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1.
Philos Trans A Math Phys Eng Sci ; 378(2183): 20200188, 2020 Oct 30.
Artigo em Inglês | MEDLINE | ID: mdl-32981442

RESUMO

We suggest that the unprecedented and unintended decrease of emissions of air pollutants during the COVID-19 lock-down in 2020 could lead to declining seasonal ozone concentrations and positive impacts on crop yields. An initial assessment of the potential effects of COVID-19 emission reductions was made using a set of six scenarios that variously assumed annual European and global emission reductions of 30% and 50% for the energy, industry, road transport and international shipping sectors, and 80% for the aviation sector. The greatest ozone reductions during the growing season reached up to 12 ppb over crop growing regions in Asia and up to 6 ppb in North America and Europe for the 50% global reduction scenario. In Europe, ozone responses are more sensitive to emission declines in other continents, international shipping and aviation than to emissions changes within Europe. We demonstrate that for wheat the overall magnitude of ozone precursor emission changes could lead to yield improvements between 2% and 8%. The expected magnitude of ozone precursor emission reductions during the Northern Hemisphere growing season in 2020 presents an opportunity to test and improve crop models and experimentally based exposure response relationships of ozone impacts on crops, under real-world conditions. This article is part of a discussion meeting issue 'Air quality, past present and future'.


Assuntos
Poluição do Ar/análise , Betacoronavirus , Infecções por Coronavirus/epidemiologia , Produtos Agrícolas/efeitos dos fármacos , Produtos Agrícolas/crescimento & desenvolvimento , Ozônio/análise , Pandemias , Pneumonia Viral/epidemiologia , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/prevenção & controle , Poluição do Ar/estatística & dados numéricos , Monitoramento Ambiental , Europa (Continente) , Humanos , Modelos Biológicos , Dióxido de Nitrogênio/análise , Dióxido de Nitrogênio/toxicidade , Ozônio/toxicidade , Medição de Risco , Estações do Ano
2.
Ecotoxicol Environ Saf ; 203: 111044, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32888613

RESUMO

BACKGROUND: Exposure to ambient fine particulate matter (PM2.5) is associated with various adverse health outcomes. Although several mechanisms have been proposed including oxidative stress and inflammatory responses, the exact mechanism is still unknown. Few studies have investigated the mechanism linking PM2.5 and blood pressure (BP). In this study, we measured urinary metabolites and BP -related renin-angiotensin-aldosterone system (RAAS) to investigate the associations between ambient PM2.5 exposure and BP in healthy C57BL/6 mice. METHODS: The C57BL/6 mice were exposed to ambient concentrated PM2.5 or filtered air (FA) for 16 weeks. Systolic BP and diastolic BP were measured by noninvasive BP system. The urine metabolites were quantified using the untargeted metabolomics approach. The expression of RAAS-related proteins angiotensin-converting enzyme (ACE)2, angiotensin (Ang) II, Ang (1-7) and aldosterone (ALD) were measured using Western blot and ELISA kits. RESULTS: The metabolomics analysis demonstrated that PM2.5 exposure induced significant changes of some metabolites in urine, including stress hormones, amino acids, fatty acids, and lipids. Furthermore, there was an elevation of BP, increase of serous Ang II and ALD, along with the decrease of ACE2 and Ang (1-7) in kidney in the PM2.5-exposed mice compared with FA-exposed mice. CONCLUSIONS: The results demonstrated that PM2.5 exposure-induced BP elevation might be associated with RAAS activation. Meanwhile, PM2.5 exposure-induced changes of stress hormone and lipid metabolism might mediate the activation of RAAS. The results suggested that the systemic stress hormone and lipid metabolism was associated with the development of hypertension.


Assuntos
Poluentes Atmosféricos/toxicidade , Angiotensina I/metabolismo , Pressão Sanguínea/efeitos dos fármacos , Hipertensão/induzido quimicamente , Material Particulado/toxicidade , Fragmentos de Peptídeos/metabolismo , Peptidil Dipeptidase A/metabolismo , Acetilglucosaminidase/urina , Angiotensina I/sangue , Animais , Biomarcadores/sangue , Biomarcadores/urina , Hipertensão/urina , Metabolismo dos Lipídeos/efeitos dos fármacos , Masculino , Metaboloma/efeitos dos fármacos , Metabolômica , Camundongos , Camundongos Endogâmicos C57BL , Fragmentos de Peptídeos/sangue , Peptidil Dipeptidase A/sangue , Sistema Renina-Angiotensina/efeitos dos fármacos , beta-Galactosidase/urina
3.
Sci Total Environ ; 741: 140465, 2020 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-32887012

