarter life). Exposure to hyperoxia or CAPS resulted in lower mean quarter life values, an effect that was further enhanced in males by combined exposure, findings consistent with delayed learning of the FI schedule. Females also initially exhibited greater reductions in quarter life values following the combined exposure to hyperoxia and CAPS and delayed reductions in response rates during extinction. Combined hyperoxia and CAPS produced greater learning deficits than either risk factor alone, consistent with enhanced neurodevelopmental toxicity, findings that could reflect a convergence of both insults on common neurobiological systems. The basis for sex differences in outcome warrants further research. This study highlights the potential for heightened risk of adverse neurodevelopment outcomes in individuals born preterm in regions with higher levels of ultrafine particle (UFP) air pollution, in accord with the multiplicity of risk factors extant in the human environment.


Assuntos
Hiperóxia/psicologia , Aprendizagem/efeitos dos fármacos , Transtornos do Neurodesenvolvimento/induzido quimicamente , Transtornos do Neurodesenvolvimento/psicologia , Tamanho da Partícula , Material Particulado/efeitos adversos , Animais , Animais Recém-Nascidos , Condicionamento Operante/efeitos dos fármacos , Condicionamento Operante/fisiologia , Feminino , Hiperóxia/complicações , Hiperóxia/metabolismo , Aprendizagem/fisiologia , Locomoção/efeitos dos fármacos , Locomoção/fisiologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Transtornos do Neurodesenvolvimento/metabolismo , Material Particulado/administração & dosagem
13.
Neurotoxicology ; 67: 169-177, 2018 07.
Artigo em Inglês | MEDLINE | ID: mdl-29879396

RESUMO

Little is known regarding the adverse effects of chronic particulate matter (PM) inhalation on the central nervous system (CNS). The present study aimed to examine how PM exposure impacts on oxidative stress and inflammatory processes, as well as the expression of interneurons and perineuronal nets (PNNs) in the CNS. BALB/c mice (6-week-old females, n = 32) were exposed to 1 to 5 µm size diesel-extracted particles (DEPs) (100 µg/m3, 5 d/week, 5 h/day) and categorized into the following four groups: 1) 4-week DEP (n = 8); 2) 4-week control (n = 8), 3) 8-week DEP (n = 8); and 4) 8-week control (n = 8). The olfactory bulb, prefrontal cortex, temporal cortex, striatum, and cerebellum were harvested from the animals in each group. The expression of antioxidants (heme oxygenase 1 [HO-1] and superoxide dismutase 2 [SOD-2]), and markers of the unfolded protein response (X-box binding protein [XBP]-1S), inflammation (tumor necrosis factor-alpha [TNF-α]), and proliferation (neurotrophin-3 and brain-derived neurotrophic factor [BDNF]) were measured using reverse transcription polymerase chain reaction (PCR) and Western blotting. The expression levels of HO-1, SOD-2, XBP-1S, TNF-α, neurotrophin-3, and BDNF were compared among groups using the Mann-Whitney U test. The temporal cortex was immunostained for parvalbumin (PV) and Wisteria floribunda agglutinin (WFA). The numbers of PV- and WFA-positive cells were counted using a confocal microscope and analyzed with the Mann-Whitney U test. HO-1 expression was elevated in the prefrontal cortex, temporal cortex, striatum, and cerebellum of mice in the 8-week DEP group compared with the control group. Expression of SOD-2 and XBP-1S was elevated in the prefrontal cortex and striatum of the 8-week DEP group compared with the control group. TNF-α expression was elevated in the prefrontal cortex, temporal cortex, striatum, and cerebellum in the 4- and 8-week DEP groups compared with the control group. Neurotrophin-3 expression was decreased in the olfactory bulb and striatum of the 8-week DEP group compared with the control group. WFA density was increased in the 8-week DEP group compared with the control group. The PV and PV + WFA densities were decreased in the 4-week DEP group compared with the control group. Chronic DEP inhalation activated oxidative stress and inflammation in multiple brain regions. Chronic DEP inhalation increased PNNs and decreased the number of interneurons, which may contribute to PM exposure-related CNS dysfunction.