RESUMO

BACKGROUND: Long-term exposure to air pollution is linked with increased risk of adverse health outcomes, but the evidence for the association between nitrogen dioxide (NO2) and mortality is weak because of the inadequate adjustment of potential confounders and limited spatial resolution of the exposure assessment. Moreover, there are concerns about the independent effects of NO2. Therefore, we examined the association between NO2 long-term exposure and all-cause and cause-specific mortality. METHODS: We included participants who were enrolled in health checkups in Okayama City, Japan, in 2006 or 2007 and were followed until 2016. We used a land-use regression model to estimate the average NO2 concentrations from 2006 to 2007 and allocated them to the participants. We estimated hazard ratios (HRs) for a 10-µg/m3 increase in NO2 levels for all-cause or cause-specific mortality using Cox proportional hazard models. RESULTS: After excluding the participants who were assigned with outlier exposures, a total of 73,970 participants were included in the analyses. NO2 exposure was associated with increased risk of mortality and the HRs and their confidence intervals were 1.06 (95% CI: 1.02, 1.11) for all-cause, 1.02 (0.96, 1.09) for cardiopulmonary, and 1.36 (1.14, 1.63) for lung cancer mortality. However, the elevated risks became equivocal after the adjustment for fine particulate matter except lung cancer. CONCLUSION: Long-term exposure to NO2 was associated with increased risk of all-cause, cardiopulmonary, and lung cancer mortality. The elevated risk for lung cancer was still observable even after adjustment for fine particulate matter.


Assuntos
Poluentes Atmosféricos/análise , Poluição do Ar , Causas de Morte , Poluentes Atmosféricos/toxicidade , Exposição Ambiental/análise , Humanos , Japão , Dióxido de Nitrogênio/análise , Material Particulado/análise
4.
Ecotoxicol Environ Saf ; 202: 110923, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32800210

RESUMO

Many studies have reported that exposure to ambient air pollution has adverse effects on health. However, there are little researches to explore the relationship between ambient air pollution and chronic sinusitis (CS). From January 1 2015 to December 31 2018, a time-series study were carried out to investigate the acute adverse roles of six criteria ambient air pollutants (fine particulate matter [PM2.5], inhalable particulate matter [PM10], nitrogen dioxide [NO2], sulfur dioxide [SO2], ozone [O3], and carbon monoxide [CO]) in hospital outpatients with CS in Xinxiang, China. Then, an over-dispersed Poisson generalized additive model was utilized to analyzed the relationships. In total, 183,943 hospital outpatient cases of CS were identified during the study period. We found that a 10 µg/m3 increase in PM2.5, PM10, SO2, NO2, and CO corresponded to 0.48% (95% confidence interval: 0.22-0.74%), 0.33% (0.16-0.50%), 0.88% (0.13-1.62%), 1.98% (1.31-2.64%), and 0.05% (0.03-0.07%) increments, respectively, in CS outpatients on the current day. The young group (<15 years of age) was more susceptible than the adult or elderly groups. These results suggested that outdoor air pollutants might increase CS outpatient, especially among youth in Xinxiang. Precautions and protective measures should be strengthened to reduce the air pollution level in the future.


Assuntos
Poluentes Atmosféricos/toxicidade , Poluição do Ar/estatística & dados numéricos , Exposição por Inalação/estatística & dados numéricos , Sinusite/epidemiologia , Adolescente , Adulto , Idoso , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Monóxido de Carbono/análise , China/epidemiologia , Doença Crônica , Feminino , Humanos , Masculino , Dióxido de Nitrogênio/análise , Pacientes Ambulatoriais , Ozônio/análise , Material Particulado/análise , Sinusite/induzido quimicamente , Dióxido de Enxofre/análise , Adulto Jovem
5.
Ecotoxicol Environ Saf ; 202: 110932, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32800216

RESUMO

Adverse health effects arising from exposure to fine particulates have become a major concern. Angiogenesis is a vital physiological process for the growth and development of cells and structures in the human body, whereby excessive or insufficient vessel growth could contribute to pathogenesis of diseases. We therefore evaluated indirect effects of carbon black (CB) and inhalable airborne particles on the angiogenic ability of unexposed Human Umbilical Vein Endothelial Cells (HUVECs) by co-culturing HUVECs with pre-exposed Small Airway Epithelial Cells (SAECs). As endothelial cells are major components of blood vessels and potential targets of fine particles, we investigated if lung epithelial cells exposed to ambient PM2.5 surrogates could induce bystander effects on neighboring unexposed endothelial cells in an alveolar-capillary co-culture lung model. Epithelial exposure to CB at a non-toxic dose of 25 µg/mL reduced endothelial tube formation and cell adhesion in co-cultured HUVECs, and decreased expression of angiogenic genes in SAECs. Similarly, exposure of differentiated SAECs to PM2.5 surrogates reduced cell reproductive ability, adhesion and tube formation of neighboring HUVECs. This indicates epithelial exposure to CB and urban PM2.5 surrogates both compromised the angiogenic ability of endothelial cells through bystander effects, thereby potentially perturbing the ventilation-perfusion ratio and affecting lung function.