Assuntos
Encéfalo/metabolismo , Mediadores da Inflamação/metabolismo , Exposição por Inalação/efeitos adversos , Estresse Oxidativo/efeitos dos fármacos , Material Particulado/administração & dosagem , Material Particulado/toxicidade , Animais , Encéfalo/efeitos dos fármacos , Encéfalo/patologia , Sistema Nervoso Central/efeitos dos fármacos , Sistema Nervoso Central/metabolismo , Sistema Nervoso Central/patologia , Feminino , Camundongos , Camundongos Endogâmicos BALB C , Estresse Oxidativo/fisiologia , Tamanho da Partícula
14.
J Allergy Clin Immunol ; 141(3): 833-844, 2018 03.
Artigo em Inglês | MEDLINE | ID: mdl-29519450

RESUMO

Inflammation is a common and essential event in the pathogenesis of diverse diseases. Decades of research has converged on an understanding that all combustion-derived particulate matter (PM) is inflammatory to some extent in the lungs and also systemically, substantially explaining a significant portion of the massive cardiopulmonary disease burden associated with these exposures. In general, this means that efforts to do the following can all be beneficial: reduce particulates at the source, decrease the inflammatory potential of PM output, and, where PM inhalation is unavoidable, administer anti-inflammatory treatment. A range of research, including basic illumination of inflammatory pathways, assessment of disease burden in large cohorts, tailored treatment trials, and epidemiologic, animal, and in vitro studies, is highlighted in this review. However, meaningful translation of this research to decrease the burden of disease and deliver a clear and cohesive message to guide daily clinical practice remains rudimentary. Ongoing efforts to better understand substantial differences in the concentration and type of PM to which the global community is exposed and then distill how that influences inflammation promises to have real-world benefit. This review addresses this complex topic in 3 sections, including ambient PM (typically associated with ground-level transportation), wildfire-induced PM, and PM from indoor biomass burning. Recognizing the overlap between these domains, we also describe differences and suggest future directions to better inform clinical practice and public health.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar em Ambientes Fechados/efeitos adversos , Material Particulado/administração & dosagem , Humanos , Inflamação/induzido quimicamente , Inflamação/patologia
15.
Toxicol Sci ; 163(1): 140-151, 2018 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-29394414

RESUMO

Particulate matter (PM) and ozone (O3) are dominant air pollutants that contribute to development and exacerbation of multiple cardiopulmonary diseases. Mature adults with cardiovascular disease (CVD) are particularly susceptible to air pollution-related cardiopulmonary morbidities and mortalities. The aim was to investigate the biologic potency of ultrafine particulate matter (UFPM) combined with O3 in the lungs of mature adult normotensive and spontaneously hypertensive (SH) Wistar-Kyoto rats. Conscious, mature adult male normal Wistar-Kyoto (NW) and SH rats were exposed to one of the following atmospheres: filtered air (FA); UFPM (∼ 250 µg/m3); O3 (1.0 ppm); or UFPM + O3 (∼ 250 µg/m3 + 1.0 ppm) combined for 6 h, followed by an 8 h FA recovery period. Lung sections were evaluated for lesions in the large airways, terminal bronchiolar/alveolar duct regions, alveolar parenchyma, and vasculature. NW and SH rats were similarly affected by the combined-pollutant exposure, displaying severe injury in both large and small airways. SH rats were particularly susceptible to O3 exposure, exhibiting increased injury scores in terminal bronchioles and epithelial degeneration in large airways. UFPM-exposure groups had minimal histologic changes. The chemical composition of UFPM was altered by the addition of O3, indicating that ozonolysis promoted compound degradation. O3 increased the biologic potency of UFPM, resulting in greater lung injury following exposure. Pathologic manifestations of CVD may confer susceptibility to air pollution by impairing normal lung defenses and responses to exposure.


Assuntos
Poluentes Atmosféricos/toxicidade , Doenças Cardiovasculares/complicações , Lesão Pulmonar/induzido quimicamente , Pulmão/efeitos dos fármacos , Ozônio/toxicidade , Material Particulado/toxicidade , Animais , Doenças Cardiovasculares/patologia , Exposição por Inalação , Pulmão/patologia , Lesão Pulmonar/complicações , Lesão Pulmonar/patologia , Masculino , Ozônio/administração & dosagem , Ozônio/química , Tamanho da Partícula , Material Particulado/administração & dosagem , Material Particulado/química , Ratos Endogâmicos SHR , Ratos Endogâmicos WKY
16.
Biochem Biophys Res Commun ; 496(4): 1291-1295, 2018 02 19.
Artigo em Inglês | MEDLINE | ID: mdl-29412164

RESUMO

Emerging evidence demonstrated that particulate matter 2.5 (PM2.5) is an important environmental risk factor for lung diseases. Serum- and glucocorticoid-inducible kinase 1(SGK1) was reported to be a crucial factor for cell survival. However, the role of SGK1 in PM2.5-induced cell injury is still unclear. In this work, we firstly found that the expression of SGK1 was decreased in PM2.5-treated human lung alveolar epithelial (A549) cells by western blot. In addition, overexpression of SGK1 significantly attenuated A549 cell apoptosis and reduced the reactive oxygen species (ROS) generation induced by PM2.5. Moreover, we found that PM2.5 exposure significantly promoted the ERK1/2 activation and inhibited the AKT activation, whereas overexpression of SGK1 could reverse that. Finally, the results of the rescue experiment showed that MK2206 (AKT inhibitor) could rescue the impact of SGK1 on A549 cell apoptosis, while PD98059 (ERK1/2 inhibitor) could not further aggravate the impact. Taken together, our results suggest that SGK1 inhibits PM2.5-induced cell apoptosis and ROS generation via ERK1/2 and AKT signaling pathway in human lung alveolar epithelial A549 cells.


Assuntos
Células Epiteliais Alveolares/citologia , Células Epiteliais Alveolares/fisiologia , Apoptose/fisiologia , Proteínas Imediatamente Precoces/metabolismo , Estresse Oxidativo/fisiologia , Material Particulado/administração & dosagem , Proteínas Serina-Treonina Quinases/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Células A549 , Células Epiteliais Alveolares/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Humanos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/fisiologia , Estresse Oxidativo/efeitos dos fármacos
17.
Am J Public Health ; 108(4): 480-485, 2018 04.
Artigo em Inglês | MEDLINE | ID: mdl-29470121

RESUMO

OBJECTIVES: To quantify nationwide disparities in the location of particulate matter (PM)-emitting facilities by the characteristics of the surrounding residential population and to illustrate various spatial scales at which to consider such disparities. METHODS: We assigned facilities emitting PM in the 2011 National Emissions Inventory to nearby block groups across the 2009 to 2013 American Community Survey population. We calculated the burden from these emissions for racial/ethnic groups and by poverty status. We quantified disparities nationally and for each state and county in the country. RESULTS: For PM of 2.5 micrometers in diameter or less, those in poverty had 1.35 times higher burden than did the overall population, and non-Whites had 1.28 times higher burden. Blacks, specifically, had 1.54 times higher burden than did the overall population. These patterns were relatively unaffected by sensitivity analyses, and disparities held not only nationally but within most states and counties as well. CONCLUSIONS: Disparities in burden from PM-emitting facilities exist at multiple geographic scales. Disparities for Blacks are more pronounced than are disparities on the basis of poverty status. Strictly socioeconomic considerations may be insufficient to reduce PM burdens equitably across populations.


Assuntos
Grupos de Populações Continentais/estatística & dados numéricos , Disparidades nos Níveis de Saúde , Exposição por Inalação/estatística & dados numéricos , Material Particulado , Pobreza/estatística & dados numéricos , Afro-Americanos/estatística & dados numéricos , Grupo com Ancestrais do Continente Europeu/estatística & dados numéricos , Humanos , Material Particulado/administração & dosagem , Material Particulado/efeitos adversos , Fatores Socioeconômicos , Estados Unidos
18.
Neurotoxicology ; 69: 217-231, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-29247674

RESUMO

Developmental exposures to ambient ultrafine particles (UFPs) can produce multiple neuropathological and neurochemical changes that might contribute to persistent alterations in cognitive-type functions. The objective of the current study was to test the hypothesis that developmental UFP exposure produced impairments in learning, memory and impulsive-like behaviors and to determine whether these were selective and thus independent of deficits in other behavioral domains such as motor activity or motivation. Performance on measures of learning (repeated learning), memory (novel object recognition, NOR), impulsive-like behavior (differential reinforcement of low rate (DRL), schedule of reward and delay of reward (DOR)), motor activity (locomotor behavior) and motivation (progressive ratio schedule) were examined in adult mice that had been exposed to concentrated (10-20x) ambient ultrafine particles (CAPS) averaging approximately 45 ug/m3 particle mass concentrations from postnatal day (PND) 4-7 and 10-13 for 4 h/day. Given the number of behavioral tests, animals were tested in different groups. Results showed male-specific alterations in learning and memory functions (repeated learning, NOR and DRL) specifically during transitions in reinforcement contingencies (changes in rules governing behavior) that did not appear to be related to alterations in locomotor function or motivation. Females did not exhibit cognitive-like deficits at these exposure concentrations, but displayed behaviors consistent with altered motivation, including increases in response rates during repeated learning, significantly increased latencies to respond on the delay of reward paradigm, and reductions in the progressive ratio break point. Consistent with our prior findings, male-specific learning and memory-related deficits were seen and occurred even at relatively low level developmental UFP exposures, while females show alterations in motivational behaviors but not final performance. These findings add to the evidence suggesting the need to regulate UFP levels.