Assuntos
Poluentes Atmosféricos/toxicidade , Material Particulado/toxicidade , Testes de Toxicidade , Técnicas de Cocultura , Células Epiteliais , Células Endoteliais da Veia Umbilical Humana/citologia , Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Células Endoteliais da Veia Umbilical Humana/metabolismo , Humanos , Pulmão/metabolismo , Neovascularização Patológica , Fuligem
6.
PLoS One ; 15(8): e0236708, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32790684

RESUMO

BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) are a kind of endocrine disruptors, which can enter human body by the inhalation of PAH-containing matter and the ingestion of PAH-containing foodstuffs. Studies showed that PAHs can cross the placental barrier and might cause adverse effects on the fetus. OBJECTIVES: This meta-analysis aimed to estimate the associations between prenatal exposure to PAHs and birth weight. METHODS: Articles published in English until May 8, 2020 and reported the effects of prenatal exposure to PAHs on birth weight were searched in multiple electronic databases including PubMed, the Web of Science, EMBASE and the Cochrane Library. The included studies were divided into three groups in accordance with the measurement of PAHs exposure. Then coefficient was extracted, conversed and synthesized by random-effects meta-analysis. And risk of bias was assessed for each study. RESULTS: A total of 3488 citations were searched and only 11 studies were included finally after double assessment. We found that there were no association between PAH-DNA adducts in cord blood (low/high) (OR: 1.0, 95%CI: 0.97, 1.03), 1-hydroxy pyrene (1-HP) concentration in maternal urine (OR: 1.0, 95%CI: 0.97, 1.03) and prenatal maternal airborne PAHs exposure (OR: 0.97, 95%CI: 0.93, 1.01) and birth weight. However, we observed ethnicity may change the effects of PAHs exposure on birth weight. CONCLUSIONS: There is no significant relationship between prenatal exposure to PAHs and birth weight in our meta-analysis. Further studies are still needed for determining the effects of prenatal PAHs exposure on birth weight.


Assuntos
Peso ao Nascer/efeitos dos fármacos , Disruptores Endócrinos/toxicidade , Exposição Materna , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Poluentes Atmosféricos/química , Poluentes Atmosféricos/toxicidade , Adutos de DNA/química , Bases de Dados Factuais , Disruptores Endócrinos/química , Feminino , Sangue Fetal/química , Humanos , Razão de Chances , Hidrocarbonetos Policíclicos Aromáticos/química , Gravidez , Pirenos/urina
7.
Chemosphere ; 260: 127521, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32688310

RESUMO

The Punchuncaví Valley is one of the most polluted areas in central Chile affected by anthropogenic emissions from the Ventanas Industrial Complex (IC) where the most important industry is the copper smelter and refinery. In this context, this research aims were to assess the usefulness of the Cupressus macrocarpa as a biomonitor. The leaf samples were taken from five selected sites, located between 0.8 and 15 km away from the source. A total of 34 elements were analyzed in leaf samples by ICP-MS and examined by enrichment factor (EF), hierarchical cluster analysis (HCA), and principal component analysis (PCA). Leaf concentration of As, Ca, Cd, Cu, Dy, Er, Gd, K, Li, Mg, Mn, Mo, Na, Nd, P, Pb, Pr, S, Sb, Sr, Ti, Yb and Zn showed statistically significant differences between sampling sites (p-value < 0.05). A clear trend to increase the concentration of Cu, Sb, S, As, Cd and Pb with the proximity to the IC. Besides, high values of Cu (93.4-369 mg kg-1) and As (7.6-12.7 mg kg-1) were observed near to industrial area exceed the phytotoxic levels reported in plants with EF > 3000% for Cu and >1300% for As. The application of PCA and HCA identified 6 factors related to the industrial complex, traffic and geogenic sources, providing the greatest variance the component related to industrial activity mainly with copper smelter and refinery. According to the results, the C. macrocarpa leaves are a good biomonitor to evaluate the high pollution load for anthropogenic elements in industrial areas.


Assuntos
Poluentes Atmosféricos , Monitoramento Biológico/métodos , Cupressus/química , Metalurgia , Folhas de Planta/química , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Chile , Cupressus/crescimento & desenvolvimento , Metais/análise , Metais/toxicidade , Folhas de Planta/crescimento & desenvolvimento , Análise de Componente Principal , Oligoelementos/análise , Oligoelementos/toxicidade
8.
Mol Immunol ; 125: 178-186, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32717666

RESUMO

PM2.5, a major component of air pollutants, has caused severe health problems. It has been reported that PM2.5 index is closely associated with severity of influenza A virus (IAV) infection. However, the underlying mechanisms have not been addressed. NLRP3 inflammasome and type I interferon signaling regulate host defense against influenza infection. The present study investigated the potential effects of air pollutants on host defense against influenza infection in vitro and in vivo. In this study, different concentrations of PM2.5 were pre-exposed to macrophages and mice before IAV infection to assess the negative effects of air pollutants in virus infection. We found that exposure to PM2.5 deteriorated influenza virus infection via compromising innate immune responses manifested by a decrease IL-1ß and IFN-ß production in vitro. Meanwhile, mice exposed with PM2.5 were susceptible to PR8 virus infection due to down-regulation of IL-1ß and IFN-ß. Mechanistically, PM 2.5 exposure suppressed the NLRP3 inflammasome activation and the AHR-TIPARP signaling pathway, by which compromised the anti-influenza immunity. Thus, our study revealed that PM2.5 could alter macrophage inflammatory responses by suppressing LPS-induced activation of NLRP3 inflammasome and expression of IFN-ß during influenza infection. These findings provided us new insights in understanding that PM2.5 combining with influenza infection could enhance the severity of pneumonia.


Assuntos
Poluentes Atmosféricos/toxicidade , Inflamassomos/efeitos dos fármacos , Interferon beta/biossíntese , Proteína 3 que Contém Domínio de Pirina da Família NLR/efeitos dos fármacos , Infecções por Orthomyxoviridae/imunologia , Material Particulado/toxicidade , Animais , Inflamassomos/imunologia , Inflamassomos/metabolismo , Vírus da Influenza A Subtipo H1N1 , Interferon beta/imunologia , Macrófagos/efeitos dos fármacos , Macrófagos/imunologia , Macrófagos/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Proteína 3 que Contém Domínio de Pirina da Família NLR/imunologia , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Infecções por Orthomyxoviridae/metabolismo
9.
Bull Environ Contam Toxicol ; 105(1): 173-179, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-32632464

RESUMO

In order to assess environmental exposure-associated human health risk of dioxin compounds for the population in the vicinity of a municipal solid waste incinerator (MSWI) in Shanghai, the atmospheric samples (n = 24) and soils samples (n = 96) were collected and analyzed to obtain the concentration level, pollution characteristics and seasonal changes of dioxin compounds in environmental medias. The toxicity equivalent concentration range of 2,3,7,8-substituted polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) was 30.9-409 fg WHO-TEQ·m-3 in atmosphere and 0.362-8.55 ng WHO-TEQ·kg-1 in soil. The non-carcinogenic health risk and carcinogenic health risk from PCDD/Fs environmental exposure of people living in the vicinity of the MSWI in Shanghai were all within the allowable range of the US Environmental Protection Agency, which implied that the MSWI in Shanghai did not produce additional risk for the population living in its vicinity.


Assuntos
Poluentes Atmosféricos/análise , Dioxinas/toxicidade , Exposição Ambiental , Incineração , Poluentes Atmosféricos/toxicidade , Atmosfera , China , Dibenzofuranos , Dibenzofuranos Policlorados/análise , Dioxinas/análise , Monitoramento Ambiental , Humanos , Dibenzodioxinas Policloradas/análise , Solo , Resíduos Sólidos/análise
10.
Ecotoxicol Environ Saf ; 203: 110956, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32678753

RESUMO

BACKGROUND: Atmospheric pollutants could induced over-expression of Muc5ac, which is a major pathological feature in acute exacerbation of Chronic Obstructive Pulmonary Disease (COPD) and fatal asthma. Notch signaling pathway could promote mucus cell proliferation and mucus secretion. However, the effects of Notch signaling pathway on the airway mucus secretion induced by PM2.5 remain unknown. In this study, we investigated the role of the Notch signaling pathway on Muc5ac by atmospheric PM2.5 in Beas-2B cell. METHODS: The mRNA and protein levels of the Notch1-4, downstream target gene Hes1 and Muc5ac in the Notch signaling pathway were detected by qPCR and western after Beas-2B cells were exposed to PM2.5 of different concentrations for 12h, 24h, and 48h. RESULTS: The longer the exposure time and the higher the concentration of PM2.5, the lower the survival rate of Beas-2B cells. The expressions of Hes1 and Muc5ac in mRNA and protein were significantly increased after PM2.5 exposure. Correlation analysis indicated that there was a positive correlation between the expression of Muc5ac and Hes1 in mRNA and protein. CONCLUSION: Atmospheric PM2.5 can induce the express of Muc5ac, the Notch signaling pathway may be involved in the regulation of Muc5ac by Hes1.