Assuntos
Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Disfunção Cognitiva/induzido quimicamente , Motivação/efeitos dos fármacos , Tamanho da Partícula , Material Particulado/toxicidade , Animais , Disfunção Cognitiva/patologia , Disfunção Cognitiva/psicologia , Feminino , Exposição por Inalação/efeitos adversos , Locomoção/efeitos dos fármacos , Locomoção/fisiologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Motivação/fisiologia , Material Particulado/administração & dosagem , Distribuição Aleatória
19.
Antioxid Redox Signal ; 28(13): 1209-1223, 2018 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-29037123

RESUMO

AIMS: Redox active ultrafine particles (UFP, d < 0.2 µm) promote vascular oxidative stress and atherosclerosis. Notch signaling is intimately involved in vascular homeostasis, in which forkhead box O1 (FOXO1) acts as a co-activator of the Notch activation complex. We elucidated the importance of FOXO1/Notch transcriptional activation complex to restore vascular regeneration after UFP exposure. RESULTS: In a zebrafish model of tail injury and repair, transgenic Tg(fli1:GFP) embryos developed vascular regeneration at 3 days post amputation (dpa), whereas UFP exposure impaired regeneration (p < 0.05, n = 20 for control, n = 28 for UFP). UFP dose dependently reduced Notch reporter activity and Notch signaling-related genes (Dll4, JAG1, JAG2, Notch1b, Hey2, Hes1; p < 0.05, n = 3). In the transgenic Tg(tp1:GFP; flk1:mCherry) embryos, UFP attenuated endothelial Notch activity at the amputation site (p < 0.05 vs. wild type [WT], n = 20). A disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) inhibitor or dominant negative (DN)-Notch1b messenger RNA (mRNA) disrupted the vascular network, whereas notch intracellular cytoplasmic domain (NICD) mRNA restored the vascular network (p < 0.05 vs. WT, n = 20). UFP reduced FOXO1 expression, but not Master-mind like 1 (MAML1) or NICD (p < 0.05, n = 3). Immunoprecipitation and immunofluorescence demonstrated that UFP attenuated FOXO1-mediated NICD pull-down and FOXO1/NICD co-localization, respectively (p < 0.05, n = 3). Although FOXO1 morpholino oligonucleotides (MOs) attenuated Notch activity, FOXO1 mRNA reversed UFP-mediated reduction in Notch activity to restore vascular regeneration and blood flow (p < 0.05 vs. WT, n = 5). Innovation and Conclusion: Our findings indicate the importance of the FOXO1/Notch activation complex to restore vascular regeneration after exposure to the redox active UFP. Antioxid. Redox Signal. 28, 1209-1223.


Assuntos
Células Endoteliais/efeitos dos fármacos , Proteína Forkhead Box O1/metabolismo , Material Particulado/farmacologia , Receptores Notch/metabolismo , Regeneração/efeitos dos fármacos , Proteínas de Peixe-Zebra/metabolismo , Animais , Células Cultivadas , Células Endoteliais/metabolismo , Oxirredução , Material Particulado/administração & dosagem , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Peixe-Zebra
20.
Regul Toxicol Pharmacol ; 93: 84-91, 2018 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-28822877

RESUMO

A four-arm study was undertaken in Japan to determine the puffing topography, mouth level exposure and average daily consumption by consumers of the tobacco heating products (THPs): the non-mentholated THP1.0(T), the mentholated THP1.0(M) and a tobacco heating system (THS). The extent of lip blocking of air inlet holes while using THP1.0(T) was also assessed. Groups 1, 2, and 4 included smokers, and group 3 included regular THP users. Smokers of 7-8 mg ISO nicotine free dry particulate matter (NFDPM) non-mentholated cigarettes took on average larger mean puff volumes from THPs than from conventional cigarettes, but puff numbers and durations were similar. Mouth level exposure to NFDPM and nicotine levels were significantly lower when using THPs than conventional cigarettes. Similar trends were observed among smokers of 7-8 mg ISO NFDPM mentholated cigarettes who used mentholated cigarettes and THP1.0(M). Regular users of commercial THS had similar puffing behaviours irrespective of whether they were using THS or THP1.0(T), except for mean puff volume which was lower with THP1.0(T). No smokers blocked the air inlet holes when using THP1.0(T). The puffing topography results support the machine puffing regime used to generate toxicant emissions data and in vitro toxicology testing.


Assuntos
Sistemas Eletrônicos de Liberação de Nicotina/métodos , Calefação/métodos , Exposição por Inalação/análise , Mucosa Bucal/efeitos dos fármacos , Nicotina/análise , Produtos do Tabaco/análise , Adulto , Sistemas Eletrônicos de Liberação de Nicotina/instrumentação , Feminino , Calefação/instrumentação , Humanos , Japão/epidemiologia , Masculino , Pessoa de Meia-Idade , Mucosa Bucal/metabolismo , Nicotina/administração & dosagem , Material Particulado/administração & dosagem , Material Particulado/análise , Adulto Jovem
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