Assuntos
Poluentes Atmosféricos/toxicidade , Células Epiteliais/efeitos dos fármacos , Mucina-5AC/biossíntese , Material Particulado/toxicidade , Receptores Notch/metabolismo , Mucosa Respiratória/efeitos dos fármacos , Linhagem Celular , Proliferação de Células/efeitos dos fármacos , Células Epiteliais/metabolismo , Células Epiteliais/patologia , Humanos , Mucosa Respiratória/metabolismo , Mucosa Respiratória/patologia , Transdução de Sinais
11.
Chemosphere ; 259: 127482, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32640380

RESUMO

Speciation of respirable particles is becoming increasingly important from an epidemiological and analytical point of view to determine the potential effects of air pollution on human health. For this reason, current laws and analytical sampling methods focus on particle size, as it turns out to be the main factor for the greater or lesser penetration into the airways. In this sense, particles of less than 10 µm in diameter (<10 µm), referred to as PM10, are the particles that have a higher capacity for access to the respiratory tract and, therefore, more significant effect on them. In this sense, one of the most important factors that have a key role in the PM10 atmospheric pollution effect is the dispersion effect with the direct influence of natural effects such as wind, rain, topography apart from others. In this work, PM10 data extracted from the Basque Government environmental stations (19 sampling points) in the Biscay province (Basque Country, north of Spain) were combined with the results obtained from the use of self-made passive samplers (SMPS) in the same sampling points areas and subsequently, the sample analysis with a non-invasive elemental technique (Scanning Electron Microscope coupled to Energy Dispersive X-ray Spectrometry) was carried out. Thanks to this methodology, it was possible to determine a wide variety of metals in PM10 such as Al, Fe, Cr, Ni, Pb, Zn, Ti, etc. Most of them present as oxides and others as part of natural aggregations such as quartz, aluminosilicates, phosphates etc.


Assuntos
Poluentes Atmosféricos/toxicidade , Poluição do Ar/estatística & dados numéricos , Monitoramento Ambiental , Material Particulado/toxicidade , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Humanos , Metais/análise , Tamanho da Partícula , Material Particulado/análise , Chuva , Espanha , Espectrometria por Raios X , Vento
12.
Ecotoxicol Environ Saf ; 202: 110896, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32622306

RESUMO

Exposure to fine particulate matter (PM) comprising toxic compounds arising from air pollution is a major human health concern. It is linked to increased mortality and incidence of various lung diseases. However, the mechanisms underlying the toxic effects of PM on lung fibroblasts have not been fully explored. We used targeted quantitative metabolomics and lipidomics analysis along with cytotoxicity studies to comprehensively characterize the alterations in the metabolite profiles of human lung fibroblasts (HEL 299) upon exposure to PM2.5 and PM10. This exposure at 50 µg/mL for 72 h induced an abnormally high apoptotic response via triggering intracellular reactive oxygen species (ROS) production and mitochondrial dysfunction through an imbalance between pro- and anti-apoptotic signaling pathways. The cytotoxic effects of PM2.5 were more severe than those of PM10. Metabolomics and lipidomics analyses revealed that PM exposure triggered substantial changes in the cellular metabolite profile, which involved reduced mitochondria-related metabolites such as tricarboxylic acid (TCA) cycle intermediates, amino acids, and free fatty acids as well as increased lysoglycerophospholipids (LPLs) containing polyunsaturated fatty acids. The decrease in mitochondria-related metabolites suggested that PM exposure led to reduced TCA cycle capacity and energy production. Apoptotic and inflammatory responses as well as mitochondrial dysfunction were likely to be accelerated because of excessive accumulation of LPLs, contributing to the disruption of membrane rafts and Ca2+ homeostasis and causing increased mitochondrial ROS formation. These results provide valuable insights regarding the toxic effects of PM exposure. Our study also provides a new direction for research on PM exposure-related health disorders using different cell lines.


Assuntos
Poluentes Atmosféricos/toxicidade , Fibroblastos/fisiologia , Material Particulado/toxicidade , Fosfolipídeos/metabolismo , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Apoptose , Linhagem Celular , Fibroblastos/efeitos dos fármacos , Homeostase , Humanos , Lipidômica , Pulmão/efeitos dos fármacos , Pneumopatias , Metabolômica , Mitocôndrias/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo
13.
Artigo em Inglês | MEDLINE | ID: mdl-32545456

RESUMO

Although exposure to ambient air pollution has been linked to mental health problems, little is known about its potential effects on youth. This study investigates the association between short-term exposure to air pollutants and emergency department (ED) visits for mental health disorders. The National Ambulatory Care Reporting System database was used to retrieve ED visits for young individuals aged 8-24 years in Toronto, Canada. Daily average concentrations of nitrogen dioxide (NO2), fine particulate matter (PM2.5), and daily maximum 8 h ozone (O3) were calculated using measurement data from seven fixed stations. A case-crossover (CC) design was implemented to estimate the associations between ED visits and air pollution concentrations. Mental health ED visits were identified using International Classification of Diseases 10th Revision (ICD-10) codes, with seven categories considered. Models incorporating air pollutants and ambient temperature (with lags of 0-5 days) using a time-stratified CC technique were applied. Multivariable regression was performed by sex, three age groups, and seven types of mental health disorders to calculate relative risk (RR). The RRs were reported for one interquartile range (IQR) change in the air pollutant concentrations. Between April 2004 and December 2015 (4292 days), there were 83,985 ED visits for mental-health related problems in the target population. Several exposures to air pollutants were shown to have associations with ED visits for mental health including same day exposure to fine particulate matter (IQR = 6.03 µg/m3, RR = 1.01 (95% confidence interval: 1.00-1.02), RR = 1.02 (1.00-1.03)) for all and female-only patients, respectively. One-day lagged exposure was also associated with ED visits for PM2.5 (RR = 1.02 (1.01-1.03)), for nitrogen dioxide (IQR = 9.1 ppb, RR = 1.02 (1.00-1.04)), and ozone (IQR = 16.0 ppb, RR = 1.06 (1.01-1.10)) for males. In this study, urban air pollution concentration-mainly fine particulate matter and nitrogen dioxide-is associated with an increased risk for ED visits for adolescents and young adults with diagnosed mental health disorders.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Serviço Hospitalar de Emergência , Transtornos Mentais , Ozônio , Adolescente , Poluentes Atmosféricos/toxicidade , Canadá/epidemiologia , Criança , Serviço Hospitalar de Emergência/estatística & dados numéricos , Feminino , Humanos , Masculino , Transtornos Mentais/epidemiologia , Dióxido de Nitrogênio , Material Particulado , Adulto Jovem
14.
Artigo em Inglês | MEDLINE | ID: mdl-32526832

RESUMO

The burden of illness resulting from adverse environmental exposure is significant. Numerous studies have examined self-care behaviors among patients with chronic obstructive pulmonary disease (COPD), but seldom assess these behaviors in relation to air pollution. The study aims to examine the effects of particulate matter (PM) education on prevention and self-care knowledge regarding air pollution, symptom changes, and indoor PM concentration levels among patients with COPD. A longitudinal, quasi-experimental design using a generalized estimating equation examined the effectiveness of the education intervention. Participants were 63 patients with COPD, of whom only 25 received intervention. Levels of PM2.5 and PM10 decreased in the first-month follow-up in the experimental group. Improvement of knowledge and prevention regarding PM in the first and third months were also greater in the experimental group compared to the control. Regarding the COPD assessment test and physical domain scores, the experimental group exhibited a greater improvement in the first-month follow-up. Scores on the psychological domain significantly changed in the sixth-month follow-up. The PM education coordinated by nurses improved the health of participants, maintaining six-month effects. Further studies should evaluate the practice barriers and effects of health education on preventive self-care behaviors regarding indoor PM among patients with COPD.


Assuntos
Poluentes Atmosféricos , Poluição do Ar em Ambientes Fechados , Poluição do Ar , Conhecimentos, Atitudes e Prática em Saúde , Material Particulado , Doença Pulmonar Obstrutiva Crônica , Autocuidado , Idoso , Idoso de 80 Anos ou mais , Poluentes Atmosféricos/toxicidade , Exposição Ambiental , Feminino , Humanos , Masculino , Material Particulado/toxicidade
15.
Toxicol Lett ; 331: 208-217, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32569800

RESUMO

Fine particulate matter 2.5 (PM2.5), one of the main components of air pollutants, seriously threatens human health. Possible neuronal dysfunction induced by PM2.5 has received extensive attention. However, there is little evidence for the specific biochemical mechanism of neuronal injury induced by PM2.5. Moreover, the pathway for PM2.5 transport from peripheral circulation to the central nervous system (CNS) is still unclear. In the current work, C57BL/6 mice were chronically exposed to ambient PM2.5 for 3, 6, 9, and 12 months. Exposure to ambient PM2.5 resulted in a significant reduction of cognitive ability in mice by Morris water maze test. PM2.5 exposure induced a neuroinflammatory reaction after cognitive impairment, while inflammation in the hypothalamus and olfactory bulb tissue occurred earlier. The expression levels of integrity tight junction proteins in the blood-brain barrier (BBB) were reduced by PM2.5 exposure. Pulmonary inflammation occurred much earlier and diminished at later stage of PM2.5 exposure. The results indicated that chronic exposure to ambient PM2.5 led to cognitive decline in mice; CNS dysfunction may be due to neuroinflammatory reactions; the reduced integrity of the BBB allowed the influence of pulmonary inflammation to neuronal alterations. The work may provide promising therapeutic or preventive targets for air pollution-induced neurodegenerative disease.


Assuntos
Poluentes Atmosféricos/toxicidade , Disfunção Cognitiva/induzido quimicamente , Exposição por Inalação/efeitos adversos , Doenças Neurodegenerativas/induzido quimicamente , Material Particulado/toxicidade , Pneumonia/induzido quimicamente , Animais , Barreira Hematoencefálica/efeitos dos fármacos , Barreira Hematoencefálica/imunologia , Disfunção Cognitiva/imunologia , Citocinas/metabolismo , Relação Dose-Resposta a Droga , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Camundongos Endogâmicos C57BL , Doenças Neurodegenerativas/imunologia , Tamanho da Partícula , Pneumonia/imunologia , Junções Íntimas/efeitos dos fármacos , Junções Íntimas/imunologia , Regulação para Cima
16.
Chemosphere ; 257: 127154, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32512328

RESUMO

Carcinogenic polycyclic aromatic hydrocarbons (cPAHs) in ambient PM2.5 and a specific molecular marker of biomass burning, levoglucosan, are used to investigate the influence on public health of biomass burning. In this work, we present an effective method for one-time analysis of cPAHs and levoglucosan by GC-MS without derivatization. The method was applied for the analysis of PM2.5 samples (64.3 ±â€¯17.6 µg m-3, n = 57) collected during a smoke haze period in Chiang Mai, Thailand. Levoglucosan was analyzed by using both the developed method (GC-MS) and a reference method (HPAEC-PAD) for comparison. Its average concentration obtained from GC-MS (0.31 ±â€¯0.21 µg m-3) was about 4 times less than the concentration obtained from the reference method (1.22 ±â€¯0.76 µg m-3). Therefore, a correcting factor (CF = 4) was used as a multiplying factor, to obtain a comparative value (1.23 ±â€¯0.86 µg m-3). The average concentration of cPAHs found in PM2.5 samples was 5.88 ±â€¯1.97 ng m-3 with the highest value of 10.86 ng m-3 indicating medium to high cancer risk due to PAHs exposure when referring to values of toxicity equivalence and inhalation cancer risk. Diagnostic ratios of BaA/(BaA + CHR) (0.48 ± 0.04) and IND/(IND + BPER) (0.58 ± 0.04) and strong correlations between PM2.5, levoglucosan and cPAHs concentrations implied that the major source of air pollution in the study period was biomass burning. PM2.5 concentration as a pollution indicator was labelled as BB-low, BB-medium, BB-high or BB-extreme; <50, 50-75, 75-100 and > 100 µg m-3, respectively. The levoglucosan and cPAHs concentration during BB-extreme pollution was 4.3 times and 2.34 times, respectively, that during BB-low pollution, and the correlation coefficient (r) between the concentrations of levoglucosan and cPAHs was as high as 0.987, indicating that the more intense the burning of biomass, the higher the carcinogenic risk in the urban air.


Assuntos
Poluentes Atmosféricos/toxicidade , Monitoramento Ambiental/métodos , Material Particulado/toxicidade , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Biomassa , Carcinógenos/análise , Poluição Ambiental/análise , Cromatografia Gasosa-Espectrometria de Massas , Glucose/análogos & derivados , Humanos , Material Particulado/análise , Hidrocarbonetos Policíclicos Aromáticos/análise , Estações do Ano , Fumaça/análise , Tailândia
18.
Proc Natl Acad Sci U S A ; 117(25): 13975-13982, 2020 06 23.
Artigo em Inglês | MEDLINE | ID: mdl-32513708

RESUMO

Arsenic is a toxic pollutant commonly found in the environment. Most of the previous studies on arsenic pollution have primarily focused on arsenic contamination in groundwater. In this study, we examine the impact on human health from atmospheric arsenic on the global scale. We first develop an improved global atmospheric arsenic emission inventory and connect it to a global model (Goddard Earth Observing System [GEOS]-Chem). Model evaluation using observational data from a variety of sources shows the model successfully reproduces the spatial distribution of atmospheric arsenic around the world. We found that for 2005, the highest airborne arsenic concentrations were found over Chile and eastern China, with mean values of 8.34 and 5.63 ng/m3, respectively. By 2015, the average atmospheric arsenic concentration in India (4.57 ng/m3) surpassed that in eastern China (4.38 ng/m3) due to the fast increase in coal burning in India. Our calculation shows that China has the largest population affected by cancer risk due to atmospheric arsenic inhalation in 2005, which is again surpassed by India in 2015. Based on potential exceedance of health-based limits, we find that the combined effect by including both atmospheric and groundwater arsenic may significantly enhance the risks, due to carcinogenic and noncarcinogenic effects. Therefore, this study clearly implies the necessity in accounting for both atmospheric and groundwater arsenic in future management.


Assuntos
Poluentes Atmosféricos/toxicidade , Intoxicação por Arsênico/epidemiologia , Arsênico/toxicidade , Saúde Global/estatística & dados numéricos , Modelos Estatísticos , Neoplasias/epidemiologia , Poluentes Atmosféricos/análise , Arsênico/análise , Atmosfera/química , Exposição Ambiental/estatística & dados numéricos , Monitoramento Ambiental , Água Subterrânea/química , Humanos , Análise Espaço-Temporal
19.
Ecotoxicol Environ Saf ; 201: 110726, 2020 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-32480160

RESUMO

BACKGROUND: Impaired in utero fetal growth trajectory may have long term health consequences of the newborns and increase risk of adulthood metabolic diseases. Prenatal exposure to air pollution has been linked to fetal development restriction; however, the impact of exposure to ambient air pollutants on the entire course of intrauterine fetal development has not been comprehensively investigated. METHODS: During 2015-2018, two cohorts of mother-infant dyads (N = 678 and 227) were recruited in Shanghai China, from which three categories of data were systematically collected: (1) daily exposure to six air pollutants during pregnancy, (2) fetal biometry in the 2nd (gestational week 24, [GW24]) and 3rd trimester (GW36), and (3) neonatal outcomes at birth. We investigated the impact of prenatal exposure to air pollutant mixture on the trajectory of fetal development during the course of gestation, adjusting for a broad set of potential confounds. RESULTS: Prenatal exposure to PM2.5, PM10, SO2 and O3 significantly reduced fetal biometry at GW24, where SO2 had the most potent effect. For every 10 µg/m3 increment increase of daily SO2 exposure during the 1st trimester shortened femur length by 2.20 mm (p = 6.7E-21) translating to 5.3% reduction from the average of the study cohort. Prenatal air pollution exposure also decreased fetal biometry at GW36 with attenuated effect size. Comparing to the lowest exposed quartile, fetus in the highest exposed quartile had 6.3% (p = 3.5E-5) and 2.1% (p = 2.4E-3) lower estimated intrauterine weight in GW24 and GW36, respectively; however, no difference in birth weight was observed, indicating a rapid catch-up growth in the 3rd trimester. CONCLUSIONS: To our knowledge, for the first time, we demonstrated the impact of prenatal exposure to ambient air pollutants on the course of intrauterine fetal development. The altered growth trajectory and rapid catch-up growth in associated with high prenatal exposure may lead to long-term predisposition for adulthood metabolic disorders.


Assuntos
Poluentes Atmosféricos/toxicidade , Desenvolvimento Fetal/efeitos dos fármacos , Exposição Materna/efeitos adversos , Material Particulado/toxicidade , Adulto , Poluentes Atmosféricos/química , China/epidemiologia , Estudos de Coortes , Feminino , Idade Gestacional , Humanos , Recém-Nascido , Material Particulado/química , Gravidez
20.
Ecotoxicol Environ Saf ; 201: 110827, 2020 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-32535366

RESUMO

Numerous experimental and epidemiological studies have demonstrated that exposure to PM2.5 may result in pathogenesis of several major cardiovascular diseases (CVDs), which can be attributed to the combined adverse effects induced by the complicated components of PM2.5. Organic materials, which are major components of PM2.5, contain thousands of chemicals, and most of them are environmental hazards. However, the contamination profile and contribution to overall toxicity of PM2.5-bound organic components (OCs) have not been thoroughly evaluated yet. Herein, we aim to provide an overview of the literature on PM2.5-bound hydrophobic OCs, with an emphasis on the chemical identity and reported impairments on the cardiovascular system, including the potential exposure routes and mechanisms. We first provide an update on the worldwide mass concentration and composition data of PM2.5, and then, review the contamination profile of PM2.5-bound hydrophobic OCs, including constitution, concentration, distribution, formation, source, and identification. In particular, the link between exposure to PM2.5-bound hydrophobic OCs and CVDs and its possible underlying mechanisms are discussed to evaluate the possible risks of PM2.5-bound hydrophobic OCs on the cardiovascular system and to provide suggestions for future studies.


Assuntos
Poluentes Atmosféricos/toxicidade , Doenças Cardiovasculares/induzido quimicamente , Sistema Cardiovascular/efeitos dos fármacos , Monitoramento Ambiental/métodos , Compostos Orgânicos/toxicidade , Material Particulado/toxicidade , Poluentes Atmosféricos/química , Humanos , Interações Hidrofóbicas e Hidrofílicas , Compostos Orgânicos/química , Material Particulado/química
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